Association of obstructive sleep apnea symptoms with all-cause mortality and cause-specific mortality in adults with or without diabetes: A cohort study based on the NHANES.

Background: The association between obstructive sleep apnea syndrome (OSAS) and mortality has not been extensively researched among individuals with varying diabetic status. This study aimed to compare the relationship of OSAS with all-cause and cause-specific mortality in US individuals with or without diabetes based on data from the National Health and Nutrition Examination Survey (NHANES).

Methods: The study included participants from the NHANES 2005-2008 and 2015-2018 cycles with follow-up information.

Preventive effects of the AMPA receptor potentiator LY450108 in an LPS-induced depressive mouse model.

Previous studies have demonstrated a close association between α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptors (AMPARs) and depressive disorders, and activation of AMPARs may represent a promising way to treat depression. However, the effects of AMPAR potentiators on depression and the underlying mechanism have not been comprehensively clarified. We used lipopolysaccharide (LPS) to establish a depressive mouse model and an in vitro damage model of SH-SY5Y cells, and the AMPAR potentiator LY450108 was introduced to the study.

Chronic ethanol exposure induced depressive-like behavior in male C57BL/6 N mice by downregulating GluA1.

Chronic ethanol exposure can increase the risk of depression. The α-amino-3‑hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor is a key factor in depression and its treatment. The study was conducted to investigate the depressive-like behavior induced by chronic ethanol exposure in mice and to explore the mechanism in cells.

Effects of Single-Dose and Long-Term Ketamine Administration on Tau Phosphorylation-Related Enzymes GSK-3β, CDK5, PP2A, and PP2B in the Mouse Hippocampus.

Ketamine is a recreational drug that causes emotional and cognitive impairments, but its specific mechanisms of action are still unclear. Recent evidence suggests that Tau protein phosphorylation and targeted delivery to the postsynaptic area are closely related to its neurotoxicity, and our recent studies have shown that long-term ketamine administration causes excessive Tau protein phosphorylation. However, the regulatory mechanism of Tau protein phosphorylation induced by ketamine has not been clarified.

Redistribution of Monocarboxylate 1 and 4 in Hippocampus and Spatial Memory Impairment Induced by Long-term Ketamine Administration.

The monocarboxylate transporters (MCTs) MCT1, MCT2, and MCT4 are essential components of the astrocyte-neuron lactate shuttle (ANLS), which is a fundamental element of brain energetics. Decreased expression of MCTs can induce cognitive dysfunction of the brain. In the present study, we established a mouse model of long-term ketamine administration by subjecting mice to a 6-month course of a daily intraperitoneal injection of ketamine.

Long-term ketamine administration causes Tau protein phosphorylation and Tau protein-dependent AMPA receptor reduction in the hippocampus of mice.

As a recreational drug of abuse and an injectable anesthetic, ketamine has been shown to cause cognitive dysfunction and induce psychotic states. Although the specific mechanism is still unclear, it may be linked to synaptic receptors, including the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor. Recent evidence suggests that Tau protein phosphorylation and targeted delivery to the postsynaptic area is involved in maintaining neuronal plasticity, indicating that the neurotoxicity induced by ketamine may be related to the transfer of Tau protein after phosphorylation.

Regulation of Tau Protein on the Antidepressant Effects of Ketamine in the Chronic Unpredictable Mild Stress Model.

Tau protein is known to play an important role in maintaining microtubule assembly and stabilization, and maintaining the normal morphology of neurons, but several studies have found that chronic stress leads to Tau hyperphosphorylation. A large number of clinical trials have found that ketamine, which is an N-methyl-D-aspartate receptor antagonist, produces a rapid, long-lasting, and potent antidepressant effect in patients suffering from major depression. This rapid antidepressant effect of ketamine, which involves many mechanisms, has attracted wide attention.

Fatal subarachnoid hemorrhage caused by rupture of variant anterior communicating artery: a case report and literature review.

Fatal subarachnoid hemorrhage (SAH) caused by anterior communicating artery (ACoA) rupture is a rare event in medicolegal practice. Anatomical variations of the ACoA tend to make its anatomical structure, and as a result, blood flow through it, more complicated, which may increase hemodynamic stress and cause weak spots in the affected blood vessels. Variant ACoAs are prone to rupture in the event of a blunt-force trauma.

A fatal case of hypothermia caused by dog bites.

Death from hypothermia usually *We presented a fatal case of hypothermia after being bitten by dog in this article. occurs among people exposed to cold and humid environmental conditions when they are homeless, aged, suffering from natural or psychiatric diseases and drug or alcohol intoxication. A normal healthy person dying from hypothermia due to dog bites is unusual and rare.

Effects of Ketamine on Levels of Inflammatory Cytokines IL-6, IL-1β, and TNF-α in the Hippocampus of Mice Following Acute or Chronic Administration.

Ketamine is an injectable anesthetic and recreational drug of abuse commonly used worldwide. Many experimental studies have shown that ketamine can impair cognitive function and induce psychotic states. Neuroinflammation has been suggested to play an important role in neurodegeneration.

Changes in hippocampal AMPA receptors and cognitive impairments in chronic ketamine addiction models: another understanding of ketamine CNS toxicity.

Ketamine has been reported to impair human cognitive function as a recreational drug of abuse. However, chronic effects of ketamine on central nervous system need to be further explored. We set out to establish chronic ketamine addiction models by giving mice a three or six month course of daily intraperitoneal injections of ketamine, then examined whether long-term ketamine administration induced cognition deficits and changed hippocampal post-synaptic protein expression in adult mice.