Objective To investigate the expression changes of the protein tyrosine phosphatase receptor T (PTPRT) in temporal lobe epileptic foci in the experimental animals and epileptic patients and the relationship between PTPRT and epileptogenesis.Methods After getting the epilepsy lobe tissue from the experimental and control groups,immunohistochemistry,immunofluorescence and Western blot analysis were used to assess the expression of PTPRT and its changes.Results In the temporal lobe tissue of intractable patients and control group,PTPRT was mainly expressed in the neurons.PTPRT was significantly increased in patients with intractable epilepsy (0.277 ± 0.048) than that in the control group(0.171 ±0.025 ; t =9.586,P ＜ 0.05).PTPRT was mainly expressed in the neurons in the temporal lobe brain tissue of the rats in the control group and experimental group.Compared with control group,the expression of PTPRT in the temporal lobe tissue was increased within 24 h post-seizure,and decreased 1 and 2 weeks post-seizure,then it was increased 1 and 2 months post-seizure (A ratio:control 0.443 ± 0.039,6 h 0.840±0.032,24 h 1.113 ±0.064,7 d 0.564 ±0.039,14 d 0.570 ±0.029,30 d 0.899 ±0.034,60 d 1.011 ± 0.074,F =256.427,P ＜ 0.05).Conclusions Through researches into the expression and function of PTPRT in the temporal lobe brain tissue of patients with intractable epilepsy and animal models,we presume that the PTPRT plays a role in the synapses reorganization and mossy fiber sprouting,and participates in the reconstruction of the neural network which leads to the intractable epilepsy.

OBJECTIVETo express and purify the protein coded by the TRAF-type zinc finger domain of myasthenia gravis (MG)-related gene P9 (P9-ZFD) and to prepare P9-ZFD antiserum for detecting expression and subcellular distribution of P9-ZFD protein in the skeletal muscles of patient with MG.

METHODSThe cDNA encoding P9-ZFD was amplified by RT-PCR. The cloned P9-ZFD cDNA was ligated into pET24a, and the P9-ZFD recombinant protein was induced via E. coli. BL21 (DE3) and purified by histidine affinity chromatography. P9-ZFD antiserum was prepared and its titer and specificity were determined by ELISA and Western blot. Expression and subcellular distribution of P9-ZFD protein in the skeletal muscles of MG and control were studied.

RESULTSThe molecular weight of purified P9-ZFD protein was about 30 kD. Its purity was more than 95%. Antiserum specific for P9-ZFD was excellent. P9-ZFD protein is fully confined to the cytoplasm membrane of skeletal muscle cell of MG, obvious immunostaining was absent in the A, I, and Z bands of cytoplasm and no immunoreactivity was observed in the skeletal muscle cell of control.

CONCLUSIONP9-ZFD protein is expressed as a cytoplasm membrane-bound protein and has obvious distribution difference in the skeletal muscle cells of patient with MG and normal control.

Adult ; Cell Membrane ; metabolism ; Escherichia coli ; metabolism ; Female ; Humans ; Muscle Proteins ; biosynthesis ; genetics ; Muscle, Skeletal ; metabolism ; pathology ; Myasthenia Gravis ; metabolism ; Peptide Fragments ; biosynthesis ; genetics ; Recombinant Proteins ; biosynthesis ; genetics ; Transfection ; Zinc Fingers

Objectives To analysis the main characteristics and changes of the internal death in pediatric intensive care unit (PICU) in the past five years. Methods The clinical data of 330 death cases in PICU internal medicine were retrospectively analyzed from January 2008 to December 2012. Results The mortality rate in PICU dropped from 5.85%to 3.96% from 2008 to 2012. Among 330 death cases, 136 cases (41.2%) were infants, 73 cases (22.1%) were toddlers, 51 cases (15.45%) were preschoolers, and 70 cases (21.21%) were school-age and adolescence. In different years, the differences of distribution of death in different age groups were statistical significance (χ2=6.90, P=0.009). In all years, the infant had the highest death rate. As the time progresses, the death rate of the infant and young children decreases, while the death rate of the school-age and adolescence increases. Among the diseases caused death, the cardiovascular disease was the most common disease (33.94%), followed by hematologic malignancy (31.52%). The difference of distribution of the diseases caused death in different age group was statistically significant (P<0.01). The cardiovascular disease was main cause of death in infant, and the hematologic malignancy was the main cause of death in other three age groups. Within 24 h admission, the pediatric critical illness score (PCIS) had been assessed, 67.49% was critical and 15.48%was extremely critical. The hospitalization time was negatively correlated with PCIS (r=-0.313, P<0.001). Conclusions In the past five years, the mortality in PICU declined year by year. Cardiovascular disease in infancy and hematologic malignancy in non infancy are the leading cause of death in children. Admission in critical or extremely critical condition is the reason of early death in hospital.

Objective To report 11 cases with the tissue defects of their upper or lower limbs repaired with the anastomsed medial sural artery perforator flaps.Methods The free medial sural artery perforator flaps,with length of 8 cm to 15 cm and width of 6 cm to 14 cm were used for tissue defect reconstruction of the distal upper or lower limbs in 11 cases,including 6 females and 5 males.The flap was harvested from the ho- mo-lateral calf,confined between the posterior-medial edge of the tibia and the middle line of the calf and a- bove the distal half part of the medial sural muscle,with a same axis of this muscle.Results Ten cases survived very well,which was relatively thin,and the donor site can be acceptable.One case resulted in a complete flap necrotized and covered with a split skin graft.No obvious motor function defect was observed of the donor leg.Conclusion The anastomsed medial sural artery perforator flap is alternative donor flap for the upper or lower limb tissue defect repair,especially for the defect in the hand or foot.

OBJECTIVE: To elucidate the correlation between CKLF-like marvel transmembrane domain containing member (CMTM5) gene and the risk of in-stent restenosis (ISR) with coronary artery disease (CAD) patients and to detect the effects and mechanisms of CMTM5-stimulated genes on human vascular endothelial cells (ECs) proliferation and migration. METHODS: A total of 124 hospitalized patients in Shijitan Hospital were enrolled in this study. All the CAD patients were detected with platelet reactivity and grouped into two groups according to platelet reactivity; ISR was conformed by coronary angiography; RT-PCR method was used to detect CMTM5 gene expression; The CMTM5 over expression, reduction and control EC lines were established; Cell count, MTT, Brdu and flow cytometry methods were used to detect the proliferation of ECs, scratch and transwell experiments to test the migration of ECs, Western blot was used to detect signal path expressions. RESULTS: CMTM5 gene expression in HAPR (High on aspirin platelet reactivity) group was 1.72 times compared with No-HAPR group, which was significantly higher than No-HAPR group. HAPR group ISR rate was 25.8% (8 cases), the incidence of No-HAPR ISR group was 9.7% (9 cases), and the results showed that in HAPR group, the incidence of ISR was significantly higher than that in No-HAPR group (P=0.04, OR=0.04, 95%CI=1.16－7.52), which showed that CMTM5 gene was significantly correlated with the risk of ISR. In HAPR group ISR rate was 25.8% (8 cases), the incidence of ISR in No-HAPR group was 9.7% (9 cases), and the results showed that the risk of ISR in HAPR group was significantly higher than that in No-HAPR group. All the results showed that CMTM5 was significantly correlated with the risk of ISR in CAD patients (P < 0.05). CMTM5 overexpression inhibited the proliferation and migration ability of ECs (P < 0.05), PI3K/Akt signaling pathways were involved in the role of regulation on ECs. CONCLUSION Our results revealed that CMTM5 gene was closely related with ISR, CMTM5 overexpression may repress ECs proliferation and migration through regulating PI3K-Akt signaling.
Chemokines ; Coronary Artery Disease/surgery* ; Coronary Restenosis ; Drug-Eluting Stents/adverse effects* ; Endothelial Cells ; Humans ; MARVEL Domain-Containing Proteins ; Phosphatidylinositol 3-Kinases ; Tumor Suppressor Proteins

OBJECTIVE: To elucidate the correlation between CKLF-like MARVEL transmembrane domain containing member 5 (CMTM5) gene and the risk of coronary artery disease (CAD), and to detect the effects of CMTM5 gene expression changes on the ability of adhesion and migration of THP-1 cells. METHODS: Using case-control method, a total of 700 hospitalized patients in Shijitan Hospital were enrolled in this study. CAD were diagnosed by coronary angiography, which was defined as at least one blood vessel diameter stenosis ≥50% according to the result of coronary angiography. Reverse transcription-polymerase chain reaction (RT-PCR) method was used to detect CMTM5 gene expression; enzyme linked immunosorbent assay (ELISA) method to detect the plasma level of CMTM5; and Logistic regression to analyze CMTM5 genes and the risk of CAD. Human vascular endothelial cells (ECs) and THP-1 cells were cultivated, adhesion and Transwells experiments were used to evaluate the chemotactic capabi-lity of CMTM5 gene on THP-1 cells. RESULTS: In this study, 350 CAD patients matched with 350 control patients were included. RT-PCR results revealed CMTM5 mRNA expression in CAD group was 3.45 times compared with control group, which was significantly higher than that in control group (P < 0.05). The levels of CMTM5 plasma protein in CAD group was (206.1±26.9) μg/L, which was significantly higher than that in control group (125.3±15.2) μg/L (P < 0.05). After adjusted for the risk factors of age, gender, BMI, smoking, hypertension, diabetes and hyperlipidemia, Logistic regression analysis results indicated that CMTM5 was the susceptibility factors of CAD, which still had significant correlation with CAD (P < 0.05). Adhesion and Transwells experiments results revealed that the numbers of adhesion and migration of THP-1 cells in CMTM5 overexpression ECs group (EO group) were significantly higher than that in lenti-mock infected ECs group (EO-MOCK group), non-infected ECs group (EN group), lenti-mock infected ECs group (ES-MOCK group), and CMTM5 suppression ECs group (ES group). On the contrary, the numbers of adhesion and migration of THP-1 cells in ES group were significantly lower than that in the other four groups (P < 0.01). CONCLUSION CMTM5 gene was closely related to the development of CAD. CMTM5 overexpression promoted the adhesion and migration of THP-1, which might play a part in the mechanisms of atherosclerosis and CAD.
Chemokines ; Coronary Angiography ; Coronary Artery Disease/genetics* ; Endothelial Cells ; Humans ; MARVEL Domain-Containing Proteins ; Tumor Suppressor Proteins

Objective To analyze the outcome of childhood B-cell acute lymphoblastic leukemia treated (ALL) with SCMC-ALL-2005 protocol. Methods Newly diagnosed B-cell ALL from May 1, 2005 to April 30, 2009 in ifve hospitals were treated and followed up according to SCMC-ALL-2005 protocol. Results A total of 601 cases with newly diagnosed B-cell ALL were enrolled. Among them, 539 cases (89.68%) were followed up until September 30, 2011. In 601 patients, there were 284 low-risk cases (LR group), 231 moderate-risk cases (MR group) and 86 high-risk cases (HR group) which were treated with SCMC-ALL-2005 protocol. The total complete remission rate during the period of induction was 98.84%and 7 cases did not achieve complete remission. The median time of the ifrst event occurring was 35 months (2.94 years). Among 539 cases completing follow-up, 403 cases (74.77%) completed treatment including 223 cases (86.43%) in LR group, 150 cases (73.17%) in MR group and 30 cases (39.47%) in HR group. The rate of cases completing treatment was signiifcantly different among three groups (P=0.001). The completion rate was highest in LR group and lowest in HR group. The 3-year overall survival (OS) rate was (83.3±1.8)%, and the 3-year EFS (event-free survival) rate was (79.2±1.9)%using a Kaplan-Meier method. The 5-year OS rate was (79.5±3.3)%, and the 5-year EFS rate was (70.9±3.7)%. There were signiifcant differences in 3-year EFS rate and 5-year EFS rate among three groups (P<0.05). Conclusions Childhood B-ALL treated with SCMC-ALL-2005 protocol achieved a better therapeutic effect and prognosis. The multi-center collaborative research is useful for the standard treatment of ALL.

Animals ; Captopril ; pharmacology ; Heart Failure ; metabolism ; Male ; Myocytes, Cardiac ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; bcl-2-Associated X Protein ; metabolism

Background: Mast cell activation is a characteristic of irritable bowel syndrome (IBS).Study on mast cell and the related inflammatory mediators in colonic mucosa is helpful for the evaluation and treatment of IBS.Aims: To assess the effect of mesalazine combined with trimebutine on colonic mucosal mast cell and related inflammatory mediators in patients with IBS.Methods: Forty patients with diarrhea-predominant IBS (IBS-D) and 40 patients with constipation-predominant IBS (IBS-C) from Oct.2014 to June 2016 at Shanghai Jiading District Central Hospital were enrolled, 20 healthy volunteers were served as controls.Forty patients with IBS-D and 40 patients with IBS-C were randomly divided into mesalazine+trimebutine group and trimebutine group, the treatment courses were all 4 weeks.Number of mast cell was counted by modified toluidine blue staining.Score of related inflammatory mediators were evaluated by immunohistochemistry.Clinical efficacy was assessed.Results: Compared with healthy controls, number of mast cell at baseline was significantly increased both in IBS-D and IBS-C patients (P<0.05).After treatment with mesalazine+trimebutine, number of mast cell was significantly decreased (P<0.05).At baseline, immunohistochemical staining score of 5-HT, IL-1, TNF-α, histamine, tryptase were significantly increased in IBS patients than in healthy controls (P<0.000 1).After treatment with mesalazine+trimebutine, above-mentioned inflammatory mediators were significantly decreased (P<0.05).In IBS-D patients, the total efficacy rate in mesalazine+trimebutine group was significantly increased than that in trimebutine group (85.0% vs.45.0%, P=0.008).In IBS-C patients, no significant difference in total efficacy rate was found between mesalazine+trimebutine group and trimebutine group (55.0% vs.25.0%, P=0.053).Conclusions: Mesalazine combined with trimebutine is an effective and safe approach to reduce mast cell infiltration and release of related inflammatory mediators, and is more efficient for patients with IBS-D.

trimester. Conclusion Moderate and severe PIH early developed during pregnancy could increase the risk of perinatal mortality, while cesarean delivery could decrease the risks in women with PIH.