Articles by Julia Grinshpun in JoVE
一种诱导大鼠抑郁症状行为的新方法 Vladimir Zeldetz*1, Dmitry Natanel*2, Matthew Boyko2, Alexander Zlotnik2, Honore N. Shiyntum3, Julia Grinshpun2, Dmitry Frank2, Ruslan Kuts2, Evgeni Brotfain2, Jochanan Peiser2 1Department of Emergent Medicine, Soroka University Medical Center, Ben-Gurion University of the Negev, 2Division of Anesthesiology and Critical Care, Soroka Medical Center, Ben-Gurion University of the Negev, 3 该协议描述了一种新的模型, 通过这种模式, 健康的大鼠可以在一定时间内收缩抑郁症, periodthrough 感染慢性不可预测的压力大鼠。
Other articles by Julia Grinshpun on PubMed
Differential Regulation of Prostaglandin Synthesis in Neonatal Rat Microglia and Astrocytes by Somatostatin European Journal of Pharmacology. Apr, 2008 | Pubmed ID: 18325491 The aim of the present study was to investigate the role of somatostatin in the regulation of brain inflammation. We used lipopolysaccharide-induced prostaglandin E2 production in neonatal rat microglia and in astrocytes as a model of brain inflammation. Our data show an unexpected differential effect of somatostatin on lipopolysaccharide-induced prostaglandin E2 synthesis in rat microglia vs. in astrocytes. Somatostatin markedly inhibited the lipopolysaccharide-induced prostaglandin E2 synthesis in microglia whereas, on the contrary, in astrocytes the lipopolysaccharide-induced prostaglandin E2 production was actually enhanced by somatostatin. These novel observations imply that somatostatin may regulate brain inflammation in a dual manner.
Establishment of an Animal Model of Depression Contagion Behavioural Brain Research. Mar, 2015 | Pubmed ID: 25523029 Depression is a common and important cause of morbidity, and results in a significant economic burden. Recent human studies have demonstrated that that depression is contagious, and depression in family and friends might cumulatively increase the likelihood that a person will exhibit depressive behaviors. The mechanisms underlying contagion depression are poorly understood, and there are currently no animal models for this condition.
Blood Glutamate Reducing Effect of Hemofiltration in Critically Ill Patients Neurotoxicity Research. Feb, 2018 | Pubmed ID: 28836163 Glutamate toxicity plays a well-established role in secondary brain damage following acute and chronic brain insults. Previous studies have demonstrated the efficacy of hemodialysis and peritoneal dialysis in reducing blood glutamate levels. However, these methods are not viable options for hemodynamically unstable patients. Given more favorable hemodynamics, longer treatment, and less needed anticoagulation, we investigated whether hemofiltration could be effective in lowering blood glutamate levels. Blood samples were taken from 10 critically ill patients immediately before initiation of hemofiltration and after 1, 2, 4, 6, and 12 h, for a total of 6 blood samples. Samples were sent for determination of glutamate, glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), hemoglobin, hematocrit, urea, creatinine, glucose, sodium, potassium, platelet, and white blood cell (WBC) levels. There was a statistically significant reduction in blood glutamate levels at all time points compared to baseline levels. There was no difference in levels of GOT or GPT. Hemofiltration can be a promising method of reducing blood glutamate levels, especially in critically ill patients where hemodialysis and peritoneal dialysis may be contraindicated.