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Luis D´Marco,Juan Salazar,Marie Cortez,María Salazar,Marjorie Wettel,Marcos Lima-Martínez,Edward Rojas,Willy Roque,Valmore Bermúdez 대한신장학회 2019 Kidney Research and Clinical Practice Vol.38 No.3
Background: Adipose tissue accumulation in specific body compartments has been associated with diabetes, hypertension and dyslipidemia. Perirenal fat (PRF) may lead to have direct lipotoxic effects on renal function and intrarenal hydrostatic pressure. This study was undertaken to explore the association of PRF with cardiovascular risk factors and different stages of chronic kidney disease (CKD). Methods: We studied 103 patients with CKD of different stages (1 to 5). PRF was measured by B-mode renal ultrasonography in the distal third between the cortex and the hepatic border and/or spleen. Results: The PRF thickness was greater in CKD patients with impaired fasting glucose than in those with normal glucose levels (1.10 ± 0.40 cm vs. 0.85 ± 0.39 cm, P < 0.01). Patients in CKD stages 4 and 5 (glomerular filtration rate [GFR] < 30 mL/min/1.73 m2) had the highest PRF thickness. Serum triglyceride levels correlated positively with the PRF thickness; the PRF thickness was greater in patients with triglyceride levels ≥ 150 mg/dL (1.09 ± 0.40 cm vs. 0.86 ± 0.36 cm, P < 0.01). In patients with a GFR < 60 mL/min/1.73 m2, uric acid levels correlated positively with the PRF thickness (P < 0.05). Conclusion: In CKD patients, the PRF thickness correlated significantly with metabolic risk factors that could affect kidney function.
Potential role of orexin and sleep modulation in the pathogenesis of Alzheimer’s disease
Roh, Jee Hoon,Jiang, Hong,Finn, Mary Beth,Stewart, Floy R.,Mahan, Thomas E.,Cirrito, John R.,Heda, Ashish,Snider, B. Joy,Li, Mingjie,Yanagisawa, Masashi,de Lecea, Luis,Holtzman, David M. The Rockefeller University Press 2014 The Journal of experimental medicine Vol.211 No.13
<P>Age-related aggregation of amyloid-β (Aβ) is an upstream pathological event in Alzheimer’s disease (AD) pathogenesis, and it disrupts the sleep–wake cycle. The amount of sleep declines with aging and to a greater extent in AD. Poor sleep quality and insufficient amounts of sleep have been noted in humans with preclinical evidence of AD. However, how the amount and quality of sleep affects Aβ aggregation is not yet well understood. Orexins (hypocretins) initiate and maintain wakefulness, and loss of orexin-producing neurons causes narcolepsy. We tried to determine whether orexin release or secondary changes in sleep via orexin modulation affect Aβ pathology. Amyloid precursor protein (APP)/Presenilin 1 (PS1) transgenic mice, in which the orexin gene is knocked out, showed a marked decrease in the amount of Aβ pathology in the brain with an increase in sleep time. Focal overexpression of orexin in the hippocampus in APP/PS1 mice did not alter the total amount of sleep/wakefulness and the amount of Aβ pathology. In contrast, sleep deprivation or increasing wakefulness by rescue of orexinergic neurons in APP/PS1 mice lacking orexin increased the amount of Aβ pathology in the brain. Collectively, modulation of orexin and its effects on sleep appear to modulate Aβ pathology in the brain.</P>
Byung-Soo Kim,Lutz Edler,Jin Joo Park,Dietrich von Fournier,Wulf Haase,Marie-Luise Sautter-Bihl,Egbert Hagmuller,Florian Gotzes,Heinz Walter Thielmann 한국독성학회 2004 Toxicological Research Vol.20 No.1
The comet assay (also called the single-cell gel electrophoresis assay) has been widely used for detecting DNA damage and repair in individual cells. Since the conventional methods of evaluating comet assay data using frequency statistics are unsatisfactory we developed a new quantitative measure of DNA damage/repair that is based on all information residing in the dose/time-response curves of a comet experiment. Blood samples were taken from 25 breast cancer patients before undergoing radiotherapy. The comet assay was performed under alkaline conditions using isolated lymphocytes. Tail DNA, tail length, tail moment and tail inertia of the comet were measured for each patient at four doses of g-rays (0, 2, 4 and 8 Gy) and at four time points after irradiation (0, 10, 20 and 30 min) using 100 cells each. The resulting three-dimensional dose-time response surface was modeled by multiple regression, and the second derivative, termed 2D, on dose and time was determined. A software module was programmed in SAS/AF to compute 2D values. We applied the new method successfully to data obtained from cancer patients to be assessed for their radiation sensitivity. We computed the 2D values for the four damage measures, i.e., tail<br/> moment, tail length, tail DNA and tail inertia, and examined the pairwise correlation coefficients of 2D both on the log scale and the unlogged scale. 2D values based on tail moment and tail DNA<br/> showed a high correlation and, therefore, these two damage measures can be used interchangeably as far as DNA repair is concerned. 2D values based on tail inertia have a correlation profile different from the other 2D values which may reflect different facets of DNA damage/repair. Using the dose-time response surface, other statistical models, e.g., the proportional hazards model, become applicable for data analysis. The 2D approach can be applied to all DNA repair measures, i.e., tail moment, tail length, tail DNA and tail inertia, and appears to be superior to conventional evaluation methods as it integrates all data of the dose/time-response curves of a comet assay.
Byung-Soo Kim,Lutz Edler,Jin Joo Park,Dietrich von Fournier,Wulf Haase,Marie-Luise Sautter-Bihl,Egbert Hagmuller,Florian Gotzes,Heinz Walter Thielmann 한국독성학회 2004 Toxicological Research Vol.20 No.2
The comet assay (also called the single-cell gel electrophoresis assay) has been widely used for detecting DNA damage and repair in individual cells. Since the conventional methods of evaluating comet assay data using frequency statistics are unsatisfactory we developed a new quantitative measure of DNA damage/repair that is based on all information residing in the dose/time-response curves of a comet experiment. Blood samples were taken from 25 breast cancer patients before undergoing radiotherapy. The comet assay was performed under alkaline conditions using isolated lymphocytes. Tail DNA, tail length, tail moment and tail inertia of the comet were measured for each patient at four doses of g-rays (0, 2, 4 and 8 Gy) and at four time points after irradiation (0, 10, 20 and 30 min) using 100 cells each. The resulting three-dimensional dose-time response surface was modeled by multiple regression, and the second derivative, termed 2D, on dose and time was determined. A software module was programmed in SAS/AF to compute 2D values.<br/> We applied the new method successfully to data obtained from cancer patients to be assessed for their radiation sensitivity. We computed the 2D values for the four damage measures, i.e., tail<br/> moment, tail length, tail DNA and tail inertia, and examined the pairwise correlation coefficients of 2D both on the log scale and the unlogged scale. 2D values based on tail moment and tail DNA<br/> showed a high correlation and, therefore, these two damage measures can be used interchangeably as far as DNA repair is concerned. 2D values based on tail inertia have a correlation profile different from the other 2D values which may reflect different facets of DNA damage/repair. Using the dose-time response surface, other statistical models, e.g., the proportional hazards model, become applicable for data analysis. The 2D approach can be applied to all DNA repair measures, i.e., tail moment, tail length, tail DNA and tail inertia, and appears to be superior to conventional evaluation methods as it integrates all data of the dose/time-response curves of a comet assay.