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Biomedical subjects

J T Cheng

Publications and source records attributed to J T Cheng.

At least 19 recordsLinked to original sources
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↗
PubMed1991

Enhancer-binding activity of the tal-1 oncoprotein in association with the E47/E12 helix-loop-helix proteins.

Almost 30% of patients with T-cell acute lymphoblastic leukemia (T-ALL) bear structural alterations of tal-1, a presumptive proto-oncogene that encodes sequences homologous to the helix-loop-helix (HLH) DNA-binding and dimerization domain. Analysis of the tal-1 gene product reveals that its HLH domain mediates protein-protein interactions with either of the ubiquitously expressed HLH proteins E47 and E12. The resultant tal-1/E47 and tal-1/E12 heterodimers specifically recognize the E-box DNA sequence motif found in eucaryotic transcriptional enhancers. Hence, the tal-1 protein shares biochemical properties with other tissue-specific HLH proteins that control cell type determination during myogenesis (e.g., MyoD1) and neurogenesis (e.g., achaete-scute). The data suggest that HLH heterodimers involving tal-1 may function in vivo as transcriptional regulatory factors that influence cell type determination during hematopoietic development.

Base Sequence↗
PubMed1991

A comparison of umbilical venous blood levels of neuropeptide Y and catecholamines between cesarean section and normal spontaneous delivery.

This study was designed to determine the presence and different levels of placental neuropeptide Y (NPY) in women at parturition between normal spontaneous delivery (NSD) and cesarean section (C/S) under spinal anesthesia and to compare it with the level of catecholamines. Umbilical vein plasma levels of neuropeptide Y and catecholamines of the placental cord were measured at delivery in 40 parturient women who were divided into two groups, with 20 patients in each. NSD group underwent vaginal delivery without the presence of intrapartum fetal distress. C/S group received elective cesarean section (C/S) under spinal anesthesia. The results showed that umbilical vein level of NPY in NSD patients was significantly less than C/S patients (160.32 pg/ml vs 346.25 pg/ml, p less than 0.01). But for catecholamines levels, C/S group were significantly less than that of NSD group.

Anesthesia, Obstetrical↗
PubMed1990

Colonoscopic diagnosis of ileocolic intussusception in an adult. A case report.

An elderly man was admitted to hospital with dull abdominal pain and marked weight loss. Ileocolic intussusception was shown on colonoscopy and later confirmed at laparotomy. The main feature was a caecal lipoma. A review of the subject and comparison with two other cases is included in the report. If the colonoscopy reveals a coil-spring polypoid mass, intussusception must be considered as a diagnosis in patients with abdominal pain.

Aged↗
PubMed1990

The chromosome translocation (11;14)(p13;q11) associated with T cell acute leukemia. Asymmetric diversification of the translocational junctions.

The t(11;14)(p13;q13) translocation associated with T cell acute lymphocytic leukemia generates two abnormal chromosomes, designated 11p+ and 14q-. To investigate the mechanism of t(11;14)(p13;q11) formation, we analyzed the translocation junctions of 11p+ and 14q- from two patients. The 11p+ junctions consisted of precise fusions of a pseudo recombination signal from chromosome 11 and the downstream recombination signal of the TCR D delta 2 gene segment from chromosome 14. In contrast, the 14q- junctions from both patients were diversified by random loss and addition of nucleotides at the translocation site. This asymmetric pattern of junctional diversification is typical of normal Ig/TCR gene rearrangement, and therefore implies that the t(11;14)(p13;q11) translocation arose due to aberrant activity of the Ig/TCR recombinase.

Adult↗
PubMed1990

Site-specific recombination of the tal-1 gene is a common occurrence in human T cell leukemia.

The tal-1 gene is altered as a consequence of the t(1;14) (p32;q11) chromosome translocation observed in 3% of patients with T cell acute lymphoblastic leukemia (T-ALL). tal-1 encodes a helix-loop-helix (HLH) domain, a DNA binding and dimerization motif found in a number of proteins involved in cell growth and differentiation. We now report that an additional 25% of T-ALL patients bear tal-1 gene rearrangements that are not detected by karyotype analysis. These rearrangements result from a precise 90 kb deletion (designated tald) that arises independently in different patients by site-specific DNA recombination. Since the deletion junctions resemble the coding joints of assembled immunoglobulin genes, tald rearrangements are likely to be mediated by aberrant activity of the immunoglobulin recombinase. Moreover, t(1;14)(p32;q11) translocations and tald rearrangements disrupt the coding potential of tal-1 in an equivalent manner, and thereby generate a common genetic lesion shared by a significant proportion of T-ALL patients.

Base Sequence↗
PubMed1990

The tal gene undergoes chromosome translocation in T cell leukemia and potentially encodes a helix-loop-helix protein.

We have analyzed t(1;14)(p32;q11) chromosome translocations from two patients with T cell acute lymphocytic leukemia. The chromosome 1 breakpoints of these patients lie within a kilobasepair of each other, and thus define a genetic locus (designated tal) involved in T cell oncogenesis. Moreover, we have identified sequences within tal that potentially encode an amphipathic helix-loop-helix motif, a DNA-binding domain found in a variety of proteins that control cell growth and differentiation. The homology domain of tal is especially related to that of lyl-1, a gene on chromosome 19 that has also been implicated in T cell oncogenesis. Hence, tal and lyl-1 encode a distinct family of helix-loop-helix proteins involved in the malignant development of lymphocytes.

Amino Acid Sequence↗
PubMed1990

Decrease of catecholamine and neuropeptide Y-like immunoreactivity in the glycerol-induced acute renal failure of rats.

Changes of catecholamine and neuropeptide Y (NPY) were investigated in experimental acute renal failure (ARF) of rats. Concentrations of noradrenaline (NA) and dopamine (DA) were determined by chromatographic analysis using electrochemical detection. Renal content of NPY, identified by radioimmunoassay, was expressed as NPY-like immunoreactivity (NPY-LI). All animals with a plasma urea value higher than 200 mg/dl induced by injection of glycerol were employed as ARF subjects for the experiment. Formation of ARF was also confirmed by histological findings showing diffused necrosis of tubular epithelia. In ARF rats, renal contents of NA and DA decreased markedly (P less than 0.001), NA (ng/g wet tissue) decreased from 186.3 +/- 19.6 to 2.81 +/- 0.67 (n = 8), and DA (ng/g wet tissue) decreased from 14.69 +/- 4.97 to 4.05 +/- 2.66 (n = 8). Similarly, NPY-LI (pg/g wet tissue) in ARF was reduced significantly (P less than 0.001) from 435.23 +/- 35.82 to 4.61 +/- 0.52 (n = 8). The decrease of NA in ARF was obtained parallel to the change of NPY-LI; degeneration of adrenergic nerve fibers was confirmed by immunohistochemical observation. Results obtained suggest damage to the adrenergic and the dopaminergic innervation in the kidneys during ARF.

Acute Kidney Injury↗
PubMed1990

Inhibitory effect of octopamine on dopamine D-1 receptor in striatal homogenates of the rat.

In the striatal homogenates of rats, octopamine produced a dose-dependent inhibition of dopamine D-1 receptor both in the receptor binding of [3H]Sch-23390 and the formation of cyclic adenosine 3',5'-monophosphate (cyclic AMP) stimulated by dopamine in the presence of sulpiride. Failure of octopamine in the displacement of binding with [3H]N-0437, one of the radioligands for the dopamine D-2 receptor, indicated the specific selectivity of octopamine to dopamine D-1 receptor sites. Lack of effect on forskolin-stimulated formation of cyclic AMP ruled out the possible direct effect of octopamine on adenylate cyclase. These results suggest that octopamine possesses the ability to bind to striatal dopamine D-1 receptors of rats.

Adenylyl Cyclase Inhibitors↗