Radiation-induced electrical degradation in crystalline Al2O3.
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Journal Article↗
Biomedical subjects
S Liu
Publications and source records attributed to S Liu.
Dietary omega-3 and polyunsaturated fatty acids modify fatty acyl composition and insulin binding in skeletal-muscle sarcolemma.
Feeding animals with diets high in saturated fat induces insulin resistance, and replacing saturated fat isocalorically with poly-unsaturated fat, especially long-chain omega-3 fatty acids, will prevent the development of insulin resistance in skeletal-muscle tissue. To investigate the mechanism, rats were fed on high-fat (20%, w/w) semipurified diets for 6 weeks. Diets containing ratios of polyunsaturated/saturated (P/S) fatty acid of 0.25 (low-P/S diet) and 1.0 (high-P/S diet) were used to study the effect of the level of saturated fat. To study the effects of omega-3 fatty acids, diets with a low-P/S ratio containing either 0 (low-omega-3 diet) or 3.3% (high-omega-3 diet) long-chain omega-3 fatty acids from fish oil were fed. Plasma membrane from skeletal muscle was purified. The content of fatty acids in sarcolemmal phospholipid was significantly related to the dietary composition. Insulin binding to intact sarcolemmal vesicles prepared from rats fed on diets high in omega-3 fatty acids increased 14-fold compared with animals fed on the low-omega-3 diet (P < 0.0001). Feeding rats on a diet with a high P/S ratio increased sarcolemmal insulin binding by 2.3-fold (P < 0.05). Increased insulin binding was due to increased receptor number at the low-affinity high-capacity binding site. Dietary effects on insulin binding were eliminated when studies were carried out on detergent-solubilized membranes, indicating the importance of the phospholipid fatty acyl composition for insulin binding. The results suggest that dietary omega-3 and polyunsaturated fatty acids increase insulin binding to sarcolemma by changing the fatty acyl composition of phospholipid surrounding the insulin receptor, and this might be the mechanism by which dietary fatty acids modify insulin action.
Animals↗
Characterization of stain-etched porous silicon.
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Journal Article↗
Mechanism of inactivation of S-adenosylhomocysteine hydrolase by (E)-5',6'-didehydro-6'-deoxy-6'-halohomoadenosines.
S-Adenosylhomocysteine (AdoHcy) hydrolase is irreversibly inactivated by (E)-5',6'-didehydro-6'-deoxy-6'-halohomoadenosines (EDDHHAs, halogen = I, Br, and Cl). The inactivation is concomitant with the reduction of the enzyme-bound NAD+ (E.NAD+) to NADH, the release of halide ion, and the formation of adenine (Ade) from the EDDHHAs. The mechanism of this inactivation involves two catalytic pathways. Pathway a involves a rapid addition of water to the 5',6'-bond of EDDHHAs and elimination of halide ion, resulting in the formation of 6'-carboxaldehyde 1 which then degrades chemically, resulting in the formation of Ade. Alternatively, 6'-carboxyaldehyde 1 can be oxidized by E.NAD+ to form 3'-keto-6'-carboxaldehyde 3 and the NADH form (inactive) of the enzyme. Like 6'-carboxaldehyde 1, the 3'-keto derivative 3 degrades chemically to form Ade. Pathway b involves the oxidation of EDDHHAs to 3'-keto-EDDHHAs 2 by E.NAD+, as the first step, and the subsequent release of halide ion to form 3'-keto-6'-carboxaldehyde 3. Evidence in support of these mechanisms includes the observations that incubation of EDDHHAs with AdoHcy hydrolase generated large molar excesses of halide ions and Ade, that Ade was shown to eliminate spontaneously from 6'-carboxaldehyde 1, and that the more rapid the halide ion release (Cl- > Br- > I-) from the EDDHHAs or the greater the partition ratios (nonlethal turnovers/lethal event), the lower the enzyme inactivation efficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine↗
Suppression of calcium-dependent membrane currents in human fibroblasts by replicative senescence and forced expression of a gene sequence encoding a putative calcium-binding protein.
Human diploid fibroblasts (HDFs) possess Ca(2+)-dependent membrane currents. These currents were suppressed in late-passage normal (senescent) HDFs and prematurely senescent HDFs derived from a subject with Werner syndrome (WS), compared with early-passage normal (young) HDFs. When young HDFs were microinjected with mRNA transcribed in vitro from a cDNA (WS3-10) which encodes a protein bearing a putative Ca(2+)-binding site and whose endogenous gene is overexpressed in senescent and WS HDFs, membrane currents fell to levels present in senescent and WS HDFs. Thus, both replicative senescence and forced expression of the WS3-10 gene sequence lead to suppression of Ca(2+)-dependent membrane currents, which suggests that a causal connection exists between these two processes.
Calcium↗
The use of molecular genetic analysis in the diagnosis of renal cell carcinoma.
The most common genetic aberration seen in nonpapillary renal cell carcinoma is believed to be the loss or inactivation of allelic material on the short arm of chromosome 3 (3p). Two patients underwent nephrectomy at our institution, each initially receiving a histologic diagnosis of renal cell carcinoma. Molecular analysis of these tissues revealed no genetic deletion on 3p, prompting further histologic and immunohistochemical evaluation of the original specimens. These additional studies confirmed alternate histologies other than renal cell carcinoma in each case. These data suggest that the loss of genetic material on the short arm of chromosome 3 may be specific for nonpapillary renal cell carcinoma. Molecular analysis may prove to be a useful adjunct in establishing the diagnosis in renal neoplasms with equivocal histologies.
Adult↗
A novel Cl- conductance in cultured chick cardiac myocytes: role of intracellular Ca2+ and cAMP.
Cl- conductance in cultured embryonic chick cardiac myocytes was characterized using whole-cell patch clamp techniques. Following elimination of cation currents in Na(+)- and K(+)-free internal and external solutions, the basal whole-cell current was predominantly a Cl- current. Cl(-)-sensitive current (ICl) was defined as the difference between the whole-cell currents recorded in normal and low [Cl-]o when measured in the same cell. The whole-cell current in the absence or presence of 10 microM cAMP was time independent, displayed outward rectification with the pipette [Cl-] < 40 mM, and was not saturated with a physiological Cl- gradient. The Cl- current was also activated by 1 microM forskolin and inhibited by 0.3 mM anthracene-9-carboxylic acid (9-AC). Forskolin was less effective than cAMP (internal dialysis) in activating the Cl- current. The cAMP- or forskolin-activated and basal Cl- current were reasonably fit by the Goldman-Hodgkin-Katz equation. The calculated PCl in the presence of cAMP was increased by five- to sixfold over the basal level. In the presence of 5 mM EGTA to decrease free [Ca2+]i, the whole-cell current could not be stimulated by cAMP, forskolin or IBMX (0.1 mM). These data suggest that cultured chick cardiac myocytes have a low basal Cl- conductance, which, as in some mammalian cardiac ventricular myocytes, can be activated by cAMP. However, this study shows that the activation process requires physiological free [Ca2+]i.
Animals↗
Anaerobic biodegradation of methyl esters by Acetobacterium woodii and Eubacterium limosum.
The ability of Acetobacterium woodii and Eubacterium limosum to degrade methyl esters of acetate, propionate, butyrate, and isobutyrate was examined under growing and resting-cell conditions. Both bacteria hydrolyzed the esters to the corresponding carboxylates and methanol under either condition. Methanol was further oxidized to formate under growing but not resting conditions. Unlike the metabolism of phenylmethylethers, no H2 requirement was evident for ester biotransformation. The hydrolysis of methyl carboxylates is thermodynamically favorable under standard conditions and the mixotrophic metabolism of ester/CO2 allowed for bacterial growth. These results suggest that the degradation of methyl carboxylates may be a heretofore unrecognized nutritional option for acetogenic bacteria.
Acetates↗
Tumor targeting in a murine tumor xenograft model with the (sFv')2 divalent form of anti-c-erbB-2 single-chain Fv.
This investigation has utilized novel forms of the single-chain Fv (sFv), wherein a cysteine-containing peptide has been fused to the sFv carboxyl terminus to facilitate disulfide bonding or specific cross-linking of this sFv' to make divalent (sFv')2. The 741F8 anti-c-erbB-2 monoclonal antibody was used as the basis for construction of 741F8 sFv, from which the sFv' and (sFv')2 derivatives were prepared. Recombinant c-erbB-2 extracellular domain (ECD) was prepared in CHO cells and the bivalency of 741F8 (sFv')2 demonstrated by its complex formation with ECD. The tumor binding properties of 125I-labeled anti-c-erbB-2 741F8 sFv, sFv', and (sFv)2 were compared with radiolabeled antidigoxin 26-10 sFv' and (sFv')2 controls. Following intravenous administration of radiolabeled species to severe combined immune-deficient (SCID) mice bearing SK-OV-3 tumors (which over-express c-erbB-2), blood and organ samples were obtained as a function of time over 24 h. Comparative analysis of biodistribution and tumor-to-organ ratios demonstrated the 741F8 sFv, sFv', and (sFv')2 had excellent specificity for tumors, which improved with time after injection. This contrasted with nonspecific interstitial pooling in tumors observed with the 26-10 sFv, sFv', and (sFv')2, which decreased with time after administration. Tumor localization was significantly better for disulfide or peptide crosslinked 741F8 (sFv')2 having Gly4Cys tails than for monovalent 741F8 sFv' or Fab. The superior properties of the 741F8 (sFv')2 in targeting SK-OV-3 tumors in SCID mice suggests the importance of further investigations of divalent sFv analogs for immunotargeting.
Amino Acid Sequence↗
Mutations of the VHL tumour suppressor gene in renal carcinoma.
Multiple, bilateral renal carcinomas are a frequent occurrence in von Hippel-Lindau (VHL) disease. To elucidate the aetiological role of the VHL gene in human kidney tumorigenesis, localized and advanced tumours from 110 patients with sporadic renal carcinoma were analysed for VHL mutations and loss of heterozygosity (LOH). VHL mutations were identified in 57% of clear cell renal carcinomas analysed and LOH was observed in 98% of those samples. Moreover, VHL was mutated and lost in a renal tumour from a patient with familial renal carcinoma carrying the constitutional translocation, t(3;8)(p14;q24). The identification of VHL mutations in a majority of localized and advanced sporadic renal carcinomas and in a second form of hereditary renal carcinoma indicates that the VHL gene plays a critical part in the origin of this malignancy.
Adenocarcinoma, Clear Cell↗
Endotoxin and steroid effects of nitric oxide synthase mRNA expression in rat lung and other tissues.
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Amino Acid Oxidoreductases↗
Prediction of the oxygen cost of the deadlift exercise.
The purpose of this study was to examine the relationship between total estimated work, bar load and total oxygen consumption (TVO2) during the deadlift exercise. Forty-two observations of TVO2 during a wide range of deadlifting bouts were made on a heterogeneous sample of 10 males and 14 females. TVO2 was measured by standard open-circuit spirometry. An R of 0.912 for work and TVO2 indicated that total estimated work during deadlifting can be used to predict oxygen cost accurately. The calculated regression equation was TVO2 (litres of O2) = 2.63 + 0.80 work (kJ) with a S.E.E. of 1.50 litres O2. An R of 0.909 for bar load and TVO2 indicated essentially the same predictability using bar load as the independent variable. The calculated regression equation was TVO2 (litres O2) = 2.88 + 0.005 bar load (kg) with a S.E.E. of 1.5 litres O2. Care should be taken when converting oxygen cost to energy expenditure values using non-protein R equivalents, since underestimations are likely, due to the heavy glycolytic involvement.
Adult↗
Effects of resistance exercise and cycling on recovery blood pressure.
The purpose of this investigation was to examine blood pressure responses during recovery from resistance exercise and cycling. Seven normotensive volunteers (5 males, 2 females) were studied. Resistance exercise consisted of three sets of five exercises (arm curl, hamstring curl, squat, 'lat pull' and bench press) on four occasions: (1) twice using 40% one-repetition maximum (1RM) for 20-25 repetitions, and (2) twice using 70% 1RM for 8-10 repetitions. The subjects also cycled for 25 min at 70% of heart rate reserve on two occasions. Measurements of recovery systolic and diastolic blood pressure were made at 2, 5, 10, 15, 30 and 60 min post-exercise with subjects in the seated position. Analysis of variance with repeated measures revealed that there were no significant differences between recovery blood pressures after the cycling or resistance exercise treatments. Average systolic blood pressure after 2 min of recovery was elevated (115 +/- 2 mmHg, P < 0.0001) and diastolic blood pressure was depressed (48 +/- 3 mmHg, P < 0.0001) in comparison to previously determined baseline values. Systolic blood pressure at 5 min and diastolic blood pressure at 15 min post-exercise were not significantly lower than resting baseline values, and remained so after 60 min of recovery. It was concluded that different intensities of resistance exercise produce the same blood pressure response in recovery and that these changes were approximately equal to those produced by cycling.
Adult↗
Protective effect of galanin on behavioral deficits in experimental traumatic brain injury.
The magnitude of behavioral deficits in traumatic brain injury (TBI) has been shown to be partly related to alterations in the balance between excitatory and inhibitory neurotransmitter release. Previous studies have demonstrated that extracellular excitatory neurotransmitter concentrations dramatically increase following experimental TBI. We examined the effects of a neuromodulatory peptide, galanin (GAL), on behavioral morbidity, as measured by sensory motor and memory performance tasks, associated with experimental TBI in the rat. A single intraventricular injection of GAL (1.0 micrograms, n = 8 or 10.0 micrograms, n = 10) or cerebrospinal fluid (CSF) vehicle (n = 10) was administered 5 minutes prior to central fluid percussion TBI in rats. Performance on sensory motor tasks was assessed prior to injury and for 5 days after TBI with beam-balance, beam-walking, and rotarod tasks. Memory performance was assessed on days 11-15 after TBI with the Morris water maze. TBI produced significant motor and memory deficits in the CSF-treated group. GAL-treated rats had significantly less magnitude of deficits compared to CSF-treated rats on beam-balance, beam-walking, and rotarod performance. The 1.0 micrograms GAL dose produced slightly greater protection than the 10.0 micrograms GAL dose. Neither GAL dose affected body weight loss or Morris water maze performance. These results suggest that the physiologic effects of GAL may reduce certain components of TBI morbidity, possibly by modulating neuronal excitability.
Animals↗
Electrodiffusive movements of chloride ion in sodium-free solution: a possible calcium activated chloride conductance in cultured heart cells.
OBJECTIVE: The aim was to demonstrate that removal of extracellular sodium (Na+o), a manoeuvre known to increase intracellular calcium (Cai2+), can activate a chloride ion conductance in cultured embryonic chick heart cells. METHODS: Intracellular chloride activity (aiCl) and membrane potentials (Em) were simultaneously measured using chloride selective and 3 M KCl filled microelectrodes. RESULTS: In Na+o-free and K+o-free solutions, a frusemide (0.3 mM) resistant decrease in aiCl of 10 mM was recorded within 10 min, along with a 5 mV hyperpolarisation, and the calculated chloride equilibrium potential (ECl) followed the change of Em, suggesting a possibly enhanced chloride conductance. When cells were exposed to Na+o-free solution, the decrease of aiCl by approximately 10 mM was associated with an initial depolarisation, followed by a hyperpolarisation to approximately -60 mV (more negative than ECl). Subsequent removal of K+o depolarised Em to -39 mV (approximately ECl), and no further loss of aiCl occurred. Restoration of K+o caused a hyperpolarisation of Em (more negative than ECl) and a continuing decline of aiCl. Prevention of K+o induced hyperpolarisation by addition of 1 mM Ba2+ stopped the decline of aiCl (Em approximately ECl), suggesting that following Na+o removal, alteration of the driving force for chloride led to a chloride efflux via an enhanced chloride conductance. When Em depolarised to -50 mV after 3 min exposure to 0.1 mM ouabain, removal of [Cl-]o caused a further depolarisation and readdition of [Cl-]o induced an 18 mV hyperpolarisation. This chloride induced hyperpolarisation was blocked by removal of [Ca2+]o (+1 mM EGTA). CONCLUSIONS: The increase in chloride conductance observed under conditions that are known to raise Ca2+i supports the presence of a Ca2+i activated chloride conductance in cultured chick heart cells.
Animals↗
Studies on an artificial trypsin inhibitor peptide derived from the mung bean trypsin inhibitor: chemical synthesis, refolding, and crystallographic analysis of its complex with trypsin.
The active fragment with Lys at the reactive site of mung bean trypsin inhibitor (MBILF) is composed of two peptide chains, A1 of 26 residues and A2 of 9 residues linked via two disulfide bonds. In the present study, a peptide of 22 residue comprising the sequence of chain A1 from position 3 to 24 was synthesized by the solid-phase method. This synthetic peptide with six Cys residues contains a reactive site at position Lys11I-Ser12I (I denotes an inhibitor residue). Air oxidation and HPLC purification resulted in two antitrypsin active components, SPC1 and SPC2. Neither SPC1 nor SPC2 can stoichiometrically inhibit trypsin. The Ki values of SPC1 and SPC2 are 1.2 x 10(-7) and 4.0 x 10(-8) M, respectively. The complexes of SPC1 and SPC2 with bovine beta-trypsin (BTRY) were crystallized by ammonium sulphate precipitation at pH 6.4 and 6.0, respectively. The two crystals have the same crystal form with space group P2(1)2(1)2(1) and cell dimension of a = 63.2(2) A, b = 63.5(6) A, and c = 69.8(4) A. The crystal structure of one complex, SPC1-BTRY, was determined and refined at 2.2 A resolution to a final R-value of 19.2%. From the resulting electron density map, 9 residues of SPC1, from position 9I to 17I, were identified clearly and three-dimension atomic model of the 9-residue reactive loop formed by a disulfide bridge, Cys9I-Cys17I, was built. No electron density corresponding to the other 13 residues was observed in the present map.(ABSTRACT TRUNCATED AT 250 WORDS)
Binding Sites↗
Women's attitudes about receiving mammographic results directly from radiologists.
PURPOSE: To learn what women think about the communication of mammographic results directly to them by radiologists. MATERIALS AND METHODS: Three hundred seven women completed a survey at the time of mammographic examination. The women were asked to indicate the strength of their agreement with seven statements about the communication of mammographic results directly to them by the radiologist. RESULTS: The majority agreed that the radiologist should give them normal (286 women [93%]) or abnormal (277 women [90%]) results directly on site. They also agreed that the radiologist should send a report written in lay language of normal (268 women [87%]) or abnormal (280 women [91%]) results directly to them and that the radiologist should inform them of recommendations for short-term follow-up examinations (93%) and monitor their compliance (88%). CONCLUSION: Because these results reflect findings for only these patients, the authors suggest that additional investigation be performed to determine what women in diverse socioeconomic backgrounds and geographic locations think about these issues.
Breast Neoplasms↗
Effect of Napip on K0 activation of the Na-K pump in adult rat cardiac myocytes.
To determine if environmental factors influence the external K (K0) dependence of Na-K pump current (Ip), we systematically varied internal (pipette) Na (Napip) and Na-K pump activity while measuring the K0 dependence in adult rat cardiac myocytes. For each Napip, reactivation of Ip by K0 was dose dependent. The maximal Ip (Ipmax) and apparent affinity for K0 binding to the Na-K pump (K0.5) increased as Napip increased. The results of making an equimolar substitution of tetramethylammonium for K and Cs, and partial Ip inhibition with ouabain, also showed that Ipmax and K0.5 increased as Napip increased. We simulated pump activity as a function of intracellular Na (Nai) and K0 using a cyclic model of the Na-K pump and found that the model predicts K0.5 for K0 binding increases as Na increases, even when the conditions are adjusted by removing pipette K and partial pump inhibition with ouabain.
Animals↗