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Biomedical subjects

M Wong

Publications and source records attributed to M Wong.

At least 253 records · Page 14Linked to original sources
PubMed1990

Human papillomavirus in oesophageal squamous cell carcinoma.

Thirty seven cases of oesophageal squamous cell carcinoma were studied by applying DNA slot blot analysis and in situ hybridisation using type specific probes for HPV 6, 11, 16 and 18. Cases of condyloma accuminata, cervical carcinoma, and laryngeal papilloma were used as controls. Blocks including areas of invasive carcinoma, intraepithelial neoplasia, and normal epithelium were studied in each case. No HPV genome was detectable in any of the oesophageal cases. It is concluded that these types of HPV do not have an association with oesophageal squamous cell carcinoma.

Carcinoma, Squamous Cell↗
PubMed1990

Confusing fat.

Explore the source record for details and available documents.

Adult↗
PubMed1990

cAMP-binding proteins in epithelial cells cultured from human sweat glands.

This study characterized the various adenosine 3',5'-cyclic monophosphate (cAMP)-binding proteins in epithelial cells cultured from human sweat glands to identify potential pathways of cAMP action in this tissue. The cAMP-binding proteins were identified by specific labeling with the photoprobe 8-azido-[32P]-cAMP and visualized by autoradiography after electrophoresis on polyacrylamide gels in the presence of sodium dodecyl sulfate. Three cAMP-binding proteins, with molecular masses of 48, 52, and 54 kDa, were identified in subcellular fractions of the cultured sweat glands. On the basis of their relative electrophoretic mobilities and reactivity with specific antisera, the 48-kDa protein was identified as the regulatory subunit of the type 1 cAMP-dependent protein isozyme, and the 54-kDa protein was identified as the regulatory subunit of the type 2 cAMP-dependent protein kinase isozyme. The 52-kDa cAMP-binding protein appeared to be a distinct isoform of the regulatory subunit, possibly related to the subclass associated with neural tissue. As determined from the relative distributions of the photolabel, the 48-, 52-, and 54-kDa binding proteins were present in the cell cytosol at a ratio of 1:2:1. The 48- and 52-kDa proteins bound the photoprobe with apparent dissociation constants (Kd) of 20-40 nM, whereas the 54-kDa protein bound the photoprobe with much lower affinity (Kd 230 nM). Only the 48- and 52-kDa proteins were associated with cell membranes. They were present in the membrane fractions in approximately equal amounts and bound the photoprobe with apparent Kd values of greater than 100 nM.(ABSTRACT TRUNCATED AT 250 WORDS)

Affinity Labels↗
PubMed1990

Neonatal excitotoxic brain injury. Physiologic, metabolic, and pathologic findings.

The mechanism of brain injury caused by excitotoxins has been explored in detail in the adult, but not the developing animal. To better define the cerebral physiologic. metabolic and pathological effects of excitotoxic damage, quisqualic acid (QA), a glutamate analogue, was injected into the parahippocampal region of the neonatal rat. Electroencephalographic monitoring showed intermittent paroxysmal discharges which persisted for more than 24 h. Metabolic alterations were consistent with disruption of membrane function with a decrease in n-acetyl aspartate and a rise in acetate. Neuropathologic examination disclosed neuronal necrosis which was maximal in the medial CA1 and hilar areas. QA produces a unique pattern of physiologic, metabolic, and pathologic alteration in the neonatal rat brain which differs from that produced by hypoxic-ischemic injury.

Animals↗
PubMed1990

Third chronological supplement to the carcinogenic potency database: standardized results of animal bioassays published through December 1986 and by the National Toxicology Program through June 1987.

This paper is the third chronological supplement to the Carcinogenic Potency Database that first appeared in this journal in 1984. We report here results of carcinogenesis bioassays published in the general literature between January 1985 and December 1986, and in Technical Reports of the National Toxicology Program between June 1986 and June 1987. This supplement includes results of 337 long-term, chronic experiments of 121 compounds, and reports the same information about each experiment in the same plot format as the earlier papers, e.g., the species and strain of animal, the route and duration of compound administration, dose level, and other aspects of experimental protocol, histopathology, and tumor incidence, TD50 (carcinogenic potency) and its statistical significance, dose response, opinion of the author about carcinogenicity, and literature citation. The reader needs to refer to the 1984 publication for a guide to the plot of the database, a complete description of the numerical index of carcinogenic potency, and a discussion of the sources of data, the rationale for the inclusion of particular experiments and particular target sites, and the conventions adopted in summarizing the literature. The four plots of the database are to be used together as results published earlier are not repeated. In all, the four plots include results for approximately 4000 experiments on 1050 chemicals. Appendix 14 of this paper is an alphabetical index to all chemicals in the database and indicates which plot(s) each chemical appears in. A combined plot of all results from the four separate papers, that is ordered alphabetically by chemical, is available from the first author, in printed form or on computer tape or diskette.

Carcinogenicity Tests↗
PubMed1990

Increased intra-articular substance P and prostaglandin E2 following injection of interleukin-1 in rabbits.

Inflammation was induced by intra-articular injection of 100 ng recombinant human interleukin-1 alpha (rhIL-1) into rabbit knees. Substance P (SP) and prostaglandin E2 (PGE2) were measured by radioimmunoassay (RIA) in the joint fluid at 4, 24 and 48 h after rhIL-1 injection. SP was increased by 4 h, further increased at 24 h and remained elevated at 48 h. PGE2 concentration was highest at 4 h and remained elevated at 48 h after rhIL-1 injection. Because of the proinflammatory activities of SP and PGE2, our studies suggest that the elevated SP and PGE2, in the joint may amplify or sustain an initial receptor-mediated inflammatory response to IL-1.

Animals↗
PubMed1990

The value of Doppler echocardiography in the treatment of tricuspid regurgitation in patients with mitral valve replacement. Perioperative and two-year postoperative findings.

The treatment for tricuspid regurgitation in patients who have mitral valve replacement remains controversial partly because of the lack of a convenient method for measuring reflux. The purpose of this study was to assess Doppler measurement of tricuspid regurgitation in selecting patients for surgical or nonsurgical management and in evaluating the results. Thirty-three patients who had mitral valve surgery had three ultrasound examinations: before operation, before discharge from hospital, and 2 years after operation. Seventeen patients were assigned to tricuspid annuloplasty and 16 to no procedure. Assignment was based on visual grading of regurgitant velocity maps and intraoperative grading by direct palpation. Before operation patients in the annuloplasty group had larger mean jet velocity areas, right atrial size, and diastolic transvalvular velocities than had the nonsurgical group. However, the overlap of data precluded the definition of thresholds for separating the patients into either of two regimens. Early after operation the patients with annuloplasties showed decreased regurgitant indexes similar to the preoperative levels of patients who had no procedure; the latter preoperative levels had not changed. Late after operation both groups showed stabilization or trends toward less regurgitation, and continued decreases in tricuspid diastolic flow velocities. Thus Doppler ultrasonography played a complementary role in selecting patients for annuloplasty or nonsurgical management and a major role in the longitudinal evaluation of treatment.

Echocardiography, Doppler↗
PubMed1989

The roles of cAMP and cAMP-dependent protein kinase in the expression of cholesterol side chain cleavage and steroid 11 beta-hydroxylase genes in mouse adrenocortical tumor cells.

The expression of the genes encoding cholesterol side chain cleavage enzyme (SCC) and steroid 11 beta-hydroxylase (11 beta-OHase) was examined in Y1 mouse adrenocortical tumor cells and in derivative cell lines defective in cAMP-dependent protein kinase activity. Y1 cells expressed both genes constitutively, and treatment with 8-bromo-cAMP (8-Br-cAMP) increased expression 5-10-fold. In three independent protein kinase mutants, expression of SCC and 11 beta-OHase was impaired to degrees dependent upon the severity of defect in cAMP-dependent protein kinase activity. In Kin-2, the least impaired mutant clone, basal expression of SCC was the same as in Y1 cells. Treatment of Kin-2 with 8-Br-cAMP increased SCC RNA to the levels seen in stimulated Y1 cells. In contrast, clone Kin-8, the most severe mutant, expressed markedly diminished basal and 8-Br-cAMP-stimulated levels of SCC mRNA. Kin-7 had basal and 8-Br-cAMP-stimulated levels of SCC mRNA which were intermediate to Kin-2 and Kin-8. None of the Kin mutants constitutively expressed detectable levels of 11 beta-OHase transcripts, and only Kin-2 responded to treatment with 8-Br-cAMP with increased expression of 11 beta-OHase; however, the time course of induction in Kin-2 was significantly delayed. The disparate patterns of expression of SCC and 11 beta-OHase in the Kin mutants suggest that these genes differ in their absolute requirement for cAMP-dependent protein kinase activity. Experiments also were performed in which Kin-7 and Kin-8 mutants were restored to cAMP-responsive states by transfection with genes encoding normal sub-units of cAMP-dependent protein kinase. These phenotypic revertants recovered 8-Br-cAMP-inducible expression of SCC and 11 beta-OHase. These results strongly support the hypothesis that impaired expression of steroidogenic enzymes in the Kin mutants results directly from defects in cAMP-dependent protein kinase activity.

Adrenal Cortex Neoplasms↗
PubMed1989

Phytochrome activation of two nuclear genes requires cytoplasmic protein synthesis.

We have investigated the effects of protein synthesis inhibitors on light-induced expression of two plant nuclear genes, Cab and rbcS, in wheat, pea and transgenic tobacco. Light activation of these two genes is very sensitive to cycloheximide, an inhibitor of cytoplasmic protein synthesis but not to chloramphenicol, an inhibitor of organellar protein synthesis. Studies with chimeric gene constructs in transgenic tobacco seedlings show that cycloheximide exerts its effect at the transcriptional level. As a control, we show that the expression of the cauliflower mosaic virus (CaMV) 35S promoter is enhanced by cycloheximide treatment, irrespective of the coding sequence used. Escape-time analyses with green wheat seedlings show that the cycloheximide block for Cab gene expression is after the primary signal transduction step linked to phytochrome photoconversion. Our results suggest that phytochrome activation of Cab and rbcS is mediated by a labile protein factor(s) synthesized on cytoplasmic ribosomes.

Blotting, Northern↗
PubMed1989

Enhancement of murine phenytoin teratogenicity by the gamma-glutamylcysteine synthetase inhibitor L-buthionine-(S,R)-sulfoximine and by the glutathione depletor diethyl maleate.

The teratogenicity of phenytoin may result from its enzymatic bioactivation to a reactive intermediate, which, if not detoxified, can interact with embryonic tissues and alter development. Glutathione (GSH) is an important cofactor/substrate for many physiological processes and for the detoxification of xenobiotic reactive intermediates. This study examined the effects of the GSH depletor diethyl maleate (DEM) and the GSH synthesis inhibitor L-buthionine-(S,R)-sulfoximine (BSO) on phenytoin embryopathy. Phenytoin, 55 mg/kg, was administered intraperitoneally (ip) to pregnant CD-1 mice at 0900 hr on gestational days 12 and 13. Pretreatment with DEM, 150 or 300 mg/kg ip, enhanced the incidence of phenytoin-induced cleft palates by 3.3-fold and 2.3-fold, respectively (P less than 0.05), without affecting the incidence of resorptions, postpartum death, or mean fetal weight. BSO, 1,800 mg/kg ip, given 0.5 hr prior to phenytoin, resulted in a 2.4-fold increase in postpartum lethality and a 5-fold increase in fetal weight loss (P less than 0.05), without altering the incidence of resorptions or cleft palates. In two subsequent studies, BSO, 680-1,018 mg/kg/day, was given in the drinking water on gestational days 9 to 13 in the first study and on days 10 to 14 in the second study. Phenytoin, 55 mg/kg ip, was given on days 11 and 12 and on days 11 to 13 in the respective studies. In the first drinking water study, BSO enhanced the incidence of phenytoin-induced fetal resorptions 3.8-fold and cleft palates 3.3-fold (P less than 0.05) but did not affect postpartum death. In the second study, BSO enhanced the incidence of resorptions, cleft palates, and postpartum death by 2-fold, 2.6-fold, and 1.7-fold, respectively (P less than 0.05). In both of the latter two studies, phenytoin-induced fetal weight loss was altered by BSO treatment (P less than 0.05). BSO alone had no embryopathic effects. These results suggest that GSH may be involved in the detoxification of a reactive intermediate of phenytoin and/or in fetal cytoprotection.

Administration, Oral↗
PubMed1989

Hydrophilic fluorescein derivatives: useful reagents for liposome immunolytic assays.

Hydrophilic derivatives of fluorescein containing hydroxyalkyl substituents were synthesized and encapsulated within liposomes. The fluorophores showed significantly more retention with time than did fluorescein, carboxyfluorescein, or calcein. Unlike calcein, the fluorophores are minimally susceptible to fluorescence quenching by Co2+. The utility of these compounds as immunodiagnostic reagents was demonstrated by encapsulating 5(6)-carboxyfluorescein trismethylolamide in haptenized liposomes which were used in an immunoassay for digoxin.

Chemical Phenomena↗
PubMed1989

Recovery of responsiveness to ACTH and cAMP in a protein kinase-defective adrenal cell mutant following transfection with a protein kinase gene.

The cause and effect relationship between mutations in cAMP-dependent protein kinase activity and resistance of adrenocortical tumor cells to ACTH and cAMP was evaluated by transfection with cloned cDNAs encoding subunits of the mouse cAMP-dependent protein kinase. Protein kinase defective, Kin 8 adrenocortical tumor cells were transfected with pRev [an expression vector encoding the regulatory subunit of the type 1 cAMP-dependent protein kinase (RI)] or with pC alpha ev [an expression vector encoding the catalytic subunit of cAMP-dependent protein kinase (C)]. The pC alpha ev transformant recovered cAMP responsive protein kinase activity, whereas the pRev transformant recovered cAMP-binding activity, but did not recover cAMP responsive protein kinase activity. The pC alpha ev transformant concomitantly recovered steroidogenic and morphologic responsiveness to ACTH- and 8-bromo-cAMP, whereas the pRev transformant remained resistant to these effects of the hormone and cyclic nucleotide. Since Kin 8 cells recovered their responsiveness to ACTH and 8-bromo-cAMP following transfection with pC alpha ev we suggest that the defect in cAMP-dependent protein kinase activity is directly responsible for the ACTH- and cAMP-resistant phenotype of the Kin 8 mutant.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Type I familial amyloid polyneuropathy in a Chinese family.

A Chinese family with at least 3 members having the typical clinical picture of type I familial amyloid polyneuropathy is presented. The pathological features, including the immunohistochemical typing of the amyloid deposits, are described and the literature is briefly reviewed.

Adult↗
PubMed1989

Influence of saline infusion on blood-tissue albumin transport.

Anesthetized rats were infused with lactated Ringer solution (LR) at constant rate for 30 or 60 min; delivered volume loads ranged from 0.03 to 0.08 ml/g body wt. Controls were given only a sustaining infusion of saline at 0.002 ml.g-1.h-1. Only 7-14% of the LR remained in the plasma at the end of the infusion; 76-88% entered the interstitial compartment, and 7-17% was excreted. The amount of plasma protein lost from the circulation with the extravasated fluid was studied simultaneously by two methods: 1) material balance in the whole animal and 2) changes in 131I-labeled albumin uptake (VA) and water content (VW) in individual tissues. The extravasation of 0.03-0.06 ml fluid/g body wt (75-160% initial plasma volume) did not significantly increase plasma protein extravasation in the whole rat. Nearly all of the sampled tissues of LR-infused rats had higher VW than controls. Tissue VA tended to increase with VW, but the regression slopes (delta VA/delta VW), a measure of the tracer albumin concentration of capillary filtrate relative to plasma, were low; skin, 0.006; paw, 0.018; skeletal muscles, 0.007; heart, 0.057; jejunum, 0.095; ileum, 0.045; cecum, 0.026; and colon, 0.027. These ratios are consistent with the very small loss of total plasma protein observed and attest to high solvent-drag reflection coefficients (sigma approximately equal to 1 - delta VA/delta VW): greater than 0.98 in capillaries of skeletal muscles, skin, and paw and 0.91-0.97 in heart and intestine.

Animals↗
PubMed1989

The effect of diazepam on neonatal seizure: in vivo 31P and 1H NMR study.

It is assumed that when anticonvulsants arrest seizure, there is rapid return of brain high energy phosphates and brain lactate to control values. To test this hypothesis, diazepam was administered to neonatal dogs during flurothyl-induced seizure. In vivo 31P nuclear magnetic resonance spectroscopy disclosed that diazepam quickly arrested electrographic seizure and restored brain phosphocreatine and inorganic phosphate to baseline values. In contrast, in vivo 1H nuclear magnetic resonance spectroscopic measurements showed that arrest of seizure with diazepam did not return brain lactate to control values. The sustained increase in cerebral blood flow and prolonged elevation of brain lactate, acetate, valine, and succinate in the postictal period indicate that metabolic recovery of the brain occurs over an extended period of time after the normalization of EEG, phosphocreatine, and brain pH.

Acetates↗
PubMed1989

3,5,3'-triiodothyroacetic acid therapy for thyroid hormone resistance.

3,5,3'-Triiodothyroacetic Acid (Triac) is reputed to suppress pituitary secretion of TSH with minimal metabolic effects. Triac has been used successfully to treat eight patients with thyroid hormone resistance. We gave Triac to a woman with selective pituitary resistance for treatment of hyperthyroidism (patient 1) and to a man with generalized resistance and chronic schizophrenia to determine whether it would improve his schizophrenia (patient 2). Patient 1 was given 0.35-3.5 mg Triac/day; patient 2 was given 0.7-4.2 mg/day. Dosages were increased by 0.7 mg/day every 2 weeks. Serum T3, T4, free T4, TSH, TSH response to TRH, systolic time intervals (STI), angiotensin-converting enzyme (ACE), and lipids were monitored bimonthly. In both patients, there was no change in symptoms, weight, lipids, or STI. In patient 1, basal TSH suppressed from 16.3 to 1.5 mU/L; in patient 2, from 2.0 to 0.5 mU/L. The peak TSH response to TRH stimulation decreased from 144 to 12.5 mU/L in patient 1 and from 14.2 to 2.8 mU/L in patient 2. Serum T4 decreased from 160 to 109 nmol/L in patient 1 and from 270 to 192 nmol/L in patient 2. ACE levels were persistently elevated in both patients. Resting energy expenditure, measured by oxygen consumption, was increased by Triac in both patients (12% in patient 1 and 9% in patient 2). Although Triac suppressed TSH and T4 secretion in both patients, it did not reduce peripheral action of thyroid hormone as expressed in STI, resting energy expenditure, and ACE. We conclude that in these two patients with resistance to thyroid hormone, at the doses used to suppress TSH and T4 secretion, the intrinsic peripheral action of Triac offset whatever decrease in thyroid hormone secretion it produced.

Adult↗