brain ischemia/obesitas

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Antioxidant Properties of Fucoidan Alleviate Acceleration and Exacerbation of Hippocampal Neuronal Death Following Transient Global Cerebral Ischemia in High-Fat Diet-Induced Obese Gerbils.

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Fucoidan, a natural sulfated polysaccharide, displays various biological activities including antioxidant properties. We examined the neuroprotective effect of fucoidan against transient global cerebral ischemia (tGCI) in high-fat diet (HFD)-induced obese gerbils and its related mechanisms. Gerbils

Trans-sodium crocetinate provides neuroprotection against cerebral ischemia and reperfusion in obese mice.

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Trans-sodium crocetinate (TSC) is a novel synthetic carotenoid compound that improves diffusion of small molecules, including oxygen, in solutions. TSC provides neuroprotection in healthy rats and rabbits. This study seeks to determine whether TSC is neuroprotective in obese mice. Sixteen-week-old

Sevoflurane postconditioning against cerebral ischemic neuronal injury is abolished in diet-induced obesity: role of brain mitochondrial KATP channels.

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Obesity is associated with increased infarct volumes and adverse outcomes following ischemic stroke. However, its effect on anesthetic postconditioning‑induced neuroprotection has not been investigated. The present study examined the effect of sevoflurane postconditioning on focal ischemic brain

Neonatal Morbidity in the Offspring of Obese Women Without Hypertension or Diabetes.

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OBJECTIVE To compare the independent risk of neonatal morbidity between the offspring of obese and nonobese women without hypertension or diabetes. METHODS This is a secondary analysis of a prospective single-center cohort study of singleton deliveries at or beyond 37 weeks of gestation from 2010 to

Neuroprotective effects of protein tyrosine phosphatase 1B inhibitor on cerebral ischemia/reperfusion in mice.

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Akt (Protein kinase B, PKB), a serine/threonine kinase, plays a critical role in cell development, growth, and survival. Akt phosphorylation mediates a neuroprotective effect against ischemic injury. Recently, a protein-tyrosine phosphatase-1B (PTP1B) inhibitor (KY-226) was developed to elicit

Acute treatment with rosuvastatin protects insulin resistant (C57BL/6J ob/ob) mice against transient cerebral ischemia.

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The purpose of this study was to investigate the short-term effects of rosuvastatin (RSV), a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on transient, focal cerebral ischemia in C57BL/6J ob/ob mice with insulin resistance (IR). Male ob/ob, lean, or wild-type (WT) mice were treated

High fructose diet-induced obesity worsens post-ischemic brain injury in the hippocampus of female rats.

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Objectives: Cerebral ischemia is caused by a reduction of the blood flow in a specific area in the brain, triggering cellular cascades in the tissue that result in neuronal death. This phenomenon leads to neurological decline in patients with stroke. The extent of the injury after stroke

Mortality after bariatric surgery: analysis of 13,871 morbidly obese patients from a national registry.

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OBJECTIVE To define mortality rates and risk factors of different bariatric procedures and to identify strategies to reduce the surgical risk in patients undergoing bariatric surgery. BACKGROUND Postoperative mortality is a rare event after bariatric surgery. Therefore, comprehensive data on

Factors associated with neonatal hypoxic ischemic encephalopathy in infants with an umbilical artery pH less than 7.00.

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Our objective was to identify factors associated with hypoxic-ischemic encephalopathy (HIE) among newborns with an umbilical pH < 7.00.Case-control study during a four-year study period in a single academic tertiary-center, including all neonates ≥35

Accelerated and exacerbated effects of high dietary fat on neuronal damage induced by transient cerebral ischemia in the gerbil septum.

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BACKGROUND Obesity induced by high-fat diet (HFD) is one of the most widespread metabolic disorders in current society. However, there has been little research regarding the effects of HFD-induced obesity in the septa of animal models of cerebral ischemia. Therefore, in the present study, we

Assessment of endothelial function in patients with initial manifestations of chronic cerebral ischemia

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Over the last decade, the number of patients with cerebrovascular diseases in Ukraine has grown by 1.5 times. This negative trend is based on the significant increase of vascular risk factors - arterial hypertension, dyslipidemia, sedentary lifestyle, excessive weight/obesity, diabetes

Preventing increased blood pressure in the obese Zucker rat improves severity of stroke.

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Obesity is a risk factor for stroke, but the determinants of increased stroke risk in obesity are unknown. We have previously reported that obese Zucker rats (OZRs) have a worse stroke outcome and display evidence of remodeling of the middle cerebral artery (MCA), in parallel with hypertension,

Obesity increases blood pressure, cerebral vascular remodeling, and severity of stroke in the Zucker rat.

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Obesity is a risk factor for stroke, but the mechanisms by which obesity increases stroke risk are unknown. Because microvascular architecture contributes to the outcome of stroke, we hypothesized that middle cerebral arteries (MCAs) from obese Zucker rats (OZRs) undergo inward remodeling and

Diet-induced obesity causes cerebral vessel remodeling and increases the damage caused by ischemic stroke.

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Hypertension, elevated fasting blood glucose and plasma insulin develop in rats fed a high fat (HF) diet. Our goal was to assess the effects of obesity, beginning in childhood, on the adult cardiovascular system. We hypothesized that rats fed a HF diet would have larger ischemic cerebral infarcts

DPP-4 inhibition with linagliptin ameliorates cognitive impairment and brain atrophy induced by transient cerebral ischemia in type 2 diabetic mice.

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BACKGROUND It is unclear whether dipeptidylpeptidase-4 (DPP-4) inhibition can counteract the impairment of cognitive function and brain injury caused by transient cerebral ischemia in type 2 diabetes. The present study was undertaken to test our hypothesis that linagliptin, a DPP-4 inhibitor,

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