Objective To explore the effect of insulin injection and protamine biosynthetic human insulin injection on basal insulin level in pregnant women with diabetes mellitus.Methods Retrospective analysis of 89 cases of pregnant women with diabetes mellitus from January 2013 to May 2016 in department of obstetrics and gynecology,tianjin red bridge hospital,the patients were divided into group A (n=38 cases) and group B (n=51 cases),the group A treatment with insulin injection,the group B treatment with protamine biosynthetic human insulin injection,compare the two groups of patients before and after treatment of three meals a day rate of blood glucose compliance, treatment compliance and satisfaction.Results Before treatment, there was no significant difference in the blood glucose compliance rate between the two groups before and after treatment;After treatment,the blood glucose compliance rate of two groups was significantly higher than before treatment ( P<0.05 ) , there was no significant difference in the compliance rate of fasting blood glucose between two groups,the compliance rate of blood glucose before dinner in group A was 81.58%,significantly higher than that in group B 60.78%(P<0.05).Conclusion Both insulin injection and protamine biosynthetic human insulin injection can maintain the basic insulin levels of pregnant women with diabetes mellitus,insulin injection can better control the blood glucose levels before dinner,with higher compliance and satisfaction.The compliance rate and satisfaction rate of pregnant women in group A were 97.37% and 97.37%,which were significantly higher than those in group B 82.35% and 80.39%(P<0.05).

This review analyzed domestic and foreign literatures on intestinal absorption,introduced the current methods and models commonly used in phenolic glycosides researches and their impacts focused on intestinal absorption,summarized the research status,aims to provide a reference for improving their oral bioavailability,improve formulations,new medicine and clinical rational use of phenolic glycosides.

Objective To analyze the clinical characteristic of Chinese autoimmune pancreatitis (AIP) patients.Methods All clinical data of 81 patients with a diagnosis of AIP in Shanghai Changhai Hospital from February 2005 to May 2012 were analyzed.Results The sex ratio was 7.1∶1 and the mean age was (57± 12) years old in 81 patients with AIP.Obstructive jaundice was the initial symptom in 51.9％ (42/81) patients.In patient receiving CT,focal and diffuse type accounted for 45 and 35 patients.respectively,and pseudocyst was the main manifestation in 1 patient,biliary tract was involved in 59(72.8％ ) patients,dilatation of main pancreatic duct was observed in 5 ( 11.1％ ) patients.In patients receiving PET-CT,diffuse increased Flourine-18 FDG uptake by the pancreas was found in 11 patients,focal increased uptake in 2patients,and significant extra-pancreatic uptake was found in 5 patients.The positive rate of serum IgG4,CA19-9,ss DNA,anti-nuclear antibody and ds-DNA antibody was 94.6％ (53/81),54.4％ (37/68),14.3％ (4/28),10.7％ (3/28),7.1％ (2/28),respectively.The pathological findings of H-E staining and IgG4 immunohistochemical analysis in 20 patients were consistent with lymphoplasmacytic sclerosing pancreatitis.Conclusions Type 1 AIP is the main subtype of AIP in China.Combining clinical symptoms,extra-pancreatic manifestations,imaging or nuclear medicine findings,serology,cytology or histology can effectively increase the correct diagnosis rate of AIP.

Objective To evaluate the role of PI3K∕Akt signaling pathway in dexmedetomidine-in-duced reduction of lung ischemia-reperfusion ( I∕R ) injury in rats undergoing cardiopulmonary bypass (CPB). Methods Twenty-four healthy adult male Sprague-Dawley rats, weighing 350-450 g, were di-vided into 3 groups (n＝8 each) using a random number table method: group I∕R, dexmedetomidine group ( group D) and dexmedetomidine plus wortmannin group (group D+W). Rats were anesthetized with pento-barbital sodium. Lung I∕R was induced by clamping the left hilum of lung for 60 min starting from 10 min of CPB, followed by 120-min reperfusion. Dexmedetomidine was injected via the tail vein in a dose of 3 μg∕kg at 10 min before clamping the left hilum of lung, followed by a continuous infusion of 1. 5 μg·kg-1·h-1 until the end of CPB in group D. Dexmedetomidine was injected via the tail vein in a dose of 3 μg∕kg at 10 min before clamping the left hilum of lung, followed by a continuous infusion of 1. 5 μg·kg-1·h-1until the end of CPB, and wortmannin was simultaneously injected via the tail vein in a dose of 15 μg∕kg, fol-lowed by a continuous infusion of 2. 0 μg·kg-1·min-1until the end of CPB in group D+W. Arterial blood samples were collected immediately before CPB ( T1), immediately after opening the left hilum of lung (T2) and at 1. 5 h after the end of CPB (T3), and oxygenation index (OI) and respiratory index (RI) were calculated. The rats were sacrificed at T3, and the left lung was removed for examination of the patho-logical changes which were scored and for determination of apoptosis rate ( by flow cytometry) and Akt, Bad, activated caspase-3, phosphorylated Akt ( p-Akt) and phosphorylated Bad ( p-Bad) in lung tissues ( by Western blot). Results Compared with the baseline at T1, OI was significantly decreased and RI was increased at T2and T3in the three groups (P＜0. 05). OI was significantly decreased and RI was increased at T3than at T2in the three groups ( P＜0. 05). Compared with group I∕R, OI was significantly increased and RI was decreased at T3, the pathological damage score and apoptosis rate were decreased, ratios of p-Akt∕Akt and p-Bad∕Bad were increased, and the expression of activated caspase-3 was down-regulated in group D, and OI was significantly decreased and RI was increased at T2in group D+W ( P＜0. 05). Com-pared with group D, OI was significantly decreased and RI was increased at T3, the pathological damage score and apoptosis rate were increased, ratios of p-Akt∕Akt and p-Bad∕Bad were decreased, and the ex-pression of activated caspase-3 was up-regulated in group D+W ( P＜0. 05). Conclusion Dexmedetomi-dine can reduce dexmedetomidine-induced reduction of lung I∕R injury through activating PI3K∕Akt signa-ling pathway and inhibiting cell apoptosis in rats undergoing CPB.

Objective: To investigate the influence of miR-520a-3p on paclitaxel (TAX) sensitivity of non-small cell lung cancer (NSCLC)A549/TAX cells via regulating frizzled class receptor 8 (FZD8). Methods: NSCLCA549 cells, TAX-resistant cell lineA549/ TAX and human lung epithelial HLF-α cells were selected. The expression level of miR-520a-3p in A549 and A549/TAX cells was detected by qPCR. According to different transfection plasmids, the experimental cells were divided into control group, miR-520a-3p mimics group, si-FZ8 group and si-FZD8+miR-520a-3p inhibitor group. After being treated with 6 μmol/L paclitaxel, the proliferation ofA549/TAX cells was determined by CCK-8 assay. Flow cytometry withAnnexin V-FLTC/PI staining was used to detect the apoptosis level of A549/TAX cells. The expression of FZD8 in A549/TAX cells was detected by WB. The targeting relationship between miR520a-3p and FZD8 was verified by the dual-luciferase reporter gene system. Results: miR-520a-3p was poorly expressed in TAX-resistant A549/TAX cells (P<0.01), and TAX up-regulated the expression of miR-520a-3p in A549/TAX cells (P<0.01). After the treatment with 6 μmol/L TAX, over-expression of miR-520a-3p significantly inhibited the proliferation of A549/TAX cells and promoted apoptosis (all P<0.01). Dual luciferase reporter gene assay showed that miR-520a-3p targetedly down-regulated the expression of FZD8 (P< 0.01). si-FZD8 could significantly inhibit the proliferation and promote cell apoptosis of A549 / TAX cells, thereby enhancing the TAX sensitivity of cells. At the same time, simultaneous knockdown of miR-520a-3p and FZD8 could reverse the enhancement of FZD8 knockdown on TAX sensitivity of A549/TAX cells (P<0.01). Conclusion: miR-520a-3p enhances the TAX sensitivity of A549/TAX cells by down-regulating the expression of FZD8.

Emerging evidence suggests that intron-detaining transcripts (IDTs) are a nucleus-detained and polyadenylated mRNA pool for cell to quickly and effectively respond to environmental stimuli and stress. However, the underlying mechanisms of detained intron (DI) splicing are still largely unknown. Here, we suggest that post-transcriptional DI splicing is paused at the Bact state, an active spliceosome but not catalytically primed, which depends on Smad Nuclear Interacting Protein 1 (SNIP1) and RNPS1 (a serine-rich RNA binding protein) interaction. RNPS1 and Bact components preferentially dock at DIs and the RNPS1 docking is sufficient to trigger spliceosome pausing. Haploinsufficiency of Snip1 attenuates neurodegeneration and globally rescues IDT accumulation caused by a previously reported mutant U2 snRNA, a basal spliceosomal component. Snip1 conditional knockout in the cerebellum decreases DI splicing efficiency and causes neurodegeneration. Therefore, we suggest that SNIP1 and RNPS1 form a molecular brake to promote spliceosome pausing, and that its misregulation contributes to neurodegeneration.
Spliceosomes/metabolism* ; Introns/genetics* ; RNA Splicing ; RNA, Messenger/genetics* ; Cell Nucleus/metabolism*

Objective To investigate the effect of LAG-3 deficiency (LAG3^-/-) on natural killer (NK) cell function and hepatic fibrosis in mice infected with Echinococcus multilocularis. Methods C57BL/6 mice, each weighing (20 ± 2) g, were divided into the LAG3^-/- and wild type (WT) groups, and each mouse in both groups was inoculated with 3 000 E. multilocularis protoscoleces via the hepatic portal vein. Mouse liver and spleen specimens were collected 12 weeks post-infection, sectioned and stained with sirius red, and the hepatic lesions and fibrosis were observed. Mouse hepatic and splenic lymphocytes were isolated, and flow cytometry was performed to detect the proportions of hepatic and splenic NK cells, the expression of CD44, CD25 and CD69 molecules on NK cell surface, and the secretion of interferon γ (IFN-γ), tumor necrosis factor α (TNF-α), interleukin (IL)-4, IL-10 and IL-17A. Results Sirius red staining showed widening of inflammatory cell bands and hyperplasia of fibrotic connective tissues around mouse hepatic lesions, as well as increased deposition of collagen fibers in the LAG3-/-group relative to the WT group. Flow cytometry revealed lower proportions of mouse hepatic (6.29% ± 1.06% vs. 11.91% ± 1.85%, P < 0.000 1) and splenic NK cells (4.44% ± 1.22% vs. 5.85% ± 1.10%, P > 0.05) in the LAG3^-/- group than in the WT group, and the mean fluorescence intensity of CD44 was higher on the surface of mouse hepatic NK cells in the LAG3^-/- group than in the WT group (t = −3.234, P < 0.01), while no significant differences were found in the mean fluorescence intensity of CD25 or CD69 on the surface of mouse hepaticNK cells between the LAG3^-/- and WT groups (both P values > 0.05). There were significant differences between the LAG3^-/- and WT groups in terms of the percentages of IFN-γ (t = −0.723, P > 0.05), TNF-α (t = −0.659, P > 0.05), IL-4 (t = −0.263, P > 0.05), IL-10 (t = −0.455, P > 0.05) or IL-17A secreted by mouse hepatic NK cells (t = 0.091, P > 0.05), and the percentage of IFN-γ secreted by mouse splenic NK cells was higher in the LAG3^-/- group than in the WT group (58.40% ± 1.64% vs. 50.40% ± 4.13%; t = −4.042, P < 0.01); however, there were no significant differences between the two groups in terms of the proportions of TNF-α (t = −1.902, P > 0.05), IL-4 (t = −1.333, P > 0.05), IL-10 (t = −1.356, P > 0.05) or IL-17A secreted by mouse splenic NK cells (t = 0.529, P > 0.05). Conclusions During the course of E. multilocularis infections, LAG3^-/- promotes high-level secretion of IFN-γ by splenic NK cells, which may participate in the reversal the immune function of NK cells, resulting in aggravation of hepatic fibrosis.