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Biomedical subjects

B Tam

Publications and source records attributed to B Tam.

11 recordsLinked to original sources
PubMed2004

Do vitamin E and selenium have beneficial effects on trinitrobenzenesulfonic acid-induced experimental colitis.

The balance between oxidant and antioxidant systems may be important in the pathogenesis and/or maintenance of tissue injury in ulcerative colitis. This study was designed to evaluate the effects of vitamin E and selenium supplementations on tissue injury and oxidative stress in trinitrobenzenesulfonic acid-induced ulcerative colitis in rats. Trinitrobenzenesulfonic acid administration severely changed the normal architecture of the colon and significantly increased the levels of malondialdehyde, protein carbonyl, and xantine oxidase (P < 0.001) in the colon homogenates of these rats. Supplementation of selenium to the trinitrobenzenesulfonic acid-treated rats neither improved the histopathological findings nor decreased the levels of malondialdehyde and protein carbonyl. Vitamin E supplementation reduced the levels of malondialdehyde and protein carbonyl but did not improve the colonic lesions. Supplementation of vitamin E + selenium significantly reduced both the severity of colonic lesions and the levels of malondialdehyde and protein carbonyl. In conclusion, we suggest that antioxidants and specific micronutrients may have beneficial effects in the treatment of ulcerative colitis.

Animals↗
PubMed2001

Stressors and coping methods among chronic haemodialysis patients in Hong Kong.

The purpose of the study was to determine the stressors and coping methods of chronic haemodialysis patients in Hong Kong. Relationships among treatment-related stressors, coping methods and length of time on haemodialysis were explored. Fifty subjects completed the Haemodialysis Stressor Scale (HSS) and Jalowiec Coping Scale (JCS). Results revealed that limitation of fluid was the most frequently identified stressor, followed by limitation of food, itching, fatigue and cost. The most common coping methods are 'accepted the situation because very little could be done', followed by 'told oneself not to worry because everything would work out fine' and 'told oneself that the problem was really not that important.' It was found that the traditional philosophies of the Chinese--Confucianism, Buddhism, and Taoism--share an approach to the understanding and management of life stressors as different from that adopted by Western philosophies. The findings of this study can further facilitate nurse practitioners in providing support, information, and alternative solutions when assisting patients in coping with long-term haemodialysis.

Activities of Daily Living↗
PubMed1998

Mutagenesis of the aspartic acid ligands in human serum transferrin: lobe-lobe interaction and conformation as revealed by antibody, receptor-binding and iron-release studies.

Recombinant non-glycosylated human serum transferrin and mutants in which the liganding aspartic acid (D) in one or both lobes was changed to a serine residue (S) were produced in a mammalian cell system and purified from the tissue culture media. Significant downfield shifts of 20, 30, and 45 nm in the absorption maxima were found for the D63S-hTF, D392S-hTF and the double mutant, D63S/D392S-hTF when compared to wild-type hTF. A monoclonal antibody to a sequential epitope in the C-lobe of hTF reported affinity differences between the apo- and iron-forms of each mutant and the control. Cell-binding studies performed under the same buffer conditions used for the antibody work clearly showed that the mutated lobe(s) had an open cleft. It is not clear whether the receptor itself may play a role in promoting the open conformation or whether the iron remains in the cleft.

Antigen-Antibody Reactions↗
PubMed1997

A kinetically active site in the C-lobe of human transferrin.

Release of iron from transferrin, the iron-transporting protein of the circulation, is a concerted process involving remote amino acid residues as well as those at the two specific iron-binding sites of the protein. Previous studies of fluoresceinated transferrin have suggested Lys 569 as a kinetically active site in the C-terminal lobe of the protein. We have therefore turned to site-directed mutagenesis to investigate the role of Lys 569 in the release process at pH 5.6, the pH of the endosome where iron is transferred from transferrin to the iron-dependent cell. Mutation of positively charged Lys 569 to an uncharged Gln results in a protein in which release of iron from the mutated lobe to pyrophosphate is slowed by a factor of 15-20 and in which release kinetics switch from a complex saturation-linear to a simple saturation function. Acceleration of release by chloride is also substantially less than in native transferrin. When Lys 569 is replaced by a positively charged Arg, in contrast, observed release rates and chloride dependence are close to those of the native protein. The mechanism of release from the C-lobe site therefore appears to be sensitive to positive charge at position 569. Binding of chloride or other simple anion accelerates and is essential for release from the C-lobe; a muted response of K569Q to chloride concentration suggests that Lys 569 may function as a kinetically active anion-binding residue in the C-lobe. Despite the kinetic effects of the K569 mutation on iron release, rates of iron uptake by K562 cells from the C-lobes of native, K569Q, and K569R proteins are almost identical. In contrast to the C-lobe, iron release from the N-lobe is insensitive to charge at residue 233, the site in that lobe homologous to residue 569, with chloride retarding rather than accelerating release. K233, therefore, is not a kinetically active anion-binding site in the N-lobe. Release mechanisms differ substantially in the two lobes of transferrin despite the identity of ligands and their nearly identical arrangements in the lobes.

Humans↗
PubMed1995

Diacylglycerol analogs inhibit the rod cGMP-gated channel by a phosphorylation-independent mechanism.

The electrical response to light in retinal rods is mediated by cyclic nucleotide-gated, nonselective cation channels in the outer segment plasma membrane. Although cGMP appears to be the primary light-regulated second messenger, cellular levels of other substances, including Ca2+ and phosphatidylinositol-4,5-bisphosphate, are also sensitive to the level of illumination. We now show that diacylglycerol (DAG) analogs reversibly suppress the cGMP-activated conductance in excised patches from frog rod outer segments. This suppression did not require nucleoside triphosphates, indicating that a phosphorylation reaction was not involved. DAG was more effective at low than at high [cGMP]: with 50 microM 8-Br-cGMP, the DAG analog 1,2-dioctanoyl-sn-glycerol (1,2-DiC8) reduced the current with an IC50 of approximately 22 microM (Hill coefficient, 0.8), whereas with 1.2 microM 8-Br-cGMP, only approximately 1 microM 1,2-DiC8 was required to halve the current. DAG reduced the apparent affinity of the channels for cGMP: 4 microM 1,2-DiC8 produced a threefold increase in the K1/2 for channel activation by 8-Br-cGMP, as well as a threefold reduction in the maximum current, without changing the apparent stoichiometry or cooperativity of cGMP binding. Inhibition by 1,2-DiC8 was not relieved by supersaturating concentrations of 8-Br-cGMP, suggesting that DAG did not act by competitive inhibition of cGMP binding. Furthermore, DAG did not seem to significantly reduce single-channel conductance. A DAG analog similar to 1,2-DiC8--1,3-dioctanoyl-sn-glycerol (1,3-DiC8)--suppressed the current with the same potency as 1,2-DiC8, whereas an ethylene glycol of identical chain length (DiC8-EG) was much less effective. Our results suggest that DAG allosterically interferes with channel opening, and raise the question of whether DAG is involved in visual transduction.

Ambystoma↗
PubMed1990

Activation of the glycine site in the NMDA receptor is necessary for the induction of LTP.

The effects of 7-chlorokynurenate (7-C1KY) were examined on N-methyl-D-aspartate (NMDA) receptor-mediated synaptic mechanisms in the CA1 region of rat hippocampal slices. 7-C1KY depressed both the NMDA receptor-mediated component of synaptic transmission recorded in Mg2(+)-free medium and the induction of long-term potentiation (LTP) in Mg2(+)-containing medium. Both of these effects were reversed by D-serine, suggesting that the action of 7-C1KY was at the allosteric glycine site on the NMDA receptor.

Action Potentials↗
PubMed1986

Stimulation of corticosterone secretion in vitro by brief ACTH exposure.

We examined the relationship between ACTH concentration and exposure duration on stimulation of corticosterone (B) secretion in vitro using perifused enzymatically dispersed rat adrenocortical cells. A modular perifusion apparatus was used that permitted evaluation of 20-24 cell chambers per experimental session. In expt 1, 20-1000 pg/ml concentrations of synthetic ACTH-(1-24) were presented to cells for 1 min. In expt 2, 100 pg ACTH-(1-24) was presented to adrenal cells in five dose-duration regimens ranging from 5 pg/min for 20 min to 100 pg/min for 1 min. Perifusal rate was 1 ml/min in all sessions. B was determined by radioimmunoassay. In expt 1 (constant-duration paradigm), 1-min presentation of ACTH-(1-24) produced log-linear dose-response effects across these concentrations (r = 0.926, P less than 0.01). In expt 2 (constant-mass paradigm), identical masses administered in different dose-duration regimens had different steroidogenic efficacies (P less than 0.02): low-dose long-duration regimens provoked greater total release than high-dose short-duration regimens. Overall, every dose-duration regimen was associated with stimulation of B secretion. These results indicate that very brief exposure to physiological concentrations of ACTH-(1-24) is a significant stimulus for corticosteroid secretion; variations in the dose-duration regimen over the physiological range modifies both the maximum rate of secretion and the duration of secretion, but not the response latency; and ACTH-(1-24) presentation mass is not the sole determinant of B secretion.

Adrenal Cortex↗
PubMed1986

Dynamics of thyrotropin-releasing hormone-induced thyrotropin and prolactin secretion by acutely dispersed rat adenohypophyseal cells. Evidence for 'all-or-none' secretion by heterogeneous secretory units, each with a specific response threshold.

We have examined the dynamics of thyrotropin-releasing hormone (TRH)-stimulated secretion of prolactin (PRL) and thyrotropin-stimulating hormone (TSH) using enzymatically dispersed rat adenohypophyseal cells suspended in a perfusion chamber with a volume of 0.2 ml to minimize mixing and dilution. One-min exposure to 3-300 nM TRH, the effective dose range, elicited immediate pulses of PRL and TSH secretion with dose-dependent amplitudes. At all TRH concentrations, following a brief burst of secretion lasting less than 1 min, release of both hormones declined precipitously. Increasing the duration of stimulation up to 30 min with half-maximal TRH concentrations did not alter the dynamics of the initial response and was ineffective in maintaining the initial amplitude of secretion. This phenomenon could not be attributed to exhaustion of readily releasable intracellular PRL and TSH, since an increment in TRH concentration elicited a second pulse of hormone secretion with temporal response characteristics identical to the first. The amplitude of the second pulse was dependent on both the initial concentration of TRH and the magnitude of the increment in TRH concentration. With a stepwise increase in TRH concentration during continuous perfusion, the sum of PRL or TSH secreted from all bursts of secretory activity approximated that achieved with a single exposure to the highest concentration of TRH employed. The high-amplitude secretory response to a given concentration of TRH was restored after an 8-min perfusion with medium alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Genetic differences in anticonvulsant sensitivity in mouse lines selectively bred for ethanol withdrawal severity.

WSP (withdrawal seizure-prone) mice exhibit approximately 10-fold more severe withdrawal convulsions than WSR (withdrawal seizure-resistant) mice after identical chronic ethanol exposure. Although WSP and WSR mice do not differ in threshold for seizures elicited by electroconvulsive shock (ECS), WSR mice are more sensitive to ethanol-induced elevation of ECS seizure thresholds. The current experiments demonstrated that WSR mice showed more ECS-induced seizure threshold elevation than WSP mice when tested after the administration of C1-C5 straight-chain alcohols. Whereas the brain concentrations of the C1 and C2 alcohols did not differ between the lines, WSP mice tended to have higher brain concentrations than WSR mice of the C3-C5 alcohols, even though they exhibited the smaller behavioral response in all cases. Thus, the difference between WSP and WSR mice was one of neurosensitivity and could not be attributed to pharmacokinetic differences. The WSR line was also more sensitive to ethchlorvynol, methyprylon, barbital, phenobarbital, pentobarbital, diazepam, valproic acid and phenytoin in this test. Examining loss of righting reflex (RR), we found that WSP and WSR mice did not differ in ED50, latency to lose RR or duration of loss of RR. Thus, the genetic anticonvulsant sensitivity difference is not simply a genetic difference in sensitivity to central nervous system depression between the lines. In summary, WSR mice were more sensitive to the anticonvulsant effects of a variety of compounds than WSP mice, suggesting that some genes influence both ethanol withdrawal seizures and ethanol's anticonvulsant effects.

Alcohol Withdrawal Delirium↗
PubMedDate not supplied

Vagus-mediated activation of mucosal mast cells in the stomach: effect of ketotifen on gastric mucosal lesion formation and acid secretion induced by a high dose of intracisternal TRH analogue.

TRH analogue, RX 77368, injected intracisternally (i.c.) at high dose (3 microg/rat) produces gastric mucosal lesion formation through vagal-dependent pathway. The gastric mucosal hyperemia induced by i.c. RX 77368 was shown to be mediated by muscarinic vagal efferent fibres and mast cells. Furthermore, electrical vagal stimulation was observed to induce gastric mucosal mast cell degranulation. The aim of the study was to assess the influence of ketotifen, a mast cell stabilizer, on RX 77368-induced gastric lesion formation and gastric acid secretion. RX 77368 (3 microg, i.c.) or vehicle (10 microL, i.c.) was delivered 240 min prior to the sacrifice of the animals. Ketotifen or vehicle (0.9% NaCl, 0.5 mL) was injected intraperitoneally (i.p.) at a dose of 10 mg x kg(-1) 30 min before RX 77368 injection. The extent of mucosal damage was planimetrically measured by a video image analyzer (ASK Ltd., Budapest) device. In the gastric acid secretion studies, the rats were pretreated with ketotifen (10 mg x kg(-1), i.p.) or vehicle (0.9% NaCl, 0.5 mL, i.p.), 30 min later pylorus-ligation was performed and RX 77368 (3 microg, i.c.) or vehicle (0.9% NaCl, 10 microL, i.c.) was injected. The rats were killed 240 min after i.c. injection, and the gastric acid secretion was measured through the titration of gastric contents with 0.1 N NaOH to pH 7.0. RX 77368 (3 microg, i.c.) resulted in a gastric mucosal lesion formation involving 8.2% of the corpus mucosa (n = 7). Ketotifen elicited an 85% inhibition on the development of mucosal lesions (n = 7, P < 0.001) whereas ketotifen alone had no effect on the lesion formation in the mucosa (n = 7). The RX 77368 induced increase of gastric acid secretion was not influenced by ketotifen pretreatment in 4-h pylorus-ligated animals. Central vagal activation induced mucosal lesion formation is mediated by the activation of mucosal mast cells in the stomach. Mast cell inhibition by ketotifen does not influence gastric acid secretion induced by i.c. TRH analogue in 4-h pylorus-ligated rats.

Animals↗