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Biomedical subjects

H Xian

Publications and source records attributed to H Xian.

At least 19 recordsLinked to original sources
PubMed2004

Neuropsychological consequences of regular marijuana use: a twin study.

BACKGROUND: Results of previous research examining long-term residual effects of marijuana use on cognition are conflicting. A major methodological limitation of prior studies is the inability to determine whether differences between users and non-users are due to differences in genetic vulnerability preceding drug use or due to the effects of the drug. METHOD: Fifty-four monozygotic male twin pairs, discordant for regular marijuana use in which neither twin used any other illicit drug regularly, were recruited from the Vietnam Era Twin Registry. A minimum of 1 year had passed since the marijuana-using twins had last used the drug, and a mean of almost 20 years had passed since the last time marijuana had been used regularly. Twins were administered a comprehensive neuropsychological test battery to assess general intelligence, executive functioning, attention, memory and motor skills. Differences in performance between marijuana-using twins and their non-using co-twins were compared using a multivariate analysis of specific cognitive domains and univariate analyses of individual test scores. Dose response relationships were explored within the marijuana-using group. RESULTS: Marijuana-using twins significantly differed from their non-using co-twins on the general intelligence domain; however, within that domain only the performance of the block design subtest of the Wechsler Adult Intelligence Scale--Revised reached a level of statistical significance. CONCLUSIONS: Out of the numerous measures that were administered, only one significant difference was noted between marijuana-using twins and their non-using co-twins on cognitive functioning. The results indicate an absence of marked long-term residual effects of marijuana use on cognitive abilities.

Adult↗
PubMed2001

A twin study of generalized anxiety disorder symptoms, panic disorder symptoms and post-traumatic stress disorder in men.

Generalized anxiety disorder (GAD), panic disorder (PD) and post-traumatic stress disorder (PTSD) often co-occur. We investigated whether and to what degree genetic and environmental contributions overlap among symptoms of GAD, symptoms of PD and PTSD. Subjects were 3327 monozygotic and dizygotic male-male twin pair members of the Vietnam Era Twin Registry who participated in a 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised (DIS3R). Genetic model fitting was performed to estimate the magnitude of genetic and environmental contributions to the lifetime co-occurrence of GAD symptoms, PD symptoms and PTSD. The liability for GAD symptoms was due to a 37.9% additive genetic contribution common to PD symptoms and PTSD. Liability for PD symptoms was due to a 20.7% additive genetic contribution common to GAD symptoms and PTSD, and a 20.1% additive genetic influence specific to PD symptoms. Additive genetic influences common to symptoms of GAD and PD accounted for 21.3% of the genetic variance in PTSD. Additive genetic influences specific to PTSD accounted for 13.6% of the genetic variance in PTSD. Remaining variance for all three disorders was due to unique environmental factors both common and specific to each phenotype. These results suggest that these disorders each have etiologically distinct components and also have significant genetic and unique environmental contributions in common.

Adult↗
PubMed2001

A twin study of the association between pathological gambling and antisocial personality disorder.

Many individuals with a history of pathological gambling (PG) also have a history of engaging in antisocial behaviors, and this has often been interpreted as a result of the former causing the latter. In a sample of 7,869 men in 4,497 twin pairs from the Vietnam Era Twin Registry, the authors examined (a) the association between PG and antisocial personality disorder (ASPD), (b) the extent to which PG might be differentially associated with childhood conduct disorder (CD) and adult antisocial behavior (AAB), and (c) the contribution of genetic and environmental factors to the association of PG with ASPD, CD, and AAB. PG was significantly associated with all 3 antisocial behavior disorders, and the association of PG with ASPD, CD, and AAB was predominantly explained by genetic factors. The results of this study suggest that the greater-than-chance co-occurrence of PG and antisocial behavior disorders is partially due to their sharing a common genetic vulnerability. The antisocial behavior observed among many individuals with PG probably cannot be interpreted as being simply a consequence of the PG.

Adult↗
PubMed2001

The genetics of pathological gambling.

Problem and pathological gambling (PG) occurs in about 5% of Americans. Gambling is associated with substantial psychosocial and psychiatric health problems, and the increasing ease of access to gambling may increase its future prevalence. Therefore, it is important to gain greater insight into the causes of PG. Family studies of PG are consistent with a substantial familial impact on vulnerability to PG. However, family studies cannot distinguish genetic from family environmental influences. By contrast, the study of twin pairs permits the genetic and environmental influences on PG to be estimated. The study of gambling behavior among 3,359 twin pair members of the Vietnam Era Twin Registry suggests that: (1) inherited factors explain a substantial proportion of the variance in the report of symptoms of gambling; (2) there is a single continuum of genetic vulnerability that underlies gambling problems of varying severities; and, (3) the co-occurrence of PG with conduct disorder, antisocial personality disorder, and alcohol abuse/dependence is partially explained by genes that influence both PG and these other psychiatric disorders. Neurophysiological correlates of gambling problems and genetically based differences in neurotransmitter systems may provide biological mechanisms that explain the genetic basis for a predisposition to PG.

Adoption↗
PubMed2001

[Immobilization of penicilin G acylase on polyacrylonitrile fiber].

The immobilization of Penicillin G Acylase from Bacillus megaterium by glutaraldehyde crosslinking on the partially acid-hydrolyed polyacrylonitrile fiber was studied. When the amount of--NH2 on fiber were 690 mumol/g and the moisture in the fiber was 64%, and the content of enzyme protein immobilized on fiber was more than 100 mg/g. The activity of 2300 IU/g was obtained with 30% of overall yield and 56% of binding efficiency. The immobilization yield was markedly influenced by ratio of the amount of free enzyme used to the weight of the fiber. The half-life of storage stability of immobilized PGA at room temperature was 130 days. The immobilized PGA kept 80% of the initial activity after 20 cycles of operation in 10% of PGK(W/V) in 0.05 mol/L phosphate buffer, pH 8.0, at 37 degrees C and an enzyme load of 150 IU/g(PGK) and 10 g(PGK) for per cycle of operation. The hydrolysis conversion of PGK in the range of 2.5%-12.5% (W/V) were over 98% for the immobilized PGA. The operation stability of immobilized PGA treated with DTT was better than that of immobilized PGA untreated.

Acrylic Resins↗
PubMed2000

Genetic and environmental influences on posttraumatic stress disorder, alcohol and drug dependence in twin pairs.

We investigated whether and to what degree genetic and environmental contributions overlap among posttraumatic stress disorder (PTSD), alcohol dependence (AD) and drug dependence (DD). Subjects were 3304 monozygotic and dizygotic male-male twin pair members of the Vietnam Era Twin Registry who participated in 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised (DIS-3R). Genetic model fitting was performed to estimate the magnitude of genetic and environmental contributions to the lifetime co-occurrence of DSM-III-R PTSD, AD and DD. The liability for PTSD was partially due to a 15.3% genetic contribution common to AD and DD and 20.0% genetic contribution specific to PTSD. Risk for AD was partially due to a 55.7% genetic contribution common to PTSD and DD. Genetic influences common to PTSD and AD accounted for 25.2% of the total risk for DD. Specific family environmental influence accounted for 33.9% of the total variance in risk for DD. Remaining variance for all three disorders was due to unique environmental factors both common and specific to each phenotype. These results suggest that PTSD, AD and DD each have etiologically distinct components and also have significant genetic and unique environmental contributions in common.

Adult↗
PubMed2000

Self-Reported zygosity and the equal-environments assumption for psychiatric disorders in the Vietnam Era Twin Registry.

The equal-environments assumption (EEA) in twin studies of psychiatric disorders assumes that the family environment which contributes to risk for a disorder is equally correlated between monozygotic (MZ) and dizygotic (DZ) twin pairs. In a study of psychiatric disorders in female twins, Kendler and colleagues (1993) have demonstrated the utility of a test of the EEA which includes a specified family environmental factor defined by using measures of perceived zygosity. We tested the EEA assumption among 3155 male-male twin pair members of the Vietnam Era Twin Registry for the following DSM-III-R lifetime disorders: alcohol dependence, marijuana dependence, any illicit drug dependence, nicotine dependence, major depression, and posttraumatic stress disorder. The majority of MZ (81.6%; n = 1593) and DZ (90.2%; n = 1086) twin pairs agreed with the investigator's assigned zygosity. The best-fitting model for each of these disorders did not allow for a specified family environmental influence. These results support the usefulness of perceived zygosity in tests of the EEA. In male twin pairs, perceived zygosity has little impact on twin similarity for common psychiatric disorders.

Adult↗
PubMed2000

Heritability of self-reported health.

OBJECTIVE: To explore the contribution of genes and environmental factors to variation in a common measure (i.e., a five-point--excellent, very good, good, fair, and poor--Likert scale) of self-reported health. DATA SOURCES: Data were analyzed from 4,638 male-male twin pair members of the Vietnam Era Twin (VET) Registry who responded to a 1987 health survey. STUDY DESIGN: Varying models for the relationship between genetic and environmental influences on self-reported health were tested in an attempt to explain the relative contributions of additive genetic, shared and nonshared environmental effects, and health conditions reported since 1975 to perceived health status. DATA COLLECTION: A mail and telephone survey of health was administered in 1987 to VET Registry twins. PRINCIPAL FINDINGS: Variance component estimates under the best-fitting model included a 39.6 percent genetic contribution to self-reported health. In a model which included the effect of health condition, genes accounted for 32.5 percent and health condition accounted for 15.0 percent of the variance in self-reported health. The magnitude of the genetic contribution to perceived health status was not significantly different in a model with or without health condition. CONCLUSIONS: These data suggest over one-third of the variability of self-reported health can be attributed to genes. Since perceived health status is a major predictor of morbidity, mortality, and health services utilization, future analyses should consider the role of heritable influences on traditional health services variables.

Aged↗
PubMed1999

Interrelationship of genetic and environmental influences on conduct disorder and alcohol and marijuana dependence symptoms.

Data from the Vietnam Era Twin (VET) Registry were analyzed to explore the degree to which the same genetic and environmental factors contribute to childhood conduct disorder symptoms and to alcohol and marijuana dependence symptoms. Data on conduct disorder and alcohol and marijuana dependence were obtained from administration of the Diagnostic Interview Schedule to 1,856 monozygotic and 1,479 dizygotic male-male twin pair members of the VET Registry. Multivariate genetic models were compared to determine the genetic and environmental influences common and or specific to all three phenotypes. A full model that allowed for common genetic and environmental influences to all three phenotypes gave a good fit to the data, but the best fitting reduced model did not allow for a genetic influence on conduct disorder symptoms. Under the best fitting reduced model, genes explained 44.7% of the variance in risk for alcohol dependence symptoms. The genetic liability for symptoms of marijuana dependence was due to a 36.3% specific contribution and a 7.6% contribution from genes common with alcohol dependence symptoms. Family environmental contributions common to all three phenotypes explained 46.7%, 11.9%, and 21.3% of variance in risk for symptoms of conduct disorder, alcohol dependence, and marijuana dependence, respectively. Common family environmental factors contribute to risk of conduct disorder symptoms and alcohol and marijuana dependence symptoms. Common genetic influences contribute to risk of symptoms of alcohol dependence and marijuana dependence. While our findings suggest genes do not contribute to co-morbid conduct disorder symptoms, comparisons with other twin studies suggest that the role of genes in risk for conduct disorder remains uncertain.

Adult↗
PubMed1999

Common genetic vulnerability for nicotine and alcohol dependence in men.

BACKGROUND: Nicotine and alcohol dependence often occur together. We examined data from male twin pairs to determine whether there are genetic or environmental influences common to nicotine and alcohol dependence, and, if so, to estimate the magnitude and correlation of these influences. METHODS: Subjects were 3356 male-male twin-pair members of the Vietnam Era Twin Registry who participated in a 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised. Genetic model fitting was performed to estimate the magnitude and correlation of genetic and environmental contributions to lifetime nicotine and alcohol dependence. RESULTS: The heritability of nicotine dependence was 60.3% (95% confidence interval [CI], 55.4%-65.2%); that of alcohol dependence, 55.1% (95% CI, 49.7%-60.5%). The best-fitting model for the co-occurrence of lifetime nicotine and alcohol dependence included a substantial genetic correlation between both disorders (r = 0.68; 95% CI, 0.61-0.74) and a modest unique environmental correlation (r = 0.23; 95% CI, 0.14-0.32). CONCLUSIONS: These data suggest a common genetic vulnerability to nicotine and alcohol dependence in men. This common genetic influence may partially explain the clinical and epidemiological observations that alcoholics are often dependent smokers.

Adult↗
PubMed1999

Genetic and environmental influences on transitions in drug use.

Genetic and environmental factors influence drug abuse, but abuse represents the culmination of a sequence of events. Different levels of use may have different determinants and these determinants may differ across drug types. Approximately 3200 male-male twin pairs from the Vietnam Era Twin Registry were interviewed by telephone. Data were obtained regarding exposure to six categories of illicit drugs, initiation of use, continuation of use, regular usage, and diagnosis of drug abuse/dependence. Genetic, common environmental, and unique environmental influences on transitions of drug involvement, defined as movement from one level of drug use to the next, were investigated. Marijuana had the highest conditional probability for the transition from exposure to use, from use to use more than five times, and from use more than five times to regular use. The rate of transition to regular use of heroin was higher than the rate for amphetamine, cocaine, sedatives, and psychedelics. Cocaine had the highest conditional probability for the transition from regular use to abuse/dependence. Significant genetic influences were observed for a number of transitions in marijuana, amphetamine, and cocaine usage.

Adult↗
PubMed1998

GABAergic cells and signals in CNS development.

GABA is formed primarily from decarboxylation of glutamate by a family of cytosolic and membrane-bound GAD enzymes. In the adult, GAD-derived GABA sustains the vitality of the central nervous system (CNS), since blockage of GAD rapidly leads to convulsions and death. In plants, cytosolic GAD synthesizes GABA in response to hormones and environmental stress. Since decarboxylation involves protonation, secretion of GABA serves to buffer cytosolic pH in plant cells. Families of GAD and GABAA receptor/Cl- channel transcripts and encoded proteins emerge early and seemingly everywhere during CNS development, with their abundance closely paralleling neurogenesis and peaking before birth. Micromolar GABA acts at receptor/Cl-channels to depolarize progenitor cells in the cortical neuroepithelium; it also elevates their cytosolic Ca2+ (Cac2+) levels. In some way, these effects decrease proliferation. GABA directs the migration of postmitotic neuroblasts at femtomolar concentrations and stimulates their random motility at micromolar concentrations via Ca2+ signaling mechanisms. Activation of GABAA receptors by micromolar GABA may limit motility via membrane depolarization and elevated Cac2+. These results indicate that in vitro GABA can affect embryogenesis of the CNS through effects on cell proliferation and migration. As neurons differentiate postnatally, Cl(-)-dependent depolarization disappears together with GABAergic Cac2+ signals. Physiologically occurring GABAergic signals at Cl-channels exist in tonic and transient forms. Since the former are found on progenitor cells while both are present in postmitotic neurons, mechanisms to generate transients differentiate in the latter. Surprisingly, tonic and transient forms of GABAergic signaling at Cl-channels are rapidly and smoothly interconvertible and seem to be derived from online GABA synthesis in a surface-accessible compartment of the membrane.

Animals↗
PubMed1997

Testing the utility of mod scores and sib-pair analysis to detect presence of disease susceptibility loci.

Linkage analyses and association studies were employed to detect disease susceptibility loci leading to elevated Q1 levels in Problem 2B. Phenotypes were defined to be the dichotomous affection status, the quantitative value for Q1, and Q1 adjusted for covariates. The method of mod-scores (for the dichotomous phenotype) and the Haseman-Elston sib-pair test on the dichotomous and quantitative phenotypes were used to screen for linkage of disease susceptibility genes to 367 markers. These analyses were performed on a sample ascertained from the first 60 replicates. The mod-score method detected linkage to MG1, MG2, and MG3 with scores of 1.5, 5.0, and 1.6 respectively. Sib-pair analysis using quantitative phenotypes signaled linkage only to the area surrounding MG1; the dichotomous phenotype detected linkage only to MG2. Association studies used ANOVA on all founders in the first 60 replicates and ASSOC on the ascertained families and on a subset of families from the 60 replicates but only confirmed an association to MG1. In conclusion, the mod-score method may be a useful tool for genomic screens.

Analysis of Variance↗
PubMed1997

[Comparison between the effects of rhCNTF on sensory and motor neuron of chicken embryo].

The effects of rhCNTF on dorsal root ganglia (DRG) sensory neurons and spinal cord (SC) motor neurons of 10-day chicken embryos were observed with serum-free culture. The results indicated that rhCNTF supported the survival and differentiation of these neurons and showed certain dose-dependent manners. No effect was found at 0.5 ng/ml rhCNTF concentration, a little survival promotive effect at 1.0-1.5 ng/ml, peak effect at 4 ng/ml and no more effects from 8.0 to 100 ng/ml. The survival number of neurons on 7th day was compared, and results showed higher sensitivity of sensory neuron to CNTF shortage than that of motoneuron. This suggests that survival effect of CNTF on motoneuron is only small part of its neurotrophic effects.

Animals↗
PubMed1997

[The method to remove nitrite from tap water by tea].

Drinking water (tap water) is polluted in pipelines by bacteria after long distance transportation. The water contains nitrite (NO2-) which is potentially harmful to human health. The nitrite concentrations range from 0.10 to 2.0 mg/L. Our experiment proved that NO2- could not be removed by boiling, but could be removed by tea. As a natural antioxidant, tea contains several antioxidants, such as ascorbic acid and catechins, which removed NO2- from tap water effectively.

Antioxidants↗
PubMed1996

Vasoactive intestinal peptide: mediator of laminin synthesis in cultured Schwann cells.

To learn more about neuropeptide-induced glial responses which accompany axon regeneration, we studied effects of VIP on laminin production by cultured Schwann cells. Schwann cells were isolated from sciatic nerves of neonatal mice, purified, and incubated for 5 days in either control medium (DMEM + 15% FCS) or control medium containing 10-7 -10-11 M VIP. At 10-7 and 10-8 M VIP, laminin levels measured by enzyme-linked immunosorbent assay were significantly higher (55% and 35%) than those in control cultures. Lower VIP concentrations (10-9 -10-11 M) produced smaller increases which were not significant. Low-affinity VIP receptors which mediated this effect were demonstrated on Schwann cells by radioligand binding studies. The increased Schwann cell synthesis of laminin induced by VIP was blocked when either a VIP antagonist or a VIP receptor antagonist was added to the VIP-containing incubation medium. In contrast to astrocytes, when Schwann cells were loaded with fura-2, VIP did not increase cytosolic Ca2+. This indicates that Schwann cells and astrocytes may have different intracellular transduction pathways; their receptor subtypes also may differ. We suggest that the VIP-induced increase in laminin synthesis which we have observed in cultured Schwann cells may also occur in vivo and might be an important component of axon-Schwann cell interactions during nerve regeneration.

Animals↗
PubMed1994

The muscarinic receptor agonist oxotremorine methiodide evokes a nicotinic response in mammalian sympathetic neurons.

Oxotremorine methiodide, a congener of oxotremorine, is used as a muscarinic receptor agonist. Responses to oxotremorine methiodide and nicotinic receptor agonists were examined in cultured guinea-pig celiac ganglion neurons using whole-cell voltage clamp techniques. At holding potentials between -30 and -60 mV, a brief application of oxotremorine methiodide produced fast and slow inward current transients, depending upon the concentration applied. Slowly developing inward current transients, characteristic of muscarinic responses, were produced by lower concentrations (EC50: 0.3 microM) and were blocked by atropine. Rapid inward current transients, characteristic of nicotinic responses, were produced by higher concentrations of oxotremorine methiodide (EC50: 168 microM) and were blocked by d-tubocurarine. Thus oxotremorine methiodide, at concentrations of 10 microM and greater, produced an initial nicotinic fast inward current transient followed by a slow muscarinic inward transient. The fast inward transients were similar to responses evoked by the nicotinic receptor agonists acetylcholine, nicotine and 1,1-dimethyl-4-phenyl-piperazinium iodide and were not antagonized by atropine. We conclude that oxotremorine methiodide acts as a nicotinic and muscarinic receptor agonist in celiac sympathetic ganglion neurons.

Animals↗