Role of TSH on Urinary Calcium Excretion In Post Menopausal Women of South Indian Population

Niranjan, G; Amrutha, P; Srinivasan, Abu Raghavan; Ramesh, Revathi; Sathishbabu, Murugaiyan; Subbaiya, Ramasamy

doi:10.7860/jcdr/2013/5290.3056

Cited by 2 publications

(1 citation statement)

References 10 publications

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“…In cultured cells, stimulation of K + efflux and intracellular K + depletion induces caspase activation, cytochrome c release and DNA degradation. Therefore, under certain circumstances, especially during sub-acute and chronic phases of an ischemic insult, intracellular K + loss is an ultimate consequence that can lead to activation of apoptotic cascades [29, 35] . This K + -mediated mechanism underlying apoptosis has been demonstrated in neurons and non-neuronal cells after ischemia, hypoxia and many other pathological insults [27, 29, 30, 36, 37] (please see the review from Aizenman’s group in this special issue).…”

Section: Apoptotic Cell Shrinkagementioning

confidence: 99%

Ionic Regulation of Cell Volume Changes and Cell Death after Ischemic Stroke

Song

2013

Transl. Stroke Res.

104

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Stroke is a leading cause of human death and disability in the US and around the world. Shortly after the cerebral ischemia, cell swelling is the earliest morphological change in injured neuronal, glial and endothelial cells. Cytotoxic swelling directly results from increased Na+ (with H2O) and Ca2+ influx into cells via ionic mechanisms evoked by membrane depolarization and a number of harmful factors such as glutamate accumulation and the production of oxygen reactive species (ROS). During the sub-acute and chronic phases after ischemia, injured cells may show a phenotype of cell shrinkage due to complex processes involving membrane receptors/channels and programmed cell death signals. This review will introduce some progress in the understanding of the regulation of pathological cell volume changes and the involved receptors and channels, including NMDA and AMPA receptors, acid-sensing ion channels (ASIC), hemichannels, transient receptor potential (TRP) channels and KCNQ channels. Moreover, accumulating evidence supports a key role of energy deficiency and dysfunction of Na+/K+-ATPase in ischemia-induced cell volume changes and cell death. Specifically, the Na+ pump failure is a prerequisite for disruption of ionic homeostasis including a pro-apoptotic disruption of the K+ homeostasis. Finally, we will introduce the concept of hybrid cell death as a result of the Na+ pump failure in cultured cells and the ischemic brain. The goal of this review is to outline recent understanding of the ionic mechanism of ischemic cytoxicity and suggest innovative ideas for future translational research.

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Section: Apoptotic Cell Shrinkagementioning

confidence: 99%

Ionic Regulation of Cell Volume Changes and Cell Death after Ischemic Stroke

Song

2013

Transl. Stroke Res.

104

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Does serum TSH level act as a surrogate marker for psychological stress and cardio-metabolic risk among adolescent and young people?

Gopal

Pune

Takhelmayum

et al. 2021

Hormone Molecular Biology and Clinical Investigation

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Objectives The incidence of metabolic syndrome is increasing even at younger ages. Metabolic syndrome constitutes a group of cardiovascular risk factors that include high cholesterol, triacylglycerol, hyperglycemia, central obesity, etc., which increases the risk of cardiovascular disease, diabetes mellitus, may be even cancer. Indian students enter colleges just after crossing their adolescent age and will be exposed to greater academic stress. Psychological stress or depression is associated with transient change in thyroid hormones level or dysfunction. To explore an association among serum Thyroid Stimulating Hormone (TSH) levels, fT3:fT4 ratio, psychological stress scores, and selected known cardio-metabolic risk markers. Methods Forty first year MBBS students were included. Their demographic, anthropometric variables, and the blood pressure were documented. Serum TSH, fT3, fT4, and salivary cortisol level was quantified. The stress level was assessed using Cohen Perceived Stress Scale Scoring. Data were expressed in mean ± standard deviation. Data (parametric/non-parametric) were compared by Independent unpaired ANOVA or Kruskal Wallis test whichever is appropriate. Spearmen correlation analysis was performed. Results Serum TSH and Cohen stress score are negatively correlated (r=−0.152), but serum cortisol showed (r=0.763) a positive correlation. TSH levels and the marks obtained in the summative assessments were negatively correlated and the correlation was not statistically significant. Conclusions The psychological stress is associated with low serum TSH, high cortisol, and poor academic performance in first year MBBS students. Blood pressure, plasma glucose, and anthropometric measures were not associated with the psychological stress.

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Role of TSH on Urinary Calcium Excretion In Post Menopausal Women of South Indian Population

Cited by 2 publications

References 10 publications

Ionic Regulation of Cell Volume Changes and Cell Death after Ischemic Stroke

Ionic Regulation of Cell Volume Changes and Cell Death after Ischemic Stroke

Does serum TSH level act as a surrogate marker for psychological stress and cardio-metabolic risk among adolescent and young people?

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