Cerebrospinal Fluid Rhinorrhea ; surgery ; Endoscopy ; methods ; Female ; Humans ; Male

Objective To investigate the role of glargine in glucose metabolism improvement and antiinflammation of skeletal muscle in Caveolin-1 silenced type 2 diabetic mice.Methods Multiple low doses of streptozotocin (STZ) intraperitoneal injection and high-fat high-glucose (HFHG) were used to induce type 2 diabetic mice model.The mice were divided into normal control group (NC group) and type 2 diabetic model group (T group).Then according to virus injection and glargine treatment,T group were further divided into type 2 diabetes group (T2DM group),type 2 diabetes with insulin treatment group (insulin group),Caveolin-1 silenced with insulin treatment group (LV-CAV1 group),and scramble virus with insulin treatment group (LV-GFP group).Glucose metabolism was accessed by the fluctuation of blood glucose.TNF-α protein expression in skeletal muscle was detected by Western blot.Results The glycemic control of LV-CAV1 group needed more dosages of glargine (P ＜ 0.05).The expression of TNFαin skeletal muscle was elevated in LV-CAV 1 group than that in LV-GFP and insulin group (P ＜ 0.05).Conclusion The anti-inflammation function and glycemic metabolism improvement of glargine may be associated with the expression of Caveoin-1 in skeletal muscle.

Objective To investigate the relationship between blood glucose levels and severity of coronary stenosis in hypertensive patients. Methods Blood pressure, fasting plasma glucose, 2 h plasma glucose, clinical features and coronary angiographic findings were analyzed retrospectively in 540 patients with essential hypertension. Acoording 2 h plasma glucose, patients were stratified into three group: group 1: 2h plasma glucose

Animals ; Chlorine Compounds ; toxicity ; Dose-Response Relationship, Drug ; Female ; Lung ; drug effects ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; biosynthesis ; genetics ; Tumor Necrosis Factor-alpha ; biosynthesis ; genetics

The aim was to construct and identify the mammalian expression vector of pCAG-IRES-SHIP-GFP and to detect whether it could express in human acute leukemia cell line K562.The cDNA fragment of SHIP obtained by RT-PCR was inserted into pCAG-IRES-GFP.The recombinant plasmid was confirmed by restriction enzyme digesiton,PCR and DNA sequecing.pCAG-IRES-SHIP-GFP was transfected into K562 cells with lipofectamine 2000.The expression of SHIP was determined by GFP fluorescence and Western blot analysis.FQ-PCR was used to quantitate SHIP mRNA.The expression of p-Akt,Akt were determined by Western blot.PI were tested by flow cytometry and MTT to verify whether exogenous SHIP could inhibit proliferation of K562 cells.The results showed that the correct constrution of the recombinant plasmid pCAG-IRES-SHIP-GFP has been shown by restriction enzyme digestion,PCR and DNA sequencing.pCAG-IRES-SHIP-GFP could express SHIP protein in K562 cells.The K562 cells viability after transfected with SHIP gene droped down.Western blot analysis showed that phospha-Akt308 and Akt473 were reduced to 38.7% and 68% respectively.It was concluded that the vector of pCAG-IRES-SHIP-GFP has been successfully constructed and it can be expressed in K562 cells.The expression of exogenous SHIP gene can lead to apoptosis of K562 cells by down-regulating the p-Akt expression.What found here might be one of the mechanisms involved in the pathogenesis of leukemia.

Leprosy is a chronic granulomatous infection caused by Mycobacterium leprae, which primarily affects the skin and peripheral nerves. In this article, we present a 45-year-old man and a 39-year-old women who suffered from asymptomatic irregular erythemas on their trunk and extremities. Since both patients denied the history of exposure to leprosy patients and were absent clinical signs of superficial sensation dysfunction and enlarged peripheral nerves, they were diagnosed of mycosis fungoides and livedo reticularis clinically. Nevertheless the biopsies of erythemas showed perineural and periadnexal foamy-cell granulomas in the dermis and Fite staining revealed a large number of acid-fast bacilli. A diagnosis of multibacillary leprosy was made finally. These cases revealed that since leprosy is still epidemic in some remote area in China and in other developing countries and its clinical manifestations may be very weird sometimes, the dermatologists should be alert of it and skin biopsy could confirm the diagnosis.
Adult ; Erythema ; pathology ; Female ; Humans ; Leprosy, Multibacillary ; diagnosis ; pathology ; Male ; Middle Aged

Objective To study the protective effect of GYY4137 on rat myocardial cells infected by Coxsackie virus B3 (CVB3) and its signal transduction mechanism.Methods Cardiomyocytes were treated with different concentrations of GYY4137(10,50,100 μmol/L) for 24 hours before addition of 100 TCID50 CVB3 for 2 hours before serum-free conditions.After treatment,the cell viability was ascertained with Cell Counting Kit-8 (CCK-8) assay.At the same time,the levels of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β),interleukin-6 (IL-6) in the supernatants were analyzed by enzyme-linked immunosorbent assay (ELISA).Western blot was used to study the expression of nuclear factor kappa-B (NF-κB) protein and the inhibitory subunit of (IκBα) in myocardial cells.Results After exposure of cardiomyocytes to GYY4137 with different concentration (10,50,100 μmol/L)for 24 hours cell viability had no change.The NF-κB expression and the levels of TNF-α,IL-1β,IL-6 [(175.80 ± 5.05) ng/L,(25.80 ± 1.97) ng/L,(65.33 ± 3.51) ng/L] in the GYY4137-treated CVB3 infection group were significantly reduced when compared with untreated CVB3 infection group (P ＜ 0.01),respectively.Compared with the normal group,the GYY4137 concentration-dependently restrained the CVB3-mediated IκBα degradation(P ＜ 0.01).Conclusions GYY4137 exerts anti-inflammatory effects in CVB3-infected cardiomyocytes.This anti-inflammatory mechanism may be associated with suppression of the activation of the NF-κB.

Objective To provide the anatomical basis for the flap based on the perforator of Plantar arch,through investigation of the morphological features of the perforator of the arch of the foot.Methods From November,2015 to March,2016,the first metatarsal base and the fifth metatarsal tuberosity were chosen as the observation point on 25 specimens of adult human feet perfused with red latex.The following contents were observed under surgical magnifier:①The origin,courses,branches and distribution of the perforator of Plantar arch.②The anastomoses among the perforator of Plantar arch and the fete arteriosum dorsale pedis.Mimic operation was performed on another fresh specimen perfused with red latex.Results There were 3 perforators in Plantar arch,which passed through the 2nd-4th metatarsal dorsal muscles to the dorsi pedis and then divided into an ascending branch and a descending branch.The ascending branch anastomosed with the rete arteriosum dorsale pedis,and the descending branch stretched to the 2nd-4th plantar arteries.The initiative outer diameters of the 1st-3rd dorsal perforators of Plantar arch were (1.5 ± 0.3)mm,(1.1 ± 0.4) mm and (0.9-± 0.3) mm respectively,and the lengths of the stem were (1.1 ± 0.2) cm,(1.5 ± 0.1) cm and (1.5 ± 0.5) cm respectively.Conclusion The flap can be used for repair of soft-tissue defects of dorsal and front foot through dorsal transposition or a V-Y advancing flap with the perforator of Plantar arch as its vascular pedicle.

Objective To synthesize N-(4-fluorophenyl)-N-(4-phenoxyphenyl) cyclopropane-1,1-dicarboxamide (NFNPDB) as small molecular c-Met kinase inhibitor analogue.Methods N-( 4-fluorophenyl )-N-( 4-phenoxyphenyl ) cyclopropane-1, 1-dicarboxamide was synthesized by nucleophilicsubstitution, amidation, etherification, reduction and condensation from diethyl malonate.Results The total yield of target compound was 3.79%, its structure was confirmed by 1 H-NMR.Conclusion The synthesis method of NFNPDB in our research can be easily operated with lost cost and short direction, which lays the foundation for designing the synthetic process of newly small molecular c-Met kinase inhibitor.

Objective To investigate the level and value of serum IgE, anti-IgE, FcεRⅠα, anti-FcεRⅠin autoimmune liver disease ( AILD) .Methods In this case-control study, the serum samples and clinical data of 77 patients with hepatosis were collected between May and November 2014 from the department of gastroenterology of Shanghai First People′s Hospital.These patients had positive results about the liver-related autoimmune antibodies, including 33 cases of AILD, 44 cases of other chronic liver disease. 64 healthy persons were collected as control group.Serum mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠwere detected by Enzyme-linked Immuno sorbent Assay ( ELISA) .Serum IgE, IgM and IgG were detected by rate scatter nephelometry.Differences among AILD, other chronic liver disease and healthy control were assessed.Results were compared using Mann-Whitney U test.Results Mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠin liver-related autoimmune antibodies positive patients were significantly higher than healthy control [1.74(1.16 -2.88)mg/L, 14.86(4.39 -26.23)mg/L, 47.22(36.89 -55.29)mg/L and 1.23(0.95-1.58)mg/L, 1.87(1.52-2.33)mg/L, 35.40(24.74-44.89)mg/L, respectively;U=1614,556.5,1319.5, P<0.01].FcεRⅠαwas significantly higher in other chronic liver disease patients than AILD patients [18.40(7.35-30.64)mg/L and 6.25(2.49-22.29), respectively;U=445, P<0.01] .Conclusion Mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠwere increased in liver-related autoimmune antibodies positive hepatosis patients.However, FcεRⅠαwas lower in AILD than other chronic liver disease.Mast cell-associated anti-IgE、FcεRⅠαand anti-FcεRⅠ molecules involved in the inflammatory lesion of liver disease.