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1.
Nat Commun ; 13(1): 7901, 2022 Dec 22.
Article in English | MEDLINE | ID: mdl-36550110

ABSTRACT

High-pressure electrical resistivity measurements reveal that the mechanical deformation of ultra-hard WB2 during compression induces superconductivity above 50 GPa with a maximum superconducting critical temperature, Tcof 17 K at 91 GPa. Upon further compression up to 187 GPa, the Tcgradually decreases. Theoretical calculations show that electron-phonon mediated superconductivity originates from the formation of metastable stacking faults and twin boundaries that exhibit a local structure resembling MgB2 (hP3, space group 191, prototype AlB2). Synchrotron x-ray diffraction measurements up to 145 GPa show that the ambient pressure hP12 structure (space group 194, prototype WB2) continues to persist to this pressure, consistent with the formation of the planar defects above 50 GPa. The abrupt appearance of superconductivity under pressure does not coincide with a structural transition but instead with the formation and percolation of mechanically-induced stacking faults and twin boundaries. The results identify an alternate route for designing superconducting materials.

2.
Exp Clin Endocrinol Diabetes ; 117(7): 354-60, 2009 Jul.
Article in English | MEDLINE | ID: mdl-19358094

ABSTRACT

We observed the effects of the combination of a high-fat diet and chronic stress on insulin resistance. Male Wistar rats were fed on either a control or a high-fat diet and given chronic stress with the electric foot shock or not for 10 weeks. After checking the glucose infusion rate (GIR) and the HOMA-IR index, the results showed that the three groups all revealed insulin resistance with increased free fatty acid (FFA), adrenocorticotropic hormone (ACTH) and corticosterone in the serum, in addition to increased tumour necrosis factor alpha (TNF-alpha) in the serum and adipose tissue, and decreased density of high affinity receptors (R1) and expression of peroxisome proliferator-activated receptor-alpha (PPARalpha) mRNA in the hepatocytes as compared with the control, but the highest alteration on aforementioned parameters revealed in the chronic stress fed with a high-fat diet. Significant interactions between high-fat diet and chronic stress were revealed on GIR, HOMA-IR index, FFA, ACTH, corticosterone, TNF-alpha (in adipose tissue) and R1. These observations strongly suggest that a combination of a high-fat diet and chronic stress can produce a synergic effect on aggravating insulin resistance associated with the abnormal hypothalamic-pituitary-adrenocortical axis, endocrine abnormality of the adipose tissue, and pathological changes of the liver.


Subject(s)
Diet, Atherogenic , Dietary Fats/adverse effects , Insulin Resistance , Stress, Physiological/physiology , Adipose Tissue, White/metabolism , Adipose Tissue, White/pathology , Animals , Dietary Fats/pharmacology , Insulin Resistance/genetics , Insulin Resistance/physiology , Liver/metabolism , Liver/pathology , Male , PPAR alpha/genetics , PPAR alpha/metabolism , Rats , Rats, Wistar , Receptor, Insulin/genetics , Receptor, Insulin/metabolism , Stress, Physiological/genetics , Time Factors , Tumor Necrosis Factor-alpha/blood , Tumor Necrosis Factor-alpha/metabolism
3.
Zhongguo Yao Li Xue Bao ; 14 Suppl: S22-5, 1993 Nov.
Article in Chinese | MEDLINE | ID: mdl-8010067

ABSTRACT

Panaxadiol saponins (PDS) contain saponins Panax notoginseng B1 and E. The spontaneous beating induced by isoproterenol in isolated rat right atria and the increase of contractile force induced by Ca2+ in isolated guinea pig colon were inhibited by PDS 75 and 150 micrograms.ml-1, respectively and perhexiline 6.25 and 12.5 mumol.L-1, respectively. It suggested that PDS could block the potential-dependent and receptor-operated calcium channel in smooth muscle. PDS 150 micrograms.ml-1 and perhexiline 6.25 mumol.L-1 depressed the contractile force induced by norepinephrine and Ca2+ in isolated rat aortic strips in Ca(2+)-free Krebs' solution. It suggested that PDS and perhexiline not only inhibited the release of intracellular Ca2+ but also blocked the inflow of extracellular Ca2+.


Subject(s)
Calcium Channels/drug effects , Calcium/antagonists & inhibitors , Ginsenosides , Heart Rate/drug effects , Muscle Contraction/drug effects , Triterpenes/pharmacology , Animals , Aorta, Thoracic/drug effects , Colon/drug effects , Female , Guinea Pigs , In Vitro Techniques , Male , Muscle, Smooth/drug effects , Muscle, Smooth, Vascular/drug effects , Rats
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