This study is to investigate the effects of phenytoin sodium, lidocaine (sodium channel blockers), propranolol (beta-adrenergic receptor antagonist), amiodarone (drugs prolonging the action potential duration) and verapamil (calcium channel blockers) on arrhythmia of mice induced by Bufonis Venenum (Chansu) and isolated mouse hearts lethal dose of Chansu. Arrhythmia of mice were induced by Chansu and then electrocardiograms (ECGs) were recorded. The changes of P-R interval, QRS complex, Q-T interval, T wave amplitude, heart rate (HR) were observed. Moreover, arrhythmia rate, survival rate and arrhythmia score were counted. Isolated mouse hearts were prefused, and the lethal dose of Chansu was recorded. Compared with control group, after pretreatment with phenytoin sodium, broadening of QRS complex and HR were inhibited, and the incidence of ventricular arrhythmia was reduced dramatically, while survival rate was improved; the isolated mouse hearts lethal dose of Chansu was increased significantly. After pretreatment with lidocaine, the prolongation of P-R interval and broadening of QRS complex were inhibited, and the incidences of ventricular arrhythmia were reduced dramatically, while survival rate was improved; the isolated mouse hearts lethal dose of Chansu was increased significantly. After pretreatment with propranolol, prolongation of P-R interval, broadening of QRS complex, prolongation of Q-T interval and HR were inhibited, and the incidences of both supraventricular and ventricular arrhythmias were reduced dramatically, while survival rate was improved. After pretreatment with amiodarone, HR was inhibited, the incidences of ventricular tachycardia were reduced dramatically. Lastly, after pretreatment with verapamil, the prolongation of P-R interval and Q-T interval were inhibited and the incidences of both supraventricular and ventricular arrhythmias were reduced dramatically; the isolated mouse hearts lethal dose of Chansu was reduced significantly. In in vivo experiments, phenytoin sodium was most effective against the mice arrhythmias induced by Chansu while cautious use of verapamil for Chansu inducing arrhythmia should be noted. It is also concluded that mice ventricular arrhythmias induced by Chansu might be most closely related to sodium channel, supraventricular arrhythmias might be related to beta-adrenergic receptor, and calcium channel plays an important role in conduction block. In in vitro experiments, phenytoin sodium was most effective, followed by lidocaine and propranolol, and amiodarone had no obvious effect and verapamil reduced the lethal dose of Chansu.

Objective To investigate the cardiac protection of Hsp27 against endotoxic cardiac depression mediated by activation of PI3K/Akt pathway and the suppression of NFκB-mediated inflammatory response in mice. Method (1) Transgenic mice with cardiac specific overexpression of Hsp27 (Hsp27 Tg) and wild littermate controls (WT) were given 10 mg/kg LPS injected intraperitoneally to induce endotoxemia, (2) The cardiac function measurement in mice was performed by using echocardiography 6 hours after LPS treatment (n = 6), (3) The activity of PBK/Akt pathway was evaluated by Western blot for [hosphor-Akt (p-Akt) and phosphor-Gsk-3β (p-Gsk-3β) one hour after LPS administration ( n = 4)], (4) Activity of inflammatory response was evaluated by protein degradation of IκBα (n = 4), (5) The apoptosis of myocardial cells was determined by TUNEL assay on the paraffin section of cardiac tissue 24 hours after LPS exposure (n = 4). Results (1) Hsp27 attenuated cardiac dysfunction significantly following LPS treatment. Compared with the primary value, LPS induced the depression of cardiac function both in WT rats and Hsp27Tg rats. However, the cardiac dysfunction was attenuated significantly in Hsp27Tg rats compared with that in WT rats ( P < 0.01 or 0.05) . (2) Hsp27 attenuated IκBα degradation after LPS administration. Compared with the primary value, LPS led to LκBα degradation by (72.92 + 9.20) % in WT rats and by (41.43 + 24.10) % in Hsp27Tg rats. The overexpression of Hsp27 lessened the IκBα degradation significantly (P < 0.05). The similar results were obtained in rat myocardial cell culture of experiments. (3) Hsp27 enhanced the activation of PI3K/Akt signaling following LPS exposure. One hour after LPS administration, the relative levels of p-Akt and p-GSK-30 were (3.11 + 0.83) and (3.19 + 1.04), respectively in WT rats, and (5.13 + 0.73) and (5.71 + 1.20) in Hsp27Tg rats, respectively. Compared with WT rats, the levels of p-Akt and p-GSK-3β were significantly higher in Hsp27Tg rats (P < 0.05). (4) The Hsp27 lessened LPS-induced the apopto-sis of myocardial cells. Twenty-four hours after LPS treatment, the percentages of myocardial cell apoptosis were (6.46+ 1.74)% in WT rats and (2.88 + 0.91)% in Hsp27Tg rats. Compared with WT rats, LPS-induced apoptosis in myocardial cells was significantly decreased in Hsp27Tg rats (P < 0.01). Conclusions The overexpression ofHsp27 attenuates cardiac dysfunction significantly during endotoxemia, and the mechanisms may be attributed to the activation of PDK/Akt signaling pathway.

Objective To explore the epidemiologic and clinical features of hand, foot and mouth disease (HFMD) caused by Coxsackie virus A16 (CA16) in Suzhou from 2010 to 2014, and analyze the relationship between the SNPs of oligoadenylate synthetase 1 (OAS1) and HFMD caused by CA16 infection.MethodsThe clinical data of children diagnosed with HFMD caused by CA16 during 2010 and 2014 were collected. The epidemiological characteristics were analyzed. Among them, 167 cases were selected to make comparison of the clinical features with 166 cases of HFMD caused by EV71 infection in the same period. The genotyping ofOAS1 rs10774671 was detected by TaqMan probe technique in 167 cases of CA16 infection children, 166 cases of EV71 infection children with HFMD and 163 healthy children. The relationship between polymorphism of gene and infection of CA 16 was analyzed.ResultsA total of 9 016 children with HFMD were included. CA16 nucleic acid detected to be positive in 762 cases. The detection rate was 8.45%. CA16 infection was most commonly in summer. Children under 5 years old accounted for 94.62% infected. Compared with EV71 infected children, CA16 infected children had shorter fever time, severer oral herpes, ulcer, and rash in hand, foot and hip, lesser nervous system involvement, fewer cases of high lactate dehydrogenase, high C reactive protein, high IgM or IgG, and signiifcant changes in the percentage of CD3+, CD3+CD4+, CD3+CD8+ and CD3-CD19+ (P all?

During past 50 years,has achieved a great progress and derived some profound lessons worthy of learning and studying for our country.This article introduces the deinstitutionalization processes of mental health institutions,reinstitutionalization and the inspiration for Chinese mental health reform.Introduced the paper are the reform of deinstitutionalization of mental health institutions in USA and some other countries,and the concept of such a reform,pointing out inspirations of such a reform for mental health reform in China.

[ABSTRACT]OBJECTIVETo study the expressions of 34βE12, Galectin-3 and HBME-1 in thyroid nodules, and to explore its diagnostic value for papillary thyroid carcinoma (PTC).METHODSEn VisionTM immunohistochemical technique was used to detect the expression of 34βE12, Galectin-3 and HBME-1 in 352 thyroid lesions. The correlation between the expressions of the 3 protein markers and clinicopathological characteristics was evaluated. The receiver operating characteristic area under the curve (ROC-AUC) and their index for diagnosis evaluation were also calculated.RESULTSThe positive rates of 34βE12, Galectin-3 and HBME-1 in 246 PTC lesions were significantly higher than those in benign nodules (P<0.001). There was no relationship between the expression of the 3 protein markers and clinicopathological characteristics (eg. gender, age, numbers of lesions, tumor size, capsular invasion, lymph node metastasis, TNM staging). The ROC-AUC of 34βE12, Galectin-3 and HBME-1 for diagnosis of PTC was 0.936, 0.915 and 0.898 respectively. The sensitivity of 34βE12, Galectin-3 and HBME-1 for diagnosis of PTC was 94.3%, 95.5% and 91.1% respectively, while the specificity was 81.1%, 71.7% and 83.0% respectively, and the diagnostic accuracy rate was 90.3%, 88.4% and 88.6% respectively.CONCLUSION The expressions of 34βE12, Galectin-3 and HBME-1 are statistically different between PTC and benign lesions, but no associations are found with clinicopathological characteristics, indicating the three protein markers have important diagnostic value for PTC.

Objective:To investigate the mechanism of programmed death 1(PD-1)/ programmed death ligand 1(PD-L1) signaling pathway and its feasibility as a potential therapeutic target and prognostic predictor by detecting the expressions, of PD-1 and PD-L1 in bone marrow mononuclear cells of children with acute lymphoblastic leukemia (ALL), and to provide new ideas for the diagnosis and treatment of ALL as well.Methods:Bone marrow samples were collected from 59 children with ALL in the First Affiliated Hospital of Zhengzhou University from September 2018 to July 2019.Flow cytometry was applied to detect the expression of PD-1 and PD-L1 in bone marrow mononuclear cells in 59 ALL patients, including 47 newly-diagnosed ALL patients and 12 relapsed ALL patients, respectively, at initial diagnosis, after induction therapy and early intensive treatment.Their relevant clinical data were collected and compared with the bone marrow specimens of 12 children suffering from non-malignant blood diseases as the control group of the same hospital during the same period.Results:There was no significant difference in the expression of PD-1 in the bone marrow mononuclear cells of the primary diagnosis group, recurrence group and control group ( H=2.402, P>0.05). The expression of PD-L1 in the relapsed and refractory group [(7.32±3.60)%] and the newly diagnosed group [(3.18±2.37)%] was higher than that in the control group [(0.84±0.39)%], and the differences were statistically significant ( H= 28.048, P<0.05). In the initial treatment group, the expression of PD-L1 in the bone marrow mononuclear cells was the strongest expression before treatment ( B=1.293), followed by after induction treatment ( B=0.036) and after early intensive treatment ( B=0.000), suggesting that there was a downward trend as the continued treatment.The expression of PD-L1 was the weakest expression in the low-risk group ( B=-3.912) than in the medium-risk group ( B=-3.595) and high-risk group ( B=0.000), revealing that the expression of PD-L1 is related to the risk grades of ALL.The higher the risk rating is, the higher the PD-L1 protein expression is. Conclusions:The high expression of PD-L1 may be involved in the pathogenesis and be used as an adverse predictor of ALL childhood and an evaluation index of chemotherapy efficacy.PD-1 / PD-L1 signaling pathway may be a potential therapeutic target of ALL childhood.

0.05)between the two groups.Conclu- sion The long-term outcomes of e-CHB is not markedly different compared with that of e+CHB.

OBJECTIVETo investigate the effect of ursolic acid (UA) on the alloxan-induced kidney injury in diabetic mice and explored its possible mechanisms.

METHODSDiabetes mellitus was induced in male Kunming mice by an injection of alloxan (70 mg/kg, i.v.). After 72 hours, blood glucose levels were detected and mice with blood glucose levels over 13.9 mmol/L were considered as diabetic and selected for further experiment. Thirty mice were randomly divided into three groups: control, diabetic and diabetic + UA(35 mg/kg/d, i.g. continuously for 8 weeks). Blood glucose concentration, organ coefficient of kidney, blood urea nitrogen (BUN), creatinine (Cr) as well as renal tissue levels of superoxide dismutase (SOD), methane dicarboxylic aldehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined. Pathology of the renal tissue was measured by hematoxylin-eosin staining.

RESULTSCompared to the control group, blood glucose, organ coefficient of kidney, BUN and Cr increased significantly. In addition, SOD activities was reduced markedly and levels of MDA and inflammatory factors (TNF-α, IL-6) increased significantly. Renal cells from model group rats showed atrophy and disordered after HE staining and infiltration of inflammatory cells also appeared in renal tissue of the model group. These changes were significantly attenuated in the diabetic group treated with UA.

CONCLUSIONUA can significantly relieve renal damage in mice with diabetic nephropathy induced by alloxan, which might be related to decreased blood glucose level, antioxidation effect and inhibiting the production of inflammatory factors such as TNF-α and IL-6.

Alloxan ; adverse effects ; Animals ; Antioxidants ; metabolism ; Blood Glucose ; Blood Urea Nitrogen ; Creatinine ; metabolism ; Diabetes Mellitus, Experimental ; physiopathology ; Diabetic Nephropathies ; chemically induced ; drug therapy ; Interleukin-6 ; metabolism ; Kidney ; physiopathology ; Male ; Mice ; Superoxide Dismutase ; metabolism ; Triterpenes ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

AIMTo observe the intracellular calcium ion spatio-temporal and dynamic changes in the hippocampal neuronal culture model of epilepsy induced by low magnesium ion medium, and to explore the relationship between calcium ion and epilepsy.

METHODSApplying both laser scanning confocal microscope and patch clamp to timely observe the changes of [Ca2+]i and electrophysiological in the hippocampal neuronal culture model of epilepsy, and the influence of NMDA receptor-gated channels retarder and non-NMDA receptor-gated channels retarder.

RESULTSAfter the hippocampal nerve cell broken into epileptiform discharges, [(Ca2+]i rapidly ascended to (620 +/- 70) nmol/L, NMIDA acceptor retarder (MK-801, 10 micromol/L) and non-NMDA acceptor retarder (NBQX, 10 micromol/L) reduced [Ca2+]i ascendance. Recovery of the elevated [Ca2+]i was obviously delay, after 90 min and 150 min epileptiform discharges, it took (114.8 +/- 5.2) min and (135.0 +/- 22.7) min (P < 0.05) respectively.

CONCLUSIONIn vitro status epilepticus causes sustained elevation of intracellular calcium levels in hippocampal neurons

Animals ; Animals, Newborn ; Calcium ; metabolism ; Cells, Cultured ; Hippocampus ; cytology ; metabolism ; Neurons ; metabolism ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus ; metabolism ; physiopathology

OBJECTIVETo study the genetic heterogeneity of autosomal dominant polycystic kidney disease (ADPKD) in Chinese.

METHODSUsing polymerase chain reaction (PCR) and non-denatured polyacrylamide gel electrophoresis, the authors analyzed eight microsatellite markers closely linked to PKD1 or PKD2 genes respectively in a Chinese ADPKD family.

RESULTSSeven informative markers were found in this family, including KG8, SM6, CW4 and CW2 which are tightly linked to PKD1, and D4S1563, D4S414 and D4S423 which are linked to PKD2. After the process of genotyping, the haplotypes were estimated with Cyrillic 2.0, and the linkage-based analysis suggested that the disease is not linked to PKD1 other than PKD2.

CONCLUSIONIn China this non-PKD1 family is the second one, but it is the first reported PKD2 family showing the genetic heterogeneity of ADPKD in Chinese. In the family the affected mother transmits the disease and the affected members' phenotypes are eterogeneous. In addition, the existing "anticipation" and the presence of the disease in a child of this family suggest that non-PKD1 linked families may have early-onset of the disease in child.

Adult ; Asian Continental Ancestry Group ; genetics ; Child ; Child, Preschool ; China ; Family Health ; Female ; Haplotypes ; genetics ; Humans ; Microsatellite Repeats ; genetics ; Middle Aged ; Pedigree ; Polycystic Kidney, Autosomal Dominant ; ethnology ; genetics ; Polymerase Chain Reaction ; TRPP Cation Channels ; genetics