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Biomedical subjects

B T Ho

Publications and source records attributed to B T Ho.

At least 19 recordsLinked to original sources
PubMed1992

Opioid-dopaminergic mechanisms in the potentiation of d-amphetamine discrimination by interferon-alpha.

In rats trained to discriminate 0.8 mg/kg IP d-amphetamine from 1 ml/kg saline, 4 x 10(6) U/kg of recombinant human interferon-alpha (rIFN-alpha) given intramuscularly 1 h prior to tests potentiated responses elicited by 0.4 mg/kg d-amphetamine. Coadministration of the opioid receptor antagonist naloxone (1 mg/kg IP) with rIFN-alpha suppressed the potentiation of d-amphetamine by the cytokine. Opioid-dopaminergic mechanisms are proposed to explain the action of rIFN-alpha.

Animals↗
PubMed1992

Analgesic activity of anticancer agent suramin.

Suramin exhibited morphine-like analgesic activity in mice. It antagonized both thermal (hot-plate) and acetic acid-evoked writhing responses with ED50 values 1/100 and 1/68, respectively, that of morphine. The suramin- and morphine-induced hot-plate analgesia was suppressed by administration of 0.5 mg/kg naloxone. However, lower doses (5-30 micrograms/kg) of naloxone produced dose-related potentiation or suppression of suramin and morphine analgesia. This potentiation effect may be due to the inhibition of writhing by naloxone itself rather than be a direct antagonism of the morphine effect.

Analgesia↗
PubMed1991

Inhibition of adenylate cyclase by tetraplatin.

In the investigation of effects of platinum-containing compounds on dopamine (DA)-activated adenylate cyclase system, tetraplatin and cisplatin were found to suppress the increase of enzyme activity by various activators. However, tetraplatin was a much more potent inhibitor than cisplatin, with its I50 values being 1/25, 1/45, and 1/130 that of cisplatin in the presence of DA/Gpp(NH)p, NaF/AlCl3, and forskolin/Gpp(NH)p respectively.

Adenylyl Cyclase Inhibitors↗
PubMed1990

Beta-adrenoceptor binding studies with LY195448 and metabolites.

LY195448(R) (a phenethanolamine derivative that has demonstrated cytotoxic activity against cell cultures in vitro but that exhibited a hypotensive side effect during phase I trials), its p-hydroxy and acid metabolites, and a noncytotoxic S-stereoisomer were evaluated with respect to competitive binding against the beta-adrenergic antagonist [3H]dihydroalprenolol in rat brain cortex and human cardiac tissues. When IC50 and Ki values were compared, the R-isomer of LY195448 in general was more potent than the S-stereoisomer. While LY195448(R) was about 10-fold more active than the p-hydroxy metabolite in cardiac tissues, the two compounds were nearly equipotent both in blocking the binding of radioligand to the brain and in reducing blood pressure in rats. In the cerebral preparation, the binding of the acid metabolite was weak, with its activity being equal to that of the S-stereoisomer.

Animals↗
PubMed1988

The effect of the experimental antitumor agent caracemide on brain choline acetyltransferase.

Caracemide was found to inhibit choline acetyltransferase (CAT) from rat brain. A concentration of 0.5 mM caracemide inhibited the enzyme by 93%, whereas a degradation product from caracemide, N-(methylcarbamoyloxy)acetamide, produced only a 50% inhibition. Two other degradation products, N-(methyl-carbamoyloxy)-N'-methylurea and N-hydroxy-N'-methylurea, lacked any inhibitory activity. With bovine brain CAT, caracemide showed noncompetitive inhibition with the substrate choline, Km 337 microM, Ki240 microM, Vmax 2.83 nmol acetylcholine formed/min/mg protein and mixed inhibition with the substrate acetyl-CoA, Km 21 microM, Ki 146 microM, Vmax 3.85 nmol acetylcholine formed/min/mg protein.

Animals↗
PubMed1987

Neurochemical and behavioral effects of N-ethyl-acetylcholine aziridinium chloride in mice.

N-ethyl-choline aziridinium (ECA) and N-ethyl-acetylcholine aziridinium (EAA) were shown to be inhibitors of high affinity choline uptake in vitro (IC50 = 0.4 microM and 1.5 microM, respectively), and intraventricular administration showed that EAA was more selective in its inhibition of hippocampal choline uptake in vivo. EAA significantly reduced the activity of choline acetyltransferase in the hippocampus 3 to 28 days following intraventricular infusion, but not in the striatum or parahippocampal cortex. Neither muscarinic receptor binding nor glutamic acid decarboxylase activity were affected in any of the three brain regions. EAA (12 or 16 nanomoles, intraventricular) significantly impaired memory performance of mice in a radial arm maze when tested two weeks after treatment. A subgroup analysis implicated long-term reference memory as the mechanism disrupted.

Animals↗
PubMed1987

Inhibition of brain choline acetyltransferase by tetraplatin.

Tetraplatin inhibited choline acetyltransferase (CAT) from rat and bovine brain with I50 values of 13.5 and 40 microM, respectively. At 0.5 mM concentration, tetraplatin exhibited inhibition of the rat brain enzyme by 89%, whereas cisplatin yielded only 18% inhibition. With bovine CAT, tetraplatin showed noncompetitive inhibition with the substrate choline, Km 337 microM, Ki 29 microM, Vmax 2.83 nmoles acetylcholine formed/min/mg protein, and competitive inhibition with the substrate acetyl-CoA, Km 21 microM, Ki 16 microM, Vmax 3.85 nmoles acetylcholine formed/min/mg protein.

Animals↗
PubMed1985

Passive avoidance deficits in mice following ethylcholine aziridinium chloride treatment.

High-affinity choline uptake (HACU) appears to be the rate-limiting step in the synthesis of the neurotransmitter acetylcholine. The present experiment was designed to examine the effects of irreversible inhibition of HACU by ethylcholine aziridinium chloride (ECA) on passive avoidance retention in mice. Animals were injected intracerebroventricularly, and one-trial passive avoidance retention evaluated 21 days later. A significant retention deficit was observed in ECA-treated animals upon retest 24 hours after training. ECA-induced changes in retention were accompanied by significant reductions in choline acetyltransferase (CAT) activity in only two of seven brain regions tested, hippocampus (48% of control) and cerebellum (76% of control). The results support the involvement of hippocampal cholinergic activity in mediation of passive avoidance learning.

Animals↗
PubMed1985

Evaluation of two distinctive beta-carbolines on serotonin binding in human platelets.

6-MeOTHBC binds to both high and low affinity receptors in human platelets. The beta-carboline is less active than chlorimipramine at the low affinity site, and it is weaker than methysergide, a known 5-HT antagonist, at the high affinity site. The other beta-carboline, B-CCE, is not active at either receptor in platelets. The data supports the view that platelets could be used as a limited model for studying 5-HT-ergic neurons.

Blood Platelets↗
PubMed1984

Haloperidol. Plasma levels and prolactin response as predictors of clinical improvement in schizophrenia: chemical v radioreceptor plasma level assays.

The relationship between clinical response of schizophrenic patients to haloperidol and (1) blood levels of the medication, determined by both gas-liquid chromatography (GLC) and radioreceptor (RR) assays, or (2) prolactin response to the medication, was examined in an inpatient study using several fixed doses of haloperidol. Regression analysis disclosed a substantial curvilinear relationship between steady-state GLC-determined plasma haloperidol levels and decrease in Brief Psychiatric Rating Scale (BPRS) Psychosis factor scores; however, no substantial relationship was found between clinical response and RR plasma haloperidol levels or serum prolactin response to haloperidol. Our results suggest that steady-state plasma levels of haloperidol determined by the GLC chemical assay are a better predictor of decreases in BPRS Psychosis factor scores than RR assayed plasma haloperidol levels or prolactin response to haloperidol.

Adult↗
PubMed1984

Prolactin response to single and multiple doses of haloperidol in schizophrenic patients.

Serum prolactin and blood levels of haloperidol were assessed in schizophrenic patients after single acute oral doses of haloperidol and during fixed dose treatment with this medication. Although significant intrapatient correlations between prolactin responses to different doses of haloperidol were found, no statistically significant interpatient relationship between haloperidol dose and prolactin response emerged. There were statistically significant relationships between steady-state plasma and red cell haloperidol levels (measured by radioreceptor or gas liquid chromatographic techniques) and serum prolactin response, but not between blood levels after the acute haloperidol dose and prolactin response.

Adolescent↗
PubMed1984

Retinal burns occurring at cataract extraction.

Paramacular changes presumably induced by operating microscope light have been described previously in six patients who had undergone extracapsular cataract extraction with posterior chamber lens implantation. Twelve additional patients are reported, including pseudophakes and nonpseudophakes, macular and paramacular burns, and no visual loss and severe visual loss. Burns occurred in spite of filters and light barriers used in some cases. Light sources were tungsten bulb or halogen/fiberoptic. Three cases had essentially normal preoperative angiography. Currently recommended safety measures have not eliminated this complication.

Aged↗
PubMed1984

Effects of 6-methoxytetrahydro-beta-carboline on 5-hydroxytryptamine binding in rat brain.

6-MeOTHBC competes for 5-HT binding sites in rat brain in-vitro and in-vivo. The beta-carboline is significantly more active at the type 1 [3H]-5-HT, than the type 2 [3H]spiperone receptors, in-vitro. Following injection, 6-MeOTHBC significantly decreases [3H]-5-HT binding in the cortex. The ineffectiveness on [3H]spiperone binding in-vivo corresponds with the low affinity in-vitro. The effect of 6-MeOTHBC on central 5-HT binding may be a significant aspect of its 5-HT-ergic activity.

Animals↗
PubMed1984

Serotonin levels and platelet uptake during premenstrual tension.

Premenstrual tension was studied in 16 females, using both biochemical and psychological parameters during the pre- and postmenstrual phases. Uptake of serotonin (5-HT) and the levels of 5-HT in platelet-rich plasma and platelet-poor plasmas were determined. Degrees of distress experienced pre- and postmenstrually were quantified via the Moos menstrual distress questionnaire. The mean Vmax was significantly lower during the premenstrual (tension) phase (8.2 +/- 0.9 pmol/min) as compared to the postmenstrual (normal) phase (14.4 +/- 3.2 pmol/min). There was no significant difference in the Km values. A highly significant (p less than 0.001) reduction in the levels of 5-HT in platelet-rich plasma (-23.2%) and platelet-poor plasma (-19.1%) was found during the premenstrual phase. There were correlations between the kinetic parameters of 5-HT uptake and some of the Moos symptoms.

Adolescent↗
PubMed1983

The residual effect of chronic neuroleptic treatment on the neuroleptic binding assay in rats.

Chronic chlorpromazine administration to rats (25 mg/Kg/day) for 30 days followed by a washout period of 10 days resulted in an increase in both the measured maximum number of binding sites, Bmax, and the apparent dissociation constant, Kd, for the binding of 3H-spiroperidol to neural membranes of the brain. When membrane suspensions were progressively diluted before the binding assay, it was found that the apparent Bmax did not change with dilution, remaining higher in membranes of chlorpromazine-treated rats than in controls. The apparent increase in Kd, on the other hand, was found to be an artifact of the assay. Thus extrapolation of the measured or apparent Kd value to infinite dilution resulted in identical value for Kd regardless of the treatment.

Animals↗
PubMed1983

Various inputs modify caudate neuronal activity.

This study investigates the input of substantia nigra (SN), dorsal raphe (DR), and medial lemniscus (ML) on caudate nucleus (CN) neurons as well as a non-specific-polysynaptic input (acoustic AC). Ninety-one units demonstrating spontaneous activity were recorded extracellularly using anesthetized rats. SN, DR, ML, and AC stimulation altered the spontaneous discharges in 79%, 90%, 86%, and 85% of the CN neurons, respectively. Only ML stimulation elicited patterns of time-locked responses in 16% of the CN units. The CN neurons showed high convergence to the four types of stimulation. Based on these results, interconnections and interrelations between SN, DR, ML, and the CN are suggested.

Animals↗
PubMed1983

Kinetic evaluation of platelet monoamine oxidase following relaxation in chronic anxiety.

The effect of relaxation training, utilizing EMG biofeedback, on platelet monoamine oxidase (MAO) activity was examined in patients with a history of chronic anxiety. Anxiety scores and MAO activity were significantly lowered after 4 weeks of therapy. Kinetic studies, using phenylethylamine as substrate, indicated a significant increase of the Km constant while the Vmax showed no significant or consistent variation. It is thought that this phenomenon represents an adaptive response by the individual to maintain a homeostatic level of the biogenic amines.

Adult↗