ABSTRACT
Background@#Estrogen is one of the most important reproductive steroidal hormones and plays a critical role in the maintenance of pregnancy, and its function is mediated by estrogen receptor 1(ESR1). The polymorphisms of ESR1 were involved in recurrent spontaneous abortion (RSA); however, the association between ESR1 polymorphisms and RSA remains controversial. The present meta-analysis was aimed to clarify the association between ESR1 PvuII (-397C/T, rs2234693) and XbaI (-351A/G, rs9340799) polymorphisms and the risk of RSA.@*Methods@#All the included articles were retrieved from PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure, and Wanfang Med Online Database up to January 3, 2018. Data were processed in the Stata 12.0 software. The odds ratios (OR s) and 95% confidence intervals (95% CI s) were calculated using fixed-effects models (FEM)/random-effects models (REM).@*Results@#Seven case-control studies with 836 cases and 1164 controls were included in the study. Generally, the ESR1 polymorphisms were not associated with RSA in any of the genetic analysis models. However, it was found that as rs9340799 polymorphism was related to increased risk of RSA in non-Asian group in the homozygous genetic model (OR = 2.40, 95% CI = 1.05-5.50, P = 0.039). Moreover, in Asian group, rs9340799 polymorphism was found to be related to decreased RSA risk in both the heterozygous model (OR = 0.53, 95% CI = 0.33-0.85, P = 0.009) and the dominant genetic model (OR = 0.55, 95% CI = 0.30-0.98, P = 0.042).@*Conclusions@#Generally, there was no significant association between the polymorphisms of ESR1 and the risk of RSA. However, subgroup analysis indicated that ESR1 rs9340799 polymorphism was related to increased RSA risk in the non-Asian group while associated with decreased RSA risk in Asian group.
Subject(s)
Female , Humans , Pregnancy , Abortion, Spontaneous , Genetics , Case-Control Studies , China , Cohort Studies , Estrogen Receptor alpha , Genetics , Genetic Association Studies , Genetic Predisposition to Disease , Iran , Polymorphism, Genetic , Polymorphism, Single Nucleotide , Risk FactorsABSTRACT
The paper discusses influence and effect of information retrieval process of biomedical literature and visualization design on user knowledge discovery,from the aspects of input and output,retieval process and information positioning,it introduces the interaction model of literature information retrieval process and analyzes approach of literature information visualization design,including color and font,statistical chart,list of categories and labels,layer structure and network pictures,etc.
ABSTRACT
<p><b>OBJECTIVE</b>Concentration of extracellular calcium ([Ca(2+)](o)) in the central nervous system decreases substantially in different conditions. It results in facilitating neuronal excitability. The goal of this study is to examine the mechanisms of enhanced neuronal excitation in low [Ca(2+)](o) in order to provide new clues to treat the hyperexcitability diseases in clinic.</p><p><b>METHODS</b>Whole-cell patch-clamp technique and neuron culture were used in the study.</p><p><b>RESULTS</b>The firing threshold of cultured hippocampal neurons decreased markedly in low [Ca(2+)](o) saline. Unexpectedly, apamine and isoprenaline, antagonists of medium afterhyperpolarization (mAHP) and slow AHP (sAHP) respectively, had no statistic significant effect on excitability of neurons. TTX at a low concentration was sufficient to inhibit I(NaP), which blocked the increase of firing frequency in low [Ca(2+)](o). It also reduced the number of spikes in normal [Ca(2+)](o).</p><p><b>CONCLUSION</b>These results suggest that in cultured hippocampal neurons, modulation of spiking threshold but not AHP may cause the increased excitability in low [Ca(2+)](o).</p>
Subject(s)
Animals , Rats , Action Potentials , Apamin , Pharmacology , Calcium , Pharmacology , Cells, Cultured , Dose-Response Relationship, Drug , Electric Stimulation , Embryo, Mammalian , Hippocampus , Cell Biology , Neurons , Patch-Clamp Techniques , Sodium Channel Blockers , Pharmacology , Tetrodotoxin , PharmacologyABSTRACT
<p><b>AIM</b>To investigate the effects of morphine on synaptic transmission of neurons of central nervous system and reveal the mechanism underlying it.</p><p><b>METHODS</b>New born wistar rats were used for primary culture of hippocampus neurons. Using whole-cell patch-clamp technique, we observed the excitatory and spontaneous inhibitory postsynaptic current (EPSC, sIPSC) and glutamate-induced current before and after morphine treatment.</p><p><b>RESULTS</b>(1) sEPSC of hippocampal neurons was markedly increased after morphine application. The effect of morphine was blocked by opioid antagonist naloxone (n=18, P < 0.01). (2) The frequency of mEPSC and the amplitude of glutamate-induced current of hippocampal neurons had no significant changes after morphine treatment (P > 0.05). (3) Morphine inhibited sIPSC of hippocampal neurons markedly and naloxone could block this effect (n=13, P < 0.01).</p><p><b>CONCLUSION</b>The results suggest that the exciting effect of morphine on hippocampal neurons are not due to direct influence of morphine on glutamate synapses transmission, but may result from the inhibition on interneurons, that is "disinhibition" way.</p>