Chronic Sleep Fragmentation Induces Endothelial Dysfunction and Structural Vascular Changes in Mice

preeclampsia can affect multiple organ systems due to hypertension and systemic endothelial dysfunction, one of the more delicate maternal systems impacted is the brain It is not always the acute risk of preeclampsia and eclampsia on the brain that impacts maternal outcome. Cortical blindness is generally reversible, and permanent blindness from retinal vascular changes is rare [8].Other than effective treatment of preeclampsia/eclampsia and termination of pregnancy, no specic therapy is indicated in pre- eclamptic women who experience ocular changes. A Similar case with Eclampsia and blindness is presented here.

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Morphological and functional vascular changes induced by childhood obesity

European Journal of Cardiovascular Prevention & Rehabilitation ◽

10.1177/1741826711398180 ◽

2011 ◽

Vol 18 (6) ◽

pp. 831-835 ◽

Cited By ~ 29

Author(s):

Marco Matteo Ciccone ◽

Vito Miniello ◽

Roberto Marchioli ◽

Pietro Scicchitano ◽

Francesca Cortese ◽

...

Keyword(s):

Body Mass Index ◽

Endothelial Dysfunction ◽

Density Lipoprotein ◽

Intima Media Thickness ◽

Carotid Intima Media Thickness ◽

Vascular Changes ◽

Obese Children ◽

Erythrocyte Sedimentation ◽

Flow Mediated Dilatation ◽

Anterior Posterior

Background: To investigate endothelial dysfunction and morphological vascular changes in childhood obesity. Methods: 93 overweight/obese children (body mass index 26 ± 5 kg/m2; median 26 kg/m2; interquartile range 22–28 kg/m2), mean age 10.9 ± 2.7 years, underwent a check-up of total, high-density lipoprotein- and low-density lipoprotein-cholesterol, triglycerides, C-reactive protein, erythrocyte sedimentation rate, and white blood cell count, together with ultrasound measures of flow-mediated dilatation, carotid intima-media thickness, and anterior-posterior diameter of the abdominal aorta. Results: The body mass index of overweight/obese children had a statistically significant linear relationship ( p < 0.05) with triglycerides, erythrocyte sedimentation rate, carotid intima-media thickness, anterior-posterior diameter of the abdominal aorta, and flow-mediated dilatation values. Conclusions: Overweight/obese children have an initial endothelial dysfunction and vascular damage, i.e., the first stage in the development of atherosclerosis.

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Chronic sleep fragmentation promotes obesity in young adult mice

Obesity ◽

10.1002/oby.20616 ◽

2013 ◽

Vol 22 (3) ◽

pp. 758-762 ◽

Cited By ~ 49

Author(s):

Yang Wang ◽

Alba Carreras ◽

SeungHoon Lee ◽

Fahed Hakim ◽

Shelley X. Zhang ◽

...

Keyword(s):

Young Adult ◽

Sleep Fragmentation ◽

Adult Mice ◽

Chronic Sleep

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Intrahepatic vascular changes in non-alcoholic fatty liver disease: Potential role of insulin-resistance and endothelial dysfunction

World Journal of Gastroenterology ◽

10.3748/wjg.v23.i37.6777 ◽

2017 ◽

Vol 23 (37) ◽

pp. 6777-6787 ◽

Cited By ~ 10

Author(s):

Marcos Pasarín ◽

Juan G Abraldes ◽

Eleonora Liguori ◽

Beverley Kok ◽

Vincenzo La Mura

Keyword(s):

Insulin Resistance ◽

Liver Disease ◽

Endothelial Dysfunction ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Potential Role ◽

Vascular Changes ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

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Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice?

Frontiers in Aging Neuroscience ◽

10.3389/fnagi.2021.759983 ◽

2021 ◽

Vol 13 ◽

Author(s):

Li Ba ◽

Lifang Huang ◽

Ziyu He ◽

Saiyue Deng ◽

Yi Xie ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Glucose Metabolism ◽

Differential Expression ◽

Mouse Models ◽

Neurological Diseases ◽

Expression Patterns ◽

Sleep Fragmentation ◽

Wild Type ◽

Chronic Sleep

Chronic sleep insufficiency is becoming a common issue in the young population nowadays, mostly due to life habits and work stress. Studies in animal models of neurological diseases reported that it would accelerate neurodegeneration progression and exacerbate interstitial metabolic waste accumulation in the brain. In this paper, we study whether chronic sleep insufficiency leads to neurodegenerative diseases in young wild-type animals without a genetic pre-disposition. To this aim, we modeled chronic sleep fragmentation (SF) in young wild-type mice. We detected pathological hyperphosphorylated-tau (Ser396/Tau5) and gliosis in the SF hippocampus. 18F-labeled fluorodeoxyglucose positron emission tomography scan (18F-FDG-PET) further revealed a significant increase in brain glucose metabolism, especially in the hypothalamus, hippocampus and amygdala. Hippocampal RNAseq indicated that immunological and inflammatory pathways were significantly altered in 1.5-month SF mice. More interestingly, differential expression gene lists from stress mouse models showed differential expression patterns between 1.5-month SF and control mice, while Alzheimer's disease, normal aging, and APOEε4 mutation mouse models did not exhibit any significant pattern. In summary, 1.5-month sleep fragmentation could generate AD-like pathological changes including tauopathy and gliosis, mainly linked to stress, as the incremented glucose metabolism observed with PET imaging suggested. Further investigation will show whether SF could eventually lead to chronic neurodegeneration if the stress condition is prolonged in time.

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