Xian Jiang - West China Hospital

Xian Jiang
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Name
Xian Jiang
Affiliation
West China Hospital
Country
China

Publications Authored By Xian Jiang

2016Dec
Exp. Mol. Pathol.
Exp Mol Pathol 2016 Dec 7;102(1):15-21. Epub 2016 Dec 7.
Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; Department of Pathology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China; Department of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), Shihezi University School of Medicine, Shihezi, 832003, China. Electronic address:

Tumor associated macrophages (TAMs) play an important role in the growth, progression, and metastasis of tumors. The distribution of TAMs in Kazakh esophageal squamous cell carcinoma (ESCC) is not determined. We aimed to investigate the role of TAMs in the occurrence and progression of Kazakh ESCC.Read More

CD163 was used as the TAM marker, and immunohistochemistry (IHC) counts were used to quantify the density of TAMs in tumor nest and surrounding stroma. IHC staining was used to evaluate the expression of vascular endothelial growth factor C (VEGF-C) in Kazakh ESCC and cancer adjacent normal (CAN) tissues. The density of TAMs in Kazakh ESCCs tumor nest and stromal was significantly higher than that in CAN tissues. The increased number of CD163-positive TAMs in tumor nest and tumor stromal was positively associated with Kazakh ESCC lymph node metastasis and clinical stage progression. Meanwhile, the expression of VEGF-C in Kazakh ESCCs was significantly higher than that in CAN tissues. Overexpression of VEGF-C in Kazakh ESCCs was significantly associated with gender, depth of tumor invasion, lymph node metastasis and tumor clinical stage. The increased number of TAMs, either in the tumor nests or tumor stroma was positively correlated with the overexpression of VEGF-C, which may promote lymphangiogenesis and play an important role in the invasion and metastasis of Kazakh ESCC.

2016Nov
Oncotarget
Oncotarget 2016 Nov;7(45):73257-73269
The Hepatosplenic Surgery Center, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.

Sorafenib resistance remains a major obstacle for the effective treatment of hepatocellular carcinoma (HCC), and a number of miRNAs contribute to this resistance. However, the regulatory networks of miRNAs are very complex, thus inhibiting a single miRNA may sequentially activate other compensatory pathways. In the present study, we generated an artificial long non-coding RNA (AlncRNA), which simultaneously targets multiple miRNAs including miR-21, miR-153, miR-216a, miR-217, miR-494 and miR-10a-5p.Read More

These miRNAs have been shown to be upregulated in sorafenib-resistant cells and participate in the mechanisms underlying sorafenib resistance. The AlncRNA contains tandem sequences of 6 copies of the complementary binding sequences to the target miRNAs and is expressed by an adenoviral vector (Ad5-AlncRNA). Infection of Ad5-AlncRNA into sorafenib-resistant HCC cells blocked the function of miRNAs, and sequentially inhibited the downregulation of PTEN and activation of AKT. Ad5-AlncRNA significantly inhibited proliferation and induced apoptosis of sorafenib-resistant cells and enhanced the effects of sorafenib in vitro and in animal models. Inhibition of autophagy decreased the sensitivity of sorafenib-resistant cells to Ad5-AlncRNA, while its induction had the opposite effect. These results indicate that targeting multiple miRNAs by the artificial lncRNA could be a potential promising strategy for overcoming sorafenib resistance in the treatment of HCC.

2016Nov
ACS Appl Mater Interfaces
ACS Appl Mater Interfaces 2016 Nov 4;8(45):31076-31082. Epub 2016 Nov 4.
Jiangsu Key Laboratory of New Power Batteries, Jiangsu Collaborative Innovation Center of Biomedical Functional Materials, School of Chemistry and Materials Science, Nanjing Normal University , Nanjing 210023, P. R. China.

For direct formic acid fuel cells (DFAFCs), the dehydrogenation pathway is a desired reaction pathway, to boost the overall cell efficiency. Elaborate composition tuning and nanostructure engineering provide two promising strategies to design efficient electrocatalysts for DFAFCs. Herein, we present a facile synthesis of porous AgPt bimetallic nanooctahedra with enriched Pt surface (denoted as AgPt@Pt nanooctahedra) by a selective etching strategy.Read More

The smart integration of geometric and electronic effect confers a substantial enhancement of desired dehydrogenation pathway as well as electro-oxidation activity for the formic acid oxidation reaction (FAOR). We anticipate that the obtained nanocatalyst may hold great promises in fuel cell devices, and furthermore, the facile synthetic strategy demonstrated here can be extendable for the fabrication of other multicomponent nanoalloys with desirable morphologies and enhanced electrocatalytic performances.

2016Nov
Chin. Med. Sci. J.
Chin Med Sci J 2016 Nov;31(4):239-246
Department of Gynaecology and Obstetrics, Hangzhou Red Cross Hospital, Hangzhou 310000, China.

Objective This study was designed to evaluate the efficacy and safety of aspirin-heparin treatment for un-explained recurrent spontaneous abortion (URSA). Methods Literatures reporting the studies on the aspirin-heparin treatment of un-explained recurrent miscarriage with randomized controlled trials (RCTs) were collected from the major publication databases. The live birth rate was used as primary indicator, preterm delivery, preeclampsia, intrauterine growth restriction, and adverse reactions (thrombocytopenia ) were used as the secondary indicators.Read More

The quality of the included studies was evaluated using RCT bias risk assessment tool in the Cochrane Handbook (v5.1.0). Meta-analysis was conducted using RevMan (v5.3) software. Subgroup analyses were conducted with an appropriately combined model according to the type of the treatments if heterogeneity among the selected studies was detected. Results Six publications of RCTs were included in this study. There were a total of 907 pregnant women with diagnosis of URSA, 367 of them were pooled in the study group with aspirin-heparin therapy and 540 women in the control group with placebo, aspirin or progesterone therapy. Meta-analysis showed that the live birth rate in the study group was significantly different from that in the control group [RR = 1.18, 95% CI (1.00-1.39), P=0.04]. Considering the clinical heterogeneity among the six studies, subgroup analysis were performed. Live birth rates in the aspirin-heparin treated groups and placebo groups were compared and no significant difference was found. There were no significant differences found between the two groups in the incidence of preterm delivery [RR=1.22, 95% CI (0.54-2.76), P=0.64], preeclampsia [RR=0.52, 95% CI (0.25-1.07), P=0.08], intrauterine growth restriction [RR=1.19, 95% CI (0.56-2.52), P=0.45] and thrombocytopenia [RR=1.17, 95% CI (0.09-14.42), P=0.90]. Conclusion This meta-analysis did not provide evidence that aspirin-heparin therapy had beneficial effect on un-explained recurrent miscarriage in terms of live birth rate, but it was relatively safe for it did not increase incidence of adverse pregnancy and adverse events. More well-designed and stratified double-blind RCT, individual-based meta-analysis regarding aspirin-heparin therapy are needed in future.

2016Aug
Int J Surg
Int J Surg 2016 Aug 21;32:150-7. Epub 2016 Apr 21.
Department of General Surgery, The First Clinical Hospital, Harbin Medical University, Harbin 150001, China. Electronic address:

Laparoscopic Roux-en-Y gastric bypass (LRYGB) is one of the most performed bariatric procedures in treating morbid obesity. There is no consensus on which technique used for gastrojejunal anastomosis is optimal. The meta-analysis aimed to solve the issue by comparing hand-sewn with mechanical gastrojejunostomy during LRYGB for morbid obesity.Read More


PubMed, Embase, Cochrane Library, Scopus, Google Scholar and Research Gate were searched (from inception to April 2016). Primary outcome was operation time. Secondary outcomes were postoperative complications (anastomotic leak, stricture, bleeding, marginal ulcer and wound infection), percent excess weight loss during one-year follow-up, reoperation, and postoperative hospital stay. Odds ratios (OR) were calculated for dichotomous outcomes and mean differences (MD) for continuous outcomes.
Twelve trials were included comprising 13,626 patients (3309 hand-sewn vs. 6791 circular vs. 3526 linear). There was no difference in operation time when hand-sewn anastomosis was compared with mechanical gastrojejunostomy (MD, -6.00; 95% confidence interval (CI), -34.85 to 22.85; P = 0.68), circular stapled anastomosis (MD, -5.24; 95% CI, -32.71 to 22.24; P = 0.71) or linear stapled anastomosis (MD, - 3.75; 95% CI, -64.81 to 57.31; P = 0.90). Hand-sewn anastomosis had significantly lower incidence rate of postoperative bleeding (OR, 0.48; 95% CI, 0.31-0.74; P = 0.001) and wound infection (OR, 0.19; 95% CI, 0.08-0.45; P = 0.0002) than circular stapled anastomosis; there were no significant differences in the other secondary outcome. And there were no significant differences in all the comparable outcomes between hand-sewn anastomosis and linear stapled anastomosis.
This meta-analysis revealed no significant differences between mechanical and hand-sewn anastomosis except for greater incidence rates of postoperative bleeding and wound infection with the use of circular staplers. Besides, more trials with adequate power are required and a cost analysis also worth trying. REGISTRATION NO.
CRD42015020025.

2016Jul
Int. J. Dermatol.
Int J Dermatol 2016 Jul 17;55(7):e404-e406. Epub 2016 Feb 17.
Department of Dermatology, West China Hospital, Sichuan University, Sichuan, Chengdu, China.
2016Jul
Mol. Cell
Mol Cell 2016 Jul;63(2):229-39
National Institute of Biological Sciences, 7 Science Park Road, Zhongguancun Life Science Park, Beijing 102206, China. Electronic address:

In response to apoptotic stimuli, mitochondria in mammalian cells release cytochrome c and other apoptogenic proteins, leading to the subsequent activation of caspases and apoptotic cell death. This process is promoted by the pro-apoptotic members of the Bcl-2 family of proteins, such as Bim and Bax, which, respectively, initiate and execute cytochrome c release from the mitochondria. Here we report the discovery of a small molecule that efficiently blocks Bim-induced apoptosis after Bax is activated on the mitochondria.Read More

The cellular target of this small molecule was identified to be the succinate dehydrogenase subunit B (SDHB) protein of complex II of the mitochondrial electron transfer chain (ETC). The molecule protects the integrity of the ETC and allows treated cells to continue to proliferate after apoptosis induction. Moreover, this molecule blocked dopaminergic neuron death and reversed Parkinson-like behavior in a rat model of Parkinson's disease.

2016May
J. Cancer Res. Clin. Oncol.
J Cancer Res Clin Oncol 2016 May 29;142(5):969-80. Epub 2016 Jan 29.
Key Laboratory of Hepatosplenic Surgery, Department of General Surgery, First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.

Hepatocyte nuclear factor 6 (HNF6) is a liver-enriched transcription factor and highly expressed in mature bile duct epithelial cells. This study sought to investigate the role of HNF6, particularly the molecular mechanisms for how HNF6 is involved in the growth and metastasis of cholangiocarcinoma (CCA) cells.
The expression of HNF6, miR-122 and key molecules was examined by Western blot analysis and real-time RT-PCR.Read More

Stable transfectants, HCCC-HNF(low) and RBE-HNF(high), were generated from human CCA HCCC-9810 and RBE cells, respectively. The regulatory effect of HNF6 on miR-122 was evaluated by luciferase reporter assay. Cell proliferation, cycle distribution, migration and invasion were analyzed. The xenograft model was used to assess the effects of HNF6 overexpression on tumorigenesis, growth, metastasis and therapeutic potentials.
Human CCA tissues and cells expressed lower levels of HNF6, which positively correlated with miR-122. HNF6 regulated the expression of miR-122 by stimulating its promoter. HNF6 overexpression inhibited cell proliferation by inducing cell cycle arrest at G1 phase through regulating miR-122, cyclin G1 and insulin-like growth factor-1 receptor. HNF6 inhibited the migration and invasion of CCA cells by regulating matrix metalloproteinase-2 and metalloproteinase-9, reversion-inducing-cysteine-rich protein with kazal motifs, E-cadherin and N-cadherin. Co-transfection of anti-miR-122 abrogated the effects of HNF6. HNF6 overexpression inhibited the ability of cells to form tumors and to metastasize to the lungs of mice, and the growth of established tumors.
The results indicate that HNF6 may serve as a tumor suppressor by regulating miR-122, and its overexpression may represent a mechanism-based therapy for CCA.

2016Mar
J Cosmet Laser Ther
J Cosmet Laser Ther 2016 6;18(1):12-5. Epub 2015 Jul 6.
a Department of Dermatology , West China Hospital of Sichuan University , Chengdu, Sichuan Province , P. R. China.

Different types of Q-switched (QS) lasers have been used successfully to treat nevus of Ota. The purpose of this study was to compare the clinical efficacy and complication of QS alexandrite (QS Alex) laser versus QS neodymium:yttrium aluminum garnet (Nd:YAG) (QS Nd:YAG) laser for bilateral nevus of Ota. Seventeen patients with bilateral nevus of Ota were treated randomly with QS Alex in one half of face and QS Nd:YAG in the other half with an interval of at least 3 months between each.Read More

Subjective assessment was made by both patients and dermatologists. Patients were also examined for evidence of complications. All patients experienced improvement (p < 0.05). There was no statistically significant difference between the two sides (p > 0.05). The pain after a short period of laser therapy was more severe for QS Alex than for QS Nd:YAG laser. Vesicles developed in 1 patient after QS Alex therapy. Both QS Alex laser and QS Nd:YAG laser were equally effective at improving bilateral nevus of Ota. Patients tolerate QS Nd:YAG laser better than QS Alex laser.

2016Mar
Oncol. Rep.
Oncol Rep 2016 Mar 9;35(3):1602-10. Epub 2015 Dec 9.
Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, P.R. China.

The rapid growth, morbidity and mortality of prostate cancer, and the lack of effective treatment have attracted great interests of researchers to find novel cancer therapies aiming to inhibit angiogenesis and tumor growth. Quercetin is a flavonoid compound that widely exists in the nature. Our previous study preliminarily demonstrated that quercetin effectively inhibited human prostate cancer cell xenograft tumor growth by inhibiting angiogenesis.Read More

Thrombospondin-1 (TSP-1) is the first reported endogenous anti-angiogenic factor that can inhibit angiogenesis and tumorigenesis. However, the relationship between quercetin inhibiting angiogenesis and TSP-1 upregulation in prostate cancer has not been determined. Thus, we explored the important role of TSP-1 upregulation in reducing angiogenesis and anti-prostate cancer effect of quercetin both in vitro and in vivo for the first time. After the selected doses were used for a certain time, quercetin i) significantly inhibited PC-3 and human umbilical vein endothelial cells (HUVECs) proliferation, migration and invasion in a dose-dependent manner; ⅱ) effectively inhibited prostate cancer PC-3 cell xenograft tumor growth by 37.5% with 75 mg/kg as compared to vehicle control group, more effective than 25 (22.85%) and 50 mg/kg (29.6%); ⅲ) was well tolerated by BALB/c mice and no obvious toxic reactions were observed; ⅳ) greatly reduced angiogenesis and led to higher TSP-1 protein and mRNA expression both in vitro and in vivo in a dose-dependent manner. Therefore, quercetin could increase TSP-1 expression to inhibit angiogenesis resulting in antagonizing prostate cancer PC-3 cell and xenograft tumor growth. The present study can lay a good basis for the subsequent concrete mechanism study and raise the possibility of applying quercetin to clinical for human prostate cancer in the near future.

2016Feb
J. Mol. Med.
J Mol Med (Berl) 2016 Feb 18;94(2):195-206. Epub 2015 Sep 18.
State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, West China Medical School, Sichuan University, 3-17 Renmin South Road, Chengdu, Sichuan, 610041, People's Republic of China.

Isoliquiritigenin (ISL) is an important flavonoid component of licorice and has been reported to possess anti-inflammatory and antioxidant properties, but its exact mechanism of action remains poorly understood. Previously, we demonstrated that ISL could suppress IL-6 expression in multiple myeloma. Here, we further characterized the anti-inflammatory effects of ISL in several psoriasis models, including the keratin 14/vascular endothelial growth factor (VEGF) transgenic mouse, the imiquimod (IMQ)-induced psoriasis-like mouse, and the human keratinocytes HaCaT and NHEK in vitro.Read More

We found that ISL ameliorated the inflammatory process in psoriasis models but not in their respective controls. Moreover, the anti-inflammatory effects of ISL were attributed to the suppression of nuclear factor-κB (NF-κB) activity, which consequently resulted in the reduction of pro-inflammation cytokines IL-6 and IL-8 expression. In conclusion, ISL exhibited anti-inflammatory effects in psoriasis models, by downregulating IL-6 and IL-8 via suppression of NF-κB activity, suggesting that ISL might serve as a potential candidate for treatment of psoriasis and other autoimmune inflammatory diseases.
ISL could ameliorate the inflammatory process of psoriasis. ISL could suppress NF-κB and subsequent production of a series of pro-inflammatory cytokines. Dual-inhibitory activity against IL-6 and IL-8 of ISL is implemented via inhibiting NF-κB. ISL exerts no inhibitory effects on normal human keratinocytes or wild-type Balb/c mice, implying its low toxicity and safety.

2016Jan
Tumour Biol.
Tumour Biol 2016 Jan 29;37(1):381-91. Epub 2015 Jul 29.
Key Laboratory of Hepatosplenic Surgery, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.

Cabozantinib is a multi-targeted tyrosine kinase inhibitor targeting vascular endothelial growth factor (VEGF) receptor (VEGFR)-2, MET (c-Met, also called hepatocyte growth factor (HGF) receptor), and other receptor tyrosine kinases. Cabozantinib has recently been approved for treating advanced medullary thyroid carcinoma (MTC), but its long-term benefit remains uncertain and dose-dependent adverse events are very common. The present study has demonstrated that 2-methoxyestradiol (2ME2), an inhibitor of hypoxia-inducible factors (HIFs) and a promising anticancer agent under investigation in clinical trials, strengthens anticancer activities of cabozantinib against MTC cells in vitro and in vivo.Read More

The activated hypoxia-inducible pathways, which are mainly regulated by HIF-1, contribute to the resistance of hypoxic MTC cells to cabozantinib. Cabozantinib upregulated HIF-1α expression at translational levels and increased the expression of the downstream factors including VEGF, lactate dehydrogenase A (LDHA), HGF, and MET. 2ME2 corrected the activated pathways by cabozantinib through downregulating HIF-1α expression and inhibiting its nuclear translocation in hypoxic MTC cells. Administration of 2ME2 enhanced the efficacy of cabozantinib in suppressing the growth of MTC cell line xenografts and patient-derived xenografts established in mice. Given that 2ME2 targets insensitive hypoxic cancer cells to cabozantinib and can inhibit the activated pathways by cabozantinib, the present results warrant further investigation of 2ME2, particularly in combination with cabozantinib, for the treatment of MTC.

2016Jan
J. Exp. Clin. Cancer Res.
J Exp Clin Cancer Res 2016 Jan 22;35:16. Epub 2016 Jan 22.
Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin, 150001, China.

Neuropilin-1 (NRP-1) is a transmembrane glycoprotein participating in the growth and metastasis of cancer cells as multifunctional co-receptors by interacting with the signaling pathways. However, its role in gastric cancer has not yet been clarified. This study aims to investigate whether NRP-1 expression is associated with the clinicopathology of gastric cancer, and involved in the growth and metastasis of gastric cancer cells.Read More


NRP-1 expression in clinical gastric cancer specimens was examined by immunohistochemistry and its association with clinicopathology analyzed. The expression of NRP-1 in a panel of human gastric cancer cells was examined by real-time RT-PCR and immunoblotting. Stable transfectants depleted of NRP-1, termed MGC-803-NRP(low), were generated from MGC-803 cells. Cell proliferation was analyzed by the Cell Counting Kit-8 and Bromodeoxyuridine incorporation assays, and migrating ability analyzed by migration assays. The xenograft model was used to assess the effects of NRP-1 depletion on tumorigenesis, growth, metastasis and therapeutic potentials. The role of NRP-1 as co-receptors in the signaling pathways stimulated by ligands was examined. The key molecules involved in cell proliferation, migration and related signaling pathways were detected by immunoblotting.
Gastric cancer tissues expressed higher levels of NRP-1 compared to normal gastric mucosa. Its expression correlated with clinical staging, tumor differentiation and pathological types. NRP-1 depletion inhibited cell proliferation by inducing cell cycle arrest in the G1/S phase by upregulating p27, and downregulating cyclin E and cyclin-dependent kinase 2. NRP-1 depletion reduced the ability of cells to migrate by inhibiting the phosphorylation of focal adhesion kinase. NRP-1 depletion suppressed tumorigenesis, tumor growth and lung metastasis by inhibiting cell proliferation and tumor angiogenesis in situ. Therapeutic NRP-1 shRNA inhibited the growth of established BGC823 tumors. Depletion of NRP-1 inhibited the activation of VEGF/VEGFR2, EGF/EGFR and HGF/c-Met pathways stimulated by respective recombinant human VEGF-165, EGF and HGF proteins.
The present results indicate that NRP-1 may be a potentially valuable biomarker and therapeutic target for gastric cancer.

2015Dec
Int J Clin Exp Med
Int J Clin Exp Med 2015 15;8(9):15828-33. Epub 2015 Sep 15.
Department of Anesthesiology, The Affiliated Hospital of Luzhou Medical College Luzhou 646000, Sichuan, China.

This study is to investigate the potential role of asiaticoside (AS) in Aβ1-42-induced apoptosis on the human umbilical vein endothelial cell (HUVEC). HUVEC cells were divided into Aβ1-42 group (treated with 50 μM Aβ1-42), AS groups (treated with 50 μM Aβ1-42 and 10 mM, 1 mM, 0.1 mM or 0.Read More

01 mM AS), and negative control group (without treatments). Cell proliferation was detected by CCK-8 assay. Apoptosis was analyzed by Hochest33342 staining and flow cytometry. Western Blot was carried out to detect the expression of Bcl-2 and Bax protein. Aβ1-42 treatment inhibited cell proliferation and increased cell apoptosis of HUVEC cells. Interestingly, AS at concentrations of 10 mM, 1 mM, 0.1 mM and 0.01 mM reversed the effects of Aβ1-42 by increasing cell survival rate and reducing apoptosis of HUVEC cells. Furthermore, the expression of Bcl-2 protein was increased whereas the expression of Bax protein was decreased in AS groups. Compared with Aβ1-42 group, the ratio of Bcl-2/Bax was significantly increased in AS groups (P < 0.05). These results suggested that AS may be effective in protecting cells from damage caused by aggregated Aβ1-42. And this effect may be attributed to the increase of Bcl-2 and decrease of Bax under AS treatment.

2015Oct
Oncotarget
Oncotarget 2015 Oct;6(30):28867-81
The Hepatosplenic Surgery Center, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.

Sorafenib resistance remains a major obstacle for the effective treatments of hepatocellular carcinoma (HCC). Recent studies indicate that activated Akt contributes to the acquired resistance to sorafenib, and miR-21 dysregulates phosphatase and tensin homolog (PTEN), which inhibits Akt activation. Sorafenib-resistant HCC cells were shown to be refractory to sorafenib-induced growth inhibition and apoptosis.Read More

Akt and its downstream factors were highly activated and/or upregulated in sorafenib-resistant cells. Inhibition of autophagy decreased the sensitivity of sorafenib-resistant cells to sorafenib, while its induction had the opposite effect. Differential screening of miRNAs showed higher levels of miR-21 in sorafenib-resistant HCC cells. Exposure of HCC cells to sorafenib led to an increase in miR-21 expression, a decrease in PTEN expression and sequential Akt activation. Transfection of miR-21 mimics in HCC cells restored sorafenib resistance by inhibiting autophagy. Anti-miR-21 oligonucleotides re-sensitized sorafenib-resistant cells by promoting autophagy. Inhibition of miR-21 enhances the efficacy of sorafenib in treating sorafenib-resistant HCC tumors in vivo. We conclude that miR-21 participates in the acquired resistance of sorafenib by suppresing autophagy through the Akt/PTEN pathway. MiR-21 could serve as a therapeutic target for overcoming sorafenib resistance in the treatment of HCC.

2015Aug
Oncol. Rep.
Oncol Rep 2015 Aug 28;34(2):663-72. Epub 2015 May 28.
Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.

Overexpression of histone deacetylases (HDACs) is associated with higher metastatic rates and a poor prognosis in gastric cancer. However, the underlying mechanisms involved remain unclear. The present study aimed to investigate the molecular pathways that are involved in HDAC1-mediated metastatic activities in gastric cancer cells.Read More

First we used a microRNA (miRNA or miR) microarray to screen potential miRNAs whose expression can be altered by HDAC1 depletion. Of these miRNAs, miR-34a is important as it is often inactivated in cancer cells and acts as a tumor suppressor for various types of cancer. The reverse transcription-quantitative polymerase chain reaction (RT‑qPCR) results confirmed that miR-34a was upregulated by HDAC1 knockdown. Cells depleted of HDAC1 had lower abilities to migrate, invade and adhere, which were restored by a miR-34a antagomiR. Depletion of HDAC1 also resulted in impaired microfilaments and microtubules, while co-transfection of the miR-34a antagomiR attenuated these changes in the cellular cytoskeleton. The HDAC1/miR-34a axis regulated the expression and activation of CD44 and its downstream factors including Bcl-2, Ras homolog family member A (RhoA), LIM domain kinase 1 (LIMK-1) and matrix metalloproteinase (MMP)-2. The latter three proteins were responsible for the organization of tubulin and actin cytoskeleton and the formation of cellular pseudopodia. In conclusion, results of the present study indicated that HDAC1 depletion inhibits the metastatic abilities of gastric cancer cells by regulating the miRNA-34a/CD44 pathway, which may be a potential target for the treatment of gastric cancer.

2015Aug
Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 2015 Aug;29(15):1392-3

The patient complained of finding on the right side of the neck fistula with discharge nine years. In recently, fistula spills significantly increased compared with the previous. Special physical examination: Right sternocleidomastoid middle 1/3 front border is seen here in a small fistula, translucence jelly secretion were spilling out when squeezeing the fistula, no smell.Read More

Ultrasound: On the right side of the upper cervical skin to submandibular gland rear could see tubular low echo area. MRI: Visible on the right side of the neck tube signal, after the submandibular gland rear. Three-dimensional CT: Visible on the right side of the neck by skin sinus crossings as deep as the tonsillar fossa lumen containing contrast agent. Clinical diagnosis: The second branchial cleft cyst and fistula.

2015Jul
Int J Clin Exp Pathol
Int J Clin Exp Pathol 2015 1;8(5):5542-8. Epub 2015 May 1.
Departemnt of Medical Research, Guangzhou General Hospital of Guangzhou Military Command 111 Liuhua Road, Guangzhou 510010, China.

microRNA-26b (miR-26b) is reported to be downregulated in many human malignancies and function as a tumor suppressor. However, the roles of miR-26b expression in cervical cancer progression are unclear. The aim of this study was to investigate the clinicopathological or prognostic significance of miR-26b in human cervical cancer.Read More


A cohort of 88 paired of cervical cancer and the adjacent normal cervical epithelial tissues were collected. Quantitative RT-PCR (qRT-PCR) assay was used to detect the expression of miR-26b and its correlations with clinicopathological factors were statistically analyzed. Finally, the survival was assessed by the Kaplan-Meier method and proportional hazards model.
The expression level of miR-26b in cervical cancer tissues was significantly lower than that in the adjacent normal cervical tissues (P<0.001). Reduced miR-26b was observed to be significantly correlated with advanced FIGO stage, higher incidence of lymph node metastasis and recurrence of cervical cancer patients (P=0.002, 0.036 and 0.029, respectively). In addition, patients with low-miR-26b expression showed poorer recurrence-free survival (RFS) and overall survival (OS) than those with high-miR-26b expression (P=0.0043 and 0.0015, respectively). Furthermore, multivariate analyses demonstrated that low miR-26b expression was an independent prognostic factor for predicting the 5-year RFS and OS of cervical cancer patients (P=0.013 and 0.007, respectively).
Our results showed that reduced miR-26b was correlated with tumor development and poor prognosis in human cervical cancer. The status of miR-26b expression may be a potential prognostic biomarker for cervical cancer patients.

Treatment of metastatic colon carcinoma with the anti-epidermal growth factor receptor antibody cetuximab/panitumumab is reported to be ineffective in KRAS-mutant tumors; therefore, it is necessary to perform KRAS mutation analysis before cetuximab or panitumumab treatment is initiated.
This study was designed to compare and evaluate the efficacy of three different methodologies--high resolution melting (HRM), Sanger sequencing, and Amplification Refractory Mutation System (ARMS)--for KRAS mutation detection in a clinical setting.
In total, 55 samples from patients with metastatic colorectal cancer were analyzed.Read More

Compared to Sanger sequencing, good consistency was found between the results of the ARMS (Kappa = 0.839) and HRM (Kappa = 0.839). The sensitivities of the methods were compared after a consensus was reached: if two of the three methodologies showed a similar result, it was considered as the consensus result. The frequency of KRAS mutations in our population was 34.5%, and discordant findings were observed in five samples. No significant difference in sensitivity was found among the three methodologies.
From the results, we can conclude that after careful in-laboratory validation, HRM is a good alternative to the ARMS and Sanger sequencing for KRAS mutation testing.

2015Apr
Tumour Biol.
Tumour Biol 2015 Apr 22;36(4):2323-34. Epub 2014 Nov 22.
Department of General Surgery, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.

Sorafenib is the standard first-line systemic drug for advanced hepatocellular carcinoma (HCC), but it also induces the activation of Akt, which contributes to the mechanisms for the resistance to sorafenib. Arsenic trioxide (ATO) is a currently clinically used anticancer drug and displays its anticancer activities by inhibiting Akt activation. Therefore, we hypothesized that ATO may potentiate the anti-cancer activities of sorafenib against HCC.Read More

The results have demonstrated that ATO synergized with sorafenib to inhibit the proliferation and promote the apoptosis of HCC cells by diminishing the increased activation of Akt by sorafenib. ATO was shown to inhibit the expression or activation of Akt downstream factors, including glycogen synthase kinase (GSK)-3β, mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (S6K), and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1), which regulate cell apoptosis and were upregulated or activated by sorafenib. Both sorafenib and ATO downregulated the expression of cyclin D1, resulting in HCC cells arrested at G0/G1 phase. ATO downregulated the expression of Bcl-2 and Bcl-xL and upregulated the expression of Bax, indicating that ATO could induce the apoptosis of HCC cells through the intrinsic pathways; but sorafenib showed little effects on these proteins of Bcl-2 family. ATO synergized with sorafenib to suppress the growth of HCC tumors established in mice by inhibiting the proliferation and inducing the apoptosis of HCC cells in situ. These results indicate that ATO may be a potential agent that given in combination with sorafenib acts synergistically for treating HCC.

2015Mar
Korean J. Physiol. Pharmacol.
Korean J Physiol Pharmacol 2015 Mar 25;19(2):159-65. Epub 2015 Feb 25.
Department of Physiology and Pathophysiology, Yanbian University College of Medicine, Yanji 133002, China.

Input signals originating from baroreceptors and vestibular receptors are integrated in the rostral ventrolateral medulla (RVLM) to maintain blood pressure during postural movement. The contribution of baroreceptors and vestibular receptors in the maintenance of blood pressure following hypotension were quantitatively analyzed by measuring phosphorylated extracellular regulated protein kinase (pERK) expression and glutamate release in the RVLM. The expression of pERK and glutamate release in the RVLM were measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or sinoaortic denervation (SAD) following hypotension induced by a sodium nitroprusside (SNP) infusion.Read More

The expression of pERK was significantly increased in the RVLM in the control group following SNP infusion, and expression peaked 10 min after SNP infusion. The number of pERK positive neurons increased following SNP infusion in BL, SAD, and BL+SAD groups, although the increase was smaller than seen in the control group. The SAD group showed a relatively higher reduction in pERK expression when compared with the BL group. The level of glutamate release was significantly increased in the RVLM in control, BL, SAD groups following SNP infusion, and this peaked 10 min after SNP infusion. The SAD group showed a relatively higher reduction in glutamate release when compared with the BL group. These results suggest that the baroreceptors are more powerful in pERK expression and glutamate release in the RVLM following hypotension than the vestibular receptors, but the vestibular receptors still have an important role in the RVLM.

2014Dec
Cancer Lett.
Cancer Lett 2014 Dec 11;355(1):96-105. Epub 2014 Sep 11.
The Hepatosplenic Surgery Center, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. Electronic address:

Sorafenib is the approved systemic drug of choice for advanced hepatocellular carcinoma (HCC), but has demonstrated limited benefits because of drug resistance. 2-Methoxyestradiol (2ME2) has been shown to be a promising anticancer drug against various types of cancers and acts by dysregulating hypoxia-inducible factor (HIF)-1. Hypoxic cancer cells are extremely resistant to therapies since they elicit strong survival ability due to the cellular adaptive response to hypoxia, which is controlled by HIF-1 and HIF-2.Read More

The present study has demonstrated that sorafenib downregulated the expression of HIF-1α, making the hypoxic response switch from HIF-1α- to HIF-2α-dependent pathways, resulting in upregulation of HIF-2α, which contributes to the insensitivity of hypoxic HCC cells to sorafenib. HIF-2α played a dominant role in regulating VEGF, thus sorafenib in turn increased the expression of VEGF (a downstream molecule of both HIF-1 and HIF-2) and cyclin D1 (a downstream molecule of HIF-2), but reduced the expression of LDHA (a downstream molecule of HIF-1), in hypoxic HCC cells. 2ME2 significantly reduced the expression of both HIF-1α and HIF-2α, and their downstream molecules, VEGF, LDHA and cyclin D1, rendering hypoxic HCC cells to increased sensitivity to 2ME2. 2ME2 also inhibited the nuclear translocation of HIF-1α and HIF-2α proteins, but had no effect on their mRNA expression. 2M2 synergized with sorafenib to suppress the proliferation and induction of apoptosis of HCC cells in vitro and in vivo, and inhibited tumoral angiogenesis. These results indicate that 2ME2 given in combination with sorafenib acts synergistically for treating HCC.

2014Dec
ACS Appl Mater Interfaces
ACS Appl Mater Interfaces 2014 Dec 11;6(24):22790-5. Epub 2014 Dec 11.
Jiangsu Key Laboratory of New Power Batteries, Collaborative Innovation Center of Biomedical Functional Materials, School of Chemistry and Materials Science, Nanjing Normal University , Nanjing 210023, People's Republic of China.

Noble metallic nanocrystals (NMNCs) with highly branched morphologies are an exciting new class of nanomaterials because of their great potential application in catalysis, sensing, optics, and electronics originating from their unique structures. Herein, we report a facile water-based method to synthesize high-quality palladium (Pd) tetrapods with the assistance of arginine molecule, which is more economical and environmentally friendly than the previous reported carbon monoxide (CO)-assisted synthesis in the organic system. During the synthesis, arginine molecule plays an essential role in controlling the tetrapod-like morphology.Read More

The as-synthesized Pd tetrapods have a potential application in the formic acid (HCOOH)-induced reduction of highly toxic hexavalent chromium (Cr(VI)) owing to their improved catalytic performance for the HCOOH decomposition.

2014Oct
Proc. Natl. Acad. Sci. U.S.A.
Proc Natl Acad Sci U S A 2014 Oct 1;111(41):14782-7. Epub 2014 Oct 1.
National Institute of Biological Sciences, Beijing 102206, China; Graduate School of Peking Union Medical College, Beijing 100730, China; and Chinese Academy of Medical Sciences, Beijing 100730, China

Intrinsic apoptotic stimuli initiate mammalian cells' apoptotic program by first activating the proteins that have only Bcl-2 homology domain 3 (BH3), such as Bcl-2 interacting mediator of cell death (Bim) and truncated BH3 interacting death domain agonist (tBid), which in turn trigger conformational changes in BCL2-associated X (Bax) and BCL2-antagonist/killer (Bak) proteins that enable oligomer formation on the mitochondria, causing cytochrome c and other apoptogenic proteins in the intermembrane space to leak out. Leaked cytochrome c then initiates apoptotic caspase activation through a well-defined biochemical pathway. However, how oligomerized Bax and Bak cause cytochrome c release from mitochondria remains unknown.Read More

We report here the establishment of cell lines in which Bim or tBid can be inducibly expressed to initiate apoptosis in a controlled, quantitative manner. We used these cell lines to examine apoptotic events after Bax and Bak oligomerization but before cytochrome c release. The mitochondrial metalloprotease OMA1 was activated in this system in a Bax- and Bak-dependent fashion. Activated OMA1 cleaved the dynamin-like GTPase, optical nerve atrophy 1, an event that is critical for remodeling of mitochondrial cristae. Knockdown or knockout of OMA1 in these cells attenuated cytochrome c release. Thus it is clear that oligomerized Bax and Bak trigger apoptosis by causing both the permeabilization of the mitochondrial outer membrane and activation OMA1.

2014Aug
Mycopathologia
Mycopathologia 2014 Aug 20;178(1-2):129-33. Epub 2014 Jun 20.
Department of Dermatovenereology, West China Hospital, Sichuan University, Chengdu, China,

We report a case of primary cutaneous mucormycosis caused by Mucor irregularis. A 47-year-old farmer was presented to our clinic with the history of progressive red plaque around the inner canthus following dacryocystectomy about a year earlier. Linear, aseptate hyphae were seen by direct KOH examination and in biopsy.Read More

Fungal culture revealed light yellow filamentous colonies that were identified as Mucor irregularis by nucleotide sequencing of rRNA gene. Amphotericin B and dexamethasone were used in gradually increasing dosage. The treatment lasted 43 days, and the patient received 760 mg total amphotericin B. The patient was discharged after 2 months of treatment. The plaque became smooth, and fungal culture was negative. There was no recurrence for half a year through telephone follow-ups. A review of published studies revealed 23 cases of Mucor irregularis infection. Most cases resulted following injuries or surgical complications. Farmers and manual laborers were most at risk with males outnumbering females among patients. Amphotericin B and its liposomal preparations remain most effective treatment choices.

2014Aug
Korean J. Physiol. Pharmacol.
Korean J Physiol Pharmacol 2014 Aug 13;18(4):353-8. Epub 2014 Aug 13.
Department of Physiology, Wonkwang University School of Medicine and Brain Science Institute at Wonkwang University, Iksan 570-749, Korea.

Control of blood pressure is maintained by the interaction between the arterial baroreflex and vestibulosympathetic reflex during postural changes. In this study, the contributions of vestibular receptors and baroreceptors to the maintenance of blood pressure following acute hypotension were compared in terms of phosphorylated extracellular regulated protein kinase (pERK) expression in the nucleus tractus solitaries (NTS). Expression of pERK in the NTS was measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or sinoaortic denervation (SAD) 5, 10, 20, and 40 min following acute hypotension induced by sodium nitroprusside (SNP) infusion.Read More

Expression of pERK increased significantly in the NTS in the control group following SNP infusion, and the expression peaked at 10 min after SNP infusion. The number of pERK positive neurons increased following SNP infusion in BL, SAD, and BL+SAD groups, although the increase was smaller than in control group. The BL group showed a relatively higher reduction in pERK expression than the SAD group, and the pERK expression in the NTS was localized to the caudal portion of the nuclei in the BL and SAD groups. These results suggest that the vestibular receptors may play a key role in maintaining blood pressure following acute hypotension; thus, the vestibular system may contribute to compensate for orthostatic hypotension.

2014Jul
Mol Med Rep
Mol Med Rep 2014 Jul 9;10(1):101-6. Epub 2014 May 9.
Department of Anesthesiology, The First Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan 646000, P.R. China.

Resveratrol, a polyphenol mainly present in grapes and red wine, demonstrated varied pharmacological activities. The protective effects of resveratrol on acute lung injury (ALI) induced by lipopolysaccharide (LPS) have remained elusive. The present study investigated whether the protective effect of resveratrol on ALI induced by LPS was via inhibiting the myeloid differentiation primary response gene (myd88)‑dependent toll‑like receptor (TLR)4 signaling pathway.Read More

Mice were pretreated with 5 or 45 mg/kg resveratrol for three days prior to bronchial perfusion with 25 mg/kg LPS. At 12 h after surgery, the ratio of the wet to the dry (w/d) lung was calculated to assess tissue edema. Histological changes of the lungs were detected using hematoxylin and eosin staining and the protein expression levels of TLR4, myd88 and nuclear factor kappa‑light‑chain‑enhancer of activated B cells (NF‑κB) were measured by western blot analysis. The concentration of interleukin (IL)‑6 and cyclooxygenase (COX)‑2 in the bronchoalveolar lavage fluid were detected by ELISA. The results showed that resveratrol can suppress the edema, inflammatory cell infiltration and alveolar structure damage of lungs in mice with ALI and decrease the lung w/d ratio. Additionally, resveratrol markedly decreased the expression of TLR4, myd88 and NF‑κB and decreased the concentration of inflammatory cytokines, including IL‑6 and COX‑2. Therefore, it can be concluded that resveratrol has a protective effect against ALI induced by LPS, at least in part by inhibiting the myd88‑dependent TLR4 signaling pathway. In conclusion, resveratrol pretreatment has a protective effect against LPS‑induced ALI in mice, which indicates that resveratrol may serve as a potential therapeutic agent for treating ALI in the clinic.

2014Jul
Nanoscale
Nanoscale 2014 Jul;6(14):8226-34
Jiangsu Key Laboratory of New Power Batteries, School of Chemistry and Materials Science, Nanjing Normal University, Nanjing 210023, PR China.

The chemical functionalization of platinum (Pt) nanostructures is becoming a new trend in electrocatalysts designs. Meanwhile, highly branched Pt nanostructures are highly exciting electrocatalysts with high activity and stability owing to their specific physical and chemical properties. In this work, the polyallylamine (PAH) functionalized Pt nanolance assemblies (Pt NLAs) have been successfully synthesized by chemical reduction of PAH-Pt(II) complex using formaldehyde (HCHO) in a two-phase water-complex system.Read More

The as-prepared Pt NLAs are highly branched and three-dimensionally (3D) interconnected nanostructures, which are composed of many long Pt nanolances in various directions. PAH functionalization improves the electrocatalytic activity of the Pt NLAs for an oxygen reduction reaction (ORR) because of high interface proton concentration on the Pt surface and excellent anti-oxidation ability of the Pt nanolances. Meanwhile, the PAH molecules bound on the Pt NLAs surface act as barrier networks to restrain accessibility of alcohol, exhibiting a high ORR selectivity. In addition, the PAH functionalized Pt NLAs show excellent durability for the ORR due to their particular 3D interconnected structure. The work demonstrates that the PAH functionalized Pt NLAs are indeed promising cathodic electrocatalysts for practical application in direct alcohol fuel cells.

2014Jun
Mol. Cancer Ther.
Mol Cancer Ther 2014 Jun 4;13(6):1589-98. Epub 2014 Apr 4.
Authors' Affiliations: The Hepatosplenic Surgery Center, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University; and Departments of Gastroenterology and General Surgery, the Fourth Affiliated Hospital of Harbin Medical University, Harbin, China

Sorafenib is the standard first-line systemic drug for advanced hepatocellular carcinoma (HCC), but the acquired resistance to sorafenib results in limited benefits. Activation of Akt is thought to be responsible for mediating the acquired resistance to sorafenib. The present study aims to examine the underlying mechanism and seek potential strategies to reverse this resistance.Read More

Two sorafenib-resistant HCC cell lines, which had been established from human HCC HepG2 and Huh7 cells, were refractory to sorafenib-induced growth inhibition and apoptosis in vitro and in vivo. Sustained exposure to sorafenib activated Akt via the feedback loop of mTOR but independent of protein phosphatase 2A in HCC cells. Autophagy participated in the resistance to sorafenib as inhibition of autophagy reduced the sensitivity of sorafenib-resistant HCC cells to sorafenib, whereas activation of autophagy by rapamycin had the opposite effect. However, rapamycin did not show a synergistic effect with sorafenib to inhibit cell proliferation, while it also activated Akt via a feedback mechanism in sorafenib-resistant HCC cells. Inhibition of Akt reversed the acquired resistance to sorafenib by switching autophagy from a cytoprotective role to a death-promoting mechanism in the sorafenib-resistant HCC cells. Akt inhibition by GDC0068 synergized with sorafenib to suppress the growth of sorafenib-resistant HCC tumors that possessed the sorafenib-resistant feature in vivo. The results have provided evidence for clinical investigation of GDC0068, a novel ATP-competitive pan-Akt inhibitor, as the second-line treatment after the failure of sorafenib-medicated molecular targeted therapy for advanced HCC.

2014May
Cell. Signal.
Cell Signal 2014 May 29;26(5):1030-9. Epub 2014 Jan 29.
The Hepatosplenic Surgery Center, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. Electronic address:

Sorafenib, the first-line systemic drug for advanced hepatocellular carcinoma (HCC), has demonstrated limited benefits with very low response rates. Thus it is essential to investigate the underlying mechanisms for the resistance to sorafenib and seek potential strategy to enhance its efficacy. Hypoxic cells inside solid tumors are extremely resistant to therapies as their survival ability is increased due to the cellular adaptive response to hypoxia, which is controlled by hypoxia-inducible factor (HIF)-1 and HIF-2.Read More

Sorafenib inhibits HIF-1α synthesis, making the hypoxic response switch from HIF-1α- to HIF-2α-dependent pathways and providing a mechanism for more aggressive growth of tumors. The present study has demonstrated that upregulation of HIF-2α induced by sorafenib contributes to the resistance of hypoxic HCC cells by activating the transforming growth factor (TGF)-α/epidermal growth factor receptor (EGFR) pathway. Blocking the TGF-α/EGFR pathway by gefitinib, a specific EGFR inhibitor, reduced the activation of STAT (signal transducer and activator of transcription) 3, AKT and ERK (extracellular signal-regulated kinase), and synergized with sorafenib to inhibit proliferation and induce apoptosis of hypoxic HCC cells. Transfection of HIF-2α siRNA into HCC cells downregulated the expression of VEGF (vascular endothelial growth factor), cyclin D1, HIF-2α and TGF-α, and inhibited the activation of EGFR. HIF-2α siRNA inhibited the proliferation and promoted the apoptosis of HCC cells in vitro, and synergized with sorafenib to suppress the growth of HCC tumors in vivo. The results indicate that targeting HIF-2α-mediated activation of the TGF-α/EGFR pathway warrants further investigation as a potential strategy to enhance the efficacy of sorafenib for treating HCC.

2014Mar
Neurosci. Lett.
Neurosci Lett 2014 Mar 29;563:70-4. Epub 2014 Jan 29.
Department of Physiology and Pathophysiology, Yanbian University College of Medicine, Yanji 133002, China. Electronic address:

Blood pressure is maintained by the interaction between the arterial baroreflexes and the vestibulo-cardiovascular reflexes during postural changes. In this study, the influence of the vestibular receptors on the maintenance of blood pressure following acute hypotension was quantitatively compared with the role of baroreceptors in terms of c-Fos protein expression in the nucleus tractus solitarius (NTS). Expression of c-Fos protein in the NTS was measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or sinoaortic denervation (SAD).Read More

Expression of c-Fos protein increased significantly in the NTS in the sham group after sodium nitroprusside (SNP) administration. However, the BL, SAD, and SAD+BL groups showed significant decreases in c-Fos protein expression compared to that of the sham group. The SAD group showed relatively more reduction in c-Fos protein expression than the BL group, and the SAD+BL group showed the least expression among the three experimental groups. The c-Fos protein expression in the NTS following acute hypotension was localized to the caudal portions of the nuclei in the BL and SAD groups. These results suggest that the role of vestibular receptors in maintaining blood pressure following acute hypotension is less potent than that of the baroreceptors but more potent than other afferent inputs in conscious rats. In addition, afferent signals for maintaining blood pressure originating from the vestibular receptors and the baroreceptors may converge in the caudal portion of the NTS.

2014Feb
Ann Dermatol
Ann Dermatol 2014 Feb 17;26(1):43-52. Epub 2014 Feb 17.
Department of Dermatology, West China Hospital, Sichuan University, Chengdu, China.

An antibiotic-free, fixed-dose combination gel with adapalene (A) 0.1% and benzoyl peroxide (BPO) 2.5% has been developed for treatment of acne vulgaris.Read More


To compare the clinical outcomes of A-BPO combination gel with vehicle gel for treatment or maintenance therapy of patients with acne vulgaris.
An electronic search of the database PubMed (1966 to September 2012), Embase (1984 to September 2012), and Cochrane Controlled Trials Register (CENTRAL; 3rd Quarter, 2012) was undertaken to identify relevant studies. Main clinical outcomes were success rate, treatment-related adverse events (AEs), AEs leading to discontinuation, satisfaction with the effectiveness, and overall satisfaction.
Six studies were finally included in this meta-analysis. The A-BPO group yielded better clinical outcomes regarding the success rate (p<0.00001), satisfaction with the effectiveness of treatment (p=0.005), and overall satisfaction (p=0.005) compared to the vehicle group. The incidence of treatment-related AEs in the A-BPO group was comparable with that of vehicle group (p=0.09), while the A-BPO group was associated with a slightly increase in the incidence of AEs leading to discontinuation when compared with the vehicle group (p=0.02).
A-BPO combination gel yields better clinical outcomes including success rate, satisfaction with the effectiveness, and overall satisfaction compared to vehicle gel, despite an increased incidence of AEs leading to discontinuation. The A-BPO combination agent most likely contributes to the treatment of moderate acne vulgaris rather than severe acne vulgaris, but it may be useful in maintenance therapy of patients with severe acne vulgaris.

2014Jan
FEBS J.
FEBS J 2014 Jan 18;281(1):115-28. Epub 2013 Nov 18.
Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, China.

This study investigated the contribution of survivin and its upstream regulators, AKT and hypoxia-inducible factor 1α (HIF-1α), to the resistance of gastric cancer cells to cisplatin (CDDP). We found that over-expression of survivin increased the resistance of SGC7901 and BGC823 gastric cancer cells to CDDP. Its over-expression abrogated CDDP-induced inhibition of cell proliferation and CDDP-induced cell apoptosis.Read More

In contrast, down-regulation of survivin expression using small hairpin RNA (shRNA) vectors and the small-molecule inhibitor YM155, or inhibition of survivin function using a recombinant cell-permeable dominant-negative survivin protein (dNSur9), promoted CDDP-induced apoptosis. CDDP-resistant sub-lines generated from the parental SGC7901 and BGC823 cells by exposure to increasing concentrations of CDDP expressed higher levels of HIF-1α and survivin in response to hypoxia, and higher levels of phosphorylated AKT (pAKT). Specific inhibition of AKT reduced the expression of HIF-1α and survivin, whereas specific inhibition or depletion of HIF-1α reduced survivin expression but had no effect on the expression of phosphorylated AKT. The expression levels of survivin affected the therapeutic efficacy of CDDP in treating gastric tumors in mice. Specific inhibition of survivin, AKT and HIF-1α enhanced the sensitivity of CDDP-resistant cells to CDDP. Specific inhibition of survivin, AKT and HIF-1α synergized with CDDP to suppress the growth of gastric tumors that had been engineered to overexpress survivin. In summary, the results provide evidence that up-regulation of survivin by AKT and HIF-1α contributes to CDDP resistance, indicating that inhibition of these pathways may be a potential strategy for overcoming CDDP resistance in the treatment of gastric cancer.

2013Nov
Acta Derm. Venereol.
Acta Derm Venereol 2013 Nov;93(6):717-8
Department of Dermatology, West China Hospital, SiChuan University, 610041 ChengDu, China.
2013Nov
Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 2013 Nov;27(21):1219-20

Patients with cervical painless mass for 3 months with swallowing not feeling a week for the chief complaint.
top right sternocleidomastoid before hitting a 7.0 by 3.Read More

0 cm size, lower limb reached 2.0 cm x 1.8 cm, the size of the mass on the left side of the supraclavicular reached 3.0 cm x 2.5 cm of the size of the mass, the three homogeneous medium hard, focally border and clear, the activity can be puncture cytological examination in return for: left supraclavicular see more protein and blood samples and a small amount of sample are arranged heap of fiber cells. Nuclear magnetic resonance (NMR): on the right side of the neck, with three at the left supraclavicular neoplasm, between 2.5-5.5 cm in size, high in T2, T1 low mixed signals, lesion boundaries clear.

2013Sep
Sichuan Da Xue Xue Bao Yi Xue Ban
Sichuan Da Xue Xue Bao Yi Xue Ban 2013 Sep;44(5):736-9, 746
Department of Dermatology , West China Hospital, Sichuan University , Chengdu 610041, China.

To investigate the expression of dual oxidase 2 (DUOX2) in psoriasis vulgaris lesions, atopic dermatitis (AD) lesions and normal skin and its role in cutaneous anti-inflammation.
Tissue samples were harvested from psoriasis lesion area, psoriasis non-lesion area, AD lesion area and AD non-lesion area, as well as normal skin, the expression level of DUOX2 protein was detected by immunohistochemical staining. The mRNA level of DUOX2 was detected by reverse transcription polymerase chain reaction (RT-PCR) analysis.Read More


The expression of DUOX2 protein was observed in all groups which mainly located in basal layer, spinous layer and dermal papilla layer. Compared with the psoriasis non-lesion group and normal skin group, the expression level of DUOX2 protein in psoriasis lesion group was significant higher (P<0. 01). The expression of DUOX2 protein in AD lesion group was stronger than that in AD non-lesion group and normal skin group (P<0. 01). In addition, the expression level of DUOX2 protein in AD lesion group was significant higher than that in psoriasis lesion group (P<0. 01). RT-PCR test revealed DUOX2 mRNA was expressed positively in psoriasis and AD lesions.
The strong expression of DUOX2 in psoriasis vulgaris lesion and AD lesion suggested that DUOX2 may play an important role in the mechanisms of cutaneous anti-inflammation.

2013Aug
Korean J. Physiol. Pharmacol.
Korean J Physiol Pharmacol 2013 Aug 30;17(4):367-73. Epub 2013 Jul 30.
Department of Physiology and Pathophysiology, Yanbian University College of Medicine, Yanji 133002, China.

Contribution of the vestibular end organ to regulation of arterial pressure was quantitatively compared with the role of baroreceptors in terms of baroreflex sensitivity and c-Fos protein expression in the rostral ventrolateral medulla (RVLM). Baroreflex sensitivity and c-Fos protein expression in the RVLM were measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or baroreceptor unloading. BL attenuated baroreflex sensitivity during intravenous infusion of sodium nitroprusside (SNP), but did not significantly affect the sensitivity following infusion of phenylephrine (PE).Read More

Baroreflex sensitivity became positive following sinoaortic denervation (SAD) during infusion of PE and attenuated sensitivity during infusion of SNP. Baroreflex sensitivity also became positive following double ablation (BL+SAD) during infusion of PE, and attenuated sensitivity during infusion of SNP. c-Fos protein expression increased significantly in the RVLM in the sham group after SNP administration. However, the BL, SAD, and SAD+BL groups showed significant decreases in c-Fos protein expression compared with that in the sham group. The SAD group showed more reduced c-Fos protein expression than that in the BL group, and the SAD+BL group showed less expression than that in the SAD group. These results suggest that the vestibular system cooperates with baroreceptors to maintain arterial pressure during hypotension but that baroreceptors regulate arterial pressure during both hypotension and hypertension. Additionally, afferent signals for maintaining blood pressure from the vestibular end organs and the baroreceptors may be integrated in the RVLM.

2013Apr
Cell. Signal.
Cell Signal 2013 Apr 17;25(4):931-8. Epub 2013 Jan 17.
Key Laboratory of Hepatosplenic Surgery, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China.

The interleukin-6 (IL-6)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway mediates cell proliferation and migration. S-phase kinase-associated protein-2 (Skp2) catalyzes the ubiquitylation of p27 and p21. Here we investigated that the cross-talk of the two pathways regulates motility and invasion of gastric cancer SGC7901 and MGC803 cells.Read More

Both cell lines endogenously secret IL-6, and blockage of IL-6 or JAK2 inhibited the activation of JAK2 and STAT3. Depletion of STAT3 downregulated Skp2 expression, and thereby increased the expression of p27 and p21. The depletion of STAT3 inhibited the ability of cells to migrate and invade, and impaired the cellular cytoskeleton mainly microtubules; while the depletion of p27 partially restored the impaired ability to migrate, and reversed the impaired microfilaments, further inhibited the ability to invade, but had little effect on microtubules and cellular adhering ability of STAT3-depleted cells. STAT3 depletion inhibited the activity of RhoA and the interaction with stathmin, downregulated the expression of pFAK (phosphorylated focal adhesion kinase), acetylated-tubulin, RECK (reversion-inducing-cysteine-rich protein with kazal motifs) and Sp1, upregulated E-cadherin, and reduced the activities of MMP (matrix metalloproteinase)-2 and -9. The depletion of p27 increased RhoA (Ras homolog family member A) activity, upregulated RECK, and downregulated E-cadherin and Sp1 in STAT3-depleted cells. The results indicate that the interaction between STAT3 and Skp2/p27/p21 pathway plays an important role in mediating the motility, migration and invasion of gastric cancer cells, and inhibition of STAT3 may be a useful therapeutic approach for metastasis of gastric cancer, but caution needs to be taken for its effects on Skp2/p27/p21 pathway.

2013Apr
Langmuir
Langmuir 2013 Apr 20;29(13):4413-20. Epub 2013 Mar 20.
Jiangsu Key Laboratory of Power Batteries, Laboratory of Electrochemistry, School of Chemistry and Materials Science, Nanjing Normal University, Nanjing 210023, P R China.

Polyallylamine (PAH) functionalized Pd icosahedra are synthesized through a simple, one-pot, seedless and hydrothermal growth method. Herein, PAH is used efficiently as a complex-forming agent, capping agent, and facet-selective agent. The strong interaction between PAH and Pd atom sharply changes the electronic structure of Pd atom in the Pd icosahedra.Read More

The protective function of PAH layers and enhanced antietching capability of Pd atom are responsible for the formation of the Pd icosahedra. Very importantly, the as-prepared PAH functionalized Pd icosahedra exhibit superior electrocatalytic activity and ethanol tolerant ability toward the oxygen reduction reaction (ORR) compared to the commercially available Pt black in alkaline media. At 0.95 V (vs RHE), the ORR specific kinetic current density at the Pd icosahedra is 4.48 times higher than that at commercial Pt black. The fact demonstrates the appropriate surface modification of the Pd nanoparticles by nonmetallic molecules can be regarded as an effective way to enhance the electrocatalytic activity toward the ORR.

2013Mar
Phys Chem Chem Phys
Phys Chem Chem Phys 2013 Mar;15(11):3793-802
Jiangsu Key Laboratory of New Power Batteries, College of Chemistry and Materials Science, Nanjing Normal University, Nanjing 210023, PR China.

The synthesis of Pt nanocrystals with controlled size and morphology has drawn enormous interest due to their particular catalytic activity. We present a facile and green hydrothermal method for synthesizing monodisperse Pt nanocubes (Pt-NCs) with polyallylamine hydrochloride (PAH) as a complex-forming agent, capping agent and facet-selective agent, and formaldehyde as a reductant. The formation mechanism, particle size and surface composition of the Pt-NCs were investigated by Ultraviolet and visible spectroscopy (UV-vis), Fourier transform infrared (FT-IR), transmission electron microscopy (TEM), selected area electron diffraction (SAED), X-ray diffraction (XRD), and X-ray photoelectron spectroscopy (XPS), etc.Read More

In the proposed PAH-K(2)PtCl(4)-HCHO synthesis system, the raw material could be reutilized to re-synthesize the Pt-NCs, and the particle size of the Pt-NCs could be readily controlled by the reduction rate of the Pt(II) species in the Pt(II)-PAH complex. After UV/Ozone and electrochemical cleaning, the residual PAH on the Pt-NC surfaces still strongly influenced the d-band centre of Pt due to the strong N-Pt interaction. The as-prepared 6 nm Pt-NCs showed superior electrocatalytic activity (mass activity and specific activity) and stability towards the oxygen reduction reaction (ORR) in both H(2)SO(4) and HClO(4) electrolytes compared to the commercial E-TEK Pt black, owing to the combination of the facets effect and electronic effect.

2013Feb
Tumour Biol.
Tumour Biol 2013 Feb 11;34(1):181-92. Epub 2012 Dec 11.
The Hepatosplenic Surgery Center, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.

S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and associated with poor prognosis. Skp2 acts as an oncogenic protein by enhancing cancer cell growth and tumor metastasis. The present study has demonstrated that small hairpin RNA (shRNA)-mediated downregulation of Skp2 markedly inhibits the viability, proliferation, colony formation, migration, invasion, and apoptosis of human gastric cancer MGC803 cells, which express a high level of Skp2.Read More

In contrast, Skp2 shRNA had only a slight effect on the above properties of BGC823 cells, which express a low level of Skp2. In accord, knockdown of Skp2 suppressed the ability of MGC803 cells to form tumors and to metastasize to the lungs of mice, and the growth of established tumors, by inhibiting cell proliferation and enhancing cell apoptosis. In contrast, overexpression of Skp2 promoted tumorigenesis of BGC823 cells in mice. Skp2 depletion induced cell cycle arrest in the G(1)/S phase by upregulating p27, p21, and p57 and downregulating cyclin E and cyclin-dependent kinase 2. Skp2 depletion also increased caspase-3 activity, impeded the ability of cells to form filopoidia and locomote, upregulated RECK (reversion-inducing cysteine-rich protein with kazal motifs), and downregulated matrix metalloproteinase (MMP)-2 and MMP-9 activity and expression. The results suggest that downregulating Skp2 warrants investigation as a promising strategy to treat gastric cancers that express high levels of Skp2.

2013Feb
Postepy Dermatol Alergol
Postepy Dermatol Alergol 2013 Feb 20;30(1):13-8. Epub 2013 Feb 20.
Department of Dermatology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Head: Prof. Zai-Pei Guo MD.

Photoaging is the superposition of chronic ultraviolet (UV)-induced damage on intrinsic aging. Telomere length is a molecular marker of cell aging, and genomic instability due to telomere shortening has been linked to several aging-related diseases.
To explore the effects of different doses of ultraviolet A (UVA) on the length of telomeres in human skin fibroblasts and partly reveal the mechanism of skin photoaging initiated by UVA irradiation.Read More


Primary cultured human skin fibroblasts were irradiated with different doses of UVA light. Cell viability, cell cycle phase, β-galactosidase, and the length of telomeres were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, cytochemical staining, and real-time polymerase chain reactions, respectively.
After UVA irradiation, inhibited proliferation, S phase accumulation and increased expression of senescence-associated β-galactosidase were observed in cultured fibroblasts. Moreover, the length of telomeres in UVA-treated cells was shortened in a dose-dependent manner as compared to controls (p < 0.05).
These results suggest that telomere length in human dermal fibroblasts can be shortened by a single high dosage of UVA radiation, and that acute photodamage might contribute to early photoaging in human skin via rapid telomere shortening. This study potentially provides the basis for better understanding of the molecular mechanism of photoaging.

2012Dec
Med. Hypotheses
Med Hypotheses 2012 Dec 20;79(6):786-9. Epub 2012 Sep 20.
West China Hospital, Sichuan University, Chengdu, China.

Vitiligo is a common, incurable skin disease with a prevalence of about 1%. Although many vitiligo therapies are available in clinics, there is almost no one method that causes significant improvement in all vitiligo patients. Some have hypothesized that melanocyte dysfunction or deficiency underlies the loss of skin pigmentation observed in vitiligo.Read More

The autoimmune-mediated apoptosis of melanocytes might be an important part of the etiology of vitiligo, which prevents the formation of melanocytes in the skin. Here we propose a novel hypothesis for vitiligo treatment using in situ melanocyte regeneration induced by melanocyte-lineage-specific genes (MLSGs). This may serve as an intelligent bioengineering prototype. The hypothesis is based on the fact that MLSGs regulate melanocyte differentiation through epigenetic reprogramming, which includes microphthalmia-associated transcription factor (MITF), paired box 3 (PAX3), and Notch signaling. MITF directs the terminal differentiation of melanocytes, and PAX3 helps to establish the properties of the melanocyte stem cells. Notch signaling promotes adult stem cell proliferation and self-renewal. This process could be mimicked by Notch intracellular domain (NICD). MLSGs could also stimulate anti-apoptotic gene expression. Recent improvements in relevant biotechniques allow the transdermal delivery of MLSG proteins into the patient, where they enter cells through protein transduction. This process may promote melanocyte regeneration in situ with little impact on the hair follicular cycle or on carcinogenesis. This simple and efficient treatment may have significant impact on the treatment of vitiligo patients.

2012May
Sichuan Da Xue Xue Bao Yi Xue Ban
Sichuan Da Xue Xue Bao Yi Xue Ban 2012 May;43(3):382-5
Department of Dermatology ,West China Hospital, Sichuan University, Chengdu 610041, China.

To study the bactericidal activity of keratinocytes to Staphylococcus aureus in the presence of TNF-alpha, IFN-gamma and their combination.
The keratinocytes were co-cultured with Staphylococcus aureus to establish the Staphylococcus invasion model of skill cell, then the differenct concentrations of TNF-alpha, IFN-gamma and their combinationt were added into the culture. 24 h later the number of intracellular viable bacteria was counted, while the same amount of sterilized PBS was used as control.Read More


Compared with the control group, each the number of intracellular viable bacteria did not change significantly under the condition of 20 ng/mL of either TNF-alpha or IFN-gamma (P > 0.05), as well as 40 ng/mL of TNF-alpha (P < 0.05). However, it was reduced significantly after the addtion of 40 ng/mL of IFN-gamma (P < 0.05), while was also decreased by the combination of TNF-alpha and IFN-gamma, of which effect was less than that achieved by IFN-gamma alone (P > 0.05).
IFN-gamma, not TNF-alpha, can enhance the bactericidal function of keratinocytes, and the bactericidal effect, is weaker when treatment is combing IFN-gamma with TNF-alpha.

2012Mar
Cancer Sci.
Cancer Sci 2012 Mar 13;103(3):528-34. Epub 2012 Jan 13.
The Hepatosplenic Surgery Center, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

The hypoxic microenvironment inside solid tumors, including hepatocellular carcinoma (HCC), is a major cause of tumor resistance to chemotherapy. The recently identified hypoxia-inducible factor (HIF)-2 executes the hypoxia response. Its expression feature and transcriptional targets indicate a possible dominance of HIF-2 in regulating genes in HCC.Read More

The aim of the present study was to determine whether transfection of siRNA targeting HIF-2α could enhance the efficacy of doxorubicin, the most commonly used drug in the treatment of HCC. Transfection of HIF-2 siRNA into human HCC cells downregulated the expression of HIF-2α, vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-α, and cyclin D1, but had little effect on the expression of HIF-1α, fms-related tyrosine kinase-1 (Flt-1), the glucose transporter (GLUT)-1, and lactate dehydrogenase A (LDHA). Doxorubicin itself only downregulated VEGF expression. Furthermore, HIF-2 siRNA inhibited proliferation, induced cell cycle arrest at the G(0)/G(1) phase, and acted synergistically with doxorubicin to inhibit the growth of human HCC cells in vitro. Transfection of HIF-2 siRNA also downregulated tumoral expression of HIF-2α, VEGF, TGF-α, and cyclin D1 in vivo, and acted synergistically with doxorubicin to suppress the growth of HepG2 tumors established in immunodeficient mice by inhibiting cell proliferation, tumor angiogenesis and microvessel perfusion. The results of the present study suggest that targeting HIF-2α with siRNA warrants investigation as a potential strategy to enhance the efficacy of doxorubicin in the treatment of HCC.

2011Oct
PLoS ONE
PLoS One 2011 14;6(10):e25943. Epub 2011 Oct 14.
Department of General Surgery, The Hepatosplenic Surgery Center, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Hydrogen sulfide (H(2)S) displays vasodilative, anti-oxidative, anti-inflammatory and cytoprotective activities. Impaired production of H(2)S contributes to the increased intrahepatic resistance in cirrhotic livers. The study aimed to investigate the roles of H(2)S in carbon tetrachloride (CCl(4))-induced hepatotoxicity, cirrhosis and portal hypertension.Read More


Sodium hydrosulfide (NaHS), a donor of H(2)S, and DL-propargylglycine (PAG), an irreversible inhibitor of cystathionine γ-lyase (CSE), were applied to the rats to investigate the effects of H(2)S on CCl(4)-induced acute hepatotoxicity, cirrhosis and portal hypertension by measuring serum levels of H(2)S, hepatic H(2)S producing activity and CSE expression, liver function, activity of cytochrome P450 (CYP) 2E1, oxidative and inflammatory parameters, liver fibrosis and portal pressure. CCl(4) significantly reduced serum levels of H(2)S, hepatic H(2)S production and CSE expression. NaHS attenuated CCl(4)-induced acute hepatotoxicity by supplementing exogenous H(2)S, which displayed anti-oxidative activities and inhibited the CYP2E1 activity. NaHS protected liver function, attenuated liver fibrosis, inhibited inflammation, and reduced the portal pressure, evidenced by the alterations of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), albumin, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and soluble intercellular adhesion molecule (ICAM)-1, liver histology, hepatic hydroxyproline content and α-smooth muscle actin (SMA) expression. PAG showed opposing effects to NaHS on most of the above parameters.
Exogenous H(2)S attenuates CCl(4)-induced hepatotoxicity, liver cirrhosis and portal hypertension by its multiple functions including anti-oxidation, anti-inflammation, cytoprotection and anti-fibrosis, indicating that targeting H(2)S may present a promising approach, particularly for its prophylactic effects, against liver cirrhosis and portal hypertension.

2011Apr
J. Surg. Res.
J Surg Res 2011 Apr 25;166(2):e187-94. Epub 2010 Dec 25.
Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.

Heme oxygenase (HO)-1 protects transplanted organs from ischemia reperfusion injury and immune rejection. This study sought to investigate whether persistent overexpression of HO-1 in donor livers could improve the survival by expanding T regulatory cells in a rat model of orthotopic liver transplantation.
Livers of Dark Agouti rats were intraportally perfused with an AAV expression vector encoding rat HO-1 (AAV-HO-1), and then transplanted into Lewis rats.Read More

The survival, HO-1 activity, Banff rejection activity index, serum levels of IL-2 and TNF-α, infiltration of CD4(+), CD8(+), and T(reg) (CD4(+)CD25(+)Foxp3(+)) cells into donor livers, and expression of Foxp3, TGF-β, and IL-10 were examined. A mixed lymphocyte reaction (MLR) was performed.
Intraportal delivery of AAV-HO-1 resulted in persistent expression of HO-1 and increased activity of HO-1 in transplanted livers, leading to prolonged survival of recipients. Overexpression of HO-1 reduced the Banff rejection activity index, and production of IL-2 and TNF-α, inhibited infiltration of CD4(+) and CD8(+) cells, and increased infiltration of T(reg) cells, into donor livers. The spleens of recipients expressed higher levels of Foxp3, TGF-β, and IL-10 than those of control rats, and the transplanted livers expressed higher levels of Foxp3 and TGF-β. Splenocytes from the tolerant recipients had higher percentages of T(reg) cells, and responded poorly to the allogeneic donor splenocytes.
Persistent expression of HO-1 in donor livers by intraportal delivery of AAV-HO-1 improves the survival by expanding T(reg) cells. HO-1-based therapies, as described herein, promise new strategies to prevent the rejection of liver transplants.

2011Apr
Cancer Biother. Radiopharm.
Cancer Biother Radiopharm 2011 Apr 21;26(2):153-7. Epub 2011 Apr 21.
Elliott-Elliott-Head Breast Cancer Research and Treatment Center, Baton Rouge, Louisiana 70816, USA.

Human leukocyte antigen G (HLA-G) is an immunotolerant nonclassical major histocompatibility complex Class Ib molecule. It is expressed by trophoblastic placental cells during pregnancy to protect the fetus from maternal alloreactivity. HLA-G is overexpressed in tumors and involved in cancer immune evasion.Read More

Reverse transcription-polymerase chain reaction and immunohistochemistry (IHC) were used to examine HLA-G expression in normal mammary and breast cancer cell lines and normal and human breast cancer tissues. Reverse transcription-polymerase chain reaction confirmed that normal epithelial MCF-12A cells had no HLA-G mRNA expression, whereas cancer cell lines MCF-7, T47D, and MDA-MB-231 and NCI/Adr-Res had various levels of HLA-G mRNA expression. Twelve (12) normal and 38 breast cancer tissues were examined by IHC. Fifty-eight (58) percent (22/38) of cancers had medium to strong staining to HLA-G, whereas only 8% (1/12) of normal breast tissues had medium to strong staining, and the difference was significant (p < 0.05). HLA-G staining was found in the membranes and cytoplasm of cancer cells. In conclusion, breast cancer cells overexpress HLA-G mRNA and protein, and this probably contributes to immune evasion.

2011Feb
Sheng Wu Gong Cheng Xue Bao
Sheng Wu Gong Cheng Xue Bao 2011 Feb;27(2):233-9
School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China.

We performed this research mainly to explore the effect of bone sialoprotein (BSP) silence by siRNA on the adhesion ability to bone matrix of bone-seeking breast cancer cells (MDA-MB-231BO). Also we aimed to provide experimental data for prevention and treatment of breast cancer bone metastasis by targeting BSP. We explored the effects of BSP gene silence on characteristics of bone-seeking breast cancer cells: proliferation by MTS[3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt] assay, bone adhesion ability by a mouse bone adhesion model in vitro, morphology of the cells by SEM, and secretion of transforming growth factor-beta1 (TGF-beta1) and receptor activator of nuclear factor-kappa B ligand (RANKL) by ELISA kits.Read More

We performed intra-cardiac injection in nude mice to explore bone metastatic ability of different cell lines. The results showed that knockdown of BSP significantly inhibited the proliferation of MDA-MB-231BO cells and their adhesion to bone matrix. We also observed bone destruction caused by bone resorption around some adhering cells. The appearances of the cells changed in BSP gene silenced group, and the secretion of TGF-beta1 and RANKL decreased. The results showed BSP gene silence can partial inhibition bone metastasis of breast cancer cells in nude mice by X-ray assay and hematoxylin-eosin staining. Based on our research, siRNA-mediated BSP silencing can inhibit proliferation and adhesion to bone matrix of bone-seeking breast cancer cells and change their surface structure, thus inhibits their bone metastatic ability.

2011Jan
Psychiatry Res
Psychiatry Res 2011 Jan 23;185(1-2):248-53. Epub 2010 May 23.
Infection and Immunology Research Laboratory, Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan Province, China, 646000.

Animal and clinical studies have demonstrated that ketamine has quick, obvious and persistent antidepressant-like effect, but such side effects as cardiovascular system excitement and hallucinogenic activity have limited its clinical application. Intravenous anesthetic propofol can remarkably inhibit or eliminate ketamine's side effects including cardiovascular system excitement and hallucinogenic activity even in a sub-anesthesia dose. However, effect of propofol on rapid antidepressant-like action induced by ketamine still remains unclear.Read More

The present study aimed to investigate effect of pretreatment with propofol on the ketamine-induced rapid antidepressant-like action in rats receiving forced swimming test. Open field test and forced swimming test were used to investigate behavior changes of rats receiving different medication. Expression of brain derived neurotrophic factors (BDNF) and a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) pGluR1-Ser845 in hippocampus was measured with sandwich-ELISA and Western Blot, respectively. Results demonstrated that rats receiving propofol alone showed neither antidepressant-like effects nor increased BDNF content; pretreatment with propofol could increase the ketamine-induced antidepressant-like effects and the expression of AMPA pGluR1-Ser845 in hippocampus, but could not further reinforce the increased BDNF content induced by ketamine in hippocampus; after AMPA receptor was antagonized, the strengthening effect of propofol on ketamine-induced antidepressant-like action significantly decreased. The results indicated that propofol in a sub-anesthetic dose could increase the ketamine-induced antidepressant-like effect.

2011Jan
Int. J. Dermatol.
Int J Dermatol 2011 Jan;50(1):74-7
Department of Dermatology, West China Hospital, Sichuan University, Sichuan, China.
2011Jan
Sichuan Da Xue Xue Bao Yi Xue Ban
Sichuan Da Xue Xue Bao Yi Xue Ban 2011 Jan;42(1):61-4, 118
Department of Dermatology, West China Hospital, Sichuan University, Chengdu 610041, China.

To investigate the protective effects of sodium selenite and aloin against ultraviolet A (UVA) radiation on the dermal fibroblasts including the suppression of proliferation, oxidative damage and collagen synthesis.
Human dermal fibroblasts were divided into the negative control group, the positive control UVA radiation group, the sodium selenite treatment plus UVA radiation group and the aloin treatment plus UVA radiation group, which were incubated with sodium selenite or aloin and irradiated with 5 J/cm2 UVA respectively. The MTT spectrophotometry and biochemical assay were used to determine the proliferation, collagen level and the SOD and GSH-Px activity of the fibroblast cells after radiation.Read More


5 J/cm2 UVA affect the proliferation, collage protein, SOD and GSH-Px activity in the fibroblast cells (P < 0.05). Sodium selenite (10-100 microg/L) and aloin (1-100 mg/L) could enhance the proliferation and the SOD and GSH-Px activity. A increased collagen synthesis in dose dependant manner was also observed (P < 0.05).
Sodium selenite and aloin in a certain range of concentration have protective effects on ultraviolet radiation induced fibroblast proliferation inhibition, oxidative injury, and decreased collagen synthesis.

2010Nov
Am. J. Chin. Med.
Am J Chin Med 2010 ;38(6):1115-30
The Hepatosplenic Surgery Center, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, China.

Matrine, one of the main components extracted from a traditional Chinese herb, Sophora flavescens Ait, has displayed anti-cancer activity in several types of cancer cells. This study aims to evaluate the therapeutic benefits of matrine on primary and metastatic breast cancer. Matrine inhibited the viability of and induced apoptosis in human MCF-7 and mouse 4T1 breast cancer cells in a dose-dependent manner in vitro as shown by MTT assay, flow cytometry and laser scanning confocal microscopy.Read More

Administration of matrine inhibited the growth of primary tumors and their metastases to lungs and livers, in a dose-dependent manner, in a highly metastatic model of 4T1 breast cancer established in syngeneic Balb/c mice. Tumors from matrine-treated mice had a smaller proliferation index, shown by immunostaining with an anti-Ki-67 antibody, a greater apoptosis index, shown by TUNEL-staining, and a less microvessel density, shown by immunostaining with an anti-CD31 A antibody, compared to the controls. Western blot analysis of tumoral homogenates indicated that matrine therapy reduced the ratio of Bcl-2/Bax, downregulated the expressions of VEGF and VEGFR-2, and increased the activation of caspase-3 and caspase-9. This study suggests matrine may be a potent agent, from a natural resource, for treating metastatic breast cancer because of its anti-apoptotic, anti-proliferative and anti-angiogenic activities.

2010Sep
Bioorg. Med. Chem. Lett.
Bioorg Med Chem Lett 2010 Sep;20(17):5123-5
Laboratory of Computer-Aided Drug Design & Discovery, Beijing Institute of Pharmacology and Toxicology, Beijing, PR China.

Based on a homology-modeled structure of PLTP and characteristic structural features of reported cholesteryl ester transfer protein (CETP) inhibitors, we designed and synthesized a novel series of 2,4,5-trisubstituted selenazole compounds. Biological evaluation reveals that compounds 12 and 17 exhibit favorable PLTP activity, and their IC(50)s are 8 microM and 10 microM, respectively.Read More

2010Mar
Int. J. Hematol.
Int J Hematol 2010 Mar;91(2):293-302
Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

This study aims to investigate the role of stromal cell-derived factor 1alpha (SDF-1alpha) and its receptor CXCR4 in cellular infiltration of the lung in differentiation syndrome (DS). The acute promyelocytic leukemia (APL) NB4 cells and freshly prepared APL cells from the patients were differentiated by all-trans retinoic acid (ATRA). The expression of SDF-1alpha in human lung tissues was examined by RT-PCR and Western blot analysis.Read More

The cells were subjected to adhesion, migration or invasion assays, and co-cultured with human lung tissues in a microgravity rotary cell culture system to examine cellular infiltration in situ. ATRA-differentiated cells expressed high levels of CXCR4, and adhered more strongly to matrigel. Their ability to migrate and invade was enhanced by SDF-1alpha and lung homogenate, and diminished by pre-treatment with an anti-CXCR4 blocking antibody. SDF-1alpha was expressed in the lung tissues of all seven human donors. ATRA-differentiated NB4 cells infiltrated into lung tissues, and this was reduced by pre-treatment with an anti-CXCR4 blocking antibody. The interaction of SDF-1alpha and CXCR4 plays an important role in pulmonary cellular infiltration during DS, suggesting that targeting SDF-1alpha and CXCR4 may provide the basis for potential treatments in the management of DS.

2010Mar
Anticancer Res.
Anticancer Res 2010 Mar;30(3):759-65
Elliott-Elliott-Head Breast Cancer Research and Treatment Center, 17050 Medical Center Drive, 4th Floor, Baton Rouge, LA 70816, USA.

Since malignant cells often have a high demand for iron, we hypothesize that breast cancer cells may alter the expression of iron transporter genes including iron importers [transferrin receptor (TFRC) and solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2 (SLC11A2)] and the iron exporter SLC40A1 (ferroportin), and additionally that the growth of breast cancer can be inhibited by manipulating iron transporter gene expression. To test our hypothesis, reverse transcription polymerase chain reaction (RT-PCR) was used to determine mRNA expression of iron transporter genes in normal human mammary epithelial MCF-12A cells and human breast cancer MCF-7 cells. Antisense oligonucleotides were employed to suppress the expression of TFRC gene in the 4T1 mammary adenocarcinoma in both cell culture and a mouse tumor model.Read More

We found the following: i) the MCF-7 cells have higher expression of TFRC and SLC11A2 compared with MCF-12A epithelia; ii) SLC40A1 was only expressed in MCF-12A epithelia but not in MCF-7 cells; iii) iron increased mRNA levels of the SLC11A2 gene in both MCF-12A and MCF-7 cells; iv) TFRC antisense oligonucleotides reduced TFRC mRNA levels and intracellular total iron, and inhibited the proliferation of the 4T1 cells in cell culture; v) TFRC antisense oligonucleotide inhibited tumor growth and lung metastases in the 4T1 mammary adenocarcinoma mouse model. In conclusion, breast cancer cells up-regulate the expression of iron importer genes and down-regulate the expression of iron exporter SLC40A1 to satisfy their increased demand for iron. Suppression of transferrin receptor by antisense results in inhibition of tumor growth and lung metastasis in the 4T1 mammary adenocarcinoma mouse model.

2010Mar
Sichuan Da Xue Xue Bao Yi Xue Ban
Sichuan Da Xue Xue Bao Yi Xue Ban 2010 Mar;41(2):280-3
Department of Dermatology, West China Hospital, Sichuan University, Chengdu 610041, China.

To investigate the effects of IPL and IPL plus 5-ALA on the proliferation, melanogenesis and tyrosinase activity of cultured B16 murine melanoma cells.
B16 cells were pretreated with or without ALA and irradiated with IPL (20, 30, 40 J/cm2), also the negative control group and the positive control UVA irradiation group (3, 4, 5 J/cm2) were designed. The proliferation of the treated B16 cells were evaluated with MTT method, the melanogenesis of the cells was tested with NaOH assay as well as tyrosinase activity was detected at 1 d, 2 d, 3 d, 4 d, and 5 d after irradiation.Read More


5 mmol/L 5-ALA did not affect the proliferation, melanogenesis and tyrosinase activity in B16 melanoma cell. The cell yielding in UVA group increased significantly (P < 0.05) compared with that of negative control group after UVA irradiation (3, 4 J/cm2), but the proliferation of the treated B16 cells were suppressed after UVA irradiation (5 J/cm2). IPL (20, 30, 40 J/cm2) or IPL plus ALA did not have any significant effects on cell proliferation. IPL or IPL plus ALA have inhibitory effects on melanogenesis without any influence on cell tyrosinase activity in B16 cells. ALA, as the photosensitizer, combined with IPL could have stronger effect than IPL alone.
We demonstrated that UVA could stimulate the proliferation of B16 cells, increase the melanogenesis and tyrosinase activity of the cells. IPL or IPL plus ALA have inhibitory effects on melanogenesis without any influence on cell proliferation and tyrosinase activity in B16 cells. IPL plus ALA had stronger effect than IPL alone.

2010Jan
Wei Sheng Wu Xue Bao
Wei Sheng Wu Xue Bao 2010 Jan;50(1):98-106
General Hospital of Guangzhou command, Guangzhou 510010, China.

To establish an experimental culture system of herpes simplex virus type II (HSV-2) latent infection and reactivation in SH-SY5Y cells.
Changes of biological character were observed after 20, 40, 60, 80,100, 120 and 140 micromoL/L ACV were added into cell cultures, and also the morphological observation was detected with phase-contrast microscopy after HSV-2 was inoculated into SH-SY5Y cells using MOI of 0.1, 1, 10 and 100.Read More

The optimum condition of time and temperature was approached using temperature of 41 degrees C, 42 degrees C, 43 degrees C, 44 degrees C and 45 degrees C, and time of 0.5 h, 1.0 h, 1.5 h, 2.0 h and 2.5 h to induce HSV-2 reactivation. The optimum concentration of Forskolin was also decided using 25, 50, 75, 100 and 125 micromoL/L to activate the virus from latency. PCR was used to authenticate HSV-2 latent infection and reactivation. The morphological changes were observed when the virus was reactivated from latency.
The optimum concentration of ACV was 60 micromoL/L to establish latency in SH-SY5Y cells. Suitable infective dose of HSV-2 was 1-10 MOI to construct latency and reactivation in SH-SY5Y cells. The time of virus latency in SH-SY5Y cells could reach up to 14 d. Heat stress of 43 degrees C, 1.5 h and 75 micromoL/L Forskolin were the optimum condition to induce virus reactivation. The morphologic changes in SH-SY5Y cells recurred by HSV-2: Cytopathic effects-were more and more obvious with time lasting from 24 h to 72 h after reactivation from latency. PCR and results of electrophoresis proved the cell model of latent infection and reactivation was set up successfully.
The cell model system of HSV-2 latent infection and reactivation in SH-SY5Y cells was established. The research provided usefulness for study on HSV-2 of latency, reactivation and pathogenic mechanism.

2009Nov
J. Biomed. Sci.
J Biomed Sci 2009 25;16:33. Epub 2008 Dec 25.
The Hepatosplenic Surgery Center, Department of General Surgery, The First Clinical College of Harbin Medical University, Harbin 150001, PR China.

Developmentally regulated endothelial cell locus-1 (Del1) is an embryonic angiogenic factor expressed in early embryonic endothelial cells, but recently has been found to be expressed in some forms of cancers including colon and breast cancers, and melanoma, and human cancer cell lines. Overexpression of Del1 accelerates tumor growth by enhancing vascular formation, implying Del1 may be a potential target for anti-angiogenic cancer therapy. The study aims to investigate whether downregulation of Del1 could inhibit the growth of tumors established in nude Balb/c mice by subcutaneous implantation of human LS-174T colon cancer cells.Read More

The shRNA expression vectors targeting human Del1, and vascular endothelial growth factor (VEGF) were constructed. Gene transfection of Del1-shRNA downregulated expression of Del1 in LS-174T cells in vivo and in vitro, but did not alter the proliferative or survival properties of cells in vitro. Gene transfection of VEGF-shRNA downregulated expression of both VEGF and Del1 in LS-174T cells in vivo and in vitro. Both Del1-shRNA and VEGF-shRNA gene therapies exhibited anti-tumor activities and they also showed a synergistic effect in suppressing growth of colon tumors by anti-angiogenesis and anti-proliferation. Although further investigation to clarify the mechanisms explaining the role of Del1 in tumor growth, and the interaction between VEGF and Del1, is required, the results indicate that downregulation of Del1 presents a potent therapeutic strategy to combat colon cancer.

2009Nov
Cancer Sci.
Cancer Sci 2009 Nov 4;100(11):2226-33. Epub 2009 Aug 4.
Hepatosplenic Surgery Center, Department of General Surgery, First Affiliated Hospital School of Harbin Medical University, Harbin, China.

Hepatocellular carcinoma (HCC) is one of the most common cancer-related causes of death, and conventional treatments offer unsatisfactory response. We have previously reported that kallistatin gene therapy suppressed the growth of HCC tumors by its anti-angiogenic activity, and meloxicam, a selective COX-2 inhibitor, inhibited proliferation and induced apoptosis of human HCC cells in vitro. The aim of this study was to determine whether combining kallistatin gene therapy and meloxicam could offer a better therapeutic effect to combat HCC in mice.Read More

A kallistatin expression plasmid was constructed and its expression was detected after intratumoral gene transfer. Both kallistatin gene therapy and meloxicam suppressed the growth of subcutaneous human HepG2 tumors established in BALB/c nude mice, and the combinational therapy showed a stronger effect in suppressing tumor growth, tumor angiogenesis and cell proliferation, and increasing cell apoptosis, than the respective monotherapies. Gene transfer of kallistatin inhibited tumor angiogenesis, and slightly inhibited cell proliferation and increased cell apoptosis in situ, but had no effect on expression of vascular endothelial growth factor, basic fibroblast growth factor, proliferating cell nuclear antigen, Bcl-2, Bax, or activation of caspase-3. Meloxicam therapy inhibited cell proliferation, induced cell apoptosis, reduced expression of proliferating cell nuclear antigen, increased activation of caspase-3, and upregulated Bax. Meloxicam also slightly inhibited tumor angiogenesis with no effect on the expression of vascular endothelial growth factor or basic fibroblast growth factor. Combining two novel anticancer agents, kallistatin targeting tumoral vascularization and meloxicam targeting cell proliferation and apoptosis, warrants investigation as a therapeutic strategy to combat HCC.

2009Apr
Hum. Gene Ther.
Hum Gene Ther 2009 Apr;20(4):314-24
Hepatosplenic Surgery Center, Department of General Surgery, First Clinical Medical School of Harbin Medical University, Harbin 150001, China.

Transcatheter arterial embolization (TAE) is a standard treatment for unresectable hepatic malignancies. It blocks the arterial blood supply to the tumor, but blockade of the blood supply can be short-lived as collateral blood vessels develop, leading to the failure of TAE. Here we report that intraportal delivery of adeno-associated viral (AAV) vectors expressing antisense hypoxia-inducible factor-1alpha (HIF-1alpha) (AAV-ASHIF) augments TAE to combat hepatocellular carcinoma (HCC).Read More

Intraportal delivery of AAV-ASHIF led to long-term localized expression of transgenic ASHIF in rat liver, and suppressed the growth of CBRH7919 HCC tumors established in rat liver by inhibiting the formation of neovessels and tumor cell proliferation. TAE therapy caused the necrosis and shrinkage of liver tumors; however, neovessels quickly formed and the residual tumors underwent rapid expansion. TAE enhanced tumor and liver hypoxia, which in turn upregulated expression of HIF-1alpha, vascular endothelial growth factor, glucose transporter-1, lactate dehydrogenase A, and proliferating cell nuclear antigen. Intraportal injection of AAV-ASHIF augmented the therapeutic effects of TAE and diminished its undesirable effects, resulting in extensive tumor cell death and suppression of the growth of liver tumors. In conclusion, this study has revealed that HIF-1 impedes the response of liver tumors to TAE. Antisense HIF-1alpha therapy is warranted as an approach for enhancing the efficacy of TAE to treat unresectable liver cancers.

Hepatocellular carcinoma (HCC), one of the most common cancers worldwide, is resistant to anticancer drugs. Hypoxia is a major cause of tumor resistance to chemotherapy, and hypoxia-inducible factor (HIF)-1 is a key transcription factor in hypoxic responses. We have previously demonstrated that gene transfer of an antisense HIF-1alpha expression vector downregulates expression of HIF-1alpha and vascular endothelial growth factor (VEGF), and synergizes with immunotherapy to eradicate lymphomas.Read More

The aim of the present study was to determine whether gene transfer of antisense HIF-1alpha could enhance the therapeutic efficacy of doxorubicin to combat HCC. Both antisense HIF-1alpha therapy and doxorubicin suppressed the growth of subcutaneous human HepG2 tumors established in BALB/c nude mice, tumor angiogenesis, and cell proliferation, and induced tumor cell apoptosis. The combination therapy with antisense HIF-1alpha and doxorubicin was more effective in suppressing tumor growth, angiogenesis, and cell proliferation, and inducing cell apoptosis than the respective monotherapies. Gene transfer of antisense HIF-1alpha downregulated the expression of both HIF-1alpha and VEGF, whereas doxorubicin only downregulated VEGF expression. Antisense HIF-1alpha and doxorubicin synergized to downregulate VEGF expression. Both antisense HIF-1alpha and doxorubicin inhibited expression of proliferating cell nuclear antigen, and combined to exert even stronger inhibition of proliferating cell nuclear antigen expression. Antisense HIF-1alpha therapy warrants investigation as a therapeutic strategy to enhance the efficacy of doxorubicin for treating HCC.

2008Sep
Mol. Biol. Rep.
Mol Biol Rep 2008 Sep 22;35(3):465-72. Epub 2007 Jun 22.
Department of Medical Research, Guangzhou Liuhuaqiao Hospital, Liuhua Road 111, Guangzhou, Guangdong Province, P. R. China.

Two approaches have been developed to construct plasmids that mediate RNA interference to inhibit the replication and expression of HBV in 2.2.15 cell.Read More

The overlapping PCR extension and restriction enzyme-digestion were used to generate DNA fragments encoding designed shRNA based on sequences of ORF C of HBV genome. The pU6 derived vectors were constructed to develop plasmid based shRNA delivery systems termed pU6/HBVi. There were significant reductions in the expression of HBsAg and HBeAg between cells transfected with pU6/HBVi and control groups (as to HBsAg: P < 0. 01; and HBeAg: P < 0. 01). Consistently, the HBV DNA copies were reduced from 2.71 x 10(7) to <5 x 10(2) copies with or without pU6/HBVi. These results suggested that shRNA delivery by recombinant plasmids harboring shRNA encoding DNA fragment of interest generated either by overlapping PCR extension or restriction enzyme-digestion, could inhibit expressions of viral proteins and reduce viral replications. The pU6 derived plasmids might be a useful shRNA delivery system in mammalian cells. In addition, we found siRNA based on stealth 2311 was a potent RNAi target of HBV genome.

2008Sep
Surg. Today
Surg Today 2008 27;38(10):931-7. Epub 2008 Sep 27.
Department of General Surgery, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.

Intestinal ischemia/reperfusion (I/R) is a common and serious clinical condition. The anti-inflammatory and anti-apoptotic properties of oxymatrine, the extract from a traditional Chinese herb, Sophora flavescens Ait, have been shown to protect the liver from I/R injury and attenuate colitis. The objective of this study was to investigate if oxymatrine could attenuate intestinal I/R injury induced in rats.Read More


The experimental design consisted of three groups of 24 Wistar rats each: a sham-operation group (control group), a group subjected to intestinal I/R and then given saline (saline group), and a group subjected to intestinal I/R and then given oxymatrine (oxymatrine group). Intestinal I/R was induced by occluding the superior mesenteric artery for 45 min. Six rats from each group were killed at selected time points, and blood and intestinal samples were collected.
Morphological alteration, reduction of gamma-glutamyl transpeptidase (gamma-GGT) activity, and increased cell apoptosis confirmed intestinal I/R injury. The oxymatrine group had a significantly lower histological score and apoptosis index than the saline group, demonstrating that the preadministration of oxymatrine attenuated gut damage. Moreover, oxymatrine inhibited the production of lipid peroxides (LPO), decreased the serum levels of tumor necrosis factor (TNF)-alpha, and downregulated expression of phosphorylated p38 mitogen-activated protein kinase, Fas, and FasL, which had been elevated by I/R.
These results provide further evidence of the anti-inflammatory and anti-apoptotic activities of oxymatrine, which may become a potent drug for protecting the intestines against I/R injury.

2008Sep
Wei Sheng Yan Jiu
Wei Sheng Yan Jiu 2008 Sep;37(5):609-12
Department of Medical Technology, West China School of Public Health, Sichuan University, Chengdu 610041, China.

To optimize the reaction conditions of enterobacteia repetitive intergenic consensus sequences-based PCR (ERIC-PCR), a molecular typing method of Salmonella, study the genomic DNA ERIC-PCR fingerprint maps of Salmonella standard strains and epidemic isolates, and supply data for a system of Salmonella epidemiology investigation and homology tracing.
Genomic DNA of S. typhimurium was abstracted and used as the template for PCR.Read More

Enterobacteia repetitive intergenic consensus sequences were used as primers to amplify the target sequences in S. typhimurium genomic DNA: Amplification products were separated by agarose gel electrophoresis, and electrophoresis maps were analyzed by gel image analysis system. To optimize template concentration, Mg2+ concentration, primers concentration and annealing temperature of PCR, the factor to be optimized was designed in different concentration grads and other factors were fixed. Analyzed 16 Salmonella strains and one E. coli strain by PCR conditions optimized.
The electrophoresis bands of amplified products were entire and most clear when template concentration was 100 ng/25 microl, Mg2+ concentration was 2.0 mmol/L, primers concentrations were 0.4 micromol/L respectively in the total volume of 25 microl of the reaction system, and annealing temperature was 52 degrees C. The ERIC-PCR fingerprint maps of different Salmonella strains with different sources were different. From 250 to 5000 bp, there were 3 to 13 bands, and in those there was a specific 250 bp band.
Important reaction conditions of ERIC-PCR had been optimized in this study. ERIC-PCR technique could discriminate Salmonella strains isolated from different regions. It could be used in Salmonella epidemiology investigation and homology tracing, so as to make up for the flaws of the traditional classification methods for salmonella.

2008Jun
Biotechnol. Lett.
Biotechnol Lett 2008 Jun 2;30(6):989-93. Epub 2008 Feb 2.
Department of Medical Research, Guangzhou Liuhuaqiao Hospital, Liuhua road 111, Guangzhou, Guangdong Province, 510010, P.R. China.

Angiogenin, a potent angiogenic factor, was cloned and expressed by Escherichia coli and then purified with gel filtration chromatography. Approximately 90% pure angiogenin was obtained to generate a monoclonal antibody. Using western immunoblotting and ELISA, we confirmed that monoclonal antibody C46 secreted from hybridoma cells stably and specifically binds to angiogenin.Read More

The fused protein angiogenin-EGF was then expressed in HUVECs, and the subcellular localization of the recombinant protein was determined by confocal microscopy and TEM assay. Recombinant angiogenin was found to mainly concentrate in the pars granulosa of the nucleus, where the protein accumulates to form ribonucleoprotein particles.

2008Jun
Zhonghua Wai Ke Za Zhi
Zhonghua Wai Ke Za Zhi 2008 Jun;46(11):851-3
Department of General Surgery, the First Clinical Hospital Affiliated of Harbin Medical University, Harbin 150001, China.

To construct and purify heme oxygenase-1, GFP gene mediated by recombinant adeno-associated-virus and identify expression rate of GFP in transplanted liver in rats.
Heme oxygenase-1 gene of rat was cloned and subcloned to rAAV vector, the gene sequence was confirmed correct by restriction enzyme and DNA sequencing. The rAAV-HO-1 was then cotransfected into 293 cell line with accessory plasmid virus helper and AAV-cap-rep through CaCl2 coprecipitation.Read More

Virus particles were purified by heparin column chromatography and titre were detected by Real-time PCR. An orthotopic liver transplantation model by Wistar to Wistar was set up using Kamada's two cuff technique. Purified rAAV-GFP was injected into portal vein and incubated for 2 hours at the donor liver cold preserved stage, and then performed OLT. Recipients were killed and visceral organs were sampled at 1 and 3 months after operation respectively, frozen section (3-5 microm) were prepared and gene expression rate in different tissues was examined under fluorescence microscope.
The inserted segment of HO-1 was identified through restriction enzyme cutting followed with electrophoresis, the result of DNA sequencing was in accordance with which found in Genbank. The GFP expression rate was over 80% in allograft at 1 and 3 month after transfection whereas there was no GFP expression in heart, lung, spleen, kidney and small bowel.
High titre rAAV carried HO-1 and GFP were constructed successfully. Steady and effective expression of GFP mediated by rAAV was demonstrated in liver allograft in rats.

2008Mar
Acta Biochim. Biophys. Sin. (Shanghai)
Acta Biochim Biophys Sin (Shanghai) 2008 Mar;40(3):235-43
Department of Breast Surgery, Qilu Hospital of Shandong University, Jinan 250012, China.

Ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis that decarboxylates ornithine to putrescine, has become a promising target for cancer research. The aim of this study is to investigate the role of ODC in breast cancer. We detected expression of ODC in breast cancer tissues and four breast cancer cell lines, and transfected breast cancer cells with an adenoviral vector carrying antisense ODC (rAd-ODC/Ex3as) and examined their growth and migration.Read More

ODC was overexpressed in breast cancer tissues and cell lines compared with non-tumor tissues and normal breast epithelial cells, and there was a positive correlation between the level of ODC mRNA and the staging of tumors. The expression of ODC correlated with cyclin D1, a cell cycle protein, in synchronized breast cancer MDA-MB-231 cells. Gene transfection of rAd-ODC/Ex3as markedly down-regulated expression of ODC and cyclin D1, resulting in suppression of proliferation and cell cycle arrest at G0-G1 phase, and the inhibition of colony formation, an anchorage-independent growth pattern, and the migratory ability of MDA-MB-231 cells. rAd-ODC/Ex3as also markedly reduced the concentration of putrescine, but not spermidine or spermine, in MDA-MB-231 cells. The results suggested that the ODC gene might act as a prognostic factor for breast cancer and it could be a promising therapeutic target.

2008Jan
J. Biomed. Sci.
J Biomed Sci 2008 Jan 18;15(1):99-109. Epub 2007 Aug 18.
Department of General Surgery, Shandong Provincial Qianfoshan Hospital, Jinan, China.

Chemotherapy combined with antiangiogenic therapy is more effective than chemotherapy alone. The aim of this study was to investigate whether endostatin, a potent anti-angiogenic agent, could enhance the efficacy of paclitaxel to combat breast cancer. An expression plasmid encoding mouse endostatin (End-pcDNA3.Read More

1) was constructed, which produced intense expression of endostatin and inhibited angiogenesis in the chorioallantoic membrane assay. 4T1 breast tumors were established in BALB/c mice by subcutaneous injection of 1 x 10(5) 4T1 cells. The End-pcDNA3.1 plasmid diluted in the transfection reagent FuGENE was injected into the tumors (around 100 mm(2)), and paclitaxel was injected i.p. into the mice. Endostatin gene therapy synergized with paclitaxel in suppressing the growth of 4T1 tumors and their metastasis to the lung and liver. Both endostatin and paclitaxel inhibited tumor angiogenesis and induced cell apoptosis. Despite the finding that endostatin was superior to paclitaxel at inhibiting tumor angiogenesis, paclitaxel was nevertheless more effective at inducing tumor apoptosis. The combination of paclitaxel and endostatin was more effective in suppressing tumor growth, metastases, angiogenesis, and inducing apoptosis than the respective monotherapies. The combinational therapy with endostatin and paclitaxel warrants future investigation as a therapeutic strategy to combat breast cancer.

2007Oct
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2007 Oct;23(10):898-900
Department of Medical Research, Guangzhou Army General Hospital, Guangzhou, China.

To construct the vector stably expressing small hair RNA(shRNA) and investigate the effect of shRNA expressed with DNA vector on HBV replication and expression.
The vector expressing shRNA designated pU6 was constructed by U6 promoter. The sequence of shRNA targeting on specific region of HBV genome against HBV was designed and synthesized, then cloned into pU6.Read More

The plasmid designated pU6B/HBVi was transfected into 2.2.15 cells using Lipofectamine 2000 reagent. The HBsAg and HBeAg in the supernatants of the transfected cells were measured by ELISA. The HBV copies in the transfected cells were measured by quantitative PCR.
Compared with controls, not only concentration of HBsAg and HBeAg but also HBV copies in transfected 2.2.15 cells decreased significantly by the plasmid expressing shRNA against HBV.
HBV replication and expression in 2.2.15 cells are inhibited by stably expressed shRNA.

2007Jan
Nan Fang Yi Ke Da Xue Xue Bao
Nan Fang Yi Ke Da Xue Xue Bao 2007 Jan;27(1):88-91
Graduate School of Southern Medical University, Guangzhou 510515, China.

To evaluate the effect of insulin-like growth factor (IGF) and its receptor-I antibody on the growth of human adrenocortical carcinoma SW-13 cell line in vitro.
The growth curves of SW-13 cell treated with IGF and its receptor-I antibody were obtained by means of MTT assay. The effects of the two agents, added either alone or in combination at different concentrations, on the cell growth were evaluated.Read More


IGF significantly promoted proliferation of SW-13 cells, and its effect was positively correlated with its concentrations (P<0.05). IGF receptor-I antibody inhibited the effect of insulin-like growth factor with direct inhibitory effect on proliferation of SW-13 cells (P<0.05).
IGF can promote the growth of human adrenocortical carcinoma SW-13 cells via its receptor-I. IGF receptor-I antibody can inhibit the effect of the growth factor, suggesting a possible role of this receptor in the treatment of adrenocortical carcinoma.

2006Jul
Lin Chuang Er Bi Yan Hou Ke Za Zhi
Lin Chuang Er Bi Yan Hou Ke Za Zhi 2006 Jul;20(14):647-8, 651
Department of Medical Research, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou 510010, China.

To determine the serum angiogenin (ANG) concentration in patients with nasopharyngeal carcinoma (NPC) and analyze its clinical significance.
Forty-two NPC patients and 30 healthy controls entered this study. Serum ANG level was quantitatively analyzed by enzyme-linked immunosorbent assay (ELISA).Read More


The mean level of serum ANG in untreated NPC was (371.4 +/- 123.5) microg/L, which was significantly higher than that in healthy controls(292.5 +/- 74.2) microg/L (P < 0.01). Furthermore, the serum level of ANG increased with the development of tumor (P < 0.05). After treatment, all patients reached a response: partial response (PR) or complete response (PR), and the serum ANG level was (340.6 +/- 112.4) microg/L, which was significantly lower than that in untreated ones (P < 0.05), but still higher than that in healthy controls (P < 0.05).
Our results indicate that the serum ANG level increases in patients with NPC, and is correlate with primary tumor progression.

2005Mar
Sichuan Da Xue Xue Bao Yi Xue Ban
Sichuan Da Xue Xue Bao Yi Xue Ban 2005 Mar;36(2):237-9
Department of Dermatology, West China Hospital, Sichuan University, Chengdu 610041, China.

To investigate the effect of ultraviolet B (UVB) on Interleukin-8 secretion in human keratinocyte cell line.
The concentration of IL-8 was detected by ELISA kit 24 h after human keratinocytes (HKC) were irradiated by different doses of UVB, and the level of IL-8 was also determined at different times after the same dose of UVB irradiation.
The secretion of IL-8 was increased after the HKC were irradiated by UVB, the effect was dose-dependent when UVB ranged from 10 to 40 mJ/cm2, and there was statistically significant difference between the IL-8 level of UVB groups (20-70 mJ/cm2) and the control (0 mJ/cm2) (P<0.Read More

01). The level of IL-8 was increased 1 h after the irradiation of 30 mJ/cm2 UVB, and it reached the peak at 12 h. There was statistically significant difference between the IL-8 levels detected at different times (3 h, 6 h, 12 h, 24 h after irradiation) and that at 0 h (P<0.01).
UVB increase the secretion of IL-8, and the effect is dose-dependent to some extent.

2005Jan
Sichuan Da Xue Xue Bao Yi Xue Ban
Sichuan Da Xue Xue Bao Yi Xue Ban 2005 Jan;36(1):143-6
Department of Dermatovenereology, West China Hospital, Sichuan University, Chengdu 610041, China.

We report here the discovery of Malassezia furfur from a groin abscess of a renal transplant patient. A 33-year-old male patient was admitted to our hospital because of a high fever and a persistent inflammatory nodule on his right groin for one week. He had received a renal transplant 3 years before and remained on immunosuppressive agents.Read More

He was treated with broad-spectrum antibiotics after hospitalization but the nodule formed a large abscess and then a deep ulcer instead of resolving. Examination of the culture by light microscopy revealed ovoid budding yeasts displaying collar-shaped structure. Subculture of the primary colonies onto Sabouraud's dextrose agar and medium containing rapeseed oil resulted in growth only on the medium containing rapeseed oil. All of the isolates was identified as Malassezia furfur. The pathogenicity of the isolates was tested in mice by intravenous injection of (3-5) x 10(8) cfu per mouse after immunosuppression with 500 mg/kg of prednisone intraporitoneally on day-2. In the mouse model, micro-abscess and inflammatory reaction and oval yeasts with budding were noted in histopathologic section of the viscera of the mice. A rib-like or serrate-like structure of the inner side of cell wall, characteristic for Malassezia spp., was observed by transmission electron microscopy. The patient received oral fluconazole and topical amphotericin B. The isolate before antifungal therapy was sensitive to both fluconazole and amphotericin B, while the isolate after antifungal treatment was only sensitive to amphotericin B. Proteinase activity of the isolates increased 1.43 times after antifungal treatment. This case indicated the invasive power of M. furfur in deep infection. Renal transplantation and reception of long-term immunosuppressive treatment are risk factors for the invasive infection of this fungus.

2004Jul
J Colloid Interface Sci
J Colloid Interface Sci 2004 Jul;275(1):172-6
Key Laboratory of Materials Cycling in Pedosphere, Nanjing Institute of Soil Science, Chinese Academy of Sciences, People's Republic of China.

The electrochemical properties on solid particle surfaces in an aqueous system have found wide application in many fields. However, for some of them there are no reliable methods of determination. What is particularly worth mentioning is the surface potentials of solid particles.Read More

Though this is a most important property and a most basic parameter in colloid interface electrochemistry, no reliable method for its determination is available yet. In the present paper, based on the diffuse double-layer theory, mathematical relations are constructed between the average concentration of ions positively adsorbed in the diffuse double layer and the surface potential of solid particles, thus transforming the determination of surface potential of solid particles into that of the average concentration of ions in the diffuse double layer, and then by applying the standard relationships of Gouy-Chapman theory, the mathematical relations of the average concentration of ions in the diffuse double layer with surface charge density, electrical field strength at surface, and specific surface area of solid particles are constructed.

2004Jul
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2004 Jul;20(4):415-8
Institute of Tumor Molecular Biology, General Hospital of Guangzhou Command, Guangzhou 510010, China.

To explore whether the promyelocytic leukemia cell line HL-60 may differentiate into activated dendritic cells (DCs) by A23187, a calcium ionophore.
The HL-60 cells were cultured in common medium alone or with various concentrations of A23187 (25-1 600 microg/L) and rhGM-CSF (100 microg/L). After culture for 24-96 hours, the cellular morphological change was observed under light microscope and electron microscope.Read More

Surface makers on treated HL-60 cells were analyzed by flow cytometry. The proliferation of allogeneic human T cells was detected by MTT colorimetry.
Under the condition of a suitable dose (200 microg/L) of A23187 treatment of HL-60 cells for 24 hours, the expression of CD83 molecule, a characteristic marker on DCs, was highest. The typical dendritic outgrowth appeared at a time when HL-60 cells were treated with A23187 for 72 hours. However, when HL-60 cells were treated with A23187 for 96 hours, the expressions of CD80 (B7.1), CD86 (B7.2), MHC-class II molecule and CD54 on HL-60 cells reached peak, and marked activation of allogeneic T cells occurred.
Calcium ionophore A23187 can induce the HL-60 cells to differentiate into activated DCs-like cells.

2004Apr
Zhong Yao Cai
Zhong Yao Cai 2004 Apr;27(4):267-9
General Hospital of Guangzhou Military Command, Guangzhou 510010.

To observe the cytotoxicity of chymopapain combined with pingyangmycin (PYM) on mouse hepatoma cell line hapa-6 in vitro.
MTT method.
Chymopapain showed cytotoxicities to hepa-6 (IC50 is about 1200 microg/ml) and had concentration dependency.Read More

Cooperation effect was showed when three different concentration chymopapain combined with PYM during 48 hours. It accorded with the change of enzyme activity of chymopapain in saline water. Cooperation effect was showed again when adding chymopapin for the second time at 48 hours.
Chymopapain has cytotoxicity on hepa-6 in vitro. Cooperation effect was showed when chymopapin was combined with PYM.

2004Feb
Zhonghua Zhong Liu Za Zhi
Zhonghua Zhong Liu Za Zhi 2004 Feb;26(2):78-81
Medical Research Department, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou 510010, China.

To develop toxin targeting vascular endothelial growth factor receptor II (VEGF-II/KDR) fused with a KDR-binling peptide screened from peptide library.
By affinity to KDR molecular which expressed specifically by new born vascular endothelial cell, peptides to KDR were screened from C7 peptide library by phage display. Among them, a peptide binding to KDR with high affinity termed as P5 was selected and fused to the N-terminal of Shiga toxin subunit A (StxA).Read More

The protein (P5-StxA) was expressed in E. coli.
ELISA and Western blot were applied to characterize the binding interaction between the fusion protein, P5-StxA and KDR. Cytotoxicity assay showed that P5-StxA maintained similar toxicity to cell as StxA. In the model of angiogenesis, P5-StxA inhibited selectively VEGF-induced growth of preexisting vessels of the chick chorioallantoic membrane.
These studies demonstrate the small peptide, P5, maybe be used as carrier of toxin targeting to KDR.

2004Jan
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2004 Jan;20(1):15-8
Department of Medical Research, General Hospital of Guangzhou Military Command, Guangzhou 510010, China.

To express the recombinant angiogenin protein in mammalian cells.
Human ANG full-length cDNA was obtained by chemical synthesis. The target gene ANG was inserted into eukaryotic expression vector pEGFP-C2.Read More

The recombinant plasmid was transfected into the human umbilical vein endothelial cells (HUVECs) via Lipofectin transfection. The expression of ANG gene in transfected HUVECs was detected by fluorescence microscopy and immunohistochemical staining.
DNA sequencing showed the sequence of the synthetic ANG was correct and amino acid sequence of ANG was right. The green fluorescence could be seen in transfected HUVECs under fluorescence microscope. Immunohistochemical staining detection showed that ANG expressed in transfected cells.
Human ANG full-length cDNA has been obtained. The ANG protein was expressed in mammalian cells successfully.

2003Jan
Anticancer Res.
Anticancer Res 2002 Sep-Oct;22(5):2685-92
Mastology Research Institute, Elliott-Hailey-Head Breast Cancer Research and Treatment Center, 17050 Medical Center Drive, 4th Floor, Baton Rouge, LA 70816, USA.

It is known that the interruption of normal iron metabolism with chelators of iron, toxic metals, toxic metals bound to transferrin, or anti-transferrin receptor antibodies leads to significant inhibition of tumor cell growth in cell culture systems and animal models. In the present study, we found that iron depletion was produced by the iron chelator deferoxamine mesylate, the free toxic metals gallium or indium, and the toxic metals gallium or indium bound to transferrin in the MCF-7 human breast cancer cell line, and this induced the condensation and fragmentation of chromatin, and the formation of DNA fragments characteristic of apoptosis. The induction of apoptosis was quantitated with acridine orange and ethidium bromide staining of apoptotic cells, separation of fragmented DNA from radiolabeled cells, and in situ terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assays.Read More

The apoptosis, caused by deferoxamine mesylate, and gallium or indium bound to transferrin in the MCF-7 cells, can be completely inhibited by excess ferric chloride or equimolar iron-loaded transferrin. Gallium-transferrin and indium-transferrin complexes induced more apoptosis than their respective salts in the MCF-7 cells. Deferoxamine mesylate induced a small increase in the endogenous expression of both the bcl-2 and bax genes in the MCF-7 cells and this can be prevented by ferric chloride. In the 13762NF rat mammary adenocarcinoma model, in situ TUNEL assays showed that the iron-deficiency following a low iron diet or intravenous injection of deferoxamine mesylate produced 5.32 +/- 3.90% and 6.46 +/- 3.58% of apoptotic cells, respectively, compared to 2.01 +/- 1.20% of apoptotic cells in the control rats maintained on a normal diet (p < 0.05 and p < 0.01, respectively, Student's t-test). This is the first report of iron depletion caused by a low iron diet or deferoxamine mesylate treatment inducing apoptosis in rats bearing the 13762NF marnmary adenocarcinoma.

2002Nov
Zhonghua Zhong Liu Za Zhi
Zhonghua Zhong Liu Za Zhi 2002 Nov;24(6):540-3
Department of Medical Research, Guangzhou PLA General Hospital, Guangzhou 510010, China.

To screen for the inhibitor of vascular endothelial growth factor (VEGF) 165 from random peptide library.
Positive phage clones were rescued after two rounds of panning and competitive elution. Its affinity activity to KDR was monitored through ELISA, immunohistochemical method, Chicken CAM assay and MTT.Read More


Five specific binding positive target molecule phage clones were obtained which were able to bind to cells whose surface had high KDR, among which, clone 3 and 13 could effectively block the vascularization of the chorioallantoic membrane of chick embryo, but they were not inhibitive on the proliferation of high KDR expression cells.
The peptides, being the inhibitors of VEGF, may be useful in the treatment of cancers.

2002Mar
Di Yi Jun Yi Da Xue Xue Bao
Di Yi Jun Yi Da Xue Xue Bao 2002 Mar;22(3):256-8
Department of Oncology, General Hospital of Guangzhou Command, Guangzhou 510010, China.

To observe whether dendritic cells (DCs) transfected with carcinoembryonic antigen (CEA)-vaccinia recombinant virus (rV-CEA) induces cytotoxic T lymphocyte-mediated CEA-specific immunity in vitro.
DCs derived from peripheral blood monocytes were transfected with rV-CEA and then cocultured with autologous T cells. The proliferation of the induced T cells and their cytotoxic activity against CEA-secreting tumor cells were assessed and compared with those of T cells induced by DCs without rV-CEA transfection.Read More


T cells induced by DCs transfected with rV-CEA showed specific cytotoxicity against CEA-secreting tumor cells.
DCs transfected with rV-CEA can elicit activation of CEA-specific T cells.

2001Nov
Di Yi Jun Yi Da Xue Xue Bao
Di Yi Jun Yi Da Xue Xue Bao 2001 ;21(11):841-843
Department of Oncology, General Hospital of Guangzhou Command, Guangzhou 510010, China.

OBJECTIVE: To detect the in vitro antitumor action of phytohemagglutinin and lymphokine activated killer (PHA- LAK) cells. METHOD: MTT colorimetric assay was used to detect the in vitro cytotoxicity of PHA-LAK cells on K562 MGc80-3 143TK Hela and LoVo. RESULTS: The significant cytotoxicity of PHA-LAK cells on these five tumor cells from different organs could be found in vitro.Read More

The PHA-LAK cell activity on 143TK could reach 57.3% when the ratio of effective cell (EC) to target cell (TC) was 7.5:1. The antitumor effect did not increased or even decreased when the ratio of EC to TC was 15:1. CONCLUSIONS: (1)PHA-LAK cell has non-specific cytotoxicity against tumor cells and can overcome the problems of the quantity and activity of immunocyte of traditional adoptive cellular immunotherapy. (2)Under some conditions does MTT colorimetric assay be a susceptible, simple and convenient method for detecting the cytotoxicity of immunocytes.