Objective:To study the protective effect of glucagon-like peptide-1 (GLP-1) on the inflammatory damage induced by high glucose(HG) in placental trophoblasts HTR8/SVneo and its molecular mechanism.Methods:Trophoblasts HTR8/SVneo cells were cultured and divided into low glucose(LG) group treated with low glucose (5 mmol/L), HG group treated with high glucose (25 mmol/L), GLP-1 group treated with high glucose combined with GLP-1, miR-137+ GLP-1 group treated with high glucose combined with GLP-1 after the transfection of miR-137 mimic, miR-137 mimic group transfected with miR-137 mimic, negative control (NC) mimic group transfected with NC mimic, and miR-137 inhibitor group transfected with miR-137 inhibitor, NC inhibitor group transfected with NC inhibitor. Apoptotic rate, expression of miR-137 and IL-6 were measured.Results:The apoptotic rate and the expression levels of miR-137 and IL-6 in HG group were significantly higher than those in LG group. The apoptotic rate and the expression levels of miR-137 and IL-6 in GLP-1 group were significantly lower than those in HG group. The apoptotic rate and the expression levels of miR-137 and IL-6 in miR-137+ GLP-1 group were significantly higher than those in GLP-1 group. The apoptotic rate and the expression level of IL-6 in miR-137 mimic group were significantly higher than those of NC mimic group, the apoptotic rate and the expression level of IL-6 in miR-137 inhibitor group were significantly lower than those in the NC inhibitor group.Conclusion:GLP-1 is able to alleviate the inflammation injury of HTR8/SVneo induced by high glucose through the miR-137/IL-6 pathway.

China ; Humans ; Industry ; Pneumoconiosis

Gastrointestinal neuroendocrine tumor(GI-NET)originates from peptide neurons and neu-roendocrine cells in gastrointestinal tract,and secrets peptide hormones,leading to carcinoid syndrome which rarely happens in clinical practice. Because of the improvement of diagnostic method and understanding of this rare disease,the morbidity is rising in recent years. The main treatments of GI-NET are surgery and compre-hensive therapy,consisting of chemotherapy and targeted therapy.

The teaching secretary of clinical department at medical university is required to be passionate,devoted,qualified and good at writing.The position is reserved for the person with healthy psychology,who knows well to deal with people,political training and sensitivity,advanced qualification.

Objective To study the immunosuppression mechanism induced by ultraviolet (UV) and cis-urocanic acid. Method The auto lymphocyte proliferation test with Langerhans＇ cell (LC) in guinea -pig was performed. Results In exposure to low dose of UVB (25 J/m2) radiation, the inhibition rate of lymphocyte proliferation stimulated by LC was 10. 5%, the inhibition rates of UVB radiation in doses of 50 J/m2 and 100 J/m2 were 22.4% or 50%, respectively. The lymphocyte proliferation was almost completely suppressed by200J/m2 UVB radiation, while the inhibition of LC function by cis-urocanic acid was weak. Conclusion UVB significantly inhibits LC auto -stimulation in dose -dependent way, which may play an important role in UVB induced immunosuppression.

Laboratory animal welfare is an important guarantee for the accuracy and reliability of experimental results, so it has been paid attention in scientific research .But the situation is not optimistic in the teaching practice .This paper has specially analyzed laboratory animal welfare and ethics in experiment teaching and provided specific measures involved in legislation , spread of animal welfare and implementation of 3R principle to ensure animal welfare .

Objective To study the immunosuppression mechanism induced by ultraviolet (UV) and cis urocanic acid. Method The auto lymphocyte proliferation test with Langerhans′ cell (LC) in guinea-pig was performed. Results In exposure to low dose of UVB (25 J/m2) radiation, the inhibition rate of lymphocyte proliferation stimulated by LC was 10.5％ , the inhibition rates of UVB radiation in doses of 50 J/m2 and 100 J/m2 were 22.4％ or 50％ , respectively. The lymphocyte proliferation was almost completely suppressed by 200 J/m2 UVB radiation, while the inhibition of LC function by cis urocanic acid was weak. Conclusion UVB significantly inhibits LC auto-stimulation in dose-dependent way, which may play an important role in UVB induced immunosuppression.

The incidence of locally recurrent rectal cancer is about 10%. Most patients have serious symptoms after tumor recurrence, which seriously affects the quality of life and prognosis of patients. Although it is more difficult to perform reoperation, it is still the main method to treat local recurrence of rectal cancer. At present, the main methods of reoperation include transabdominal anterior resection, combined pelvic organ resection, combined pelvic organ resection, and sacral resection. Open surgery is the main method. In recent years, with the extensive development of laparoscopic technology, laparoscopic techniques have been tried at home and abroad to perform reoperations for locally recurrent rectal cancer, showing good short-term results. The authors systematically introduce the application of laparoscopic technology in the reoperation of locally recurrent rectal cancer based on relevant research advances at home and abroad, in order to explore its clinical application prospects and promotion value.

Objective To assess the value of magnetic resonance imaging for acute pancreatitis.Methods 77 patients of acute pancreatitis were examined with holding breath MRI sequence.Transverse scan:2D Flash T 1WI/T 1W+FS,TSE T 2WI+FS or HASTE+FS,Trufisp.Coronals scan:2D Flash T 1W+FS.MRCP was used in 34 patients.2D Flash dynamic contrast enhanced were used in 77 patients.Results 59 cases of acute edematous pancreatitis showed swelling and low signal intensity on T 1WI and higher signal intensity on T 2WI.Excepted the above findings,18 cases of hemorrhagic necrosis pancreatitis alos showed the higher signal intensity on T 1WI and peripancreatic exudative hydrops.Conclusion MRI is a reliable method for demonstrating acute pancreatitis.

Objective To observe the effect of nicotine(NIC) on the activation and resultant death of microglia induced by LPS. Methods The animal model that exposed to chronic nicotine treatment was established and LPS was injected intraperitoneally to induce the activation of microglia. Furthermore, the CD11b-positive microglia in cerebral cortex, hippocampal and substantia ngra were observed through immunohistochemical staining. BV2 cells(Microglial cell line of mouse) were subcultured, simultaneously the following kits were used including CCK-8 kit assay for cell activity, Nitric oxide assay kit assay for NO release, RT-PCR assay for the iNOS,TNF-α,IL-1β,IL-6,COX-2,IRF-1,Caspase-11 mRNA expression, Western blotting assay for the protein expression of P-I-κB and Caspase-3. Results Nicotine suppressed the CD11b-positive microglia expression in cerebral cortex,hippocampal and substantia ngra induced by LPS;Nicotine inhibited the activation-induced cell death (AICD), attenuated NO release, reduced iNOS,TNF-α,IL-1β,IL-6,COX-2,IRF-1,Caspase-11 mRNA expression, decreased the protein expression including P-I-κB and Caspase-3 of BV2 cells. Conclusion Nicotine pretreatment can suppress the activation and resultant death of microglial cells induced by LPS, which suggests that nicotine may play a neuroprotective role on inflammatory reaction of brain.;