Search PubMed⌕ Search

Biomedical subjects

J T Cheng

Publications and source records attributed to J T Cheng.

At least 163 records · Page 9Linked to original sources
PubMed1994

Propofol does not reduce infarct volume in rats undergoing permanent middle cerebral artery occlusion.

As propofol has been reported to have effects similar to those of thiopentone on cerebral blood flow, intracranial pressure and cerebral metabolic rate, we postulated that it might also have a protective effect on focal cerebral ischemia. This experiment was designed to test whether or not propofol can alter infarct volume resulting from permanent focal cerebral ischemia in rats. Forty-five rats were randomly assigned to three groups, all of which received xylaxine (5 mg kg-1 im) and ketamine (100 mg kg-1 ip) anesthesia. Rectal temperatures were controlled at 36-37 degrees C. A right temporal craniotomy was performed and the middle cerebral artery (MCA) was ligated with a 10-O suture. Both common carotid arteries (CCAs) were then occluded for 60 minutes using aneurysm clips. In Group 1 rats (n = 15), normal saline (1 ml kg-1 i.v.) was given right after MCA and CCAs ligation. In Group 2 rats (N = 15), propofol (10 mg kg-1 i.v. bolus) was given right after MCA and CCAs ligation. In Group 3 rats (n = 15), continuous intravenous infusion of propofol (16 mg kg-1 hr-1) was given for four hours following MCA and CCAs ligation, during which time mean arterial pressure was maintained approximately 90 mmHg. Twenty-four hours after ischemia, the brains were removed, frozen, sectioned and stained with 2% 2,3,5-triphenyltetrazolium chloride. The cross-sectional area of infarction on each brain slice was measured using computer imaging analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Inhibitory effect of xylamine on the uptake of [3H]dopamine into isolated striatal synaptosomes of the rats.

The synaptosomal preparations from Wistar rat striata show a Na(+)-dependent, nomifensine-sensitive uptake of [3H]dopamine([3H]DA). Xylamine, a nitrogen mustard, attenuated this uptake of [3H]DA into the synaptosomes (IC50 = 0.2 microM). The dose-dependent reduction of [3H]DA uptake by xylamine indicated competitive kinetics. Action of xylamine was modified if the active transport inhibitor, ouabain or iodoacetate, was also incubated during the pretreatment period or if the content of Na+ in medium was changed. Also, xylamine displaced the binding of [3H]mazindol in a correlative way with the inhibition of [3H]DA uptake. However, the activity of Na+, K(+)-ATPase in synaptosomes was not modified by xylamine at concentrations sufficient to block the uptake of [3H]DA. These findings suggest that xylamine has the ability to compete with the transport of [3H]DA into striatal synaptosomes through an effect on the carrier instead of an action on enzymatic activity.

Animals↗
PubMed1993

Labeling of tyrosines in proteins with [15N]tetranitromethane, a new NMR reporter for nitrotyrosines.

Lysozyme and ribonuclease were used as model proteins to explore the feasibility of detecting protein-bound nitrotyrosines by 15N-NMR spectroscopy. The reporter group was introduced via synthesized [15N]tetranitromethane. Several experiments for detection of the 15N resonance in the model [3-15N]nitrotyrosine demonstrated a substantial pH-dependence of the chemical shift. When lysozyme was nitrated, either two or three 15N resonances were detected, depending on the extent of nitration. The pH-dependence of the detected resonances clearly described an apparent microscopic pK in accord with reported values, while addition of Gd(III) gave selective line broadening, indicating that the 15N reporter group could also monitor relative distances from paramagnetic sources. Nitration of ribonuclease showed five 15N resonances, of which three persisted in the purified monomer. The pH-dependence of these resonances also described apparent microscopic pK values. The [3-15N]nitrotyrosine model was reduced to the [3-15N]aminotyrosine and its 15N resonance was easily monitored by several methods, including selective population inversion. When the protein-bound nitrotyrosines were similarly reduced, much sample decomposition resulted, a possible result of photooxidation, and/or reduction of disulfide bond(s), thereby making interpretation difficult.

Animals↗
PubMed1993

Antihypertensive principles from the leaves of Melastoma candidum.

Three active principles were isolated from the leaf of Melastoma candidum using the screening of hypotensive effects on spontaneously hypertensive rats (SHR). Intravenous injection of castalagin, procyanidin B-2, or helichrysoside into SHR lowered the mean blood pressure in a dose-dependent manner, with helichrysoside being the most potent compound. Plasma noradrenaline (NA) levels, both basal in SHR and elevated in normal rats through cold-stress stimulation, were attenuated by these compounds in a way which was not influenced by adrenalectomy. Decrease of NA release from sympathetic nerves was assumed to be responsible. Moreover, the hypertensive effect of various vasoconstrictors in anesthetized rats was reduced by helichrysoside. The same results were also observed in castalagin or procyanidin B-2 treated animals. The results indicate that the three principles possess the ability to lower blood pressure through a decrease of sympathetic tone as well as due to direct vasodilatation in SHRs.

Animals↗
PubMed1993

Down-regulation of beta-adrenergic receptors on mononuclear leukocytes induced by dobutamine treatment in patients with congestive heart failure.

(+/-)-Dobutamine is a positive inotropic drug usually used to improve ventricular function in patients with congestive heart failure (CHF). However, it has been found that haemodynamic responses to dobutamine become blunted during continuous treatment. In this study we determined the time-dependent changes of beta-adrenergic receptors in CHF patients treated with dobutamine. Seven CHF patients received a continuous intravenous infusion of dobutamine (5 micrograms.kg-1 x min-1) for 96 h. Blood samples were obtained before and every 24 h after starting the therapy. The density of beta-adrenergic receptors on mononuclear leukocytes and the plasma concentrations of norepinephrine and epinephrine were determined. During dobutamine treatment the receptor density (fmol.mg-1, mean +/- SEM) gradually decreased from 42.8 +/- 4.4 (baseline) to 31.4 +/- 3.3 (P < 0.05), 25.2 +/- 4.0 (P < 0.01), 18.8 +/- 5.5 (P < 0.01) and 13.4 +/- 3.4 (P < 0.01) at 24, 48, 72 and 96 h, respectively. However, the plasma concentrations of norepinephrine and epinephrine were not significantly changed during the 96 h period of treatment. Thus, the beta-adrenergic receptors down-regulated as early as 24 h after the dobutamine treatment was begun in CHF patients. This receptor down-regulation was not associated with changes of plasma catecholamine concentrations, but was related rather to the development of drug tolerance to dobutamine.

Adult↗
PubMed1993

Inhibitory effect of octopamine on the release of endogenous acetylcholine from isolated myenteric synaptosomes of guinea-pig.

1. The effect of octopamine on the release of endogenous acetylcholine (ACh) from isolated ileal synaptosomal preparations of guinea-pigs was examined using high pressure liquid chromatography with electrochemical detection. Release of ACh was induced by substance P or by depolarization with high potassium (50 mmol/L) in medium containing atropine, propranolol and naloxone. 2. Octopamine produced a dose-dependent inhibition of substance P-induced ACh release. A similar inhibitory action of octopamine was found in the samples depolarized by high potassium as a reference. 3. The action of octopamine was not reversed by the dopamine receptor antagonists either for the DA-2 subtype, domperidone, or for the DA-1 subtype, SCH23390, or by haloperidol. However, idazoxan and yohimbine antagonized this octopamine-induced inhibition at concentrations sufficient to abolish the action of clonidine. 4. Failure of guanethidine or nomifensine to inhibit octopamine ruled out mediation by noradrenergic neurotransmitters. 5. Octopamine decreased the influx of [45Ca] stimulated by substance P into synaptosomal preparations and this was reversed by idazoxan or yohimbine at concentrations sufficient to block the action of clonidine. 6. Pertussis toxin abolished the inhibitory action of octopamine at a dose high enough to block the action of clonidine. 7. These results indicate that octopamine suppresses the influx of calcium ions into cholinergic nerve terminals of ileal synaptosomes of guinea-pigs via an activation of alpha 2-adrenoceptors coupled with a pertussis toxin-sensitive GTP-binding protein which results in a decrease of ACh release.

Acetylcholine↗
PubMed1993

Phosphorylation of the TAL1 oncoprotein by the extracellular-signal-regulated protein kinase ERK1.

Alteration of the TAL1 gene is the most common genetic lesion found in T-cell acute lymphoblastic leukemia. TAL1 encodes phosphoproteins, pp42TAL1 and pp22TAL1, that represent phosphorylated versions of the full-length (residues 1 to 331) and truncated (residues 176 to 331) TAL1 gene products, respectively. Both proteins contain the basic helix-loop-helix motif, a DNA-binding and protein dimerization motif common to several known transcriptional regulatory factors. We now report that serine residue 122 (S122) is a major phosphorylation site of pp42TAL1 in leukemic cell lines and transfected COS1 cells. In vivo phosphorylation of S122 is induced by epidermal growth factor with a rapid time course that parallels activation of the ERK/MAP2 protein kinases. Moreover, S122 is readily phosphorylated in vitro by the extracellular signal-regulated protein kinase ERK1. These data suggest that TAL1 residue S122 serves as an in vivo substrate for ERK/MAP2 kinases such as ERK1. Therefore, S122 phosphorylation may provide a mechanism whereby the properties of TAL1 polypeptides can be modulated by extracellular stimuli.

Amino Acid Sequence↗
PubMed1993

Products of the TAL1 oncogene: basic helix-loop-helix proteins phosphorylated at serine residues.

TAL1 gene rearrangement is observed in nearly 30% of patients with T-cell acute lymphoblastic leukemia (T-ALL), and thus it represents the most common genetic lesion associated with this disease. Nevertheless, the presence of TAL1 gene products in normal or leukemic cells has not been reported. Therefore, immunoprecipitation with anti-TAL1 antisera was used to demonstrate the presence of TAL1 phosphoproteins, pp42TAL1 and pp22TAL1, in both T-ALL and erythroleukemia cell lines. The pp42TAL1 and pp22TAL1 proteins appear to be phosphorylated forms of full-length and truncated TAL1 gene products respectively. Phosphoamino acid analysis revealed that pp42TAL1 contains phosphoserine residues. The TAL1 phosphoproteins were detected in all of the T-ALL cell lines that harbor obvious TAL1 gene rearrangements. Interestingly, pp42TAL1 and pp22TAL1 were also present in some, but not all, of the T-ALL lines without detectable TAL1 gene alterations. Therefore, TAL1 activation may promote leukemogenesis in a far greater proportion of T-ALL patients than the 30% that bear gross TAL1 gene rearrangements.

Basic Helix-Loop-Helix Proteins↗
PubMed1992

Inhibitory effect of xylamine on the uptake of [3H]norepinephrine into primary astrocyte cultures.

Primary astrocyte cultures from neonatal rat brains show a Na+-dependent, desipramine-sensitive uptake of [3H]norepinephrine ([3H]NE). Xylamine, a nitrogen mustard, attenuated this uptake of [3H]NE into the astrocytes (IC50 = 0.8 microM). The dose-dependent reduction of [3H]NE uptake by xylamine indicated competitive kinetics. However, xylamine lost the effect if the active transport inhibitor, ouabain or iodoacetate, was also incubated during the pretreatment period of if Na+ was absent. The activity of Na(+)-K(+)-ATPase in astrocytes was not modified by xylamine at the concentrations sufficient to block the uptake of [3H]NE. These findings suggest that xylamine has the ability to compete with the transport of [3H]NE into astrocytes through an effect on the carrier instead of an action on enzymatic activity.

Animals↗
PubMed1992

Increase of plasma neuropeptide Y-like immunoreactivity following chronic hypoxia in the rat.

In an attempt to understand the changes of circulating neuropeptide Y (NPY) during hypoxia, the plasma level of NPY was investigated by radioimmunoassay. Exposure of rats to hypobaric hypoxia at an altitude of 18,000 ft for 4 weeks causes an increase of pulmonary pressure and an elevation of plasma NPY-like immunoreactivity (NPY-LI). However, the systemic blood pressure was not elevated by this chronic hypoxia. Also, plasma noradrenaline (NA) estimated by chromatographic analysis (HPLC-ECD) was not markedly raised. Failure of bretylium and guanethidine, sympathetic neuron blockers, in reducing the plasma NPY-LI level of these rats ruled out the participation of adrenergic nervous terminals. Adrenal medulla seems responsible for this elevation of plasma NPY-LI because this magnitude disappeared in adrenalectomized rats. These data suggest that chronic hypoxia induced an elevation of circulating NPY from the adrenal gland of rats.

Adrenal Glands↗
PubMed1992

Inhibitory effect of neuropeptide Y (NPY) on the in vitro activity of dopamine-beta-hydroxylase.

Neuropeptide Y (NPY) is found to be costored with norepinephrine (NE) in vesicles of the nerve terminals. An endogenous inhibitor of dopamine-beta-hydroxylase (DBH), the synthetic enzyme of NE, has been mentioned. In an attempt to clarify the effect of NPY on DBH activities, an in vitro assay is carried out using chromatographic analysis of NE formation from dopamine. NPY (20-80 pmol/ml) produced a dose-dependent depression of NE formation catalysed by the purified bovine adrenal DBH. Lineweaver-Burke plots (Km = 1.1 mM, Vmax = 10 pmol/min/mg protein) showed a non-competitive inhibition in NPY (30 pmol/ml, IC50)-treated samples. Moreover, failure of denatured NPY even at maximum concentration to influence the DBH activities suggested the essential of natural form of NPY. Participation of sulfhydryl compound seems also negligible, because N-ethylmaleimide did not overcome the effect of NPY. These results indicate that NPY has the ability to inhibit the catalytic action of DBH.

Animals↗
PubMed1992

Proto-oncogene erbA expression and increased abundance of progesterone receptors in the mouse uterus after passive immunisation against progesterone before implantation.

Passive immunisation with a monoclonal anti-progesterone antibody (DB3) prevents pregnancy in the mouse, and antibody is localised in the endometrium before the onset of implantation. BALB/c female mice were injected intraperitoneally with 9 nmol of DB3 (a dose known to cause 100% infertility) 32 h post coitum, and the uterus was removed at various times after injection. Using a monoclonal anti-progesterone receptor antibody (PR6), expression of progesterone receptors was found to be abundant in uterine tissue of DB3-treated mice; this was associated with substantial progesterone receptor mRNA levels and with maximum localisation of DB3 antibody as detected by anti-idiotype antibody. Control animals treated with an equal amount of the mouse myeloma protein P3 showed very low levels of progesterone receptor in the uterus. DB3 treatment also affected uterine expression of the proto-oncogene erbA product (which shows primary sequence homology with the progesterone receptor) as revealed by specific antiserum to the ERBA protein and by in situ hybridisation with a cDNA probe to v-erbA. Time-course studies indicated that the erbA gene was expressed at a high level before progesterone receptor expression increased, that its expression was dependent on the presence of the embryo and that erbA expression persisted longer in DB3-treated females. The observations suggest that anti-progesterone immunisation has a direct effect within the uterus, involving persistence of proto-oncogene erbA expression (which itself may represent an early maternal response to pregnancy) and increased progesterone receptor levels resulting from an unopposed oestrogen effect derived from local ligand withdrawal.

Amino Acid Sequence↗
PubMed1992

Enhancement of the mutagenicity of IQ and MeIQ by nitrite in the Salmonella system.

The fried food mutagens IQ, MeIQ, Glu-P-1 and Trp-P-2 were treated with nitrite at pH 3.0 for 1 h at 37 degrees C. The resulting reaction mixtures were tested for mutagenicity towards Salmonella typhimurium TA97, TA98, TA100 and TA1535. Glu-P-1 and Trp-P-2 were readily converted to weak or non-mutagenic deaminated compounds, whereas IQ and MeIQ were converted to extremely strong mutagenic derivatives in both the presence and the absence of rat liver S9 mix. The mutagenicity of MeIQ in TA98 was enhanced by nitrite up to 3-fold, while that of nitrosated MeIQ was further enhanced by S9 mix up to 15-fold. The nitrosation products of MeIQ were resolved into 7 bands by TLC on silica gel plate. Bands I, III, V and VI were highly mutagenic to both TA98 and TA100. The experimental results suggest that the non-enzymatic formation of direct-acting mutagens from indirect-acting mutagens such as IQ or MeIQ might be physiologically important, especially with regard to the etiology of human gastrointestinal tract tumors.

Amines↗
PubMed1992

Effect of premedication on the changes of neuropeptide Y (NPY) in anesthesia.

Premedication is one of the popular techniques in anesthesia, not only for the decrease of side effects but also for the increase of actions. Clinically, we found that plasma neuropeptide Y-like immunoreactivity (NPY-IR) was lowered in patients who had received premedication. In rats, plasma NPY-IR was not modified by the intravenous injection of diazepam. Pethidine reduced the plasma NPY-IR level which could be reversed by naloxone. Direct inhibition of plasma NPY-IR through an activation of opioid receptors can thus be considered. To the cold-stress stimulation, plasma NPY-IR was markedly raised. Diazepam reduced this stimulation-induced increase of plasma NPY-IR in a dose-dependent manner. Similar derivative of benzodiazepine produced an inhibition in a way following the potency as that to produce anxiolytic action. Also, this inhibition was reversed by PK11195, an antagonist of peripheral benzodiazepine receptors. Moreover, pain-stimulated increase of plasma NPY-IR in rats was also reduced by pethidine. This action was totally reversed in the presence of naloxone, indicating the participation of opioid receptors in the process. The obtained results suggest that premedication of diazepam and/or pethidine has the ability to decrease plasma NPY-IR in animals.

Animals↗
PubMed1992

Pharmacological characterization of alpha 2-adrenoceptors in isolated jejunum of rabbits.

In the isolated jejunum of rabbits, norepinephrine (NE) lowered the muscle tone in a dose-dependent manner which was potentiated by yohimbine, an antagonist of alpha 2-adrenoceptors. Guanethidine and/or bretylium, the adrenergic neuron blockers, attenuated this action of yohimbine, indicating the participation of neuronal alpha 2-adrenoceptors. In the presence of guanethidine and atropine, clonidine and guanabenz reduced the relative responses to forskolin, but they did not modify the responses to dibutyryl cAMP. The inhibition mediated by these alpha 2-adrenergic agonists was abolished by pertussis toxin, an inhibitor of Gi protein. The actions of clonidine and guanabenz were also blocked by yohimbine and/or rauwolscine. Thus, the Gi protein mediated inhibition of adenylate cyclase by postsynaptic alpha 2-adrenoceptors in muscle cells can be considered. The obtained data indicate that alpha 2-adrenoceptors are presented in adrenergic nerve terminals and smooth muscle of jejunum of rabbits to function as the feed-back autoreceptors in autonomic neurotransmission.

Animals↗
PubMed1992

The effect of exogenous dopamine on ileal smooth muscle of guinea-pigs.

In the isolated ileum of guinea-pig, treatment with dopamine produced a lowering of muscle tone in a dose-dependent manner. Dopamine-induced relaxation at low concentration was reversed by haloperidol, the specific antagonist of dopamine receptors. The relaxations by dopamine induced at concentration of 1 microM or higher were abolished by haloperidol with propranolol. At the concentration sufficient to block beta-adrenoceptors, propranolol attenuated this relaxation by dopamine at high concentrations. Similar results were also observed in tissues concerning the dopamine-stimulated formation of cyclic AMP. Mediation of dopamine receptor and beta-adrenoceptor in this cyclic AMP-related relaxation can thus be considered. Failure of sulpiride, an antagonist of dopamine DA-2 receptors, to reverse the actions of dopamine ruled out the participation of DA-2 receptor. Otherwise, SCH23390, the blocker of dopamine DA-1 receptors, reversed the responses to dopamine at low concentration only. Actions of dopamine induced at high concentration were disappeared in the presence of SCH23390 with propranolol. Thus, the obtained data suggest that dopamine induced relaxation of ileal smooth muscle through an activation of dopamine DA-1 receptors and/or a stimulation of beta-adrenoceptors at the concentrations over 1 microM to result in an increase of cyclic AMP in guinea-pigs.

Animals↗
PubMed1992

A prospective study of urine and serum myoglobin levels in patients with acute rhabdomyolysis.

Serum and urine myoglobin levels, measured by radioimmunoassay, were determined prospectively in eight patients with acute rhabdomyolysis, within 24 hours of admission. Five patients had urine myoglobin concentrations greater than 1,000 ng/ml (normal < 5 ng/ml); four of these patients subsequently developed acute renal failure. In three patients whose urinary myoglobin levels ranged from 19 to 275 ng/ml, acute renal failure did not occur. This difference in the occurrence of acute renal failure between the two patient groups was statistically significant (p < 0.05). Mean peak serum creatinine was significantly higher in the patients with high urine myoglobin (6.4 +/- 1.3 mg/dl) compared to those with low urine myoglobin (2.2 +/- 0.3 mg/dl), p < 0.02. There was no statistical correlation between level of serum creatine phosphokinase and serum or urine myoglobin, although the serum and urine myoglobin levels correlated well with each other. These findings suggests that among other factors, urine myoglobin may need to reach a critical level in order for myoglobinuric renal failure to ensue.

Acute Disease↗