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Biomedical subjects

A Chiu

Publications and source records attributed to A Chiu.

At least 37 records · Page 2Linked to original sources
PubMed2000

Effects of carbohydrate ingestion before and during exercise on glucose kinetics and performance.

We investigated the effect of carbohydrate (CHO) ingestion before and during exercise and in combination on glucose kinetics, metabolism and performance in seven trained men, who cycled for 120 min (SS) at approximately 63% of peak power output, followed by a 7 kJ/kg body wt time trial (TT). On four separate occasions, subjects received either a placebo beverage before and during SS (PP); placebo 30 min before and 2 g/kg body wt of CHO in a 6.4% CHO solution throughout SS (PC); 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and placebo throughout SS (CP); or 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and 2 g/kg of CHO in a 6.4% CHO solution throughout SS (CC). Ingestion of CC and CP markedly (>8 mM) increased plasma glucose concentration ([glucose]) compared with PP and PC (5 mM). However, plasma [glucose] fell rapidly at the onset of SS so that after 80 min it was similar (6 mM) between all treatments. After this time, plasma [glucose] declined in both PP and CP (P < 0.05) but was well maintained in both CC and PC. Ingestion of CC and CP increased rates of glucose appearance (R(a)) and disappearance (R(d)) compared with PP and PC at the onset of, and early during, SS (P < 0.05). However, late in SS, both glucose R(a) and R(d) were higher in CC and PC compared with other trials (P < 0.05). Although calculated rates of glucose oxidation were different when comparing the four trials (P < 0.05), total CHO oxidation and total fat oxidation were similar. Despite this, TT was improved in CC and PC compared with PP (P < 0.05). We conclude that 1) preexercise ingestion of CHO improves performance only when CHO ingestion is maintained throughout exercise, and 2) ingestion of CHO during 120 min of cycling improves subsequent TT performance.

Adult↗
PubMed1999

Cr(IV) causes activation of nuclear transcription factor-kappa B, DNA strand breaks and dG hydroxylation via free radical reactions.

Electrophoretic mobility shift, DNA strand breakage assays and electron spin resonance (ESR) spin trapping were used to investigate the activation of nuclear transcription factor (NF)-kappa B, DNA strand breakage and 2'-deoxyguanosine hydroxylation induced by Cr(IV), as well the role of free radical reactions in these processes. Incubation of synthesized Cr(IV)-glutathione complex with cultured Jurkat cells resulted in activation of DNA binding activity of NF-kappa B. Cr(VI) is also able to induce NF-kappa B activation through Cr(V) and Cr(IV) intermediates generated during the reduction of Cr(VI) by the cells. Cr(III) did not cause observable NF-kappa B activation due to its inability to cross cell membranes. Cr(IV)-induced NF-kappa B activation is dose-dependent. Catalase inhibited the activation while superoxide dismutase enhanced it. The metal chelator, deferoxamine, and hydroxyl (.OH) radical scavengers, sodium formate and aspirin, also inhibited the NF-kappa B activation. Electrophoretic assays using lambda Hind III linear DNA showed that, in the presence of H2O2, Cr(IV) is capable of causing DNA strand breaks. Deferoxamine, sodium formate and aspirin inhibited the DNA strand breaks. HPLC measurements also show that .OH radical generated by the Cr(IV)-mediated reaction with H2O2 was capable of causing 2'-deoxyguanosine (dG) hydroxylation to generate 8-hydroxyguanosine (8-OHdG). The relative magnitude of 8-OHdG formation correlated with the generation of .OH radicals. ESR spin trapping measurements showed that reaction of Cr(IV) with H2O2 generated .OH radicals, which were inhibited by deferoxamine, sodium formate and aspirin. The results show that Cr(IV) can cause NF-kappa B activation, DNA strand breaks and dG hydroxylation through .OH radical-initiated reactions. This reactive chromium intermediate may play an important role in the mechanism of Cr(VI)-induced carcinogenesis. The results also suggest that the Cr(IV)-glutathione complex may be used as a model compound to study the role of Cr(IV) in Cr(VI) carcinogenicity.

Antioxidants↗
PubMed1999

Risk factors for falls in hospitalized older medical patients.

BACKGROUND: The incidence of falls among older hospitalized patients is higher than that of community-dwelling older persons. Prevention is important, but factors associated with these falls are less well studied than falls occurring in the community or nursing homes. METHODS: This study was conducted in an acute-care general hospital in Hong Kong. During November 1995 to March 1997, all older inpatients who fell during hospitalization were assessed by a geriatrician, a physiotherapist, and an occupational therapist. A standardized protocol to study the clinical and performance-oriented functional factors was employed. A sex- and age-matched hospital control was recruited for each case. In total, 51 cases and controls (mean ages 77.8 +/- 7.3 years and 77.5 +/- 7.0 years, respectively) were studied. RESULTS: Among the multiple clinical and functional risk factors for falls identified, lower limb weakness (i.e., power less than MRC grade 4 in one or both lower limbs) and poor tandem walk ability emerged as two significant predictive factors for falls in the hospital. The overall classification accuracy of fallers and nonfallers was 79%. The sensitivity was 84% and specificity was 75%. Clinical factors were the underlying causes for the lower limb weakness and poor tandem walk performance. CONCLUSIONS: Among clinical and functional risk factors for falls in the older medical patient, lower limb weakness and poor tandem walk ability were most predictive. Falls prevention programs in hospitals should employ these two tests as screening instruments.

Accidental Falls↗
PubMed1999

Troponin-I, myoglobin, and mass concentration of creatine kinase-MB in acute myocardial infarction.

Myoglobin, creatine kinase-MB (CKMB) mass concentration and troponin-I are newer biochemical markers for the diagnosis of acute myocardial infarction (AMI). We conducted a prospective study to formulate a model for the collective interpretation of these three markers in the diagnosis of AMI. Eighty-seven patients with AMI had serial serum samples taken to establish the time-frame sensitivity of individual markers. None of the markers had a good sensitivity within the first 4 h of infarction. Myoglobin and CKMB (mass) had sensitivities of 92.3% and 96.2%, respectively, at 4-8 h post infarct. CKMB (mass) and troponin-I had sensitivities >92% at 8-24 h. Troponin-I maintained sensitivity >93% until 72 h. A guideline was formulated based on the results. Our data suggest that troponin-I, myoglobin and CKMB (mass) yield satisfactory diagnostic sensitivity when used with reference to specific time frames. The combined use of these markers can provide valuable information for clinicians in managing AMI patients.

Adult↗
PubMed1999

Inhaled nitric oxide protects against hyperoxia-induced apoptosis in rat lungs.

Inhaled nitric oxide (NO), frequently administered in combination with hyperoxic gas mixtures, was recently shown to protect against the injurious consequences of prolonged hyperoxia. We investigated the possibility that this protective effect is attributable to the ability of NO to block pulmonary apoptosis. We show that rats exposed to 100% O2 for 60 h develop severe lung injury consisting of pronounced vascular leak and alveolar apoptosis as inferred from the presence of positive terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and DNA ladders in agarose gels and a decrease in constitutive procaspase-3 levels. However, the inclusion of NO (20 parts/million) in the hyperoxic gas mixture significantly attenuated both the vascular leak and apoptosis. NO reversed the hyperoxia-associated changes in the activity of the redox-sensitive transcription factors nuclear factor-kappaB, activator protein-1, and Sp1 after 24 h, lowered intercellular adhesion molecule-1 levels, and increased glutathione content. We therefore show, for the first time, that NO can protect against both hyperoxia-induced apoptosis and inflammation. The data suggest that this protection may occur at the transcriptional and caspase-activation levels.

Administration, Inhalation↗
PubMed1999

Ten-year cardiovascular risk in a Hong Kong population.

BACKGROUND: Cardiovascular disease is a major health issue in Hong Kong. We conducted a screening program to assess the 10-year risk for the population and to assess the potential benefit of large-scale screening in Hong Kong. METHOD: A local screening program for cardiovascular risk was carried out in a health service network with a total of 17,716 participants. Retrospective data analysis for the prevalence and distribution of the various risk factors was performed. The data were then applied to calculate the 10-year risk of each individual, according to the European Task Force coronary risk chart. RESULTS: Of the participants, 54.2% had total cholesterol levels > 5.2 mmol/l; 28.7% had body mass index > 25 kg/m2; 18.5% were hypertensive; 15.1% were smokers; and 3.7% had diabetes mellitus. There were 35.5% of the screened population who had at least two risk factors and 10.9% had at least three risk factors. A total of 9049 individuals satisfied the criteria for the European Task Force guidelines and were selected for 10-year cardiovascular risk analysis. We calculated that 68.0% of the male population had at least 10% risk and 41.5% had at least 20% risk of developing a coronary heart event within 10 years. Among women, 48.2% of the population carried at least 10% risk and 2.8% carried at least 20% risk. CONCLUSION: The calculated 10-year risk of the population, particularly for men, is significant. Our study demonstrated that mass screening is feasible, and has the benefit of early identification of high-risk individuals, which could be a reasonable strategy for cost-effective medicine.

Adolescent↗
PubMed1998

Arterial blood pressure responses to cell-free hemoglobin solutions and the reaction with nitric oxide.

Changes in mean arterial pressure were monitored in rats following 50% isovolemic exchange transfusion with solutions of chemically modified hemoglobins. Blood pressure responses fall into three categories: 1) an immediate and sustained increase, 2) an immediate yet transient increase, or 3) no significant change either during or subsequent to exchange transfusion. The reactivities of these hemoglobins with nitric monoxide (.NO) were measured to test the hypothesis that different blood pressure responses to these solutions result from differences in .NO scavenging reactions. All hemoglobins studied exhibited a value of 30 microM-1 s-1 for both .NO bimolecular association rate constants and the rate constants for .NO-induced oxidation in vitro. Only the .NO dissociation rate constants and, thus, the equilibrium dissociation constants varied. Values of equilibrium dissociation constants ranged from 2 to 14 pM and varied inversely with vasopressor response. Hemoglobin solutions that exhibited either transient or no significant increase in blood pressure showed tighter .NO binding affinities than hemoglobin solutions that exhibited sustained increases. These results suggest that blood pressure increases observed upon exchange transfusion with cell-free hemoglobin solutions can not be the result of .NO scavenging reactions at the heme, but rather must be due to alternative physiologic mechanisms.

Animals↗
PubMed1997

Disposition and metabolism of olanzapine in mice, dogs, and rhesus monkeys.

Olanzapine (OLZ) is a novel antipsychotic agent with a high affinity for serotonin (5-HT2), dopamine (D1/D2/D4), muscarinic (m1-m5), adrenergic (alpha 1), and histamine (H1) receptors. The pharmacokinetics, excretion, and metabolism of OLZ were studied in CD-1 mice, beagle dogs, and rhesus monkeys after a single oral and/or intravenous dose of [14C]OLZ. After oral administration, OLZ was well absorbed in dogs (absolute bioavailability of 73%) and to the extent of at least 55% in monkeys and 32% in mice. The terminal elimination half-life of OLZ was relatively short in mice and monkeys (approximately 3 hr) and long in dogs (approximately 9 hr). In mice and dogs, radioactivity was predominantly eliminated in feces; but, in monkeys, the major route of elimination of radioactivity was urine. Dogs and monkeys excreted in urine, respectively, 38% and 55% of the dose over a 168-hr period, whereas the fraction of the dose excreted in urine of mice over the collection period (120 hr) was 32%. OLZ was subject to substantial first-pass metabolism; at the tmax, OLZ accounted for 19%, 18%, and 8% of the radioactivity, in mice, dogs, and monkeys, respectively. The ratio of AUC OLZ to AUC radioactivity was, respectively, 10%, 14%, and 4% in mice, dogs, and monkeys. The principal urinary metabolites in mice were 7-hydroxy OLZ glucuronide, 2-hydroxymethyl OLZ, and 2-carboxy OLZ accounting for approximately 10%, 4%, and 2% of the dose. Metabolites that were present in urine in lesser amounts were 7-hydroxy OLZ, N-desmethyl OLZ, and N-desmethyl-2-hydroxymethyl OLZ. In dogs, the major metabolite accounting for approximately 8% of the dose was 7-hydroxy-N-oxide OLZ. Other metabolites identified were 2-hydroxymethyl OLZ, 2-carboxy OLZ, N-oxide OLZ, 7-hydroxy OLZ, and its glucuronide and N-desmethyl OLZ. The major metabolite in monkey urine was N-desmethyl-2-carboxy OLZ, and accounted for approximately 17% of the dose. In addition, N-oxide-2-hydroxymethyl, 2-carboxyl OLZ, and 2-hydroxymethyl OLZ were identified in monkey urine. Thus, in mice and dogs, OLZ was metabolized through aromatic hydroxylation, allylic oxidation, N-dealkylation, and N-oxidation reactions. In monkeys, OLZ was biotransformed mainly through double oxidation reactions involving the allylic carbon and methyl piperazine nitrogen. Whereas the oxidative metabolic profile of OLZ in animals was similar to that of humans, animals were notable for not forming appreciable amounts of the principal human metabolite (i.e. 10-N-glucuronide OLZ).

Administration, Oral↗
PubMed1993

Hypersensitivity pneumonitis: a diagnostic dilemma.

Hypersensitivity pneumonitis is an important but underdiagnosed form of interstitial lung disease. Its clinical hallmark is recurrent or chronic pulmonary symptoms of variable severity associated with an array of systemic symptoms but without extrapulmonary structural abnormalities. Clinical suspicion is the key to diagnosis, which is supported by establishing an environmental or occupational exposure to a causative inhaled antigen; by excluding infectious and other causes of recurrent, migratory, or progressive radiologic lung abnormalities; and by demonstrating antigen-specific antibodies in the serum. Two cases of hypersensitivity pneumonitis are described that illustrate the widely variable clinical, laboratory, and radiologic presentations and emphasize the importance of diagnosing this treatable condition.

Aged↗
PubMed1992

Separation and purification of high molecular weight glycoproteins using agarose gel electrophoresis.

Several components of the extracellular matrix in the molecular weight range of 220 kDa to 150 kDa were purified by preparative electrophoresis on 2.5% Pro-Sieve agarose gels. These high molecular weight glycoproteins, separated under reducing conditions, were recovered in solution by extraction of individual agarose gel slices and analyzed on sodium dodecyl sulfate polyacrylamide gels and Western blots. This simple method permitted the separation and recovery of the laminin B chains (220 kDa and 205 kDa) and entactin (150 kDa) and may prove useful for the purification of other high molecular weight species.

Animals↗
PubMed1990

Environmental carcinogenesis and biotechnology.

Numerous environmental and host factors, some of which are known and some unknown, contribute to cancer development. While data and studies abound, our current understanding of the relation between cancer and the environment is still very limited. Understanding environmental carcinogenesis is critical to its effective management. Biotechnology has revolutionalized the study of biological and biomedical sciences. This minireview provides an overview of environmental carcinogenesis with emphasis on the contributions and prospects of biotechnology in advancing an understanding of environmental carcinogenesis for its prevention and intervention.

Animals↗