Publications by authors named "Li-Li Shao"

13 Publications

  • Page 1 of 1

Effect of renin-angiotensin-aldosterone system inhibitors on all-cause mortality and major cardiovascular events in patients with diabetes: A meta-analysis focusing on the number needed to treat and minimal clinical effect.

J Diabetes Complications 2021 Mar 31;35(3):107830. Epub 2020 Dec 31.

Department of Epidemiology and Statistics, School of Public Health, Hebei Medical University, 361 East Zhongshan Road, Shijiazhuang 050017, China; Hebei Province Key Laboratory of Environment and Human Health, 361 East Zhongshan Road, Shijiazhuang 050017, China. Electronic address:

Aims: To assess the effectiveness of renin-angiotensin-aldosterone system (RAAS) inhibitors, angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) separately to prevent all-cause mortality, myocardial infarction (MI), stroke and heart failure (HF) in patients with diabetes considering the number needed to treat (NNT) and minimal clinical effect (MCE).

Methods: Data from 17 morbidity-mortality trials in patients with diabetes were used to calculate NNTs and evaluate MCE to prevent all-cause mortality, myocardial infarction, stroke, and heart failure.

Results: A total of 17 trials involving 42,037 patients were included in this meta-analysis. Mean follow-up was 3.7 years. ACEIs significantly reduced the risk of all-cause mortality, MI and HF; the corresponding mean NNTBs were 48, 62 and 78, respectively, but ARBs were only associated with a reduction in heart failure. The clinical significance assessment of the included trials indicated that most of the statistically significant trial results had no definitive clinical significance, and only some of them had possible clinical significance.

Conclusions: Among patients with diabetes, ACEIs reduced all-cause mortality, MI and HF, whereas ARBs could only prevent HF. However, none of the results of these trials had clear clinical significance, and most had only possible clinical significance.
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http://dx.doi.org/10.1016/j.jdiacomp.2020.107830DOI Listing
March 2021

Biological effects of chlamydiaphage phiCPG1 capsid protein Vp1 on chlamydia trachomatis in vitro and in vivo.

J Huazhong Univ Sci Technolog Med Sci 2017 Feb 22;37(1):115-121. Epub 2017 Feb 22.

Department of Dermatology and Venereology, Tianjin Medical University General Hospital, Tianjin, 300052, China.

The researches on chlamydia in recent years show that chlamydia bacteriophage may be a potential and effective means to solve the clinical infection of chlamydia trachomatis (Ct). We investigated the biological effect of chlamydiaphage phiCPG1 capsid protein Vp1 on Ct both in McCoy cells and genital tract of mice. Different concentrations of Vp1 were co-incubated with Ct E serotype strain in McCoy cells. Female BALB/c mice were used to establish Ct E strain-induced urogenital infection model. They were randomly divided into five groups and given different treatments on the fifth day after Ct inoculation. Animals in groups 1 and 2 were given 30 μL different concentrations of Vp1 in the genital tract respectively, those in group 3 were intramuscularly injected with 30 μL Vp1, those in the infected group did not receive any intervention, and those in the control group received 30 μL PBS in the genital tract. The vaginal discharge was collected to identify the live chlamydia by cell culture and gene fragment by real time PCR different days after infection. Inhibition rate of 100 μg/mL and 50 μg/mL Vp1 proteins against Ct E strain in the McCoy cell cultures was 91% and 79% respectively. The number of intracellular Ct inclusion in the McCoy cells co-cultured with vaginal discharge of group 1 and group 2 was less than in the infected group, and that in group 1 was less than in group 2, on the 7th day after Ct inoculation. Real-time PCR showed that chlamydia concentration of the vaginal discharge in group 2 was lower than in the infected group, and that in group 1 was lower than in group 2 on the 10th day. It was suggested that Vp1 capsid proteins had inhibitory effect on the proliferation of Ct serovar E strain in cell culture and mouse genital tract.
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http://dx.doi.org/10.1007/s11596-017-1704-1DOI Listing
February 2017

Could lengthening minocycline therapy better treat early syphilis?

Medicine (Baltimore) 2016 Dec;95(52):e5773

Department of Dermatovenereology, Tianjin Medical University General Hospital, Tianjin, China.

Syphilis is a sexually transmitted disease caused by Treponema pallidum. Minocycline, a representative tetracycline derivative, has the greatest antimicrobial activity among all tetracyclines. There are few reports about treating syphilis with minocycline because there is a lack of efficacy data from controlled trials. We compared the rates of serological cure in patients with early syphilis who were treated with minocycline or benzathine penicillin G (BPG).During the study period, a total of 40 syphilis patients received the BPG treatment, which was a single intramuscular dose of 2.4 million units of BPG, and 156 patients were treated with minocycline; 77 patients were placed in the 2-week, standard minocycline therapy group and received 100 mg of minocycline orally, twice daily for 14 days, and 79 patients were placed in the 4-week, lengthened minocycline therapy group and received 100 mg of minocycline orally, twice daily for 28 days. The outcome of interest was the rate of serological cure in these patients.At the end of the 2-year follow-up, the serological cure rate of the 4-week, lengthened minocycline therapy group (87.34%) was higher than that of both the 2-week, standard minocycline therapy group (72.73%) and the BPG treatment group (77.50%). In addition, the curative effect of the 4-week, lengthened minocycline therapy was significantly greater than that of the 2-week, standard minocycline therapy in patients who were aged >40 years; exhibited an initial rapid plasma reagin titer ≥1: 32; or exhibited secondary syphilis (P = 0.000, 0.008, 0.000; <0.05).Minocycline appears to be an effective agent for treating early syphilis, especially when applied as a 4-week, lengthened therapy.
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http://dx.doi.org/10.1097/MD.0000000000005773DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207593PMC
December 2016

Semaphoring mAb: a new guide in RIT in inhibiting the proliferation of human skin carcinoma.

Asian Pac J Cancer Prev 2015 ;16(3):941-5

Department of Dermatovenereology, Tianjin Medical University General Hospital, Tianjin, China E-mail :

Semaphoring is a transmembrane receptor which participates in many cytokine-mediated signal pathways that are closely related to the angiogenesis, occurrence and development of carcinoma. The present study was designed to access the effect of mono-antibody (mAb) guided radioimmunotherapy (RIT) on skin carcinoma and investigate the potential mechanisms. Semaphoring mAb was acquired from mice (Balb/c), purified with rProtein A column; purity, concentration and activity were tested with SDS-PAGE and indirect ELISA; specificity and expression on the cutanuem carcinoma line and tissue were tested by Western blotting; morphology change was assessed by microscopy. MTT assay and colony inhibition tests were carried out to test the influence on the proliferation of tumor cells; Western blotting was also carried out for expression of apoptosis-associated (caspase-3, Bax, Bcl-2) and proliferation-related (PI3K, p-Akt, Akt, p-ERK1/2, ERK1/2) proteins and analyse the change in signal pathways (PI3K/Akt and MEK/ERK). The purity of purified semaphorin mAb was 96.5% and the titer is about 1?106. Western blotting showed semaphoring mAb to have specifically binding stripes with semaphoring b1b2 protein, B16F10, and A431 cells at 39KDa, 100KDa and 130KDa, respectively. Positive expression was detected both in cutanuem carcinoma line and tissue and it mostly located in cell membranes. MMT assay revealed dose-relate and time-relate inhibitory effect of semaphorin mAb on A431 and B16F10. Colony inhibition tests also showed dose-relate inhibitory effects. Western blotting demonstrated the expression of apoptosis and proliferation-related protein and changes in signal pathway. In conclusion, we demonstrated that semaphorin is highly expressed on the tumor cell-surfaces and RIT with semaphorin mAb has effect in inhibiting proliferation and accelerating apoptosis of tumor cells.
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http://dx.doi.org/10.7314/apjcp.2015.16.3.941DOI Listing
December 2015

[Expression of TFPI-2 gene and its promoter methylation in acute myeloid leukemia].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2014 Aug;22(4):920-6

Department of Hematology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong Province, China.

The aim of this study was to detect the mRNA expression of tissue factor pathway inhibitor-2 ( TFPI-2) and its methylation in bone marrow mononuclear cells from acute myeloid leukemia (AML) patients and to explore its significance in AML. Bone marrow mononuclear cells were isolated from newly diagnosed AML patients (n = 33), complete remission AML patients (n = 19), relapsed/refractory AML patients (n = 12) and iron deficiency anemia patients (control group, n = 15). Expression of TFPI-2 mRNA was detected with real-time quantitative PCR (RT-PCR) and the methylation of CpG island in its promoter was detected with methylation-specific PCR (MSP). The results showed that the expression of TFPI-2 mRNA in newly diagnosed AML, complete remission AML and relapsed/refractory AML patients was much lower than that in the controls (P < 0.05). Furthermore, its expression in relapsed/refractory AML patients was lower than that in newly diagnosed AML patients (P = 0.006). Compared with complete remission AML patients, the expression of TFPI-2 mRNA in newly diagnosed AML patients was significantly reduced (P = 0.030). The percentage of TFPI-2 promoter methylation in AML patients was 64.63% (42/64). In newly diagnosed AML group, complete remission AML group and relapsed/refractory AML group,the percentages of TFPI-2 promoter methylation were 66.67% (22/33), 52.63% (10/19) and 83.33% (10/12) (P > 0.05), respectively. The optical density ratio of TFPI-2 mRNA expression was 0.165 (0.005-2.099) in methylated AML patients, and 0.597 (0.011-2.787) in unmethylated AML patients (P < 0.05). Methylation of TFPI-2 gene promoter was not detected in control patients. After 2 courses of chemotherapy, the level of TFPI-2 mRNA was much higher in the CR group than that in the non-CR group (P < 0.05). It is concluded that the down-regulation or silence of TFPI-2 gene potentially results from its promoter methylation, and the expression level of TFPI-2 and the methylation status of its promoter may be used as indicators of risk stratification and evaluation of disease progress.
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http://dx.doi.org/10.7534/j.issn.1009-2137.2014.04.008DOI Listing
August 2014

[One case of ascaris larva migrans].

Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi 2013 Dec;31(6):493

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December 2013

The complete mitochondrial genome of the Hybris subjacens (Neuroptera:Ascalaphidae).

Mitochondrial DNA 2014 Apr 17;25(2):109-10. Epub 2013 Apr 17.

Laboratory of Molecular Evolution and Biodiversity, College of Life Sciences, Anhui Normal University , Wuhu , P.R. China and.

The mitochondrial genome of Hybris subjacens (Neuroptera: Ascalaphidae) is a circular molecule of 15,873 bp in length, containing 37 typical animal mitochondrial genes: 13 protein-coding genes (PCGs), 2 ribosomal RNAs, 22 transfer RNAs and a non-coding AT-rich region. Its gene order and arrangement are identical to the common type found in most insect mitogenomes. All PCGs start with a typical ATN codon except for COI and ND1 which use CTT and TTG as their start codon, respectively; all PCGs terminate in the common stop codon TAA or TAG, except for the COI and ND5 which use single T as their stop codons. The non-coding AT-rich region is 1051 bp long, located between rrnS and tRNA(lle) genes. It contains some structures of repeated motifs and microsatellite-like elements characteristic of the neuropterids.
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http://dx.doi.org/10.3109/19401736.2013.786708DOI Listing
April 2014

Ischemic postconditioning mediates cardioprotection via PI3K/GSK-3β/β-catenin signaling pathway in ischemic rat myocardium.

Shock 2012 Aug;38(2):165-9

Anesthesiology Department, the First Hospital Affiliated at China Medical University, Shenyang, China.

Previous studies have shown that PI3K/GSK-3β/β-catenin signaling pathway plays a vital role in ischemic preconditioning. The present study attempts to evaluate whether PI3K/GSK-3β/β-catenin signaling pathway might be responsible for the cardioprotection in ischemic postconditioning. Male Sprague-Dawley rats underwent 30 min of left anterior descending coronary artery occlusion and 2 h of reperfusion. One hundred twenty rats were randomized into six groups: sham, ischemia/reperfusion (I/R), ischemic postconditioning (Post), 15 μg · kg wortmannin (PI3K inhibitor) plus ischemic postconditioning (Wort + Post), wortmannin plus I/R (Wort + I/R), and 0.6 mg · kg SB216763 (GSK-3β inhibitor) plus I/R (SB + I/R). Wortmannin and SB216763 were administered, respectively, 10 and 5 min before reperfusion. Myocardial infarct size; number of apoptotic cardiomyocytes; total Akt, GSK-3β; phosphorylated Akt, GSK-3β; β-catenin in cytosol and nucleus; and Bcl-2 protein were assessed. It was found that Post and SB + I/R reduced infarct size (32.3% [SD, 2.8%], 32.7% [SD, 2.1%], vs. 53.4% [SD, 3.2%], respectively, P < 0.05) and apoptotic index of cardiomyocytes (23.2% [SD, 1.8%], 23.8% [SD, 1.8%], vs. 47.3% [SD, 5.8%], respectively, P < 0.05); compared with I/R, wortmannin abolished the cardioprotection of ischemic postconditioning. Post and SB + I/R increased phosphorylated Akt, phosphorylated GSK3β, β-catenin in cytosol and nucleus, and Bcl-2 expression versus I/R. These results indicate that ischemic postconditioning could induce myocardial protection via PI3K/GSK-3β/β-catenin signaling pathway, activation of which results in accumulation of β-catenin and upregulation of its target genes Bcl-2.
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http://dx.doi.org/10.1097/SHK.0b013e31825b5633DOI Listing
August 2012

Synthesis, structure, and bioevaluation of 2,5-bis(arylmethenyl)cyclopentanones.

J Asian Nat Prod Res 2008 Sep-Oct;10(9-10):957-65

School of Pharmacy, Wenzhou Medical College, Wenzhou, China.

Curcumin is an excellent lead compound with a variety of bioactivity. Recent articles reported that curcumin's instability and low bioavailability in vivo are mainly due to its easily decomposable beta-diketone moiety. With the aim of bioactive curcumin analogs with better pharmacokinetic property, we present here 11 bis(arylmethenyl)cyclopentanones similar to curcumin and without beta-diketone moiety by reacting relevant arylaldehydes and cyclopentanones. The analogs were structurally determined by 1HNMR and MS spectra, and the crystal structure of 6 was analyzed by X-ray diffraction. Their antibacterial activities in vitro against seven Gram-positive and Gram-negative bacteria were tested, and their inhibition of TNF-alpha and IL-6 secretion in LPS-induced mouse macrophages was investigated using enzyme-linked immunosorbent assay. It was observed that several derivatives displayed higher activity when compared with curcumin, and most of the analogs exhibited activities against the ampicillin-resistant Gram-negative Enterobacter cloacae.
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http://dx.doi.org/10.1080/10286020802181257DOI Listing
March 2009

[The antitumor effect and immuno-mechanism of IL-23 in mouse mammary cancer].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2008 Sep;24(9):853-6

The Fourth Hospital, Hebei Medical University, Shijiazhuang 050011, China.

Aim: To study the antitumor effect of IL-23 in mouse mammary cancer and the change of its immune function.

Methods: IL-23/MA-891, LXSN/MA-891 and the parental MA-891 cells were inoculated in the subcutaneous tissues of mice, respectively. The mouse models were used to observe the tumorigenic activity of IL-23/MA-891 cells. On the thirtieth day, the spleens and tumors of the mice in three groups were extracted and then IFN-gamma, TNF-alpha, IL-12 and IL-4 were detected by ELISA. The expression of MHC-I, MHC-II, CD80 and CD86 in tumor cells, the ratio of positive cells of CD11c, and the selection of CD4 and CD8 in the spleens were detected by flow cytometry, respectively. CD4 and CD8 in three groups were immuno-stained and then they were examined by microscope.

Results: The tumor in the mouse inoculated with IL-23/MA891 cells developed much more slowly than that in the other two groups. Meanwhile, the spleen cells of this group secreted higher IFN-gamma, TNF-alpha and IL-12 than the other two groups (P<0.01), but the secretion of IL-4 in the three groups had no difference (P>0.05). In IL-23/MA891 group, CD4+, CD8+ lymphocytes, CD11c+ cells in spleens and infiltration of CD4+, CD8+ lymphocytes in tumor tissues were also markedly higher than those in LXSN/MA-891 and MA-891 groups (P<0.01). The expression of MHC-I, MHC-II, CD80 and CD86 in IL-23/MA-891 groups was also higher than that in the other two groups (P<0.01).

Conclusion: In the mice the antitumor effect of the mammary cancer cells transferred by IL-23 gene is obvious, which can enhance the cellular immune function and play an important role in inhibiting the growth of tumor.
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September 2008

[Inhibitory effect of IL-27 gene on tumor formation activity of Eca109 cells in nude mice and its mechanisms].

Ai Zheng 2008 Jan;27(1):12-7

Research Center, The Fourth Affiliated Hospital, Hebei Medical University/Hebei provincial Cancer Institute, Shijiazhuang, Hebei, PR China.

Background & Objective: Cytokine-based biotherapy is a hot spot in tumor research. This study was to explore the inhibitory effect of interleukin-27 (IL-27) on tumor formation activity of human esophageal carcinoma cell line Eca109 in nude mice, and investigate its antitumor mechanisms.

Methods: IL-27 gene was transfected into Eca109 cells with retrovirus vector and stable clones were selected by G418. The expression of IL-27 gene was detected by reverse transcription-polymerase chain reaction (RT-PCR). The secretion of IL-27 from Eca109/IL-27 cells and interferon-gamma (IFN-gamma) in peripheral blood mononuclear cells (PBMCs) were detected by ELISA. Cell proliferation in vitro was assessed by MTT assay. Eca109/IL-27, Eca109/LXSN and Eca109 cells were subcutaneously injected into nude mice to observe the growth of transplanted tumors. The expression of CD16 and FasL in tumor-infiltrating lymphocytes (TIL) and the expression of Fas in tumor cells were detected by flow cytometry.

Results: IL-27p28 and IL-27EBI3 were expressed in Eca109/IL-27 cells, but not in Eca109/LXSN and Eca109 cells (P<0.01). IL-27 secretion was significantly higher in Eca109/IL-27 cells than in Eca109/LXSN and Eca109 cells (P<0.01). The proliferation rates of the 3 cell lines were similar (P> 0.05). IFN-gamma secretion was significantly higher in Eca109/IL-27 cell-stimulated PBMCs than in Eca109/LXSN cell-and Eca109 cell-stimulated PBMCs [(56.28+/-1.61) pg/mL vs. (12.70+/-0.82) pg/mL and (11.06+/-0.64) pg/mL, P<0.01]. As compared with those in Eca109 and Eca109/LXSN groups, the tumor growth in nude mice was significantly slower in Eca109/IL-27 group (P<0.05), the expression of CD16 and FasL in TIL and the expression of Fas in tumor cells were up-regulated in Eca109/IL-27 group (P<0.05).

Conclusion: IL-27 gene may inhibit the tumor formation activity of Eca109 cells in nude mouse by activating natural killer (NK) cells through Fas/FasL pathway.
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January 2008

Safety and efficacy of oral nonsteroidal anti-inflammatory drugs in patients with rheumatoid arthritis : a six-month randomised study.

Clin Drug Investig 2004 ;24(2):89-101

Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China.

Objective: To monitor the safety and efficacy profile of long-term treatment with diclofenac, nabumetone, meloxicam and celecoxib in patients with rheumatoid arthritis.

Design And Methods: This randomised, prospective clinical trial included a total of 461 subjects (313 females and 148 males) with clinically diagnosed rheumatoid arthritis. Their average age was 46.9 +/- 14.4 years (range 20-69 years), and the average disease duration was 1333.7 +/- 992.85 days. Subjects were randomly assigned daily administration of one of the following: diclofenac 75-100mg, meloxicam 15mg, nabumetone 1000mg or celecoxib 200mg. During the 6-month treatment period, a monthly patient interview was conducted to evaluate drug efficacy and safety.

Results: 407 subjects successfully completed the 6-month treatment. Sixteen patients (12.2%) withdrew from the diclofenac group, 16 (12.2%) from the nabumetone group, 17 (11.8%) from the meloxicam group and five (9.1%) from the celecoxib group. Most withdrawals occurred during the first 3 months of treatment. Reasons for withdrawals in the first three groups were lack of efficacy (44.9%) and adverse effects (38.8%). For the celecoxib group, high cost (80%) was the main reason for withdrawal. Adverse drug reactions to NSAIDs mostly occurred at an early stage of treatment, with an incidence rate of 31.9% for the diclofenac group, 19.9% for the nabumetone group, 25.2% for the meloxicam group, and 7.27% for the celecoxib group. Clinical efficacy rates for the four NSAIDs were positively related to the length of treatment. During the first 4 months, diclofenac, meloxicam and celecoxib showed better efficacy than nabumetone. There were no significant differences in efficacy during the fifth and sixth months. The overall 6-month effectiveness rates were 68.8% for diclofenac, 59.8% for nabumetone, 67.6% for meloxicam and 69.1% for celecoxib.

Conclusions: Adverse drug reactions and their related withdrawals occurred mostly at an early stage of NSAID treatment, so it is crucial to strengthen pharmacovigilance during this period. Among the investigated NSAIDs, celecoxib did not prove to be superior to diclofenac, nabumetone or meloxicam with respect to its efficacy in the treatment of rheumatoid arthritis; however, it did show good patient compliance and safety profiles.
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http://dx.doi.org/10.2165/00044011-200424020-00004DOI Listing
October 2012

[Clinic experience in treating two cases].

Authors:
Li-Li Shao

Zhong Xi Yi Jie He Xue Bao 2003 Sep;1(3):170, 176

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http://dx.doi.org/10.3736/jcim20030306DOI Listing
September 2003
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