Biomedical subjects
Publications and source records attributed to L Abel.
Extracts of decidual tissue produced in pseudopregnant rats were found to suppress in vitro antibody response to alpha-2,4-dinitrophenyl-polylysine. The peak levels of both the total antibody response and the 2-mercaptoethanol-resistant fraction were reduced. Extracts prepared in a similar manner from uteri of normal untreated or pseudopregnant rats did not exert such an effect.
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This study investigated the relationships between the relatively mild manifestations in verbal behavior of social alienation and disorganized thinking in normal subjects and cerebral glucose metabolic rates measured by positron emission tomography (PET). Three groups of 10 young normal male subjects were injected with D-[18F]deoxyglucose (FDG) during either wakefulness, rapid eye movement (REM), or non-REM (NONREM) sleep, and 32 to 45 minutes later they were asked to report their thoughts, emotions, or dreams and free-associations to these mental events. Nonparametric correlations were obtained between measures of interpersonal social alienation, intrapsychic conflicts, and thought disorder derived from the typescripts of these reports by content analysis--using the Gottschalk-Gleser Social Alienation-Personal Disorganization Scale--and regional cerebral glucose metabolic rates obtained from PET scans. Total social alienation-personal disorganization scores obtained from the reports of wakeful, silent mentations showed significant positive correlations with glucose metabolic rates in the left temporal lobe. The patterns of significant correlations involving these verbal behavior measures derived from the content analysis of verbal reports of dreams or other mental events occurring during REM and non-REM sleep were in different cerebral locations from those found with these variables during silent, waking mentation. Previous observations suggesting that increased left temporal lobe glucose may typify chronic schizophrenia may instead be indicative of a wide range of thought disorder and/or social alienation manifestations occurring, at times transiently and minimally, in normal people.
Sib pair linkage studies are now widely used to investigate the genetic factors implicated in complex quantitative traits. To increase the power of these approaches, it has been proposed to select extremely discordant (ED) sib pairs which are expected to contain the highest linkage information. However, it is known that sibships of larger size contain more linkage information than independent sib pairs. In this paper we compare, in terms of power and cost considerations, the ED strategy, which uses information on sib pairs only, to the recently developed 'Maximum Likelihood Binomial' sibship-oriented method performed on the whole sibships from which the ED sib pairs have been extracted. We show that the use of these whole sibships is an efficient alternative to approaches focusing on ED sib pairs only.
BACKGROUND: Previous studies examining the relationship of anxiety scores, derived from the content analysis of speech of normal individuals, have revealed that the anxiety scores occurring in the dreams associated with rapid eye movement (REM) sleep are significantly correlated with localized cerebral glucose metabolic rates assessed by positron emission tomography (PET) scanning. These significant intercorrelations occur in different cerebral areas when the anxiety scores are obtained from mental experiences reported during non-REM sleep or during wakeful silent mentation. OBJECTIVE: The purpose of the present study was to examine the intercorrelations found between anxiety attributed to the self, anxiety-displacement, and anxiety denial measured from computerized content analysis of 5-min verbal reports of subjective thoughts and feelings obtained from wakeful normal subjects and localized cerebral glucose metabolic rates during PET scanning. METHODS: The subjects were 10 wakeful young males. Their anxiety scores were derived from computerized content analysis of 5-min reports they gave of their subjective thoughts, feelings and fantasies during a 30-min period following an intravenous injection of F D-deoxyglucose (FDG). The subjects were moved 32--45 min after this injection to obtain a PET scan, which records all of the localized cerebral glucose metabolic rates during the 30 min following the FDG injection. RESULTS: Significant intercorrelations of localized cerebral glucose metabolic rates with the scores of self-anxiety, anxiety displacement, and anxiety-denial were found in dissimilar cerebral locations depending on the type of anxiety involved. The significant correlations occurred in brain regions known to be associated with the functions of emotions, cognition, memory, and vision. CONCLUSIONS: Specific combinations of cerebral areas, based on glucose metabolic rates, appear to distinguish and be associated with different verbal expressions of anxiety. Replication of this preliminary research will be carried out.
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The spread and clinical manifestations of an infection in human populations depend on a variety of factors, among them host genetics. Familial linkage studies used in genetic epidemiology to identify host genes test for nonrandom segregation of a trait with a few candidate chromosomal regions or any regions in the genome (genomewide search). When a clear major gene model can be inferred and reliable epidemiologic information is collected (e.g., in schistosomiasis), parametric linkage studies are used. When the genetic model cannot be defined (e.g., in leprosy and malaria), nonparametric linkage studies (e.g., sibling-pair studies) are recommended. Once evidence of linkage is obtained, the gene can be identified by polymorphisms strongly associated with the trait. When the tested polymorphism is in strong linkage disequilibrium with the disease allele or is the disease allele itself (e.g., in HIV infection and malaria), association studies can directly identify the disease gene. Finally, the role of the detected polymorphism in causing the trait is validated by functional studies.
Genetic factors have clearly been shown to play a role in controlling malarial infection in animal models. There is now also increasing evidence for the genetic control of malaria in man. We carried out a segregation analysis based on blood parasite load phenotype for a population of the town of Bobo-Dioulasso (Burkina-Faso). This analysis demonstrated a strong genetic effect. Our results were not consistent with the segregation of a major gene and thus suggest that parasite load is under the control of minor genes. The genetic effect was stronger in children than in adults. We carried out a regression analysis in children and found that there was an association between the phenotype for blood parasite load and the q31-33 region of chromosome 5. We identified a gene in this region, Pfil1 (Plasmodium falciparum infection levels 1), which accounted for almost 50% of the variance in blood parasite load and which played a fundamental role in the control of infection. The 5q31-33 region contains several genes encoding cytokines that regulate T lymphocytes. The identification of genes controlling malarial infection opens up new possibilities for preventive and treatment strategies. It should be possible in the near future to identify individuals at risk of malaria, who would derive the greatest benefit from preventive and therapeutic measures. Finally, a deeper understanding of these genes controlling protective immune responses could be of value for the development of vaccines.
The development of genetic epidemiology methods using recent human genetic map together with the growing availability of candidate genes have led to substantial advances in the identification of host genes in human malaria. Investigation of these genes has progressed along two complementary ways: 1) The search for genes influencing the severe malaria clinical phenotype by means of population based case-control studies which showed the protective role of several red cell genetic defects (sickle cell anemia, a-thalassaemia ...) and that some polymorphisms of the TNF-alpha promoter region could predispose to cerebral malaria; 2) The investigation of the genetic regulation of malaria-related biological phenotypes (infection levels, immune response) by means of familial studies which underlined the influence of the 5q31-q33 chromosomal region in the control of Plasmodium falciparum blood parasitemia and the role of major histocompatibility complex (MHC) and non-MHC genes in the regulation of humoral and cellular response to various malarial antigens. Ongoing studies will precise the role of these genes and probably reveal the existence of other genes not identified yet. The impact of these findings on the understanding of malaria pathogenesis and on the design of future preventive and therapeutic strategies should be considerable.