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Biomedical subjects

J Greenberg

Publications and source records attributed to J Greenberg.

At least 91 records · Page 5Linked to original sources
PubMed1994

Using socially fair treatment to promote acceptance of a work site smoking ban.

Announcements of a work site smoking ban were made to 732 clerical workers. The presentations differed in the amount of information given about the need for the ban and the degree of interpersonal sensitivity shown over the personal impact of the ban. Immediately after the announcement, questionnaires were completed to assess participants' acceptance of the ban. High amounts of information thoroughness and of social sensitivity, given separately, enhanced acceptance of the ban, but their combined effects were even greater. Although heavy smokers were least accepting of the ban, they showed the greatest incremental gain in acceptance after exposure to thorough information presented in a highly sensitive manner. By contrast, nonsmokers' acceptance of the ban was uniformly unaffected by the way it was presented to them. Regardless of how much they smoked, all participants recognized the procedural fairness associated with giving thorough information in a socially sensitive manner.

Adult↗
PubMed1994

DNA haplotype analysis of Huntington disease reveals clues to the origins and mechanisms of CAG expansion and reasons for geographic variations of prevalence.

This study of allelic association using three intra- and two extragenic markers within 150 kb of the Huntington disease (HD) mutation has provided evidence for linkage disequilibrium for four of five markers. Haplotype analysis of 67 HD families using markers in strong linkage disequilibrium with HD identified two haplotypes underlying 77.6% of HD chromosomes. Normal chromosomes with these two haplotypes had a mean number of CAG repeats significantly larger than and an altered distribution of CAG repeats compared with other normal chromosomes. Furthermore, haplotype analysis of five new mutation families reveals that HD has arisen on these same two chromosomal haplotypes. These findings suggest that HD arises more frequently on chromosomes with specific DNA haplotypes and higher CAG repeat lengths. We then studied CAG and CCG repeat lengths in the HD gene on 896 control chromosomes from different ancestries to determine whether the markedly reduced frequency of HD in Finland, Japan, China and African Blacks is associated with an altered frequency of DNA haplotypes and subsequently lower CAG lengths on control chromosomes compared to populations of Western European descent. The results show a highly significant inverse relationship between CAG and CCG repeat lengths. In populations with lowered prevalence rates of HD, CAG repeat lengths are smaller and the distribution of CCG alleles is markedly different from Western European populations. These findings suggest that, in addition to European emigration, new mutations make a contribution to geographical variation of prevalence rates and is consistent with a multistep model of HD developing from normal chromosomes with higher CAG repeat lengths.

Africa↗
PubMed1994

A new locus for autosomal dominant retinitis pigmentosa on the short arm of chromosome 17.

Retinitis pigmentosa (RP) is a group of genetically and clinically heterogeneous retinopathies, some of which have been shown to result from mutations in two different known retinal genes, rhodopsin (3q) and peripherin-rds (6p). Three additional anonymous loci at 7p, 7q and pericentric 8 have been implicated by linkage studies. There are still, however, a few families in which all known loci have been excluded. In this report we present data indicating a location, on the short arm of chromosome 17, for the autosomal dominant RP (ADRP) locus in a large South African (SA) family of British ancestry. Positive two-point lod scores have been obtained for nine markers (D17S938, Z = 5.43; D17S796, Z = 4.82; D17S849, Z = 3.6; D17S786, Z = 3.55; TP53, Z = 3.55; D17S578, Z = 3.29; D17S960, Z = 3.16; D17S926, Z = 1.51; D17S804, Z = 0.47 all at theta = 0.10 except D17S804 and D17S926, theta = 0.20). These data provide definitive evidence for the localization of an ADRP gene on chromosome 17p. The human recoverin gene has been localized to 17p13.1 and was consequently a prime candidate for ADRP in the family studied. However, mutation screening of the three exons of this gene failed to produce any evidence of recoverin being the gene involved in the pathogenesis of ADRP in this SA family.

Calcium-Binding Proteins↗
PubMed1994

Metabolic and environmental origins of volatile organic compounds in breath.

Although more than 200 volatile organic compounds (VOCs) have been identified in human alveolar breath, their origins are still mostly unknown. An attempt was made to determine whether the major VOCs in breath were derived from inside or outside the body--that is, were they products of metabolism or contaminants from the environment? The concentrations were measured of the 24 most abundant VOCs in the alveolar breath of 12 normal volunteers and also in the air they inspired. The polarity of the mean alveolar gradient (concentration in breath minus concentration in inspired air) was positive in 15 VOCs and negative in nine. The mean alveolar gradient varied from strongly positive (for example, 2,3,3-trimethylpentane), consistent with a metabolite manufactured in the body, to strongly negative (for example, isoprene), consistent with ingestion of an air pollutant which was then catabolised in vivo or excreted via an extra-pulmonary pathway.

Breath Tests↗
PubMed1994

Alveolar gradient of pentane in normal human breath.

Previous studies have raised the question of whether pentane is a normal constituent of human breath, since its concentrations in inspired room air and expired breath are often similar. Using a highly sensitive assay for volatile organic compounds, we studied 37 normal subjects in order to determine the alveolar gradient of pentane in their breath (i.e. concentration in alveolar breath minus concentration in the inspired air). The chemical identity of pentane was confirmed by mass spectroscopy. The alveolar gradient of pentane was zero +/- 0.175 nmol/l in 54.1% of subjects, and distributed in an approximately bell-shaped curve. Determination of the alveolar gradient divided the normal subjects into three groups: the "passive equilibrators" who did not appear to excrete pentane in the breath (the majority), "metabolizers" who actively catabolized inhaled pentane, and "manufacturers" who excreted more pentane than they inhaled.

Breath Tests↗
PubMed1994

Genetic mapping of retinitis pigmentosa--implications for South African patients.

The term 'retinitis pigmentosa' (RP) encompasses a group of hereditary degenerative disorders of the retina, which are both genetically and clinically heterogeneous. The finding of molecular markers for certain forms of RP potentially allows for presymptomatic and prenatal diagnosis of a proportion of RP families. These developments and their implications for affected South African families are highlighted in this article.

Chromosome Mapping↗
PubMed1994

Computed tomography or endoscopic ultrasonography in preoperative staging of gastric and esophageal tumors.

BACKGROUND: Accurate preoperative staging of tumors of the esophagus and stomach is important in selecting treatment and determining prognosis. To date, no exact preoperative test has been useful in assessing stage of these tumors. Until recently, computed tomographic (CT) scanning has been the most frequently used examination to predict operative findings. Endoscopic ultrasonography (EUS) is a relatively new modality used by some centers to assess extramural anatomy of tumors in these two locations. METHODS: We described 28 patients with tumors involving the esophagus and gastroesophageal junction, and the stomach, who underwent both EUS and CT before surgical exploration. We compared these two tests with the final pathologic interpretation and paid particular attention to presence of lymph nodes and wall penetration by primary tumor. RESULTS: For wall penetration by an esophageal-gastroesophageal junction carcinoma, EUS was 85% accurate versus 15% for CT. For absence of nodal spread by these tumors, EUS was 100% accurate versus 67% for CT. In the presence of nodal spread EUS was 60% accurate versus 50% for CT. For wall penetration by a gastric carcinoma, EUS was 71% accurate versus 0% for CT. In the absence of nodal spread EUS and CT were both 100% accurate. In the presence of nodal spread EUS was 50% accurate versus 25% for CT. CONCLUSIONS: EUS is more accurate than CT in the preoperative staging of upper gastrointestinal malignancies.

Aged↗
PubMed1994

Locus heterogeneity for Waardenburg syndrome is predictive of clinical subtypes.

Waardenburg syndrome (WS) is a dominantly inherited and clinically variable syndrome of deafness, pigmentary changes, and distinctive facial features. Clinically, WS type I (WS1) is differentiated from WS type II (WS2) by the high frequency of dystopia canthorum in the family. In some families, WS is caused by mutations in the PAX3 gene on chromosome 2q. We have typed microsatellite markers within and flanking PAX3 in 41 WS1 kindreds and 26 WS2 kindreds in order to estimate the proportion of families with probable mutations in PAX3 and to study the relationship between phenotypic and genotypic heterogeneity. Evaluation of heterogeneity in location scores obtained by multilocus analysis indicated that WS is linked to PAX3 in 60% of all WS families and in 100% of WS1 families. None of the WS2 families were linked. In those families in which equivocal lod scores (between -2 and +1) were found, PAX3 mutations have been identified in 5 of the 15 WS1 families but in none of the 4 WS2 families. Although preliminary studies do not suggest any association between the phenotype and the molecular pathology in 20 families with known PAX3 mutations and in four patients with chromosomal abnormalities in the vicinity of PAX3, the presence of dystopia in multiple family members is a reliable indicator for identifying families likely to have a defect in PAX3.

Chromosome Mapping↗
PubMed1994

An acute dose of desmethylimipramine inhibits brain uptake of [125I]3,3',5-triiodothyronine (T3) in thyroxine-induced but not T3-induced hyperthyroid rats: implications for tricyclic antidepressant therapy.

The tricyclic antidepressant, desmethylimipramine (DMI), a highly selective inhibitor of presynaptic uptake of norepinephrine (NE), has also been shown to reduce [125I]3,3',5-triiodothyronine (T3) uptake in rat brain synaptosomes. Using DMI as a probe to examine 1) possible noradrenergic influences on thyroid hormone (TH) actions in brain and 2) TH:affective disorder relationships, we found that a single dose of DMI produces a small (7.4-25%) but significant (P < or = .05) decrease in brain uptake of both labeled T3 (T3) and labeled thyroxine (T4) across the spectrum of thyroid states from hypothyroid (HYPO) to euthyroid to T4-induced hyperthyroid. Therefore, it was noted with considerable interest that DMI appeared not to interfere with brain T3 uptake in T3-induced hyperthyroid (T3-HYPER) rats. To confirm this finding, thyroidectomized male rats were made T3-HYPER through administration of T3 (20 micrograms/kg) for 3 weeks or maintained without TH supplement for 6 weeks, becoming HYPO. Rats were given i.v. T3 and 5 min later i.p. DMI or saline. They were decapitated at 3 hr and brains retrieved for radiochemical analysis. Each experiment was run in three separate trials, with three to four rats in each treatment category (DMI or saline). Evaluation by analysis of variance showed that T3 concentrations (percentage of dose) were significantly lower in DMI than in saline-treated rat brain for HYPO (-15%; P = .0034) but not T3-HYPER rats (-2%; P = .6595). These results suggest that, as it does in the case of NE, DMI tends to block TH uptake sites in rat brain. The data also demonstrate a differential affinity for those sites in which T3 > DMI > T4 and suggest that T3 might augment tricyclic antidepressant therapy more effectively than T4.

Analysis of Variance↗
PubMed1993

Desmethylimipramine, a potent inhibitor of synaptosomal norepinephrine uptake, has diverse effects on thyroid hormone processing in rat brain. I. Effects on in vivo uptake of 125I-labeled thyroid hormones in rat brain.

Several lines of evidence point to an interaction between amine uptake inhibitors (tricyclic antidepressants) and thyroid hormones. To examine this issue under conditions which would minimize secondary effects of drug treatment, desmethylimipramine (DMI), a highly specific norepinephrine uptake inhibitor, was given acutely as a single i.p. dose one hour before i.v. [125I]triiodothyronine (T3*) or [125I]thyroxine (T4*). Tissues were analysed after rat decapitation at 3, 5, 10, and 20 min intervals thereafter. DMI had a small but significant inhibitory effect on the brain uptake of both T3* (7.4%) and T4* (19%) over their respective 20-min time courses as indicated by two-way ANOVA. To examine the drug response further and to determine the effect of thyroid status on the response, hypothyroid (HYPO) and T4-induced hyperthyroid (HYPER) rats, were given i.v. T3* and, 5 min later, i.p. DMI or saline. They were killed 3 h later and tissue analysed. Because DMI effects on T4* uptake could not be evaluated over a 3 h period without blocking T4* to T3* conversion, sodium ipodate (60 mg/kg) was given in 2 doses before i.v. T4*. Under these conditions, DMI significantly reduced brain concentrations of the administered T3* and T4* in HYPO (15% and 19%) and in HYPER rats (13% and 25%). These results suggest that, as it does in the case of norepinephrine, DMI blocks the uptake site for T3 and T4 in rat brain. No information is available regarding the relationship, if any, between the thyroid hormone and norepinephrine uptake sites.

Animals↗
PubMed1993

Emotional expression and the reduction of motivated cognitive bias: evidence from cognitive dissonance and distancing from victims' paradigms.

Two experiments tested whether expression of emotions from which motivated cognitive biases presumably provide protection would reduce the extent of such biases. In Study I, we hypothesized that expressing any tension produced by writing a counterattitudinal essay would reduce the extent of dissonance-reducing attitude change. To test this hypothesis, Ss were induced to write an essay arguing for higher tuition. High-choice Ss were either encouraged to express their emotions, to suppress them, or to do neither. As expected, high-choice-express Ss exhibited the least attitude change. Study 2 tested the hypothesis that expressing fear of cancer would reduce the extent of defensive distancing from cancer patients, but expressing sympathy would not. Although control Ss clearly distanced from cancer patients, fear-expression Ss did not. Implications for understanding the role of affect in defense are discussed.

Adult↗
PubMed1993

Molecular analysis of juvenile Huntington disease: the major influence on (CAG)n repeat length is the sex of the affected parent.

Juvenile Huntington disease (HD), characterised by onset of symptoms before the age of 20 with rigidity and intellectual decline, is associated with a predominance of affected fathers. In order to investigate the molecular basis for the observed parental effect, we have analysed the CAG trinucleotide repeat within the HD gene in 42 juvenile onset cases from 34 families. A highly significant correlation was found between the repeat length and age of onset (r = -0.86, p < 10(-7) and it was determined that the sex of transmitting parent was the major influence on CAG expansion leading to earlier onset. Neither the size of the parental upper allele, the age of parent at conception of juvenile onset child, nor the grandparental sex conferred a significant effect upon expansion. Affected sib pair analysis of CAG repeat length, however, revealed a high correlation (r = 0.91, p < 10(-7). Furthermore, analysis of nuclear and extended families showed a familial predisposition to juvenile onset disease. This study demonstrates that the sex of transmitting parent is the major influence on trinucleotide expansion and clinical features in juvenile Huntington disease.

Adolescent↗
PubMed1993

Retinitis pigmentosa in southern Africa.

Retinitis pigmentosa (RP) is a heterogeneous group of inherited retinal disorders which are a common cause of genetic blindness. The relative frequencies of the different forms of RP in South Africa, as determined from the register at the DNA banking centre for RP at the Department of Human Genetics, University of Cape Town, are presented and discussed. Of the 125 families analysed, 29 (23%) showed autosomal dominant, 33 (27%) autosomal recessive and 3 (3%) X-linked inheritance. In 10 families the pedigree data were insufficient to allow accurate genetic subtyping and a further 50 patients were sporadic without a family history of RP or other syndromic features which would allow categorization.

Asia↗
PubMed1993

Increased pentane and carbon disulfide in the breath of patients with schizophrenia.

AIMS: To determine the concentrations of pentane (a marker of lipid peroxidation) and other volatile organic compounds in the breath of patients with schizophrenia. METHODS: Volatile organic compounds were assayed by gas chromatography/mass spectroscopy (GC/MS) in 88 subjects--25 with acute schizophrenic psychosis, 26 with psychiatric disorders other than schizophrenia, and 37 normal volunteers. RESULTS: The mean alveolar gradients of pentane and carbon disulfide (CS2) were significantly higher in the patients with schizophrenia than in the control groups. CONCLUSIONS: Schizophrenia may be accompanied by accelerated lipid peroxidation in cell membranes, as well as increased manufacture of CS2, a known neurotoxin.

Adult↗
PubMed1993

Comparison of single-dose diethylcarbamazine and ivermectin for treatment of bancroftian filariasis in Papua New Guinea.

This double-blind study compared the clinical safety and parasitologic efficacy of single-dose regimens of diethylcarbamazine (DEC) and ivermectin for treatment of bancroftian filariasis in Papua New Guinea. Five groups of 10 men each with mean levels of parasitemia ranging from 2,985 to 5,185 microfilariae (mf)/ml were given DEC (6 mg/kg of body weight one time or 1 mg/kg, then 6 mg/kg four days later) or ivermectin (220 micrograms/kg; 20 micrograms/kg, then 200 micrograms/kg four days later or 20 micrograms/kg, then 400 micrograms/kg four days later). No significant side effects (e.g., acute adenolymphangitis, fever lasting more than eight hours, hypotension) were observed in any of the five treatment groups. The magnitude of reduction in microfilaremia was greater (P < 0.01) for the three ivermectin groups versus the two DEC groups in the first 30 days after drug administration (mf levels < 1% of pretreatment values versus 22.6-41.5%, respectively). At 90 and 180 days, mf levels continued to decrease in the DEC groups whereas they increased in the ivermectin groups given a total dose of 220 micrograms/kg. Eighteen months after drug administration, individuals given DEC or 420 micrograms/kg of ivermectin had the greatest degree of reduction in microfilaremia (86-90% compared with the pretreatment values). Decreases in parasite antigenemia measured by enzyme-linked immunosorbent assay for a secreted 200-kD adult worm antigen were greatest for the single-dose DEC group (39.7% decrease relative to the pretreatment level versus 7.8-15.7% for the ivermectin groups). These results indicate that single-dose DEC and ivermectin are well-tolerated by Wuchereria bancrofti-infected individuals with high levels of microfilaremia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Linkage of Usher syndrome type I gene (USH1B) to the long arm of chromosome 11.

Usher syndrome is the most commonly recognized cause of combined visual and hearing loss in technologically developed countries. There are several different types and all are inherited in an autosomal recessive manner. There may be as many as five different genes responsible for at least two closely related phenotypes. The nature of the gene defects is unknown, and positional cloning strategies are being employed to identify the genes. This is a report of the localization of one gene for Usher syndrome type I to chromosome 11q, probably distal to marker D11S527. Another USH1 gene had been previously localized to chromosome 14q, and this second localization establishes the existence of a new and independent locus for Usher syndrome.

Base Sequence↗