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Biomedical subjects

T T Chau

Publications and source records attributed to T T Chau.

At least 37 records · Page 2Linked to original sources
PubMed1991

[A preliminary study of family Apgar index in the Chinese].

The present study was designed to evaluate the clinical availability of family Apgar index in Chinese people. From August 1987 to February 1988, 113 samples from 45 Chinese families were collected from our record family patients. The family members who were over 12 years of age were asked to complete a family Apgar questionnaire and CHQ during a family visit. The patients age, sex, marital status, education, religion, family role, socioeconomic status were also recorded. The result showed that there was no significant correlation between the family Apgar scores and all of the patient's characteristics (sex, age, marital status, education, religion, family role, socioeconomic status) except the score of CHQ. It is suggested that the family Apgar index is a simple and useful instrument to screen out family dysfunctional patients in daily office practice.

Asian People↗
PubMed1991

[The use of extended family APGAR index in OPD].

The present study was designed to evaluate the clinical availability of extended family APGAR in OPD. Five hundred and twenty two patients were collected from three different out-patient departments were studied during a 6 month period. All 522 patients were over 12 years of age and asked to completed an extended family function questionnaire. The patient's age, sex, marital status, occupation, education, family role, socioeconomic status and religion were also recorded. The results showed that there were significant difference among the extended scores of patient's marital status and the socioeconomic status. We also found that patients suffering from family problems, psychosomatic problems and multiple problems have significantly lower extended scores. Because only 3 patients were diagnosed as having family problems by a chart reviewed in all 522 patients, we suggest further research on the extended family APGAR before widely using it in OPD.

Adult↗
PubMed1989

Effects of analgesics on bradykinin-induced writhing in mice presensitized with PGE2.

The intraperitoneal injection of 1 mg/kg PGE2 (which by itself was inactive) enhanced the writhing response induced by a subnociceptive dose of bradykinin (BK, 0.5 mg/kg ip) in male mice. The BK1 agonist, DesArg9-BK and the BK1 antagonist DesArg9-Leu8-BK did not affect writhing. The BK2 agonists, Lys-BK and Tyr-BK, like BK, induced writhing in the PGE2-treated mice. On the other hand, the DPhe7-analogs of BK, which antagonize BK at the BK2 subtype of receptors, potently inhibited the writhing response induced by BK. The writhing was also inhibited by morphine, but in contrast, non-steroidal antiinflammatory drugs (NSAIDs) only weakly inhibited the writhing response in this assay, suggesting that the nociceptive effect of BK was not significantly dependent upon the biosynthesis of PGE2. These results suggest that the algesic effect of BK in this mouse model is mediated via a BK2 receptor subtype.

Analgesics↗
PubMed1989

Pharmacologic modulation of D-49 phospholipase A2-induced paw edema in the mouse.

Paw edema was produced in CD-1 mice by the injection of 0.3 micrograms of snake venom PLA2 (A.p. piscivorus D-49) into the hind paw. Edema peaked at 10 min, remained elevated until 60 min, and then declined slowly. The PLA2 inhibitors, luffariellolide and aristolochic acid, reduced the edema but only when coinjected with the PLA2. The histamine/serotonin antagonists were the most effective drug class against PLA2-induced paw edema. The PAF antagonists, CV-6202 (iv) and kadsurenone (coinjected) reduced the PLA2-induced edema, whereas high doses of the corticosteroids, dexamethasone and hydrocortisone, were also effective. NSAIDs only partially inhibited the paw edema. The LO/CO inhibitors yielded varying activities, with only BW755C and NDGA inhibiting the edema. These results suggest that PLA2 induces paw edema in the mouse via the action of several classes of inflammatory mediators.

Animals↗
PubMed1989

[A study of the effect of patient load and diseases upon resident training in a family medicine clinic].

Patient appointments and scheduling of patients and physicians are the first step in family medicine practice. The goals of outpatient services are to train the family physicians, to provide comprehensive and continuing health care for the family and its members. We evaluated the effect of the appointment system upon residents' training in a family medicine clinic of the Kaohsiung Medical College Hospital. The results were as follows: during the period between Aug. 1985 and Nov. 1986, a total of 2,220 patients and 5,891 out-patient encounters was recorded in this module. The subject age was mostly in the range of 16-64 years for all trainees. The distribution of the chronic diseases was relatively even for all except two trainees. For 4 residents, there were 40-60% more than the ideal patient numbers per session. This abnormal situation interferes with the normal functioning of family medicine clinics. The provocative results of this study suggest at least two important avenues for improvement. The first is to modify the appointment system. The second is to schedule the ideal amount of patients and kinds of diseases in order to provide comprehensive and continuous care for the family and its members.

Adolescent↗
PubMed1989

Pemedolac: a novel and long-acting non-narcotic analgesic.

Pemedolac [cis-1-ethyl-1,3,4,9-tetrahydro-4-(phenylmethyl)-pyrano [3,4-b]indole-1-acetic acid; AY-30,715] exhibited potent analgesic effects against chemically induced pain in rats and mice and against inflammatory pain in rats. In each of the animal models used the analgesic potency of pemedolac was defined by an ED50 of 2.0 mg/kg p.o. or less. Significant analgesic activity was detected in rats at 16 hr after administration of 1 mg/kg p.o. (paw pressure test) and at 10 hr after administration of 10 mg/kg p.o. to mice (p-phenylbenzoquinone writhing). Inasmuch as pemedolac was inactive in the hot plate and tail-flick tests; and its analgesic activity was not antagonized by naloxone (1 mg/kg s.c.), and tolerance did not develop upon multiple administration; this drug does not exert its analgesic effects through an opiate mechanism. Pemedolac differed from standard nonsteroidal anti-inflammatory drugs (NSAIDs) in that the doses which produced analgesia were much lower than those required for either anti-inflammatory or gastric irritant effects. In acute anti-inflammatory tests, pemedolac exhibited only weak activity as evidenced by an ED50 approximately 100 mg/kg p.o. in the carrageenan paw edema procedure. This demonstrates for pemedolac a separation of at least 50-fold between the acute analgesic and anti-inflammatory activities, which was greater than that observed with reference NSAIDs. The compound also had a low ulcerogenic liability with an acute UD50 = 107 mg/kg p.o. and a subacute UD50 estimated to be 140 mg/kg/day p.o. In contrast, the reference NSAIDS (piroxicam, indomethacin, naproxen and ibuprofen) exhibited similar dose-response relationships for the analgesic, anti-inflammatory and gastric irritant effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗
PubMed1988

Temporal relationships of the anti-inflammatory effect of etodolac in the adjuvant arthritic rat.

Using the curative model of adjuvant arthritis, adult male Sprague-Dawley rats were treated with vehicle or etodolac (1, 3, and 8 mg/kg/day, po) for 9 days. Rats were sacrificed after 1, 2, 4, or 9 daily doses, and paw volume, PGE2 concentrations, and N-acetyl-beta-D-glucosaminidase (NAG) activity were determined in the left adjuvant-injected hindpaws. All three doses of etodolac caused a significant decrease in PGE2 concentrations after the first dose, and the decreases persisted for 2, 4, and 9 days of treatment, respectively. In rats given four daily doses of 3 and 8 mg/kg/day of etodolac, the paw volume was significantly decreased by about 50%, compared with that of the arthritic controls. A significant decrease in NAG activity was observed only after nine daily doses of 8 mg/kg/day etodolac. The sequence of anti-inflammatory events manifested following etodolac treatment would appear to be an initial inhibition of PGE2 synthesis, followed by resorption of fluid, and then by a reduction in macrophage infiltration.

Acetates↗
PubMed1987

Histopathologic evaluation of the effects of etodolac in established adjuvant arthritis in rats: evidence for reversal of joint damage.

Histopathologic evaluation of hindpaws from control rats with established adjuvant arthritis showed severe alterations in soft tissue and bone, as well as progressive, moderate-to-severe articular changes. Following treatment with etodolac for 28 days, soft tissue and articular changes were rated mild, and bone changes were rated moderate, but with remodeling. These findings indicate that etodolac partially reversed the joint damage in these rats.

Acetates↗
PubMed1986

Synthesis and analgesic evaluation of 4-(2-heptyloxy)-7-[(Z)-(3-hydroxycyclohexyl)]indole: a caveat on indole-phenol bioisosterism.

The synthesis of 4-(2-heptyloxy)-7-[(Z)-(3-hydroxycyclohexyl)]indole (7) is described. Compound 7 was tested for analgesic properties in the phenylbenzoquinone writhing test and was found to be essentially devoid of activity. In contrast, cis-3-[4-(2-heptyloxy)-2-hydroxyphenyl]cyclohexanol (8), the analogue in which the pyrrolo ring is replaced by a hydroxyl group, had an ED50 of 8.3 mg/kg, sc, in the same model. The absence of bioisosterism between the pyrrolo ring and the phenolic hydroxyl group, in this instance, is discussed in terms of the circumstances that control the manifestation of bioisofunctionality between a pyrrolo ring and a phenolic hydroxyl group, which functions as a hydrogen-bond donor.

Analgesics↗
PubMed1983

Antitussive effect of the optical isomers of mu, kappa and sigma opiate agonists/antagonists in the cat.

The optical isomer of mu and kappa opiates, when given i.v., inhibited the cough reflex in the lightly anesthetized cat, the levoisomers being, in general, 2 to 14 times more potent than the dextro-isomers. The optical isomers of the sigma agonist, SKF 10,047, did not show any antitussive activity up to near lethal or lethal doses (5 mg/kg i.v.). Naloxone (1 mg/kg i.v.) did not block or reverse the antitussive effects of (-)- and (+)-codeine but completely antagonized the effects of an ED84 of (-)-, (+)-morphine, (-)-, (+)-methadone, levomethorphan and dextromethorphan. The cough suppressant effects of the kappa opiates were partially blocked by naloxone, (+/-)-ketocyclazocine being more sensitive to the effect of naloxone than (-)-cyclazocine. (-)-SKF 10,047 at 3.0 mg/kg i.v. and the ED16 of (-)-cyclazocine did not inhibit the antitussive effect of codeine but blocked that of morphine, behaving like naloxone. (+)-SKF 10,047 and (+)-cyclazocine did not show in vivo antagonistic effect vs. codeine or morphine. The ED16 of ketocyclazocine partially antagonized codeine but not morphine. The optical isomers of opiates showed good correlation between the in vivo antitussive potencies and their in vitro inhibitory potencies against (-)-codeine binding in homogenates of the guinea-pig medulla. The data confirm the hypothesis that the cough suppressant effects of opiates are mediated by receptors which are less stereoselective and less naloxone-sensitive than the analgesic receptors. The possible involvement of mu and kappa sites as well as their interactions are discussed.

Animals↗
PubMed1982

3H-Codeine binding in the guinea pig lower brain stem.

Saturable binding of (-)-3H codeine was found in the guinea pig medulla (KD = 5.6 x 10(-7) M, Bmax = 1.4 pmol/mg protein), whereas little stereospecific binding was detected (KD = 4.4 x 10(-5) M). The saturable binding of (-)-3H codeine was slightly enhanced by Na+ and by Mg++ but not by Li++ and Ca++. The enhancement appears to be due to an increase in the number of receptor sites. (-)-3H-Codeine binding was displaced by (-)- and (+)-codeine, morphine, (-)- and (+)-methadone but not by barbiturates. Naloxone, at a high concentration (1 x 10(-5) M), inhibits the binding by only 40%. This agrees with our previously published data which shows that the optical isomers of codeine had significant antitussive effects in the cat, these effects not being antagonized by naloxone. A class of opiate antitussive receptors, which are less naloxone-sensitive and less stereoselective than the mu receptors, is implicated.

Animals↗
PubMed1982

Evidence for the existence of peptide and nonpeptide morphine-like materials in mouse brain: effect of an analgesic intracerebroventricular dose of acetylcholine on their levels.

Brains of mice pretreated with saline or 40 micrograms of acetylcholine (ACh) i.c.v. were fractionated according to published procedures. The fractions yielded four peaks of inhibitory activity in the radioreceptor assay. Intraventricular ACh decreased the inhibitory activity of peak I (fractions 10-19), increased that of peak II (fractions 20-24) and peak III (fractions 25-29) and did not change the activity of peak IV in the radiotracer binding assay. Peaks I, III and IV were potent inhibitors of the coaxially stimulated guinea-pig ileum and such inhibitory activity was not destroyed by incubation with trypsin, carboxypeptidase or by naloxone. Intraventricular ACh did not alter the activity of the three peaks on coaxially stimulated ileum bioassay. Peaks II and III both caused a contraction of the nonstimulated guinea-pig ileum and their effect was reduced either by enzymatic treatment (peak II) or by atropine (peak III). No difference was observed between the effects of each peak in saline or ACh-treated mice in this test. All four peaks were active in the writhing test. The results suggest the presence of several opiate-like materials in the brain. The endogenous opioids appear to be a mixture of endorphin-like peptides as well as nonpeptides. The data also indicate the presence of spasmogenic peptides with some opiate properties.

Acetylcholine↗
PubMed1980

Comparative studies of the pharmacological effects of the d- and l-isomers of codeine.

Opiates are known for their stereospecificity. The following studies show that l-codeine was active in the mouse tail-flick test as well as in the hot plate test whether given p.o. or s.c. The ED50 in the first test was 4.09 mg/kg s.c. (2.01-8.34 mg/ kg) and 13.41 mg/kg p.o. (6.91-26.0 mg/kg). In the second antinociceptive test, the ED50 was 20.66 mg/kg s.c. (11.52-37.08 mg/kg) and 20.47 mg/kg p.o. (14.63-28.57 mg/kg). The d-isomer of codeine was inactive ina both tests up to 100 mg/kg but caused hyperexcitability, convulsions and ultimately death. Although l-codeine was more potent than d-codeine inhibiting the cough reflex in the anesthetized cat, the d-compound did have good activity. The ED50 of the l-isomer was 0.27 mg/kgi.v. (0.14-0.47 mg/kg) and that of the d-isomer was 1.61 mg/kg i.v. (0.98-2.65 mg/kg). In these animals, l-codeine did not significantly affect the cardiovascular parameters at the doses tested, whereas d-codeine caused a significant but transient decrease in the blood pressure and heart rate. The specific and nonspecific properties of d- and l-codeine were further delineated in the opiate receptor binding assay. l-Codeine inhibited the stereospecific binding of 2.2 x 10(-9) M [3H]dihydromorphine in mouse brain homogenate with the IC50 being 1.6 x 10(-5) M (1.2 x 10(-5)--2.0 x 10(-5) M). d-Codeine had no effect up to 10(-4) M.

Analgesia↗