Objective To analyze functioning and disability, unmet needs and the service for people with disabilities in Shenzhen, Guangdong, China. Methods Based on International Classification of Functioning, Disability and Health (ICF) and World Report on Disabil-ity, the theoretical framework had been constructed, and the unmet needs and service status for people with disabilities in Shenzhen in 2015 had been statistically analyzed. Results For the statistics of disability by categories, physical disability composed of 42.5%, speech disability composed of 1.5%;people with severe and extremely severe disabilities composed of 52.8%;Futian District composed of 19.7%, Yantian District composed of 2.2%;people aged 0 to 18 years composed of 17.4%, and people aged over 60 years (27.0%) were the larger group. For the unmet needs of people with disabilities, 25%needed rehabilitation therapy, 18.8%needed functional training, 23.2%needed assis-tive devices, and 32.9%had no need. For rehabilitation sevice in Shenzhen, 24.4%received rehabilitation therapy, 17.4%received function-al training, 20.4%received assistive devices, and 37.6%did not receive any service. For the barrier-free reconstruction, 4.6%needed bath-room reconstruction, and 0.7%needed internet access screen software. Conclusion The status of functioning and disability, unmet needs and service development of rehabilitation in Shenzhen had been analyzed. There was still a gap between unmet needs and services of rehabilita-tion. It recommended to construct precise services delivery based on unmet needs, improve the full coverage and quality of service of reha-bilitation.

Colorectal cancer (CRC) is a common malignancy burdening people globally, with increasing morbidity and mortality nowadays, due to the alternation in the diet type and lifestyle in modern society. Berberine, a type of benzylisoquinoline alkaloid, is widely present in numerous medicinal plants, particularly including Coptidis Rhizoma. Mounting evidence reveals that berberine possesses an array of pharmacological effects, such as anti-inflammation, anti-bacterium, anti-cancer, anti-diabetes mellitus and so on. In particular, berberine exhibits substantial inhibition on various types of cancers including CRC. Hereby, we sought to systematically review the suppressive effect of berberine on CRC through the diminishment of the proliferation and metastasis, induction of apoptosis, arrest of cell cycle, regulation of inflammatory reaction, the reverse of chemotherapeutic resistance and restoration of gut microbiota in CRC, so as to shed light on the in-depth mechanisms underlying the treatment of CRC with berberine in the clinical setting.

BACKGROUND: Studies have confirmed that monosialotetrahexosyl ganglioside can induce human umbilical cord mesenchymal stem cells to differentiate into neuron-like cells, but little is reported on its optimal concentration. OBJECTIVE: To explore the optimal concentration of monosialotetrahexosyl ganglioside that induces human umbilical cord mesenchymal stem cells to differentiate into neuron-like cells in vitro. METHODS: Human umbilical cord mesenchymal stem cells were isolated by using collagenase digestion method, and after expansion, passage 3 cells were randomly allocated into five groups. When 70%-80% of cells were confluent, 50, 100, 150 and 200 mg/L monosialotetrahexosyl ganglioside induction solutions were added in corresponding experimental groups, while cells in the blank control group were cultured in the same volume of L-DMEM medium. Cell morphology was observed under inverted phase contrast microscope. Expression levels of microtubule-associated protein 2, neurofilament protein and glial fibrillary acidic protein were measured by using immunohistochemistry at 6 hours after induction. RESULTS AND CONCLUSION: Human umbilical cord mesenchymal stem cells were isolated successfully and sub-cultured stably. These cells could express surface markers of mesenchymal stem cells. Monosialotetrahexosyl ganglioside at the optimal concentration of 150 mg/L was confirmed to induce the neuron-like differentiation of human umbilical cord mesenchymal stem cells, and differentiated cells could express microtubule-associated protein 2 and neurofilament protein as neuron-specific markers.

OBJECTIVETo evaluate the efficacy and safety of Capsule metadoxine in the treatment of alcoholic liver disease.

METHODSA randomized double blind multicenter placebo-controlled clinical study was performed to evaluate the therapeutic effectiveness and safety of capsule metadoxine. Patients in metadoxine group received capsule metadoxine 500mg tid po. Patients in placebo group received placebo 2 pillows tid po. The treatment duration was 6 weeks. Patients were followed up 2 weeks after the treatment. Patients were visited once every 3 weeks during the treatment period. Clinical symptoms and liver function were evaluated in all the patients before treatment, at week 3, week 6 and 2 weeks after therapy. CT scan was done in some patients before treatment and at the end point of therapy.

RESULTS254 patients were recruited in the study, 126 in metadoxine group and 128 in placebo group. Median ALT, AST, GGT level in metadoxine group were decreased from 80.0 U/L, 59.2 U/L, 123.0 U/L (before treatment) to 41.1 U/L, 36.0 U/L, 57.0 U/L (after 6 weeks therapy). The improvement in liver function was more significant in metadoxine group than in placebo group (P less than 0.05). For the patients who stopped drinking during the study, the total effective rate of improvement in liver function was 82.8% in metadoxine group, much higher than that in placebo group (55.7% , P=0.0000). For the patients who did not stop drinking during the study, the total effective rate of improvement in liver function was 65.4% in metadoxine group, which is not significantly higher than that in placebo group (44.8%, P=0.1767). The CT value ratio of liver to spleen was significantly improved in metadoxine group (P=0.0023), and there was no significant difference between the two groups (P=0.6293). The rate of adverse was 1.6% in both of groups.

CONCLUSIONCapsule metadoxine is an effective and safe treatment for alcoholic liver disease.

Administration, Oral ; Adult ; Aged ; Alanine Transaminase ; blood ; Alcohol Deterrents ; administration & dosage ; therapeutic use ; Analysis of Variance ; Aspartate Aminotransferases ; blood ; Capsules ; Double-Blind Method ; Drug Combinations ; Fatty Liver, Alcoholic ; blood ; drug therapy ; pathology ; Female ; Follow-Up Studies ; Humans ; Liver ; diagnostic imaging ; pathology ; Liver Diseases, Alcoholic ; blood ; drug therapy ; pathology ; Liver Function Tests ; Male ; Middle Aged ; Pyridoxine ; administration & dosage ; therapeutic use ; Pyrrolidonecarboxylic Acid ; administration & dosage ; therapeutic use ; Treatment Outcome ; Ultrasonography ; Young Adult ; gamma-Glutamyltransferase ; blood

OBJECTIVESTo observe the role of PPARgamma during the activation process of hepatic stellate cells (HSC).

METHODSBy morphology and RT-PCR, we study the changes of expression of PPARgamma in culture-activated HSC or in vivo activated HSC induced by dimethylnitrosamine (DMN).

RESULTSIn vitro, the expression level of PPARgamma in freshly isolated HSC (0.72+/-0.01) significantly reduced to 0.48+/-0.03 on the third day of culture (t = 19.8372, P<0.01), and reduced 70% on the seventh culture-day and could not be detected after the second passage. In vivo, HSC freshly isolated from normal control rats expressed PPARgamma (0.76+/-0.01). During the development of rat liver fibrosis induced by DMN, the expression level significantly reduced to 0.46+/-0.02 after the third injection of DMN (t = 29.5318, P<0.01), and reduced 66% on the end of first week and could not be detected on the end of second and third week.

CONCLUSIONThe expression of PPARgamma might play an important role on the maintenance of resting-form of HSC, and the reduction of expression of PPARgamma might be an early event during the activation process of HSC.

Animals ; Liver ; cytology ; Liver Cirrhosis ; etiology ; pathology ; Male ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear ; physiology ; Transcription Factors ; physiology

OBJECTIVESTo investigate the effect of magnesium isoglycyrrhizinate on the proliferation and oxidative stress of rat hepatic stellate cells (HSCs).

METHODSThe effect of various concentrations of maganesium isoglycyrrhizinate on the proliferation of primary rat HSCs and HSCs strains were measured by making cell growth curves and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphennylterazolium bromide (MTT) colorimetric assay. Morphological changes of the rat HSCs were also studied. After rat HSCs were incubated with various concentrations of maganesium isoglycyrrhizinate and ferric nitrilotriacetate (Fe-NTA) for 24 hours, the activity of superoxide dismutase (SOD) and contents of malondialdehyde (MDA) in supernates were measured to observe the effect of magnesium isoglycyrrhizinate on the oxidative stress of rat HSCs.

RESULTSCompared with the control group, the proliferation of rat HSCs was significantly inhibited when the concentration of magnesium isoglycyrrhizinate in the medium reached a certain level range. In the oxidative stress induced by Fe-NTA, magnesium isoglycyrrhizinate, within a certain strength range, obviously enhanced the activity of SOD and decreased the contents of MDA in supernates of rat HSCs culture media.

CONCLUSIONSMagnesium isoglycyrrhizinate could significantly inhibit the proliferation of rat HSCs and it, within a certain strength range, exert protective effects in the oxidative stress induced by Fe-NTA.

Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Hepatocytes ; cytology ; Male ; Malondialdehyde ; metabolism ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Saponins ; pharmacology ; Superoxide Dismutase ; metabolism ; Triterpenes ; pharmacology

OBJECTIVE To investigate the therapeutic effect of scutellarin on colitis-associated cancer (CAC) and its underlying mechanism based on Wnt/β-catenin signaling pathway. METHODS The mouse model of CAC was estab?lished by azomethane oxide (AOM) and sodium dextran sulfate (DSS), followed by scutellarin treatment, with recording the body weight, diarrhea and hematochezia. After sacrificing the mice, the colorectal length and colorectal tumor were assessed. The levels of pro-inflammatory factors TNF-α and IL-6 in mice's sera were measured by the enzyme-linked immunosorbent assay (ELISA). The colorectal lesions were appraised by hematoxylin and eosin (H&E) staining. Theβ-catenin level in CAC tissues was probed by immunofluorescent analysis. The apoptosis-related genes Bax and Bcl-2, and Wnt signaling pathway-related genes β-catenin, GSK-3β, TCF4, c-Myc and cyclin D1 were detected by real-time quantitative RT-PCR (RT-qPCR). Finally, Western blotting analysis (WB) was employed to examine the expressions of the apoptosis and Wnt signaling pathway-related proteins. RESULTS Scutellarin significantly improved AOM/DSS-caused weight loss, colorectal length shortening, and tumor growth in mice (P<0.01). Meanwhile, colorectal lesions could be substantially alleviated by scutellarin. ELISA results showed that the levels of pro-inflammatory factors TNF-αand IL-6 were drastically lessened (P<0.01). Scutellarin also sharply inhibited the nuclear translocation of β-catenin, as evidenced by the reduction in the nuclear level ofβ-catenin protein. In addition, scutellarin attenuated the mRNA expres?sion of Wnt signaling pathway-relatedβ-catenin, TCF4, c-Myc and cyclin D1, whereas it heightened GSK-3βmRNA level. These results were consolidated by WB analysis, which indicated that scutellarin could mitigate the protein levels of phospho-GSK-3β,β-catenin, TCF4, c-Myc and cyclin D1, with the increase in GSK-3β protein in CAC tissue. Moreover, scutellarin could induce the apoptosis of CAC, demonstrated by enhanced expression of Bax and diminished expression of Bcl-2 in both mRNA and protein levels. CONCLUSION Scutellarin may ameliorate colitis-associated colorectal cancer by weakening Wnt/β-catenin signaling cascade.

Objective To explore the existence of natural loci on Marmota himalayana plague in Sichuan province and to provide basis for prevention and control of the disease. Methods Both epidemiological investigation and laboratory tests were used to provide the host animal and fleas of the vectors with Yersinia pestis carriers. Results 30 species of animals were found to belong to 10 orders. Ochotona curzoniae and M.himalayana were the most common ones while 7 species of the fleas belonged to 7 genera and 3 families. M.himalayana was the main reservoirs while Callopsylla dolabris and Oropsylla silantiewi served as vectors. The 13 Y.pestis were identified from 43 Marmota samples. 8 samples were identified under IHA, with the highest titer of herding-dogs serum as 1 : 10 240. 19 samples were F1 antigen positive using RIHA and the highest titer of M.himalayana serum was 1:409 600. The major foci was 4545 km2, distributed at Dege county in Sichuan province. Conclusion We have confirmed the existence of natural foci on M. Himalayana plague in Sichuan province.

We evaluated the role of IL-10- in IL-33-mediated cholesterol reduction in macrophage-derived foam cells (MFCs) and the mechanism by which IL-33 upregulates IL-10. Serum IL-33 and IL-10 levels in coronary artery disease patients were measured. The effects of IL-33 on intra-MFC cholesterol level, IL-10, ABCA1 and CD36 expression, ERK 1/2, Sp1, STAT3 and STAT4 activation, and IL-10 promoter activity were determined. Core sequences were identified using bioinformatic analysis and site-specific mutagenesis. The serum IL-33 levels positively correlated with those of IL-10. IL-33 decreased cellular cholesterol level and upregulated IL-10 and ABCA1 but had no effect on CD36 expression. siRNA-IL-10 partially abolished cellular cholesterol reduction and ABCA1 elevation by IL-33 but did not reverse the decreased CD36 levels. IL-33 increased IL-10 mRNA production but had little effect on its stability. IL-33 induced ERK 1/2 phosphorylation and increased the luciferase expression driven by the IL-10 promoter, with the highest extent within the −2000 to −1752 bp segment of the 5′-flank of the transcription start site; these effects were counteracted by U0126. IL-33 activated Sp1, STAT3 and STAT4, but only the STAT3 binding site was predicted in the above segment. Site-directed mutagenesis of the predicted STAT3-binding sites (CTGCTTCCTGGCAGCAGAA→CTGCCTGGCAGCAGAA) reduced luciferase activity, and a STAT3 inhibitor blocked the regulatory effects of IL-33 on IL-10 expression. Chromatin immunoprecipitation (CHIP) confirmed the STAT3-binding sequences within the −1997 to −1700 and −1091 to −811 bp locus regions. IL-33 increased IL-10 expression in MFCs via activating ERK 1/2 and STAT3, which subsequently promoted IL-10 transcription and thus contributed to the beneficial effects of IL-33 on MFCs.
Binding Sites ; Cholesterol ; Chromatin Immunoprecipitation ; Computational Biology ; Coronary Artery Disease ; Foam Cells* ; Humans ; Interleukin-10* ; Interleukin-33* ; Luciferases ; Macrophages* ; Mutagenesis, Site-Directed ; Phosphorylation ; RNA, Messenger ; Transcription Initiation Site

Adolescent ; Adult ; Aged ; Blood Banks ; legislation & jurisprudence ; Blood Donors ; legislation & jurisprudence ; Child ; Female ; Hepatitis C ; epidemiology ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Young Adult