Quadriceps kinesiology (emg) with varying hip joint flexion and resistance.
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Biomedical subjects
Publications and source records attributed to D C Lin.
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Benzoylecgonine, a polar metabolite of cocaine, was extracted and purified from urine using a reversed-phase high-performance liquid chromatographic column. The portion of the eluent corresponding to elution of the drug was collected, derivatized, and quantified using gas chromatography-mass spectrometry with selected ion monitoring. Using this procedure, analysis of 1 ng/ml of benzoylecgonine in urine can be achieved.
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The ethanol level in brain and blood and the blood level of acetaldehyde upon waking from an anesthetic dose of ethanol were found to be significantly higher in C57BL/6J mice which prefer to drink ethanol solution over water than in DBA/2J mice which avoid the drinking of an ethanol solution. The brain level of acetaldehyde did not differ significantly between the two mouse strains. Possible explanations for the difference in brain sensitivity toward ethanol are discussed.
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The cation-complexing carboxylic-acid antibiotic X-537A, at concentrations far below that required for ionophorous activity, selectively inhibits the oxidation of glutamate and isocitrate by liver mitochondria in steady-state 3. The site of inhibition has been localized specifically at the reduction of NADP(+). Glutamate and isocitrate dehydrogenases, the oxidation of NAD(+)-dependent substrates, pyridine nucleotide transhydrogenations, and the respiratory chain between NADH (or NADPH) and O(2) are unaffected by the antibiotic X-537A. Kinetic evidence, i.e., competition between chlorotetracycline (a fluorescence probe for membrane-bound bivalent cation) and X-537A, indicates that the NADP(+)-reducing, antibiotic-sensitive site is most probably associated with the inner mitochondrial membrane.
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hOAT1 is a renal membrane protein able to efficiently transport acyclic nucleoside phosphonates (ANPs). When expressed in CHO cells, hOAT1 mediates the uptake and cytotoxicity of ANPs suggesting that it plays an active role in the nephrotoxicity associated with cidofovir CMV therapy and high-dose adefovir HIV therapy. Although efficiently transported by hOAT1, tenofovir did not show any significant cytotoxicity in isolated human proximal tubular cells, which correlates with the lack of nephrotoxicity observed in HIV-infected patients on prolonged tenofovir therapy.