Objective: This study was undertaken to explore the effect of left ventricular assist device (LVAD) on failing heart after myocardial ischemia. By detecting the changes of plasma atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and cardiac troponin I (cTnI) levels within 6 hours after the implantation of LVAD, we review the basis on which neurohormones may be used to determine prognoses of failing heart and choose an optimal predictor. Methods: 15 adult healthy dogs were divided into 3 groups randomly. The LVAD was implanted in LA-AO bypass in all three groups. Myocardial ischemia was induced by ligating the main left anterior descending coronary artery (LAD). In group A, after a ligation of 10 minutes, the myocardium was reperfused for 6 hours. In group B, after a ligation of 40 minutes, the myocardium was reperfused for 6 hours. In group C, after a ligation of 40 minutes, the LVAD was used for LV support for 6 hours. Results: After 6 hours reperfusion,in group C, the hemodynamics was significantly improved, the ANP, BNP and cTnI were return to normal level, and myocardial ultrastructure was recovered significantly. While in group B, the hemodynamic, the neurohormones, and myocardial ultrastructure were worse. Relational analysis demonstrated that ANP and cTnI levels were influenced by hemodynamics obviously, but there was a weak relationship between circulating BNP and hemodynamics. Plasma BNP level was able to identify the cardiac function status. Conclusion: LVAD can be beneficial to improve cardiac function and can reduce the plasma levels of ANP, BNP and cTnI. Plasma BNP level can identify the cardiac function status. Those findings indicated that plasma BNP determination provides important prognostic information about cardiac function and may be a better prognostic indicator.

Objective In human,both in vivo and in vitro,telomere shortening appears to be a major component of cell senescence and aging. However, gender specific human telomere shortening needs to be further characterized. Therefore our study is aimed at clarifying gender-dependent profiles of telomere shortening. Methods 123 peripheral blood samples were collected from healthy individuals of different ages. The mean telomeric restricted fragment (TRF) was measured using Southern Blotting with Dig-labeled probe. Results Distinguished dynamics profiles of telomere shortening were observed among different age groups. Conclusion The result indicates that there are gender specific dynamic profiles of telomere shortening. Therefore, the gender must be considered when an individual age is estimated by telomeric restricted fragment length assay.

Objective To investigate the hypothesis that food allergy in infants may be associated with variation in their intestinal microflora. The formation of intestinal microflora in healthy infants and changes in food allergic infants were detected.Methods 16S rRNA gene sequences specific for bifidobacterium, lactobacillus and escherichia coli in fecal were quantitatively detected by real-time PCR. The three fecal floras were assessed in 71 healthy infants and 100 infants with food allergy. Results After birth,there were bifidobacteria colonized in infantile intestine,then the number increased rapidly up to 5 times at the sixth month, which was always the preponderant flora. Lactobacilli was also presented in infantile intestine 1 month after birth and augment gradually. The number of Escherichia coli was less than bifidobacteria and lactobacilli and appeared to decline during the early infants. The number of bifidobacteria and lactobacilli in the infants with food allergy were markedly less than that in the healthy infants, but escherichia coli was significantly more than that in the healthy infants.Conclusions During the first year of life,the intestinal microflora in infants is in a developing process. Compared with the healthy infants,bifidobacteria and lactobacilli decrease, but escherichia coli increase in the food allergic infants.These results indicate that the probiotics may be benefit to the prevention and treatment of food allergy.

Calcium Channel Blockers ; pharmacology ; Cell Survival ; drug effects ; Drug Antagonism ; Humans ; Kidney ; cytology ; drug effects ; Lead ; toxicity

AIM: To study the expression of nuclear factor kappa B (NF-?B) in the L 1-L 4 spinal ganglions of adjuvant arthritis (AA) rats, to explore the neuroendocrinoimmunological mechanism of rheumatoid arthritis (RA). METHODS: The expression of the NF-?B protein was detected by immunohistochemistry method and the alteration of the active NF-?B protein (nuclear protein) was investigated by Western blotting analysis. RESULTS: The expression of NF-?B protein in L 1-L 4 spinal ganglions of AA rats was much higher than that in the healthy controls ( P

Objective To study whether p38 mitogen-activated protein kinases (p38MAPK) signal pathway were activated in the process of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) which then induces rheumatoid arthritis (RA) fibroblast-like synoviocyte (FLS) to synthesize matrix metalloproteinase-1 (MMP-1) and look for the relative mechanisms of how TWEAK was involved in the destruction of articular bones and cartilage. Methods RA FLS were primarily cultured and stimulated with TWEAK. FLS were pretreated with SB203580 or not. ELISA was used to detect the concentration of MMP-1 in cell-cultured supernatant. Western blotting was used to detect the expression of p-p38MAPK and P65 in RA FLS. Results TWEAK (100 ng/ml) could induce RA FIS to synthesize MMP-1. SB203580 could partially inhibite the expression of MMP-1 producted by RA FLS which was induced by TWEAK. TWEAK could make p38MAPK phosphorylated and increase the expression of P65 protein in the cell nucleus. Conclusion TWEAK induces RA FLS to synthesize MMP-1. In this process, p38MAPK signal transduction pathway is activated and then induce the expression of NF-κB.

Objective To explore the effect of the JAK/STAT signal pathway on the apoptosis-related gene in the synovial tissue of rat rheumatoid arthritis (RA).Methods Fifty rat models of collagen-induced arthritis,whose arthritis index was more than 2,were divided into the model group,the low dose of AG490 group,the medium dose of AG490 group and the high dose of AG490 group.In addition,6 rats were treated intraperitoneal injection.Then,the arthritis index and the change of apoptosis-related genes were compared.Multiple-sample average was analyzed by single-factor x2 test and LSD-t or Tamhane's T 2 test were used for two-two comparison.Results The arthritis index of the model group increased evidently,and the apoptosis inhibitor Bcl-2,Bcl-xl gene and protein expression was up-regulated,which was significantly different when compared with that of the control group(0.931±0.035 vs 0.351±0.024,0.920±0.037 vs 0.271±0.029,0.322±0.047 vs 0.230±0.031 ).The expression of apoptosis promoting factor Bax wasslightly up-regulated.The blockage of JAK/STAT pathway cotld down-regulate the expression levels of the gene and protein of survivins Bcl-2 and Bcl-xl,and up-regulate the gene and protein expressions of Bax.Conclusion In the process of RA development,apoptosis inhibitor Bcl-2,Bcl-xl gene and protein expression is up-regulated.JAK/STAT signal transduction pathway regulates the apoptosis process.

Ataxia Telangiectasia ; genetics ; Humans

Adenocarcinoma, Mucinous ; pathology ; Breast Neoplasms ; pathology ; Carcinoma, Ductal, Breast ; pathology ; Carcinoma, Renal Cell ; pathology ; Carcinoma, Squamous Cell ; pathology ; Cystadenocarcinoma, Mucinous ; pathology ; Cystadenoma, Mucinous ; pathology ; Female ; Giant Cells ; pathology ; Humans ; Osteoclasts ; pathology ; Ovarian Neoplasms ; pathology ; Pancreatic Neoplasms ; pathology ; Thyroid Carcinoma, Anaplastic ; Thyroid Neoplasms ; pathology ; Tongue Neoplasms ; pathology ; Urologic Neoplasms ; pathology

italic>γ-Aminobutyric acid (GABA) is a crucial inhibitory neurotransmitter found in various cells in the human body. While the GABAergic system is typically associated with the nervous system, recent research has revealed that immune cells and tumor cells also express components of this system. In the tumor microenvironment (TME), GABA is secreted to act extracellularly on other cells. GABA is metabolized via the GABA shunt and is involved in the tricarboxylic acid (TCA) cycle by generating succinate, which can provide energy for tumor cells. Activation of GABA receptors (GABARs) is a major pathway through which GABA participates in the regulation of antitumor immune responses. The activation of GABA type A receptors (GABA_ARs) can inhibit the activation and proliferation of T cells, elicit anti-inflammatory macrophages, and promote tumor cell growth and migration, while activation of GABA type B receptors (GABA_BRs) is generally considered to inhibit cancer cell migration and induce cancer cell apoptosis. In general, receptor activation inhibits immune cells, but the effect on tumor cells varies. Additionally, the downregulation of the expression levels of GABA transporters (GATs) is involved in tumor progression. Although antagonists of GABA metabolism and drugs that act on GABA receptors are considered therapeutic drugs for tumors, there have been few clinical studies conducted on them.