Üsküdar mesireleri

Taha Toros Arşivi, Dosya No: 63-Salacak-Üsküdarİstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033

Nonadiabatic coupling between C-O stretching and Pt substrate electrons enhanced by frustrated mode excitations

We report the transient enhancement of coupling between adsorbate internal stretching vibration and substrate electrons induced by femtosecond laser excitation. A Pt(111) surface covered with carbon monoxide (CO) is irradiated with a 150 fs pump pulse at 400 nm. Transient changes in the imaginary part of nonlinear susceptibility in the C-O stretching region are probed by using femtosecond time-resolved infrared-visible sum-frequency generation with phase-sensitive detection. The line shape of C-O stretching shows remarkable asymmetry due to Fano interference with a continuum of electron-hole pair excitation. Excitations of CO-Pt frustrated modes play a key role in the enhancement of the nonadiabatic coupling

Effect of Nobiletin on Lipid Metabolism in Rats

Nobiletin enhances differentiation and lipolysis of 3T3-L1 adipocytes and improves hyperglycemia and insulin resistance in obese (ob) diabetic ob/ob mice. We investigated the effects of nobiletin on lipid metabolism and accumulation of body fat in rats. The control group was fed a 20% high-fat diet and 1% cholesterol, and the nobiletin group was fed same diet supplemented with 0.1% (w/w) nobiletin. The rats were fed for 4 weeks. Weights of epididymal, perirenal, total white adipose tissues (WAT: mesenteric, perirenal, and epididymal), and the subcutaneous WAT in the nobiletin group were significantly lower than those in the control group. This decrease was brought about by nobiletin without affecting triglyceride (TG) levels in the liver and skeletal muscle. Plasma TG levels tended to be decreased by nobiletin. The size and diameter of WAT adipocytes in the nobiletin group were significantly lower than those in the control group. This decrease may be partly due to lower lipoprotein lipase (a major determinant for the development of obesity) levels in WAT of the nobiletin group than that of the control group. Plasma levels of high density lipoprotein cholesterol and apolipoprotein A-I increased significantly with administration of nobiletin. These results suggested a beneficial effect of nobiletin on lipid metabolism. However, no significant differences were observed between the nobiletin and the control groups in proteins such as ATP-binding cassette transporter A1, and sterol regulatory element-binding protein-1 in the liver, PPARγ and tumor necrosis factor-α (TNF-α) in WAT, and adiponectin and TNF-α in plasma.Nobiletin enhances differentiation and lipolysis of 3T3-L1 adipocytes and improves hyperglycemia and insulin resistance in obese (ob) diabetic ob/ob mice. We investigated the effects of nobiletin on lipid metabolism and accumulation of body fat in rats. The control group was fed a 20% high-fat diet and 1% cholesterol, and the nobiletin group was fed same diet supplemented with 0.1% (w/w) nobiletin. The rats were fed for 4 weeks. Weights of epididymal, perirenal, total white adipose tissues (WAT: mesenteric, perirenal, and epididymal), and the subcutaneous WAT in the nobiletin group were significantly lower than those in the control group. This decrease was brought about by nobiletin without affecting triglyceride (TG) levels in the liver and skeletal muscle. Plasma TG levels tended to be decreased by nobiletin. The size and diameter of WAT adipocytes in the nobiletin group were significantly lower than those in the control group. This decrease may be partly due to lower lipoprotein lipase (a major determinant for the development of obesity) levels in WAT of the nobiletin group than that of the control group. Plasma levels of high density lipoprotein cholesterol and apolipoprotein A-I increased significantly with administration of nobiletin. These results suggested a beneficial effect of nobiletin on lipid metabolism. However, no significant differences were observed between the nobiletin and the control groups in proteins such as ATP-binding cassette transporter A1, and sterol regulatory element-binding protein-1 in the liver, PPARγ and tumor necrosis factor-α (TNF-α) in WAT, and adiponectin and TNF-α in plasma

Comprehensive Genetic Evaluation in Patients with Special Reference to Late-Onset Sensorineural Hearing Loss

Hearing loss (HL) is a common and multi-complex etiological deficit that can occur at any age and can be caused by genetic variants, aging, toxic drugs, noise, injury, viral infection, and other factors. Recently, a high incidence of genetic etiologies in congenital HL has been reported, and the usefulness of genetic testing has been widely accepted in congenital-onset or early-onset HL. In contrast, there have been few comprehensive reports on the relationship between late-onset HL and genetic causes. In this study, we performed next-generation sequencing analysis for 91 HL patients mainly consisting of late-onset HL patients. As a result, we identified 23 possibly disease-causing variants from 29 probands, affording a diagnostic rate for this study of 31.9%. The highest diagnostic rate was observed in the congenital/early-onset group (42.9%), followed by the juvenile/young adult-onset group (31.7%), and the middle-aged/aged-onset group (21.4%). The diagnostic ratio decreased with age; however, genetic etiologies were involved to a considerable degree even in late-onset HL. In particular, the responsible gene variants were found in 19 (55.9%) of 34 patients with a familial history and progressive HL. Therefore, this phenotype is considered to be a good candidate for genetic evaluation based on this diagnostic panel