As a pleiotropic cytokine, interleukin-6 (IL-6) participates in many physiological activities in vivo. IL-6 plays an important role in the physiology and pathology of chronic inflammation, autoimmune diseases, tumors and other diseases through diverse mechanisms. At present, inhibitors targeting IL-6/IL-6R have been shown to improve treatments for some inflammatory diseases such as rheumatoid arthritis and systemic juvenile idiopathic arthritis. IL-6 binds to a specific receptor to activate the downstream JAK/STAT3 signaling pathway. However abnormally activated STAT3 often appears in various types of malignant tumors and participates in the occurrence and development of tumors. In addition, studies have shown that IL-6 is a key factor in the cytokine storm associated with COVID-19 patients. The physiological participation of IL-6/STAT3 pathway in complex diseases makes this pathway become a research hotspot for drug discovery. Therefore, we summarize the latest research progress of small molecular inhibitors on IL-6/STAT3 signaling pathway, in order to provide a reference for the development of IL-6/STAT3 related drug in the future.

OBJECTIVETo investigate the therapeutic effects of peptide YY against hepatic fibrosis in rats and explore the possible mechanism.

METHODRat models of hepatic fibrosis were established with a subcutaneous injection of carbon tetrachloride and randomized into normal control group, model group, peptide YY (PYY)-treated group, octreotide-treated group, and interferon gamma-treated group. Serum levels of the hepatic function indices and hepatic fibrotic index were detected, and the hepatic fibrosis grade was assessed using HE staining. The expression of transforming growth factor beta1 (TGFbeta1) were determined with immunohistochemical staining method.

RESULTSThe rats in PYY-treated group showed significantly different serum levels of TBIL, HA and LN from the rats in the model group (P<0.05). PYY significantly reduced hepatic fibrosis scores and lowered TGFbeta1 expression as compared with the model group.

CONCLUSIONSPYY can down-regulate TGFbeta1 expression to inhibit the development of hepatic fibrosis with comparable efficacy with interferon gamma and octreotide.

Animals ; Carbon Tetrachloride ; Immunohistochemistry ; Liver Cirrhosis, Experimental ; chemically induced ; drug therapy ; metabolism ; Male ; Peptide YY ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; biosynthesis

Adult ; Aluminum Silicates ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Occupational Exposure ; adverse effects ; statistics & numerical data ; Quartz ; adverse effects ; analysis ; Silicosis ; epidemiology ; mortality

Objective To investigate the effect of two different odontoblast inducer on the proliferation and apoptosis of rat adiposed-derived stem cells.Methods Adiposed-derived stem cells were collected by enzyme digestion from inguinal fat pads of 4 days post natal mice.Immunocytochemistry was performed to identify the cells.MTT and flow cytometry were tested the prolifera-tion and apotosis of adiposed-derived stem cells by co-cultured with tooth germ cell conditioned medium(TGC-CM)or dentin non-collagenous protein medium (DNCPM).Results Cells displayed a fibroblast-like appearance and positively expressed CD44 and CD105 when cufured to the secend yeneration.After 3 day the cells polarity changed by co-cultured.Count of cells were no obvious change by TGC-CM co-cultured,while that ruduced significantly by DNCPM co-cultured.It confirmed that the proliferation rate of ADSCs in TGC-CM group and control group is higher than DNCPM group(P <0.05),while the apotosis of that in DNCPM group is higher TGC-CM group(P <0.05).Compared with control group,the results had no significant difference(P >0.05).Conclusion TGC-CM may have more advantage as inducer in rat adiposed-derived stem cells differentiate into dentin like cells than DNCPM.

Background and purpose: Researches demonstrated that the butyric acid sodium salt (sodium butyrate, NaB) has effect on the inhibition of tumor cell proliferation, differentiation and apoptosis-promoting, while the mechanism on salivary adenoid cystic carcinoma(SACC) is still uncertain. This study mainly probed into the impact of different concentration of sodium butyrate on the migration and invasion of SACC cell line ACC-M, and its mechanism of action. Methods:MTT assay explored the optimal concentration of sodium butyrate on the cell ACC-M and the observation of cell growth. Transwell assay was used to detect the effects of sodium butyrate on the ACC-M cells on the aspact of invasion and migration ability. Fluorescence real-time quantitative PCR (RT-PCR) and Western blot were used to test respectively the expression of HMGB1, TLR4 mRNA and protein in ACC-M after functioned by 5 group drugs with different concentrations. Results:Compared with the control group, on the one hand, the concentration 0.625, 1.25, 2.5, 5 and 10 mmol/L of sodium butyrate could effectively inhibit cell proliferation and apparently showing concentra-tion-dependence (P<0.05);On the other hand, 5 sets concentration of sodium butyrate could also effectively inhibit invasion and migration ability of ACC-M cells in vitro (P<0.05), as well as reducing the expression of HMGB1, TLR4 mRNA and protein in ACC-M cells (P<0.05). Furthermore related analysis showed that the decline of TLR4 protein expression was positively correlated with inhibition of HMGB1 (r=0.810, P<0.05). Conclusion:Sodium butyrate has an effect on inhibiting ACC-M cell proliferation, signiifcantly reducing ACC-M cell invasion and migration capabilities, and reducing expression of HMGB1, TLR4 mRNA and protein, and both expression amount are positively correlated, Meanwhile the positively correlation suggests that sodium butyrate probably achieve the inhibition ability by lowering the expression of HMGB1, TLR4 mRNA and protein in ACC-M cell.

Objective To observe the effect of sodium butyrate on the invasion and migration of human salivary gland ade‐noid cystic carcinoma cell line ACC‐2 in vitro and to investigate the underlying mechanisms .Methods The cultured ACC‐2 cells were treated with different concentrations of sodium butyrate for 24 h ,and detected the viability rate of the cells by methyl thiazolyl tetrazolium(MTT) assay ;the drug′s influence on invasion and migration on ACC‐2 were detected by Transwell experiment ,while the protein and mRNA expression of HMGB1 and TLR4 explored by Western‐blot and RT‐PCR assay ;the relationship between TLR4 expression and HMGB1 was investigated .Results Compared with control group ,0 .625 ,1 .250 ,2 .500 ,5 .000 ,10 .000 mmol/L groups of sodium butyrate inhibited the proliferation of ACC‐2 cells(P<0 .05);the influence of sodium butyrate on the in‐vasion of ACC‐2 cells of all groups had no significant difference(P>0 .05);only 2 .500 ,5 .000 and 10 .000 mmol/L groups inhibited ACC‐2 cells migration and down‐regulated the protein and mRNA of HMGB1 and TLR4(P<0 .05) .Correlation analysis showed a positive correlation between the TLR4 protein and HMGB1 protein(r=0 .810 ,P<0 .05) .Conclusion Sodium butyrate could inhib‐it ACC‐2 cells proliferation and high concentration gropes inhibit ACC‐2 cells migration ,while reducing HMGB1 and TLR4 mRNA and protein expression ,suggesting that NaB might inhibite ACC‐2 cells migration through down‐regulated the mRNA and protein expression .

Objective To investigate the effects of mirror visual feedback (MVF) and electromyographic biofeedback (EMGBF) on upper extremity function in hemiplegic patients after stroke based on task-oriented training. Methods 90 patients with hempiplegia after stroke were randomly divided into control group (n=30), EMGBF group (n=30) and MVF group (n=30). All patients accepted routine rehabilitation and task-oriented training once a day for 8 weeks. The EMGBF group also accepted EMGBF, and the MVF group accepted MVF in addition. They were assessed with Fugl-Meyer Assessment (FMA) and the Upper Extremity Function Test (UEFT), and their integrated electromyogram (iEMG) of affected upper extremities were recorded before and after treatment. Results All the groups improved in scores of FMA and UEFT, as well as the iEMG after treatment (P<0.05), and ranked as the MVF group, the EMGBF group and the control group from improving more to less (P<0.05). Conclusion Mirror visual feedback combined with electromyographic biofeedback may further promote the recovery of upper limb function in patients with hemiplegia after stroke based on task-oriented training.

AlM:To discuss the protective effect ofα-mangostin on retinal light damage in mice.METHODS:Totally 30 Balb/c mice, aged 6~8wk, were randomly divided into the control group, light-exposure group and α-mangostin group. Every group contained 10 mice. Mice of α-mangostin group were treated with alpha-mangostin at the dose of 30mg/( kg · d ) body weight by intragastric administration daily for 7d, and then exposed to white light at the 5th d. The light-exposure group and α-mangostin group were exposed to 5 000 ± 200lx white light-emmiting diodes (LEDs) for continuously 1h to establish the mice model of retinal light damage. Flash -electroretinograme was recorded 72h after light exposure. The changes in retinal morphology of mice were observed by light microscopy. Retinas were extracted to detect the malondialdhyde ( MDA ) content change of the retinal homogenate.RESULTS: Flash-electroretinogram ( F-ERG ) showed that retinal dysfunction was less severe in α-mangostin group than in light-exposure group ( P<0. 05 ). Light microscopy test showed that retina structural damage was less severe in α-mangostin group than in light-exposure group (P<0. 05). The level of MDA in retinal tissue of α-mangostin group was significantly lower when compared with light-exposure group (P<0. 05).CONCLUSlON: α-mangostin inhibits lipid peroxidation induced by light damage and protect retina against light damage.

Objective To study sleep characteristics in patients with temporal lobe epilepsy (TLE) through polysomnography (PSG). Methods Twenty-five TLE patients (TLE group) and eighteen healthy volunteer subjects (control group) were recruited to our study. Patients of two groups were evaluated by whole-night PSG, including total time in bed (TIB), total sleep time (TST), sleep efficiency (SE), sleep latency (SL), rapid eye movement latency (REML), wake after sleep onset (WASO), the percentages of non-REM (NREM) 1, 2 and 3 stages and the percentages of rapid eye movement (REM) occupied TST (N1％, N2％, N3％and REM％), the apnea-hypopnea index (AHI), hypopnea index, mean oxygen saturation (SpO2) and nadir SpO2, periodic leg movements (PLMs) index and PLMs index of REM sleep, sleep stage shifts (SSS) and sleep stage shifts per hour (SSS/h), NREM1, NREM2, NREM3 and REM sleep stage and wake shifts (abbreviated as N1, N2, N3, REM and W) and their proportions of SSS (abbreviated as N1/SSS, N2/SSS, N3/SSS, REM/SSS and W/SSS). Results Compared with control group, WASO, PLMs, PLMs index of REM sleep, SSS, SSS/H and N2 were significantly increased in TLE group. Moreover, compared with control group, SpO2 was decreased in TLE group (P<0.05). Conclusion Our results suggest that TLE patients have sleep disorder manifested as disorder of sleep structure, increased incidents of respiratory and motion events.

OBJECTIVETo investigate the epidemiological features of the pathogens responsible for prostatitis in the Changshu area, and offer some evidence for the clinical treatment of prostatitis.

METHODSThis study included 2 306 cases of prostatitis that were all clinically confirmed and subjected to pathogenic examinations in 3 hospitals of Changshu area from 2008 to 2012. Neisseria gonorrhoeae, mycoplasma urealyticum and chlamydia trachomatis were detected by nucleic acid amplification ABI 7500, the bacterial data analyzed by VITEK-2 Compact, the drug-resistance to antibacterial agents determined using the WHONET 5.6 software, and the enumeration data processed by chi-square test and curvilinear regression analysis using SPSS 19.0.

RESULTSThe main pathogens responsible for prostatitis were found to be Staphylococcus haemolyticus (30%), Staphylococcus epidermidis (12%), Enterococcus faecalis (9%), Escherichia coli (6%), Staphylococcus warneri and Staphylococcus aureus (3%), Mycoplasma urealyticum (8%), chlamydia trachomatis (5%) and Neisseria gonorrhoeae (6%). Statistically significant increases were observed in the detection rates of Escherichia coli (chi2 = 17.56, P<0.05), Mycoplasma urealyticum (chi2 = 8.73, P<0.05), Chlamydia trachomatis (chi2 = 8.73, P<0.05) and Enterococcus (chi2 = 8.22, P<0.05), but not in other pathogens. The resistance rates of Gram-positive bacteria to erythromycin and benzylpenicillin G were both above 45%, but with no significant difference between the two, those of Oxacillin (chi2 = 10.06, P<0.05) and Cefoxitin (chi2 = 9.89, P<0.05) were markedly increased, but those of quinolones, gentamycin and clindamycin remained low, except rifampicin (chi2 = 11.09, P<0.05). The resistance rates of Gram-negative bacteria to cefazolin and ampicillin were relatively high (mean 57.3%), and those to ceftriaxone (chi2 = 11.26, P<0.05) and trimethoprim sulfamethoxazole (chi2 =11.00, P< 0.05) significantly high; those to amikacin, cefepime, piperacillin/tazobactam and imipenem remained at low levels with no significant changes. However, the resistance rates of mycoplasma urealyticum to ciprofloxacin (chi2 = 11.18, P<0.05) and azithromycin (chi2 = 9.89, P<0.05) were remarkably increased.

CONCLUSIONGram-positive bacteria are the major pathogens responsible for prostatitis, but Escherichia coli, enterococcus and sexually transmitted disease pathogens are found to be involved in recent years. Quinolones and aminoglycosides are generally accepted as the main agents for the treatment of Gram-positive bacterial infection. However, rational medication for prostatitis should be based on the results of pathogen isolation and drug sensitivity tests in a specific area.

Anti-Bacterial Agents ; pharmacology ; Drug Resistance, Bacterial ; Gram-Negative Bacteria ; drug effects ; Gram-Positive Bacteria ; drug effects ; Humans ; Male ; Prostatitis ; epidemiology ; microbiology