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At least 469 records · Page 26Linked to original sources
PubMed2003

Clinical, hormonal, behavioral, and genetic characteristics of androgen insensitivity syndrome in a Brazilian cohort: five novel mutations in the androgen receptor gene.

Androgen insensitivity syndrome (AIS) is caused by mutations in the androgen receptor gene and is associated with a variety of phenotypes in 46,XY individuals, ranging from phenotypic women [complete form (CAIS)] to men with minor degrees of undervirilization or infertility [partial form (PAIS)]. We studied 32 subjects with male pseudohermaphroditism from 20 families (9 CAIS, 11 PAIS) with the following criteria for AIS: 46,XY karyotype, normal male basal and human chorionic gonadotropin-stimulated levels of serum testosterone and steroid precursors, gynecomastia at puberty, and, in prepubertal patients, a family history suggestive of X-linked inheritance. The entire coding region of the androgen receptor gene was analyzed, and mutations were found in all families with CAIS and in eight of 11 families with PAIS. Fifteen different mutations were identified, including five (S119X, T602P, L768V, I898F, and P904V) that have not been described previously. Detailed clinical and hormonal features were compared with genotype in 25 subjects with AIS and confirmed by mutational analysis. LH hormone levels and the LH x testosterone product were high in all postpubertal subjects with AIS. All subjects with PAIS maintained at postpubertal age the gender identity and social sex that was assigned to them in infancy, in contrast to other forms of pseudohermaphroditism.

Adolescent↗
PubMed1995

Sex differences in ethanol-related behaviors in genetically defined murine stocks.

Over the past 30 years, there have been a number of important developments in our understanding of the etiology and consequences of excessive drinking among humans. Probably one of the most important findings to date is that there are large individual differences among humans in appetite for alcohol and age of onset of problem drinking. We recognize this finding in at least two different alcoholic types, each with its own estimate of genetic influence. We have also come to realize that there are important differences between men and women, both in etiology of problem drinking and in the consequences of chronic alcohol use. In this chapter, the advantages and limitations of applying genetically defined animal models, primarily, selected lines and inbred strains of mice, are evaluated with examples from the literature.

Alcohol Drinking↗
PubMed1999

The effect of drug-injection behavior on genetic evolution of HIV-1.

The effect of injection-drug use on human immunodeficiency virus type 1 (HIV-1) env genetic evolution was examined in 15 seroconverting injection-drug users followed up for 4 years. After adjustment for non-drug-related independent variables significantly associated with genetic diversity (time since seroconversion and progressor status), injection frequency was positively and highly significantly associated with HIV-1 env genetic diversity (P=.003). The mutation rate in those who had injected at least once a day during the previous 6 months was estimated to be 62% greater than the rate in those who had not injected at all. If the positive effect of drug-injection frequency on env genetic diversity extends to the HIV-1 pol gene, the risk of emergence of resistance to antiretroviral drugs may be enhanced by increased drug-injection frequency, especially under the selection pressure of antiretroviral therapy.

Adult↗
PubMed2002

Using a telephone survey to acquire genetic and behavioral data related to cigarette smoking in "made-anonymous" and "registry" samples.

In the Smokers and Nonsmokers Study, the authors investigated the feasibility of using random digit dialing telephone interviews to locate adults in the continental United States who were willing to provide DNA from buccal swabs through the mail. Interviews with 3,383 adults regarding their smoking-related behaviors (response rate = 70%) were conducted in 1999-2000; swab returns continued into early 2001. Overall, 57% of interviewees agreed to receive mailed information explaining the study. Better-educated persons (odds ratio (OR) = 1.3, 95% confidence interval (CI): 1.1, 1.6), younger persons (OR = 0.988, 95% CI: 0.983, 0.992), persons with symptoms of depression (OR = 1.8, 95% CI: 1.4, 2.4), and current smokers (OR = 2.25, 95% CI: 1.8, 2.8) were likelier to agree to receive a mailing. Approximately 26% of interviewees (45% of those receiving kits) returned buccal swabs, and 18% were successfully genotyped. Older (OR = 1.02, 95% CI: 1.01, 1.03), better-educated (OR = 1.4, 95% CI: 1.1, 1.7), and White (OR = 1.8, 95% CI: 1.4, 2.5) participants were more likely to return DNA samples, but current smokers (OR = 0.6, 95% CI: 0.5, 0.8) were less likely to do so. Participants were randomly assigned to one of two forms of participation: the "registry" group (names were kept on file) or the "made-anonymous" group (names were unassociated with samples). The two groups were equally likely to return kits, but registry respondents were more likely to nominate siblings for participation in the study (OR = 1.6, 95% CI: 1.2, 2.1). The participants in this study were similar demographically to the national population. The authors conclude that random digit dialing surveys coupled with mail collection of DNA may constitute a practical method of obtaining DNA samples for biobehavioral research.

Adult↗
PubMed1988

In vivo behavior of genetically engineered herpes simplex viruses R7017 and R7020: construction and evaluation in rodents.

The herpes simplex virus (HSV) recombinant R7017 was constructed from HSV-1 (strain F) by deleting a portion of the thymidine kinase (tk) gene and by replacing the sequences representing the internal inverted repeats and adjacent genes in the L component with a fragment of the HSV-2 genome encoding the glycoproteins G, D, I, and a portion of E. In addition, the R7020 recombinant contains an HSV-1 DNA fragment encoding the tk gene fused to the alpha 4 gene promoter. The results of studies in mice, guinea pigs, and rabbits were as follows: Both recombinants remained unchanged after nine serial, intracerebral passages in mice; the recombinants could not be differentiated with respect to attenuation in mice injected intracerebrally, in vaginally infected guinea pigs, and in rabbits inoculated on the scarified cornea. Given intradermally or intramuscularly, the recombinants prevented severe infections by virulent challenge viruses, and R7020 established latent infections (at a low frequency) in all species tested, whereas latent R7017 virus was detected in rabbits only.

Animals↗
PubMed1990

In vivo behavior of genetically engineered herpes simplex viruses R7017 and R7020. II. Studies in immunocompetent and immunosuppressed owl monkeys (Aotus trivirgatus).

The genetically engineered herpes simplex virus strains R7017 and R7020 were tested in owl monkeys (Aotus trivirgatus) previously shown to model herpetic diseases of immunocompromised patients and neonates. In contrast to the lethal disease seen in monkeys receiving 100-1,000 plaque-forming units (pfu) of wild-type virus, inoculation of greater than or equal to 10(6) pfu of recombinant viruses produced local lesions and viral shedding but not disseminated disease. Latent recombinant viruses were recovered from some ganglia innervating the sites of inoculation. Monkeys protected from lethal infection with wild-type virus exhibit recurrent lesions that increase in frequency and severity after total lymphoid gamma irradiation (TLI). In contrast, monkeys immunosuppressed by TLI and inoculated with R7020 could not be differentiated from irradiated controls with respect to morbidity or mortality. Moreover, the virus was not transmitted from immunosuppressed infected females to normal male cage mates.

Animals↗
PubMed2005

Family, twin, adoption, and molecular genetic studies of juvenile bipolar disorder.

Juvenile bipolar disorder (JBD) has been a subject of significant research and debate. Phenotypic differences between JBD and adult-onset bipolar disorder have led researchers to question whether or not similar neuropathologic mechanisms will be found. While much is known about the genetic and environmental contributions to the adult-onset phenotype, less is known about their contributions to JBD. Here, we review family, twin, adoption, and molecular genetic studies of JBD. Behavioral genetic data suggest both genetic and environmental contributions to JBD, while molecular genetic studies find linkage to age of onset of bipolar disorder to chromosomes 12p, 14q, and 15q. Additionally, changes associated with symptom age of onset have been recently reported in the brain-derived neurotrophic factor (BDNF) and glycogen synthase kinase 3-beta (GSK3-beta) genes. We contend that further progress in discovering the precise genetic and environmental contributions to JBD may depend on advances in phenotypic refinement, an increased appreciation of comorbid conditions, and more investigation of the longitudinal course of the disorder.

Adoption↗
PubMed1991

Why are siblings so different? The significance of differences in sibling experiences within the family.

Siblings, who are 50% similar genetically and grow up within the same family, nevertheless differ markedly in personality and psychopathology, and most of these sibling differences cannot be explained by genetic factors. These findings from the field of behavioral genetics imply that within-family processes that lead to sibling differences, called nonshared environment, are crucial for understanding environmental influences on individual development. Such nonshared environmental influences cannot be identified by the conventional strategy of comparing one child per family on a family-by-family basis; what is needed are studies of siblings that focus on why they are so different. The implications of these findings for investigating family process are outlined, and research is reviewed that explores the extent to which siblings in a family have different experiences, and that begins to assess links between such differential experiences and developmental outcomes.

Family↗
PubMed2001

Corpus callosum morphology of Williams syndrome: relation to genetics and behavior.

As the largest interhemispheric commissure in the brain, the corpus callosum is of particular interest in disorders that may preferentially affect white matter development such as Williams syndrome (WS). Individuals with WS possess a remarkable array of neurobehavioral peaks and valleys, including deficits in visuospatial ability, mathematics, and attention, but with relative preservation of language and affect. Our study measured the corpus callosum and its primary subdivisions using high-resolution MRI in 20 individuals with WS (13 females and seven males; mean age 28.5, SD 8.3 years; range 19 to 44 years) and 20 age- and sex-matched control participants (mean age 28.5, SD 8.2 years; range 19 to 48 years). Total midsagittal corpus callosum area was reduced (F=4.5, p=0.04, df=36) in the WS population. The area of the splenium (F=12.4, p=0.001, df=36) and isthmus (F=9.4, p=0.004, df=36) were disproportionately reduced in WS beyond the absolute reduction of the entire corpus callosum. These reductions are in concordance with other neuroanatomical findings of decreased parietooccipital volumes as well as the observed visuospatial problems associated with WS.

Adult↗