Publications by authors named "Yanan Jiang"

121 Publications

Controllable Plexcitonic Coupling in a WS-Ag Nanocavity with Solvents.

ACS Appl Mater Interfaces 2021 Sep 31;13(36):43554-43561. Epub 2021 Aug 31.

Hubei Key Laboratory of Optical Information and Pattern Recognition, Wuhan Institute of Technology, Wuhan 430205, China.

Strong coupling between emitters and cavities underlies many of the current strategies aiming at generating and controlling quantum states at room temperature. Recent experiments reveal strong coupling between two-dimensional transition metal dichalcogenides (TMDCs) and individual plasmonic structures; however, the coupling strength is quite limited (<200 meV), and the active control of the coupling strength is challenging. Here, we demonstrate the active tuning of plexcitonic coupling in monolayer WS coupled to a plasmonic nanocavity by immersing into a mixed solution of dichloromethane (DCM) and ethanol. By adjusting the mixture ratio, continuous tuning of the Rabi splitting energy ranged from 183 meV (in ethanol) to 273 meV (in DCM) is achieved. The results are mainly attributed to the remarkable increase of the neutral exciton density in monolayer WS as the concentration of DCM is increased. It offers an important stepping stone toward a further study on plexcitonic coupling in layered materials, along with potential applications in quantum information processing and nonlinear optical materials.
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http://dx.doi.org/10.1021/acsami.1c10295DOI Listing
September 2021

Tegaserod Maleate Inhibits Esophageal Squamous Cell Carcinoma Proliferation by Suppressing the Peroxisome Pathway.

Front Oncol 2021 4;11:683241. Epub 2021 Aug 4.

Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.

Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) are the two major types of esophageal cancer (EC). ESCC accounts for 90% of EC. Recurrence after primary treatment is the main reason for poor survival. Therefore, recurrence prevention is a promising strategy for extending the 5-year survival rate. Here, we found tegaserod maleate could inhibit ESCC proliferation both and . Proteomics analysis revealed that tegaserod maleate suppressed the peroxisome signaling pathway, in which the key molecules peroxisome membrane protein 11B (PEX11B) and peroxisome membrane protein 13 (PEX13) were downregulated. The immunofluorescence, catalase activity assay, and reactive oxygen species (ROS) confirmed that downregulation of these proteins was related to impaired peroxisome function. Furthermore, we found that PEX11B and PEX13 were highly expressed in ESCC, and knockout of PEX11B and PEX13 further demonstrated the antitumor effect of tegaserod maleate. Importantly, tegaserod maleate repressed ESCC tumor growth in a patient-derived xenograft (PDX) model . Our findings conclusively demonstrated that tegaserod maleate inhibits the proliferation of ESCC by suppressing the peroxisome pathway.
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http://dx.doi.org/10.3389/fonc.2021.683241DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8372369PMC
August 2021

PDIA6 promotes pancreatic cancer progression and immune escape through CSN5-mediated deubiquitination of β-catenin and PD-L1.

Neoplasia 2021 Sep 26;23(9):912-928. Epub 2021 Jul 26.

Department of Pathophysiology, Zhengzhou University, Zhengzhou, China.

Protein Disulfide Isomerase Family A Member 6 (PDIA6) is an endoplasmic reticulum protein that is capable of catalyzing protein folding and disulfide bond formation. Abnormally elevated expression of PDIA6 has been reported to predict poor outcomes in various cancers. Herein, gain-of- and loss-of-function experiments were performed to investigate how PDIA6 participated in the carcinogenesis of pancreatic cancer (PC). By analyzing the protein expression of PDIA6 in 28 paired PC and para carcinoma specimens, we first found that PDIA6 expression was higher in PC samples. Both the overall survival and disease-free survival rates of PC patients with higher PDIA6 expression were poorer than those with lower PDIA6 (n = 178). Furthermore, knockdown of PDIA6 impaired the malignancies of PC cells - suppressed cell proliferation, invasion, migration, cisplatin resistance, and xenografted tumor growth. PDIA6-silenced PC cells were more sensitive to cytotoxic natural killer (NK) cells. Overexpression of PDIA6 had opposite effects on PC cells. Interestingly, COP9 signalosome subunit 5 (CSN5), a regulator of E3 ubiquitin ligases known to promote deubiquitination of its downstream targets, was demonstrated to interact with PDIA6, and its expression was increased in PC cells overexpressing PDIA6. Additionally, PDIA6 overexpression promoted deubiquitination of β-catenin and PD-L1 and subsequently upregulated their expression in PC cells. These alterations were partly reversed by CSN5 shRNA. Collectively, the above results demonstrate that PDIA6 contributes to PC progression, which may be associated with CSN5-regulated deubiquitination of β-catenin and PD-L1. Our findings suggest PDIA6 as a potential target for the treatment of PC.
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http://dx.doi.org/10.1016/j.neo.2021.07.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8329431PMC
September 2021

Downregulation of miR-135b-5p Suppresses Progression of Esophageal Cancer and Contributes to the Effect of Cisplatin.

Front Oncol 2021 1;11:679348. Epub 2021 Jul 1.

Department of Gastroenterology and Hepatology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Esophageal cancer (EC) is one of the commonest human cancers, which accompany high morbidity. MicroRNAs (miRNAs) play a pivotal role in various cancers, including EC. Our research aimed to reveal the function and mechanism of miR-135b-5p. Our research identified that miR-135b-5p was elevated in EC samples from TCGA database. Correspondingly real-time PCR assay also showed the miR-135b-5p is also higher expressed in Eca109, EC9706, KYSE150 cells than normal esophageal epithelial cells (Het-1A). CCK8, Edu, wound healing, Transwell assay, and western blot demonstrated miR-135b-5p inhibition suppresses proliferation, invasion, migration and promoted the apoptosis in Eca109 and EC9706 cells. Moreover, the miR-135b-5p inhibition also inhibited xenograft lump growth. We then predicted the complementary gene of miR-135b-5p using miRTarBase, TargetScan, and DIANA-microT. TXNIP was estimated as a complementary gene for miR-135b-5p. Luciferase report assay verified the direct binding site for miR-135b-5p and TXNIP. Real-time PCR and western blot assays showed that the inhibition of miR-135b-5p remarkably enhanced the levels of TXNIP in Eca109 and EC9706 cells. Furthermore, cisplatin (cis-diamminedichloroplatinum II, DDP) decreased miR-135b-5p expression and increased TXNIP expression. Enhanced expression of miR-135b-5p attenuated the inhibitory ability of cisplatin (cis-diamminedichloroplatinum II, DDP) in Eca109 cells, accompanied by TXNIP downregulation. In conclusion, the downregulation of miR-135b-5p suppresses the progression of EC through targeting TXNIP. MiR-135b-5p/TXNIP pathway contributes to the anti-tumor effect of DDP. These findings may provide new insight into the treatment of EC.
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http://dx.doi.org/10.3389/fonc.2021.679348DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8281352PMC
July 2021

Cloperastine inhibits esophageal squamous cell carcinoma proliferation in vivo and in vitro by suppressing mitochondrial oxidative phosphorylation.

Cell Death Discov 2021 Jun 21;7(1):166. Epub 2021 Jun 21.

The Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.

Esophageal squamous cell carcinoma (ESCC) is a major type of esophageal cancer. The prognosis of patients with ESCC remains poor because of the high morbidity and mortality of the disease. One strategy for drug discovery for ESCC treatment or prevention is screening FDA-approved drugs. In the present study, we found that the antitussive agent cloperastine can inhibit the proliferation of ESCC cells. However, the underlying mechanism was unclear. To determine the mechanism of this inhibitory effect, we performed proteomic analysis using KYSE150 cells treated with cloperastine and DMSO. The results identified several down-regulated signaling pathways included those of three key proteins (NADH dehydrogenase [ubiquinone] 1 alpha subcomplex 1, NADH ubiquinone oxidoreductase subunit S5, and cytochrome C oxidase subunit 6B1) involved in oxidative phosphorylation. Meanwhile, we observed that oxidative phosphorylation in mitochondria was inhibited by the drug. Importantly, cloperastine suppressed ESCC growth in a xenograft mouse model in vivo. Our findings revealed that cloperastine inhibits the proliferation of ESCC in vivo and in vitro by suppressing mitochondrial oxidative phosphorylation.
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http://dx.doi.org/10.1038/s41420-021-00509-wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8257628PMC
June 2021

Micrometer-scale transient ion transport for real-time pH assay in living rat brains.

Chem Sci 2021 Apr 19;12(21):7369-7376. Epub 2021 Apr 19.

Beijing National Laboratory for Molecular Sciences (BNLMS), Key Laboratory of Analytical Chemistry for Living Biosystems, Institute of Chemistry, The Chinese Academy of Sciences (CAS), CAS Research/Education Center for Excellence in Molecular Science Beijing 100190 China

Ion transport has been widely used for various applications such as sensing, desalination and energy conversion; however, nearly all applications are based on steady-state ion transport. Herein, we for the first time demonstrate the capability of transient ion transport for sensing with both high spatial (∼μm) and temporal (∼ms) resolution by using pH as the model target. Transient ion transport behavior (, time-dependent ion current change) was observed by applying high-frequency pulse potential. Importantly, we proposed the ion distribution transient model for this time-dependent ion transport behavior. With this model, the temporal resolution of the as-developed pH microsensor based on ion current was improved to the ms level, thus satisfying the requirement of neurochemical recording. Moreover, our microsensor features good reproducibility, selectivity, and reversibility, and can thus real-time monitor the pH change in living rat brains. This study demonstrates the first example of sensing based on ion transport, opening a new way to neurochemical monitoring with ultrahigh spatiotemporal resolution. This study is also helpful to understand the transient process of asymmetric ion transport.
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http://dx.doi.org/10.1039/d1sc00061fDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8171349PMC
April 2021

Structural basis of copper-efflux-regulator-dependent transcription activation.

iScience 2021 May 16;24(5):102449. Epub 2021 Apr 16.

Section of Transcription & Gene Regulation, The Hormel Institute, University of Minnesota, Austin, MN, USA.

The copper efflux regulator (CueR), a representative member of mercury resistance regulator (MerR) family metalloregulators, controls expression of copper homeostasis-regulating genes in bacteria. The mechanism of transcription activation by CueR and other MerR family regulators is bending the spacer domain of promoter DNA. Here, we report the cryo-EM structures of the intact CueR-dependent transcription activation complexes. The structures show that CueR dimer bends the 19-bp promoter spacer to realign the -35 and -10 elements for recognition by σ-RNA polymerase holoenzyme and reveal a previously unreported interaction between the DNA-binding domain (DBD) from one CueR subunit and the σ nonconserved region (σNCR). Functional studies have shown that the CueR-σNCR interaction plays an auxiliary role in CueR-dependent transcription, assisting the activation mechanism of bending promoter DNA by CueR dimer. Because DBDs are highly conserved in sequence and structure, this transcription-activating mechanism could be generally used by MerR family regulators.
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http://dx.doi.org/10.1016/j.isci.2021.102449DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8169799PMC
May 2021

Bestatin Cream Impairs Solar Simulated Light‒Driven Skin Inflammation and Skin Carcinogenesis in Mice.

J Invest Dermatol 2021 May 26. Epub 2021 May 26.

Department of Pathophysiology, School of Basic Medical Sciences, Academy of Medical Science, College of Medicine, Zhengzhou University, Zhengzhou, China. Electronic address:

Leukotriene A4 hydrolase (LTA4H) is an enzyme that catalyzes the production of the inflammatory mediator leukotriene B4, which is involved in inflammatory responses mediated through the leukotriene B4/leukotriene B4 receptor type 1 (BLT1) signaling pathway. In this study, we investigated whether bestatin, an LTA4H inhibitor, could suppress skin acute inflammation and carcinogenesis. In the clinical sample, BLT1 was significantly induced in human skin tissues after acute solar simulated light (SSL) exposure. BLT1 and NF-κB p65 expressions were also increased in acute SSL‒induced mouse skin tissue. Furthermore, LTA4H and BLT1 were highly expressed in skin chronic inflammation and squamous cell carcinomas. More importantly, topical administration of bestatin cream dramatically inhibited BLT1 expression in acute SSL‒induced human skin tissues. BLT1 and NF-κB p65 expressions were also suppressed in acute SSL‒induced Lta4h-knockout and bestatin-treated mice skin tissues. Moreover, we conducted long-term prevention and therapeutic studies, which showed that bestatin significantly attenuated SSL-induced skin carcinogenesis. Mechanistic studies showed that bestatin inhibited skin carcinogenesis by suppressing cell proliferation and inducing cell apoptosis through LTA4H‒BLT1‒protein kinase B‒NF-κB p65 pathway. Overall, our results suggest that topical application of novel cream containing bestatin might open a helpful avenue for SSL-induced skin carcinogenesis.
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http://dx.doi.org/10.1016/j.jid.2021.03.032DOI Listing
May 2021

Comparison of Pancreatic Damage in Rats for Two Methods of Paraquat Administration.

Front Pharmacol 2021 20;12:611433. Epub 2021 Apr 20.

Emergency Department, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

It is noted that elevated serum amylase levels suggesting pancreatic damage has an association with prognosis in PQ patients. This study aimed to determine whether PQ can cause pancreatic damage. The two conventional models (intragastric infusion (iG) and intraperitoneal injection (iP)) may exhibit different effects on the pancreas depending on whether or not they pass through the digestive tract. In this study, the rats were divided into four groups: the intragastric infusion group (PQ-iG, = 45), intraperitoneal injection group (PQ-iP, = 53), normal control group 1 (NC-iG, = 6) and normal control group 2 (NC-iP, = 6). Pancreatic damage was compared between groups using serum amylase activity assay, hematoxylin and eosin (H&E) staining, TUNEL assay, and transmission electron microscopy (TEM). Serum amylase levels in group PQ-iG were significantly higher than in group PQ-iP ( < 0.05). Examination of the H&E sections showed damage to the pancreas. Both experimental groups were displayed inflammatory infiltration within 9 h of PQ treatment. After 9 h, patchy necrosis was observed in group PQ-iP, when inflammatory infiltration was still the dominant pathology. Necrosis appeared and gradually worsened in group PQ-iG, in which necrosis was the dominant pathology. The TUNEL assay showed significantly higher numbers of apoptotic cells in the pancreas of PQ-groups than in the control NC- groups ( < 0.05). TEM showed expansive endoplasmic reticulum lumens and mitochondria swelling in the pancreas of the PQ-groups. It is concluded that both methods of modeling could cause pancreatic damage and the type and degree of damage would change over time. Note that pancreatic damage in group PQ-iG was more severe than that in group PQ-iP. Therefore, clinical practitioners should pay close attention to pancreatic damage caused by PQ, especially when the route of PQ administration was oral.
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http://dx.doi.org/10.3389/fphar.2021.611433DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8099104PMC
April 2021

Cisatracurium inhibits the growth and induces apoptosis of ovarian cancer cells by promoting lincRNA-p21.

Bioengineered 2021 12;12(1):1505-1516

Department of Anesthesiology, Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.

As a common muscle relaxant, cisatracurium has shown good antitumor effect on some tumors. Recent studies reported that cisatracurium could inhibit the progression of colon cancer by upregulating tumor suppressor gene p53. However, its role in ovarian cancer and its regulatory effect on p53 and p53 downstream targeting gene long intergenic noncoding RNA p21 (lincRNA-p21) is still unknown. Quantitative Real-time Polymerase Chain Reaction (qRT-PCR) was used to assess the expression of p53, lincRNA-p21 and miR-181b. Cell viability and proliferation were detected by CCK-8 assay and Edu staining, respectively. Wound-healing and Transwell assays were performed to determine the abilities of cell migration and invasion. Apoptosis was evaluated by TUNEL staining. Luciferase reporter assay was conducted to detect the relationship between lincRNA-p21 and miR-181b. As a result, cisatracurium could increase the expressions of p53 and lincRNA-p21 of ovarian cancer cell line (OVCAR-3) in a dose-dependent manner. In addition, cisatracurium significantly inhibited the proliferation, migration and invasion of OVACR-3 cells, and induced apoptosis. However, these above changes in biological function can be attenuated by lincRNA-p21 knockdown. Next, lincRNA-p21 could directly target miR-181b and negatively regulate its expression by luciferase reporter assay. In conclusion, cisatracurium inhibited the progression of OVCAR-3 cells through upregulation of lincRNA-p21 expression activated by p53 inhibiting miR-181b expression. The experimental results provide a new research idea for the application of cisatracurium in ovarian cancer.
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http://dx.doi.org/10.1080/21655979.2021.1916271DOI Listing
December 2021

Hypoxia enhances the production and antitumor effect of exosomes derived from natural killer cells.

Ann Transl Med 2021 Mar;9(6):473

School of Pharmacy, Binzhou Medical University, Yantai, China.

Background: Exosomes are a subgroup of extracellular vesicles that are naturally released by almost all types of cells. However, the factors that promote the capacity of natural killer (NK) cells to release exosomes are unclear. In this study, we investigated whether hypoxia can enhance the yield of NK cell-derived exosomes and improve the immunotherapeutic effects of these cells.

Methods: Exosomes from NK92 or NK92-hIL-15 cells were isolated from culture medium under normoxic (NK92-Exo and NK92-hIL-15-Exo) or hypoxic (hypoxic NK92-Exo and hypoxic NK92-hIL-15-Exo) conditions. NK92-Exo and hypoxic NK92-Exo were characterized by transmission electron microscopy (TEM), nanoparticle-tracking analysis (NTA), and western blot. Real-time cell assay, wound healing assay, flow cytometry, and western blot were then performed to assess cytotoxicity, cell proliferation, cell migration, apoptosis, and the expression levels of cytotoxicity-associated proteins.

Results: After 48 hours of hypoxic treatment, NK92-Exo exhibited significantly increased cytotoxicity, enhanced inhibition of cell proliferation, and elevated levels of molecules associated with NK cell cytotoxicity. The hypoxia-treated NK92-Exo and NK92-hIL-15-Exo showed increased expression of three functional proteins of NK cells-specifically FasL, perforin, and granzyme B-as compared with their NK92-Exo counterparts exposed to normoxia.

Conclusions: As an approach that supports overproduction of exosomes, hypoxic treatment of NK cells may serve as a promising therapeutic option for cancer immunotherapy.
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http://dx.doi.org/10.21037/atm-21-347DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8039676PMC
March 2021

From hair to pancreas: transplanted hair follicle mesenchymal stem cells express pancreatic progenitor cell markers in a rat model of acute pancreatitis.

Am J Transl Res 2021 15;13(3):1389-1399. Epub 2021 Mar 15.

Department of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, P. R. China.

Acute pancreatitis (AP) is commonly accompanied by intense pain and is associated with high mortality rates. However, the effectiveness of existing therapeutic approaches remains unsatisfactory. Stem cell therapy, which can promote the regeneration of damaged tissue and alleviate systemic inflammatory responses, has brought new possibility for patients suffering from AP. In particular, hair follicle-derived mesenchymal stem cells (HF-MSCs) are proposed as a suitable cell source for treating pancreatic diseases, but further research on their effectiveness, safety, and underlying mechanisms is warranted for clinical implementation. In this work, the therapeutic potential of HF-MSC transplantation was studied in an L-arginine-induced AP rat model. HF-MSCs were extracted from infant Sprague-Dawley (SD) rats, expanded , and detected by flow cytometry. HF-MSCs were labeled by PKH67 and transplanted into rats with AP via tail vein injection. Serum specimens were collected at 24 h, 48 h, and 72 h after transplantation, and the levels of amylase, lipase, and anti-inflammatory factors, namely interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), were analyzed. Pancreas samples were collected and assayed by immunofluorescence and immunohistochemistry 1 week after transplantation to monitor the differentiation of HF-MSCs and the functional recovery of the damaged pancreas. Intravenously delivered rat HF-MSCs spontaneously homed to the damaged pancreas and expressed pancreatic progenitor cell markers, relieved inflammation, and boosted pancreatic regeneration. These findings indicate that HF-MSC transplantation is a potentially effective treatment for AP.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8014427PMC
March 2021

Relationship between changes in the course of COVID-19 and ratio of neutrophils-to-lymphocytes and related parameters in patients with severe . common disease.

Epidemiol Infect 2021 03 29;149:e81. Epub 2021 Mar 29.

School of Pharmacy, Binzhou Medical University, Yantai, China.

To assess the relationship between the neutrophil-to-lymphocyte ratio (NLR) and related parameters to the severity of coronavirus disease 2019 (COVID-19) symptoms. Clinical data from 38 COVID-19 patients who were diagnosed, treated and discharged from the Qishan Hospital in Yantai over the period from January to February 2020 were analysed. NLR and procalcitonin (PCT) were determined in the first and fourth weeks after their admission, along with the clinical characteristics and laboratory test results of these patients. Based on results as obtained on the first and fourth weeks after admission, five indices consisting of NLR, white blood cells, neutrophils, lymphocytes (LY) and monocytes (MON) were selected to generate receiver operating characteristic curves, while optimal cutoff values, sensitivities and specificities were obtained according to the Yuden index. Statistically significant differences in neutrophils, LY and the NLR were present in the severe vs. moderate COVID-19 group from the first to the fourth week of their hospitalisation. The cut-off value of NLR for predicting the severity of COVID-19 was 4.425, with a sensitivity of 0.855 and a specificity of 0.979. A statistically significant positive correlation was present between PCT and NLR in the severe group as determined within the first week of admission. NLR can serve as a predictor of COVID-19 disease severity as patients' progress from the first to the fourth week of their hospitalisation. The statistically significant positive correlation between levels of NLR and PCT in severe patients indicated that increases in NLR were accompanied with gradual increases in PCT.
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http://dx.doi.org/10.1017/S0950268821000674DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8027554PMC
March 2021

Comprehensive characterization of a drug-resistance-related ceRNA network across 15 anti-cancer drug categories.

Mol Ther Nucleic Acids 2021 Jun 15;24:11-24. Epub 2021 Feb 15.

College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, P.R. China.

Cancer is still a major health problem around the world. The treatment failure of cancer has largely been attributed to drug resistance. Competitive endogenous RNAs (ceRNAs) are involved in various biological processes and thus influence the drug sensitivity of cancers. However, a comprehensive characterization of drug-sensitivity-related ceRNAs has not yet been performed. In the present study, we constructed 15 ceRNA networks across 15 anti-cancer drug categories, involving 217 long noncoding RNAs (lncRNAs), 158 microRNAs (miRNAs), and 1,389 protein coding genes (PCGs). We found that these ceRNAs were involved in hallmark processes such as "self-sufficiency in growth signals," "insensitivity to antigrowth signals," and so on. We then identified an intersection ceRNA network (ICN) across the 15 anti-cancer drug categories. We further identified interactions between genes in the ICN and clinically actionable genes (CAGs) by analyzing the co-expressions, protein-protein interactions, and transcription factor-target gene interactions. We found that certain genes in the ICN are correlated with CAGs. Finally, we found that genes in the ICN were aberrantly expressed in tumors, and some were associated with patient survival time and cancer stage.
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http://dx.doi.org/10.1016/j.omtn.2021.02.011DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7933708PMC
June 2021

Comprehensive circRNA Expression Profile and Construction of circRNAs-Related ceRNA Network in a Mouse Model of Autism.

Front Genet 2020 16;11:623584. Epub 2021 Feb 16.

Translational Medicine Research and Cooperation Center of Northern China, Heilongjiang Academy of Medical Sciences, Harbin, China.

Autism is a common disease that seriously affects the quality of life. The role of circular RNAs (circRNAs) in autism remains largely unexplored. We aimed to detect the circRNA expression profile and construct a circRNA-based competing endogenous RNA (ceRNA) network in autism. Valproate acid was used to establish an model of autism in mice. A total of 1,059 differentially expressed circRNAs (477 upregulated and 582 downregulated) in autism group was identified by RNA sequencing. The expression of novel_circ_015779 and novel_circ_035247 were detected by real-time PCR. A ceRNA network based on altered circRNAs was established, with 9,715 nodes and 150,408 edges. Module analysis was conducted followed by GO and KEGG pathway enrichment analysis. The top three modules were all correlated with autism-related pathways involving "TGF-beta signaling pathway," "Notch signaling pathway," "MAPK signaling pathway," "long term depression," "thyroid hormone signaling pathway," etc. The present study reveals a novel circRNA involved mechanisms in the pathogenesis of autism.
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http://dx.doi.org/10.3389/fgene.2020.623584DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7928284PMC
February 2021

Dihydroartemisinin Inhibits the Proliferation of Esophageal Squamous Cell Carcinoma Partially by Targeting AKT1 and p70S6K.

Front Pharmacol 2020 20;11:587470. Epub 2020 Nov 20.

Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.

Dihydroartemisinin (DHA), a sesquiterpene lactone with endoperoxide bridge, is one of the derivatives of artemisinin. In addition to having good antimalarial properties, DHA exhibits anticancer effects including against malignant solid tumors. However, the mechanism by which DHA inhibits the progression of esophageal cancer, especially esophageal squamous cell carcinoma (ESCC), is unclear. In this study, DHA was found to inhibit the proliferation of ESCC, and the underlying molecular mechanisms were explored. DHA inhibited ESCC cells proliferation and anchorage-independent growth. Flow cytometry analysis revealed that DHA significantly blocked cell cycle in the G1 phase. The results of human phospho-kinase array revealed that DHA downregulated the levels of p70S6K and p70S6K. Furthermore, the levels of mTOR, p70S6K, p70S6K and RPS6 were decreased after DHA treatment in KYSE30 and KYSE150 cells. We then explored the proteins targeted by DHA to inhibit the mTOR-p70S6K-RPS6 pathway. Results of the kinase assay revealed that DHA significantly inhibited phosphorylation of mTOR by binding to AKT1 and p70S6K kinases. , DHA inhibited the tumor growth of ESCC patient-derived xenografts and weakened p-mTOR, p-p70S6K, and p-RPS6 expression in tumor tissues. Altogether, our results indicate that DHA has antiproliferative effects in ESCC cells and can downregulate mTOR cascade pathway partially by binding to AKT1 and p70S6K. Thus, DHA has considerable potential for the prevention or treatment of ESCC.
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http://dx.doi.org/10.3389/fphar.2020.587470DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7919191PMC
November 2020

Differences in aluminum tolerance and immobilization between two indigenous ectomycorrhizal fungi Lactarius deliciosus and Pisolithus tinctorius from Southwest China's forest stands.

Ecotoxicol Environ Saf 2021 Apr 16;213:112042. Epub 2021 Feb 16.

College of Resources and Environment, Centre of Excellence for Soil Biology, Southwest University, 2 Tiansheng Road, Beibei, Chongqing 400715, China; School of Biological Sciences, University of Western Australia, 35 Stirling Highway, Perth, WA 6009, Australia. Electronic address:

Aluminum (Al) toxicity severely decreases plant growth and productivity in acidic soil globally. Ectomycorrhizal (ECM) fungi can promote host plant's Al-tolerance by acting as a physical barrier or bio-filter. However, little information is available on the role of ECM fungus on Al immobilization with respect to Al-tolerance. This present study aimed to screen a promising indigenous ECM fungus with high Al-tolerance and to understand its role in Al immobilization related to Al-tolerance. Two ECM fungal strains (Lactarius deliciosus 2 and Pisolithus tinctorius 715) isolated from forest stands in Southwest China were cultured in vitro with 0.0, 1.0 or 2.0 mM Al addition for 21 days to compare their Al accumulation and Al-tolerance. Meanwhile, fungal mycelia were incubated in 0.037 mM Al solutions, and then Al concentrations in the solution were determined at time 2, 5, 10, 20, 40, 60, 120, 180, and 240 min, and the Al immobilization characteristics were evaluated using the pseudo-first order, pseudo-second order and intraparticle diffusion models. Results showed that 1.0 or 2.0 mM Al addition significantly increased fungal biomass production by 23% or 41% in L. deliciosus 2, not in P. tinctorius 715. Fungal Al concentrations in L. deliciosus 2 and P. tinctorius 715 were significantly increased by 293% and 103% under 2.0 mM than under 1.0 mM Al addition. The pH values in the culture solution were significantly decreased by 0.43 after 21 d fungus growth but no changes between these two fungi under the same Al addition. Fungal Al immobilization showed a three-stage trend with initially a rapid rate followed a relatively slower rate until reaching equilibrium. The pseudo-second order model was the best (R = 0.98 and 0.99 for L. deliciosus 2 and P. tinctorius 715) to fit the experimentally observed data among the three models. Compared to P. tinctorius 715, L. deliciosus 2 also had greater intercept value, cation exchange capacity (CEC), and extracellular Al proportion in fungal mycelia. Additionally, bio-concentration on Al, active site numbers for Al, boundary layer thickness, CEC, and immobilization on the cell wall in fungal mycelia were involved in ECM fungal Al-tolerance. These results show that both ECM fungi are Al-tolerant while L. deliciosus 2 is a promising indigenous ECM isolate with higher Al-tolerance in Southwest China, and they can be hence applied to the afforestation and ecological restoration in acidic soil.
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http://dx.doi.org/10.1016/j.ecoenv.2021.112042DOI Listing
April 2021

Sex-specific survival benefit in early skin melanoma based on 8th AJCC edition: an analysis of data from the Surveillance, Epidemiology, and End Results (SEER) database.

Ann Transl Med 2021 Jan;9(1):53

Department of Burns & Plastic Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, China.

Background: Females have been found to have a survival benefit over males in past studies. However, in early melanoma patients, this benefit occurred in only those aged >60 years. The 8th edition of the American Joint Committee on Cancer (AJCC) readjusted the melanoma staging system, specifically stage I. This study aims to verify whether the sex-specific benefit in females exists in different age groups according to the 8th edition of the staging system.

Methods: We collected the data of individuals diagnosed with skin melanoma between 2004 and 2015 from the Surveillance, Epidemiology, and End Results (SEER) database. Based on the 8th edition of the melanoma staging system, patients diagnosed with pathological stage T1a-T3a, N0 and M0 melanoma were enrolled.

Results: A total of 115,576 patients, including 62,938 male patients and 52,638 female patients, were enrolled in this study. The survival rates of males and females in each stage from IA-IIA were significantly different (P<0.001). In further analyses of each age group, it was found that the proportions of patients with stages IA, IB and IIA were significantly different in each age group. Cox analysis showed that females with stage IA in all age groups benefited significantly, but those in stage IB benefited only when they were aged >60 years. In stage IIA patients, there were significant differences between the <50 and 61-70 years age groups.

Conclusions: Based on data from the SEER database, we found that according to the 8th edition of the AJCC melanoma staging system, females had a higher survival rate than males, and this difference was significant in all age groups in the stage IA group but fluctuated with age in the stage IB and IIA groups.
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http://dx.doi.org/10.21037/atm-20-3845DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7859735PMC
January 2021

A novel salt inducible WRKY transcription factor gene, AhWRKY75, confers salt tolerance in transgenic peanut.

Plant Physiol Biochem 2021 Mar 17;160:175-183. Epub 2021 Jan 17.

Shandong Dry-land Farming Technology Key Laboratory, College of Agronomy, Qingdao Agricultural University / Peanut Industry Cooperative Innovation Center, Qingdao, 266109, Shandong, China. Electronic address:

Peanut is an important oilseed crop whose production is threatened by various abiotic and biotic stresses. Study of the molecular mechanism of salt tolerance could provide important information for the salt tolerance of this crop. WRKY transcription factors (TFs) are one of the largest TF families in plants and are involved in growth and development, defense regulation and the stress response. Here, we cloned a novel WRKY transcription factor gene belonging to the WRKY IIc subfamily, AhWRKY75, from the salt-tolerant mutant M34. The expression of AhWRKY75 was induced by NaCl stress treatment. After salt treatment, AhWRKY75-overexpressing peanuts grew better than wild-type plants. Furthermore, several genes related to the reactive oxygen species (ROS) scavenging system were up-regulated; the activities of superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT) were significantly higher in transgenic lines than in non-transgenic control plants; and the malondialdehyde (MDA) and superoxide anion contents were significantly lower in transgenic lines than in control plants. The net photosynthetic rate (Pn), stomatal conductance (GS) and transpiration rate (Tr) of transgenic lines were significantly higher in transgenic plants than in control plants, and the intercellular CO concentration (Ci) was significantly lower in transgenic plants than in control plants. These results demonstrated that the AhWRKY75 gene conferred salt tolerance in transgenic peanut lines by improving the efficiency of the ROS scavenging system and photosynthesis under stress treatment. This study identifies a novel WRKY gene for enhancing the tolerance of peanut and other plants to salt stress.
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http://dx.doi.org/10.1016/j.plaphy.2021.01.014DOI Listing
March 2021

Characterizing heterogeneity of non-small cell lung tumour microenvironment to identify signature prognostic genes.

J Cell Mol Med 2020 12 12;24(24):14608-14618. Epub 2020 Nov 12.

College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.

Growing evidence has highlighted the immune response as an important feature of carcinogenesis and therapeutic efficacy in non-small cell lung cancer (NSCLC). This study focused on the characterization of immune infiltration profiling in patients with NSCLC and its correlation with survival outcome. All TCGA samples were divided into three heterogeneous clusters based on immune cell profiles: cluster 1 ('low infiltration' cluster), cluster 2 ('heterogeneous infiltration' cluster) and cluster 3 ('high infiltration' cluster). The immune cells were responsible for a significantly favourable prognosis for the 'high infiltration' community. Cluster 1 had the lowest cytotoxic activity, tumour-infiltrating lymphocytes and interferon-gamma (IFN-γ), as well as immune checkpoint molecules expressions. In addition, MHC-I and immune co-stimulator were also found to have lower cluster 1 expressions, indicating a possible immune escape mechanism. A total of 43 differentially expressed genes (DEGs) that overlapped among the groups were determined based on three clusters. Finally, based on a univariate Cox regression model, prognostic immune-related genes were identified and combined to construct a risk score model able to predict overall survival (OS) rates in the validation datasets.
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http://dx.doi.org/10.1111/jcmm.16092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7754023PMC
December 2020

Development of methods for detecting the fate of mesenchymal stem cells regulated by bone bioactive materials.

Bioact Mater 2021 Mar 19;6(3):613-626. Epub 2020 Sep 19.

State Key Laboratory of New Ceramics and Fine Processing, School of Materials Science and Engineering, Tsinghua University, Beijing, 100084, People's Republic of China.

The fate of mesenchymal stem cells (MSCs) is regulated by biological, physical and chemical signals. Developments in biotechnology and materials science promoted the occurrence of bioactive materials which can provide physical and chemical signals for MSCs to regulate their fate. In order to design and synthesize materials that can precisely regulate the fate of MSCs, the relationship between the properties of materials and the fate of mesenchymal stem cells need to be clarified, in which the detection of the fate of mesenchymal stem cells plays an important role. In the past 30 years, a series of detection technologies have been developed to detect the fate of MSCs regulated by bioactive materials, among which high-throughput technology has shown great advantages due to its ability to detect large amounts of data at one time. In this review, the latest research progresses of detecting the fate of MSCs regulated by bone bioactive materials (BBMs) are systematically reviewed from traditional technology to high-throughput technology which is emphasized especially. Moreover, current problems and the future development direction of detection technologies of the MSCs fate regulated by BBMs are prospected. The aim of this review is to provide a detection technical framework for researchers to establish the relationship between the properties of BMMs and the fate of MSCs, so as to help researchers to design and synthesize BBMs better which can precisely regulate the fate of MSCs.
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http://dx.doi.org/10.1016/j.bioactmat.2020.08.035DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7508719PMC
March 2021

Mefloquine Inhibits Esophageal Squamous Cell Carcinoma Tumor Growth by Inducing Mitochondrial Autophagy.

Front Oncol 2020 28;10:1217. Epub 2020 Jul 28.

Department of Pathophysiology, School of Basic Medical Sciences, AMS, Zhengzhou University, Zhengzhou, China.

Esophageal squamous cell carcinoma (ESCC) has a worldwide impact on human health, due to its high incidence and mortality. Therefore, identifying compounds to increase patients' survival rate is urgently needed. Mefloquine (MQ) is an FDA-approved anti-malarial drug, which has been reported to inhibit cellular proliferation in several cancers. However, the anti-tumor activities of the drug have not yet been completely defined. In this study, mass spectrometry was employed to profile proteome changes in ESCC cells after MQ treatment. Sub-cellular localization and gene ontology term enrichment analysis suggested that MQ treatment mainly affect mitochondria. The KEGG pathway enrichment map of down-regulated pathways and Venn diagram indicated that all of the top five down regulated signaling pathways contain four key mitochondrial proteins (succinate dehydrogenase complex subunit C (SDHC), succinate dehydrogenase complex subunit D, mitochondrially encoded cytochrome c oxidase III and NADH: ubiquinone oxidoreductase subunit V3). Meanwhile, mitochondrial autophagy was observed in MQ-treated KYSE150 cells. More importantly, patient-derived xenograft mouse models of ESCC with SDHC high expression were more sensitive to MQ treatment than low SDHC-expressing xenografts. Taken together, mefloquine inhibits ESCC tumor growth by inducing mitochondrial autophagy and SDHC plays a vital role in MQ-induced anti-tumor effect on ESCC.
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http://dx.doi.org/10.3389/fonc.2020.01217DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400730PMC
July 2020

Ranolazine protects against diabetic cardiomyopathy by activating the NOTCH1/NRG1 pathway.

Life Sci 2020 Nov 21;261:118306. Epub 2020 Aug 21.

Department of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, China; Translational Medicine Research and Cooperation Center of Northern China, Heilongjiang Academy of Medical Sciences, Harbin, China; Department of Pharmacology and Therapeutics, Melbourne School of Biomedical Sciences, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Australia. Electronic address:

Aims: Diabetic cardiomyopathy (DCM) is a common diabetes complication that can cause arrhythmia, heart failure, and even sudden death. Ranolazine is an antianginal agent used to treat chronic stable angina and has been demonstrated as an effective treatment for many cardiovascular diseases. However, the mechanism by which ranolazine alleviates DCM is unclear, motivating this study investigating the effects of ranolazine in DCM.

Materials And Methods: DCM rats were treated with one of three doses of ranolazine (10, 30, and 90 mg/kg/day) for 12 weeks. B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), cysteinyl aspartate specific proteinase-3 (Caspase-3), Notch homolog 1 (NOTCH1), and Neuregulin 1 (NRG1) expression was assayed using western blot and qRT-PCR. Cardiac changes were assayed using echocardiography, CT, HE staining, and Masson's trichrome staining. TUNEL staining and flow cytometry were used to detect cell apoptosis. NOTCH1 inhibitor (DAPT) was used to explore the mechanism of ranolazine.

Key Findings: Compared with the DCM group, the ranolazine groups had no obvious weight loss and significantly decreased blood glucose levels. Ranolazine prevented diabetes-caused cardiac injury. Ranolazine also decreased the number of apoptotic cells and altered the expression of apoptosis-related mRNAs and proteins. Ranolazine-induced NOTCH1 activated NRG1 and inhibited the downstream apoptosis-related pathway, while DAPT partially inhibited ranolazine-induced NOTCH1 and NRG1 expression.

Significance: To our knowledge, this study is the first to demonstrate that ranolazine protects against DCM-induced apoptosis by activating the NOTCH1/NRG1 signaling pathway. Moreover, our study identified new mechanisms involved in DCM.
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http://dx.doi.org/10.1016/j.lfs.2020.118306DOI Listing
November 2020

Structural basis of bacterial σ -mediated transcription reveals roles of the RNA polymerase zinc-binding domain.

EMBO J 2020 07 2;39(14):e104389. Epub 2020 Jun 2.

Section of Transcription & Gene Regulation, The Hormel Institute, University of Minnesota, Austin, MN, USA.

In bacteria, σ is the flagella-specific sigma factor that targets RNA polymerase (RNAP) to control the expression of flagella-related genes involving bacterial motility and chemotaxis. However, the structural mechanism of σ -dependent promoter recognition remains uncharacterized. Here, we report cryo-EM structures of E. coli σ -dependent transcribing complexes on a complete flagella-specific promoter. These structures reveal how σ -RNAP recognizes promoter DNA through strong interactions with the -10 element, but weak contacts with the -35 element, to initiate transcription. In addition, we observed a distinct architecture in which the β' zinc-binding domain (ZBD) of RNAP stretches out from its canonical position to interact with the upstream non-template strand. Further in vitro and in vivo assays demonstrate that this interaction has the overall effect of facilitating closed-to-open isomerization of the RNAP-promoter complex by compensating for the weak interaction between σ4 and -35 element. This suggests that ZBD relocation may be a general mechanism employed by σ family factors to enhance transcription from promoters with weak σ4/-35 element interactions.
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http://dx.doi.org/10.15252/embj.2020104389DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7360974PMC
July 2020

Emodin succinyl ester inhibits malignant proliferation and migration of hepatocellular carcinoma by suppressing the interaction of AR and EZH2.

Biomed Pharmacother 2020 Aug 25;128:110244. Epub 2020 May 25.

Department of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang Province, 150081, PR China. Electronic address:

Emodin is a promising anti-cancer reagent. To improve the physicochemical and anti-cancer property, we modified its structure and get a derivative called emodin succinyl ester (ESE). Here, we investigated the effect of ESE on the suppression of hepatocellular carcinoma (HCC) and the underlying mechanism. Our results showed that ESE strongly inhibited HCC cell proliferation and migration in vitro. Further study revealed that ESE treatment decreased transcription level and protein expression of androgen receptor (AR) and enhancer of zeste homolog 2 (EZH2), two key factors interacting to promote aggressive HCC development. Conversely, overexpression of AR attenuated the inhibitory effect of ESE on EZH2 expression, and vice versa. Importantly, overexpression of AR or EZH2 could counteract ESE-suppressed cell proliferation and migration. The association of ESE-targeted AR and EZH2 with the suppression of tumorigenicity was further confirmed in xenograft and diethylnitrosamine (DEN)-induced HCC mouse models. These findings validate the therapeutic effect of ESE on HCC aggression by targeting the interaction of AR and EZH2, suggesting ESE may be a potent drug in the clinical treatment of HCC.
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http://dx.doi.org/10.1016/j.biopha.2020.110244DOI Listing
August 2020

Construction and Analysis of Human Diseases and Metabolites Network.

Front Bioeng Biotechnol 2020 30;8:398. Epub 2020 Apr 30.

College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.

The relationship between aberrant metabolism and the initiation and progression of diseases has gained considerable attention in recent years. To gain insights into the global relationship between diseases and metabolites, here we constructed a human diseases-metabolites network (HDMN). Through analyses based on network biology, the metabolites associated with the same disorder tend to participate in the same metabolic pathway or cascade. In addition, the shortest distance between disease-related metabolites was shorter than that of all metabolites in the Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic network. Both disease and metabolite nodes in the HDMN displayed slight clustering phenomenon, resulting in functional modules. Furthermore, a significant positive correlation was observed between the degree of metabolites and the proportion of disease-related metabolites in the KEGG metabolic network. We also found that the average degree of disease metabolites is larger than that of all metabolites. Depicting a comprehensive characteristic of HDMN could provide great insights into understanding the global relationship between disease and metabolites.
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http://dx.doi.org/10.3389/fbioe.2020.00398DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7203444PMC
April 2020

Characteristics of myeloid sarcoma in mice and patients with deficiency.

Oncol Lett 2020 Jun 27;19(6):3789-3798. Epub 2020 Mar 27.

Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin 300060, P.R. China.

Myeloid sarcoma (MS) carries a poor prognosis, and information on epigenetic modifications in MS is currently limited. In the present study, 214 ten-eleven translocation-2 () mice were successfully constructed. In addition, 436 patients with myelodysplastic syndrome (MDS) and 354 with acute myeloid leukemia (AML) patients were recruited. The incidence of MS in mice and patients with deficiency was examined, and the efficiency of hypomethylating agents (HMAs) was also be evaluated. A total of 93% of the mice developed myeloid malignancies, 5.5% of which were accompanied by MS (n=11). The survival of these mice ranged between 3 and 25 months. No significant difference was observed between the survival of MS and non-MS mice with loss (P>0.05). In addition, MS cells were transplantable, and their recipients exhibited myeloproliferative characteristics, such as increased white blood cell counts, monocytosis, low erythrocyte counts and hepatosplenomegaly. Their median survival duration was 94.8 days. In the clinical setting, 9.7% of MDS and 11.6% of AML patients with deficiency developed MS, which was higher compared with previous reports (1.5-9.1%). The median age of the MS patients was 44 years old. 5-Aza-2'-deoxycytidine (5-Aza-dC) reduced the incidence of MS in mice, and decitabine was a suitable treatment strategy for MS patients. These data indicate that deficiency plays a key role in MS and its prognostic significance requires further investigation. HMAs may be a useful treatment for MS patients with mutations.
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http://dx.doi.org/10.3892/ol.2020.11479DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202316PMC
June 2020

Metal-Organic Framework Membrane Nanopores as Biomimetic Photoresponsive Ion Channels and Photodriven Ion Pumps.

Angew Chem Int Ed Engl 2020 07 25;59(31):12795-12799. Epub 2020 May 25.

Beijing National Laboratory for Molecular Science, Key Laboratory of Analytical Chemistry for Living Biosystems, Institute of Chemistry, Chinese Academy of Sciences (CAS), CAS Research/Education Center for Excellence in Molecule Science, Beijing, 100190, P. R. China.

Biological ion channels and ion pumps with sub-nanometer sizes modulate ion transport in response to external stimuli. Realizing such functions with sub-nanometer solid-state nanopores has been an important topic with wide practical applications. Herein, we demonstrate a biomimetic photoresponsive ion channel and photodriven ion pump using a porphyrin-based metal-organic framework membrane with pore sizes comparable to hydrated ions. We show that the molecular-size pores enable precise and robust optoelectronic ion transport modulation in a broad range of concentrations, unparalleled with conventional solid-state nanopores. Upon decoration with platinum nanoparticles to form a Schottky barrier photodiode, photovoltage across the membrane is generated with "uphill" ion transport from low concentration to high concentration. These results may spark applications in energy conversion, ion sieving, and artificial photosynthesis.
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http://dx.doi.org/10.1002/anie.202005084DOI Listing
July 2020

Reply to the letter "GAS5/MiR-135b axis is a potential target for myocardial infarction".

Int J Cardiol 2020 07 16;311:20. Epub 2020 Mar 16.

Department of Pharmacology (State-Province Key Laboratories of Biomedicine- Pharmaceutics of China, Key Laboratory of Cardiovascular Medicine Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150081, PR China.

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http://dx.doi.org/10.1016/j.ijcard.2020.03.033DOI Listing
July 2020
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