Octopamine: an endogenous blocker of dopamine D-1 receptors.
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Animals↗
Biomedical subjects
J T Cheng
Publications and source records attributed to J T Cheng.
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↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗
Neuropeptide Y (NPY) inhibits dimethylphenylpiperazinium (DMPP)-induced gastric acid secretion in isolated rat stomach.
The effect of neuropeptide Y (NPY) on gastric acid secretion was investigated on an everted preparation of isolated rat stomach. Perfusion with synthetic NPY did not modify the basal secretion of gastric acid. However, NPY reduced dimethylphenylpiperazinium (DMPP)-stimulated acid secretion at concentrations insufficient to affect acid secretion stimulated by muscarine, histamine or gastrin. The decrease in acetylcholine (ACh) release from postganglionic cholinergic neurons by NPY is therefore considered to be responsible. Determination of NPY content by radioimmunoassay, in mucosal and muscular layers of the stomach, indicates that NPY possibly produces cholinergic inhibition under physiological levels. The present study suggests, therefore, that NPY has the ability to inhibit the release of ACh from postganglionic cholinergic neurons, thus producing a decrease in gastric acid secretion.
Animals↗
Study of plasma neuropeptide Y (NPY) and catecholamines levels during spinal anesthesia.
Plasma levels of neuropeptide Y (NPY) and catecholamines were investigated during spinal anesthesia. Ten ASA physical status I-II patients were studied after obtaining institutional approval and informed contents. All patients were free from endocrine and metabolic disease underwent elective low risk operation. No premedication was given before operation. Spinal anesthesia was performed on lateral position from L3-4 interspace with 15 mg tetracaine without added epinephrine. The analgesic level was about at T6 dermatone. Blood samples were obtained from radial artery catheter, 15 minutes before spinal anesthesia and 5', 15', 30', 60', 120', during operative period and 30' after operation in postanesthesia recovery room. The results showed that there were significant elevation in plasma level of NPY during spinal anesthesia compared with the level before anesthesia. However, no statistically significant changes of plasma catecholamines were found.
Adolescent↗
Study of plasma neuropeptide Y (NPY) and catecholamines levels during isoflurane anesthesia.
Twelve ASA physical status I-II patients were studied after obtaining institutional approval and informed contents. All patients were free from endocrine and metabolic disease undergoing elective low risk operation. Pethidine 1 mg/kg i.m. and benzodiazepine 0.01 mg/kg p.o. were given as premedication one hour before anesthesia. Anesthesia was induced with thiopental 4 mg/kg and succinylcholine 1.5 mg/kg for tracheal intubation. Anesthesia was maintained with 2% isoflurane and 50% N2O in oxygen. Ventilation was controlled and adjusted to maintain an end-tidal CO2 concentration of 25-35 torr. Atracurium 0.4 mg/kg was given as muscle relaxant. Blood samples were obtained from radial arterial catheter, 15 minutes before induction of anesthesia and 5 min after anesthesia, 15 min, 30 min, 60 min during operation and 30 min after operation in postanesthesia recovery room. The results showed that there were no statistically significant changes in plasma levels of NPY and catecholamines during operation underwent isoflurane anesthetic technique. This result indicates that isoflurane anesthesia can block the plasma NPY as well as catecholamines during surgical stress.
Adult↗
4-Aminopyridine induces the release of neuropeptide Y (NPY) to produce an atropine- and tetrodotoxin-resistant contraction in rabbit isolated jejunum.
4-Aminopyridine (4-AP) induced an atropine- and tetrodotoxin (TTX)-insensitive contraction (resistant contraction), in a concentration-dependent manner, in the isolated jejunum of rabbits. The failure of specific antagonists of histamine, serotonin and substance P to affect this resistant contraction ruled out the participation of histamine, serotonin and/or substance P. Antiserum against neuropeptide Y (NPY) reduced this resistant contraction in a concentration-dependent manner and inhibited the action of 4-AP totally at a high concentration (1.25% dilution) whereas normal serum lacked this ability. This suggested that the release of NPY was involved in this 4-AP-induced resistant contraction. Radioimmunoassay of NPY-like immunoreactivity in isolated synaptosomal preparations indicated that 4-AP possessed the ability to induce the release of NPY. However, guanethidine did not affect the actions of 4-AP, indicating that NPY is released mainly from non-adrenergic nerves. Our results indicate that 4-AP induces the release of NPY from non-adrenergic nerves to produce an atropine- and TTX-resistant contraction in the isolated jejunum of rabbits.
4-Aminopyridine↗
Noradrenergic potentiation of cerebellar Purkinje cell responses to GABA: evidence for mediation through the beta-adrenoceptor-coupled cyclic AMP system.
Previous in vivo studies from our laboratory have consistently shown that iontophoretically applied norepinephrine (NE) can potentiate gamma-aminobutyric acid (GABA)-induced depressant responses of cerebrocortical, cerebellar and hypothalamic neurons. Additional experiments have further suggested that this noradrenergic facilitating action is specific for GABA and results from the activation of a beta-type adrenoceptor. The goal of the present studies was to determine if the cAMP second messenger system might also be a component of the mechanism responsible for this NE modulatory action on GABA-mediated inhibition. In one set of in vitro experiments, we examined cerebellar neuronal responses to GABA before, during and after iontophoretic application of NE, 8-bromo-3',5'-cyclic AMP (BcAMP) or 3-isobutyl-1-methyl xanthine (IBMX) or bath application of forskolin (10-30 microM). In a second group of in vivo studies, extracellularly recorded responses of individual cerebellar Purkinje (P) cells to iontophoretic pulses of GABA or beta-alanine were examined before, during and after NE or BcAMP microiontophoresis. In 20 of 25 cerebellar cells recorded from tissue slices, iontophoretically applied NE markedly enhanced responses to GABA in a manner similar to that observed previously in vivo. In these in vitro preparations, bath application of forskolin was also capable of potentiating GABA-induced inhibition in each of 4 cases tested whereas dideoxy-forskolin was not. Iontophoretic application of IBMX further enhanced the facilitating effects of NE on GABA-induced inhibition in 10 of 11 cases tested. Furthermore, under in vitro conditions, BcAMP augmented inhibitory responses to GABA in all cerebellar neurons tested. In the intact rat brain, iontophoretic administration of BcAMP caused a marked NE-like augmentation of P-cell responses to GABA in 73% of the cells tested. As with NE, BcAMP was ineffective in enhancing P-cell inhibitory responses to beta-alanine, an agent which like GABA causes hyperpolarization, by increasing Cl conductance. In summary, these results indicate that a membrane permeant analog of cAMP, a phosphodiesterase inhibitor and an agent which directly activates adenyl cyclase can mimic the previously observed GABA-potentiating actions of NE. Thus, these findings provide further support for the contention that noradrenergic enhancement of GABA inhibition results from a cascade of transmembrane events which includes beta-receptor activation, adenyl cyclase stimulation and increased intracellular production of cAMP.
1-Methyl-3-isobutylxanthine↗
The molluscan neuropeptide FMRFamide stimulates the release of [14C]acetylcholine from isolated ileal synaptosomal preparations of guinea-pig.
FMRFamide stimulated, in a dose-dependent manner, the efflux of [14C]acetylcholine (ACh) from isolated synaptosomes of guinea-pig ileum preloaded with labelled choline. Participation of the cholinergic mechanism and/or substance P was ruled out by the finding that antagonists failed to affect the FMRFamide-induced release of ACh. The ACh-releasing action of FMRFamide was negated by the deletion of calcium ion from the bathing medium and it was also abolished by tetrodotoxin. The results obtained suggest that FMRFamide possesses the ability to induce the release of ACh from enteric synaptosomes of guinea-pig.
Acetylcholine↗
Course and prognosis of human immunodeficiency virus-associated nephropathy.
PURPOSE: Patients infected with the human immunodeficiency virus (HIV) have been described to have an unusual form of renal disease known as HIV-associated nephropathy. This condition is characterized by severe proteinuria, rapid progression to renal insufficiency, and a morphologic pattern of focal segmental glomerulosclerosis (FSGS) on renal biopsy. Despite increasing awareness of this entity, the epidemiology and clinical course of HIV-associated nephropathy are not yet well defined. We therefore decided to study HIV-infected patients with this biopsy-proven pattern of focal sclerosis. PATIENTS AND METHODS: Using life-table analysis, we evaluated the clinical features and course of 26 patients with HIV infection and biopsy-proven FSGS and compared them with those in 24 subjects with HIV infection who had no glomerular disease at autopsy. RESULTS: The group with FSGS had a higher percentage of blacks (96% versus 46%) and intravenous drug abusers (42% versus 17%), and had a higher mean serum creatinine level (5.4 mg/dL versus 1.0 mg/dL) than the group of HIV-infected subjects without glomerular disease. At the time of diagnosis of FSGS, six patients had clinical acquired immunodeficiency syndrome (AIDS), eight had AIDS-related complex (ARC), and 12 patients had no evidence of AIDS or ARC. The progression to end-stage renal disease for all patients was rapid, with a median time to dialysis of 10.9 weeks. Duration of patient survival was dependent upon the stage of HIV infection at the time of diagnosis of renal disease. Patients who presented with AIDS had a median survival of 1.9 months, compared to a median survival of 3.6 months for those with ARC and 9.7 months for initially asymptomatic HIV carriers (p less than 0.05). Fifteen patients either presented with or developed AIDS during the course of the study, and all died as a consequence of their immunodeficiency. Survival curves from the diagnosis of AIDS to death were similar in the group with HIV-associated nephropathy (7.3 weeks) compared to the control AIDS group without renal disease (6.9 weeks). CONCLUSION: Our data indicate that FSGS associated with HIV infection can occur before other manifestations of AIDS, is more common in blacks and in intravenous drug abusers, and is rapidly progressive to uremia. Patient survival is dependent upon the stage of HIV infection. These findings may prove useful in devising more effective strategies for the care of this growing patient population.
AIDS-Related Complex↗
Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study.
Clinical and pathologic findings in the kidneys of 30 consecutive acquired immunodeficiency syndrome (AIDS) autopsies and in 34 consecutive renal biopsies performed on HIV infected patients at our institution between 1983 and 1987 were studied. To determine if the lesions of HIV-associated nephropathy have morphologic specificity, a subgroup of 13 biopsies with a diagnosis of HIV-associated nephropathy (HIVN) were compared to 13 biopsies each of heroin-associated nephropathy (HAN) and of idiopathic focal segmental glomerulosclerosis (IFSGS) matched for patient age, proteinuria and serum creatinine. A diagnosis of HIVN was made in 1 of 30 (3.3%) AIDS autopsies and 26 of 34 (76.5%) renal biopsies. When compared to HAN and IFSGS, HIVN had more globally "collapsed" glomeruli (P less than 0.001), less glomerular hyalinosis (P less than 0.02), more severe visceral epithelial cell swelling (P less than 0.05), more numerous visceral epithelial cell droplets (P less than 0.002), more prevalent and severe tubular microcystic dilatation (P less than 0.02), and tubular cell degenerative changes (P less than 0.001). Focal glomerular electron-dense deposits were present in 14 of 26 cases. Tubuloreticular inclusions were extremely numerous in glomerular and interstitial capillary endothelial cells as well as in interstitial leukocytes (P less than 0.001). Granular degeneration of nuclear chromatin was present in 10 of 26 cases. Nuclear bodies were more numerous in tubular and interstitial cells of HIVN (P less than 0.01), particularly type 3 (P less than 0.001). Reversal of tissue T4/T8 ratio was observed. We conclude that while no single morphologic feature of HIVN is specific, the combination of clinical and pathologic findings is quite distinctive and permits a presumptive diagnosis of HIVN in otherwise asymptomatic carriers.
Acquired Immunodeficiency Syndrome↗
L-ascorbic acid produces hypoglycaemia and hyperinsulinaemia in anaesthetized rats.
L-Ascorbic acid (Vitamin C) produced a marked reduction in the blood glucose concentration following intravenous injection (20-100 mg kg-1) to anaesthetized rats. This hypoglycaemic effect was accompanied by an increase in plasma insulin concentration. D-ascorbic acid produced a similar hypoglycaemic effect.
Anesthesia↗