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PubMed1987

The role of genetic factors in the immunomodulating effect of thymosin.

The possible role of hypothetical genetic factors involved in the immunomodulating effect of thymosin fraction 7 (T7) was investigated. The model system was the in vitro immunization of murine spleen cell cultures with sheep red blood cells (SRBC), and the generation of antigen specific B cells in T7 treated cultures was compared to that of control values. It was found that T7 treatment enhanced the plaque forming cell (PFC) response of BALB/c spleen cells, while it proved to be suppressive in CBA cultures. Moreover, the T7 treatment of athymic BALB/c nude spleen cells resulted in a marked PFC response to SRBC, while a similar treatment of CBA nude cultures was ineffective in the same assay. The role of possible genetic factors was further confirmed using H-2 congenic and recombinant mouse strains on the C3H and B10 background. T7 elevated the PFC values in all B10 strains tested, and was suppressive in the case of C3H strains. It seems that the outcome of T7 treatment of murine target cells is determined by the genetic background and is independent of the H-2 haplotype.

Animals↗
PubMed2003

Peripheral vascular disease in Type 2 diabetic Chinese patients: associations with metabolic indices, concomitant vascular disease and genetic factors.

AIMS: Conventional and genetic risk factors have been reported to play a role in the pathogenesis of vascular disease, but do not explain the lower burden of cardiac and peripheral vascular disease (PVD) in Chinese compared with Caucasians. The role of renin-angiotensin system (RAS) gene polymorphisms and conventional vascular risk factors has not been determined. METHODS: A total of 3097 Chinese diabetic subjects were screened for PVD, which was identified in 194 of the 2967 patients with Type 2 diabetes. Biochemical parameters and the genotype and allele frequencies of three RAS gene polymorphisms, the angiotensin-converting enzyme (ACE) insertion/deletion, angiotensinogen (AGT) M235T and angiotensin II type 1 receptor (AT1R) A1166C polymorphisms were then compared between the PVD patients and 1046 age, gender and diabetes duration-matched patients without PVD. RESULTS: PVD identified in 6.5% was associated with significantly worse glycaemic control, lipid profile and renal function. Smoking was more common, as were the other macro- and microvascular diseases. The prevalence of hypertension was similar between the groups, yet diastolic blood pressure was slightly lower in the PVD group. The ACE D allele was significantly more frequent in patients with PVD compared with the matched diabetic controls (38.1 vs. 29.8%, P = 0.039). No differences in the AT1R or AGT polymorphisms were observed. CONCLUSIONS: PVD was associated with a worse metabolic profile and greater concomitant vascular disease than controls. The ACE I/D polymorphism was associated with PVD in these Type 2 diabetic patients.

Aged↗
PubMed2002

Non-familial Alzheimer's disease is mainly due to genetic factors.

This team takes the position that what is commonly referred to as non-familial Alzheimer's disease (AD) is predominantly due to genetic factors. Population-based studies suggest that genetic factors cause the majority of cases that begin after age 60. There are several lines of evidence supporting this position: Data from the Nun Study suggest that the risk for AD is largely established by early adulthood, implying that later adult exposures likely play only a small role in causation. Family studies show that first-degree blood relatives of persons with non-familial AD have a substantially increased risk of AD relative to controls. Twin studies suggest that the heritability of AD exceeds 60%. Environmental factors, such as socioeconomic status, education, and head injury, are strong risk factors for AD only in individuals with a genetic predisposition. The APOE genotype is a powerful risk factor for AD and accounts for as much as 50%. There are numerous other candidate genes with strong associations with AD that presumably explain the remaining population risk. This paper further reviews the mechanisms associated with AD causation for APOE and other candidate genes and implications for the development of prevention strategies.

Adult↗
PubMed1993

Genetic factors in hypertension.

Genetic approaches to hypertension have the potential to identify many of the primary abnormalities that underlie this disorder. Approaches in experimental animals and humans have advanced to the point that this is no longer merely a possibility but is a tangible reality. Successes in the past year include the mapping of a number of relevant loci and the identification of several mutations that contribute to the pathogenesis of hypertension in animals and humans.

Animals↗
PubMed2004

A common genetic factor underlies hypertension and other cardiovascular disorders.

BACKGROUND: Certain conditions characterised by blood vessel occlusion or vascular spasm have been found to cluster together in epidemiological studies. However the biological causes for these associations remain controversial. This study used a classical twin design to examine whether these conditions are linked through shared environmental exposures or by a common underlying genetic propensity to vasospasm. METHODS: We investigated the association between hypertension, migraine, Raynaud's phenomenon and coronary artery disease in twins from a national register. Phenotype status was determined using a questionnaire and the genetic and environmental association between phenotypes was estimated through variance components analysis. RESULTS: Responses were obtained from 2,204 individuals comprising 525 monozygotic and 577 dizygotic pairs. There was a significant genetic contribution to all four traits with heritabilities ranging from 0.34 to 0.64. Multivariate model-fitting demonstrated that a single common genetic factor underlies the four conditions. CONCLUSIONS: We have confirmed an association between hypertension, migraine, Raynaud's phenomenon and coronary artery disease, and shown that a single genetic factor underlies them. The demonstration of a shared genetic factor explains the association between them and adds weight to the theory of an inherited predisposition to vasospasm.

Adolescent↗
PubMed1991

[The contribution of genetic factors to perinatal pathology and infant mortality].

The authors consider the contribution made by genetic factors to perinatal and infant mortality on the basis of many-year studies performed in the Minsk Teratology Center and analysis of the data available in the literature. In 1972-1984 there was an increase in the incidence of congenital malformations among deceased children. Genetic factors predispose to at least 7-8% postimplantation embryonal and fetal elimination. Perinatal and neonatal mortality is caused by congenital malformations in 19.1 and 37% of cases, respectively. A genetic analysis has indicated that 23.2% of them are induced by genic, chromosomal, and genomic mutations and 51.0% are caused multifactorially. The prevention of genetically determined perinatal mortality is most effective in implementing the screening programs for detection of heterozygous carriage along with subsequent prospective examination and prenatal diagnosis.

Anemia, Hemolytic, Congenital↗
PubMed1997

[Relationship between learning behavior and genetic factor on immobility shown during forced swimming test].

The relationship between learning and genetic factor on immobility in mice during a forced swimming test (FST) has been studied. The duration of immobility during the FST did not change significantly after the administration of either scopolamine (2.5 mg/kg, ip) or cyclohexamine (150 mg/kg, ip), although both drugs produced impairment in the learning task. This suggests that the increase in immobility observed during the second trial of the FST may not be related to learning which could occur during the first trial. Concerning the strain difference, first, the duration of immobility in C3H mice was shorter than that in ICR, ddY, C57BL and BALB mice. Second, after receiving shock stress in a box, ICR, ddY and C57BL mice, but not C3H mice showed a marked decrease in locomotor activity when placed in the box again without shock. Also during the FST, both C57BL and ddY mice, but not C3H mice showed prolongation of immobility and reduction in swimming after shock stress. The changes in locomotor activity, and immobility and swimming during the FST caused by shock stress in ddY mice recovered to normal levels after treatment with imipramine. From these results, it is suggested that the immobility shown during the FST, which may be independent of learning and dependent on some genetic factor, is a suitable model of depression in animals.

Animals↗
PubMed1999

[Genetic factors and a polygenic model of Alzheimer's disease].

Genetic factors are responsible, to a certain degree, for many, if not all, Alzheimer's disease (AD) cases. A certain proportion of early-onset (below 65 years of age) AD cases follows an autosomal dominant mode of inheritance. Three genes were identified whose mutations account for 50-70% of early-onset monogenic AD cases in AD pedigrees. These are the genes of the amyloid precursor protein (APP) and two presenilins (PS I and PS II). The polymorphic variant of apolipoprotein E, APOE epsilon 4, is a genetic causative factor in familial and sporadic cases of various early- and late-onset AD forms (it is found, in general, in 20-50% of all AD cases). The action of the epsilon 4 allele is codominant, with the AD risk increased in homozygotes (epsilon 4/epsilon 4 > epsilon 4 > epsilon 3 or epsilon 2). In contrast to the mutations in the PS I and APP genes, the APOE epsilon 4 allele is not a necessary and sufficient condition for AD development. Mutations in these genes have not been found in a proportion of familial early-onset AD cases and are not causative factors in the majority of late-onset familial and sporadic forms. The genes determining AD are evolutionarily conservative and are expressed in all human tissues as early as at initial ontogenetic stages. This raises the question as to why AD is a progressive disorder affecting certain cerebral regions only at middle or old age. A hypothesis and model are suggested to explain the interaction between evolutionary, ontogenetic, and epigenetic factors of the development of the central nervous system and the products of genes whose mutations result in AD. Findings of different mutant genes indicate that AD is a set of genetic disorders (ADs) with a common pathological manifestation.

Age of Onset↗
PubMed2002

[Effects of genetic factors on the response to hormone replacement therapy].

Hormone Replacement Therapy (HRT) is currently recognized as the potential tool for menopause medicine. But it is also well known that the effects of HRT on bones and blood vessels show interindividual variances. Among the candidate factors to explain these variances, genetic factors may play an important role. Several reports have shown associations between some genetic markers, such as polymorphisms of estrogen receptor alpha gene, and the effect of HRT on bone mineral density. Phenotype of apolipoprotein B, E, and angiotensin-converting enzyme, as well as polymorphisms of estrogen receptor alpha gene, have been reported to influence the lipid metabolic or vasodilatic response to HRT. This information can be applicable to tailor-made therapy. But the results of reports are conflicting and relationships between genetic markers and the response to HRT are still controversial. Further investigations will reveal the potential of genetic markers in disease managements near future.

English Abstract↗
PubMed1999

Genetic factors in IgA nephropathy.

Immunoglobulin A glomerulonephritis (IgA-GN) or Berger's disease is the most common glomerulonephritis when diagnosis is based on renal biopsy. The disease has a variable clinical course. Abnormalities in the production and/or catabolism of IgA are thought to play an important role in the etiology and pathogenesis of IgA-GN. Some evidence suggests that genetic factors determine the susceptibility to develop IgA-GN. Furthermore it has been proposed that genetic factors determine also the rate of progression. Since hypertension is an important predictor of progression, genes involved in blood pressure regulation have been analysed. A polymorphism in the gene for the angiotensin converting enzyme has been reported to be associated with progression. Further studies and progress in molecular biology will help to further elucidate the genetic factors which contribute to the development and progression of IgA-GN.

Biopsy↗
PubMedDate not supplied

[Genetic factors in the etiology of anorexia nervosa].

Anorexia nervosa (AN) is a disease of complex ethiopatogenesis. Population genetics studies suggest a significant role of genetic factors in the morbidity risk. Family and twin studies allow for the estimation of the heritability--the influence of genetic factors on the specific phenotype--of the anorexia nervosa in 50-80%. Due to the low prevalence of the disease, the adoption studies have not been performed. The rapid development of the molecular biology methods gives possibility for the searching of the specific genes increasing the risk of anorexia nervosa. Linkage studies are based on scanning the whole genome for loci associated with susceptibility to a certain disease. In the preliminary studies, no linkage was found between anorexia nervosa and the markers on the chromosomes 1-5, 13 and X. In the association studies, relationship between vulnerability to AN and polymorphism in 5-HT2a receptor and uncoupling proteins gene were reported. These results need further confirmation.

Anorexia Nervosa↗
PubMed2005

Bone mass in young adults: relationship with gender, weight and genetic factors.

OBJECTIVES: To determine the relationship of the bone mass attained in young adults with anthropometric and genetic factors. DESIGN: Cross-sectional study of normal individuals. METHODS: We studied 341 healthy subjects between 22 and 45 years of age. Bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry (DXA) and correlated with body weight, height and nine polymorphisms in six genes involved in sex steroid metabolism (17-hydroxylase, aromatase and 5-reductase) and activity (oestrogen receptors (ER)-alpha and -beta, and androgen receptor). RESULTS: The BMD was higher in men than in women (spine: 1.048 +/- 0.120 vs. 1.034 +/- 0.112; hip: 0.907 +/- 0.131 vs. 0.822 +/- 0.104 g cm(-2), P < 0.001). However, the difference was due, at least in part, to the larger body size in men and diminished markedly after height adjustment. There was a negative correlation between age and hip BMD. Body weight was the single most influential factor on spine and hip BMD in both sexes, explaining 8-9% of BMD variance. Amongst the genetic factors studied, a common CA repeat polymorphism in ER-beta showed a significant association with BMD in women (P = 0.03 at the spine, and 0.008 at the hip). The relationship between ER-beta genotype and BMD persisted after adjustment by body weight and age, explaining a further 2-3% of BMD variance. Allelic variants of other genes studied were not related with BMD. CONCLUSIONS: Body weight and allelic variants of ER-beta are associated with BMD in young adults.

Absorptiometry, Photon↗
PubMed2004

WRN gene and other genetic factors affecting immortalization of human B-lymphoblastoid cell lines transformed by Epstein-Barr virus.

The immortalization of human B-lymphoblastoid cell lines (LCL) transformed by Epstein-Barr virus (EBV) is accompanied by two major events: increase in telomerase activity and change in karyotype from normal diploid to aneuploidy. We investigated the effect of genetic factors on the incidence of immortalization by putting old and new data together to collect enough samples for statistical analysis. Among 50 LCL from normal individuals, 5 LCL (10.0%) were immortalized and the remaining 45 LCL were mortal. None of the 44 LCL (0%; P < 0.031 against normal individuals by chi square test) from patients having Werner syndrome (WS), a recessive genetic disorder showing premature aging, were immortalized. Among 11 LCL from a family with a tendency to have hereditary type 2 diabetes mellitus, 5 LCL (45.5%; P < 0.0040 against normal individuals, P < 0.00001 against WS patients) were immortalized. Duplicated measurements of the lifespan of 33 LCL showed a good coincidence (r=0.785) between the first and second estimations, indicating that each mortal LCL has a predetermined lifespan. These results strongly suggest that the normal WRN gene, the causative gene of WS, is essential for LCL to immortalize, and genetic factor(s) of a family having diabetes mellitus increases immortalization, implicating that host genetic factors affect immortalization of EBV and probably carcinogenesis by EBV.

Adolescent↗
PubMed1996

Association of factor VII:C levels with environmental and genetic factors in patients with ischaemic heart disease and coronary atheroma characterised by angiography.

Elevated Factor VII:C (FVII:C) levels are an independent risk factor for acute myocardial infarction. To examine the association between FVII:C levels, genetic and environmental factors in patients with a history suggestive of ischaemic heart disease, 270 patients were studied. FVII:C levels were significantly associated with the Msp I and promoter insertion polymorphisms. FVII:C correlated with environmental factors, and these correlations remained when analysed by genotype. In a multiple regression model, genotype, body mass index, cholesterol, triglycerides and gender remained as independent and significant predictors of FVII:C levels. There was no significant difference in FVII:C concentrations with severity of atheroma, or in patients with a history of myocardial infarction. These findings provide further evidence linking FVII:C with Msp I and promoter insertion genotypes and with environmental factors in established IHD, but suggest there is not a genotype-environment interaction or a relationship between FVII:C levels and severity of ischaemic heart disease.

Aged↗
PubMed2004

Effect of environmental and genetic factors on education-associated disparities in weight and weight gain: a study of Finnish adult twins.

BACKGROUND: Disparities in body mass index (BMI) between persons with different educational levels in Western countries are well documented, but the background of these education-associated disparities remains poorly understood. OBJECTIVE: The objective was to examine the influence of environmental and genetic factors on education-associated disparities in self-reported BMI and weight change. DESIGN: Longitudinal postal surveys were performed in 1975, 1981, and 1990. The data were analyzed by using multivariate genetic models for twin data. The data derived from the Finnish Twin Cohort included 2482 monozygotic and 5113 dizygotic same-sex male and female twin pairs born between 1915 and 1957. RESULTS: Education-associated differences in BMI and in weight change were clear in 1975 and 1981, respectively, whereas no differences were seen in weight change between 1981 and 1990 when age and baseline BMI were adjusted for. The trait correlation between baseline BMI and educational attainment (-0.15 in men and women) was mainly due to correlations between additive genetic factors that contributed to BMI and education in men (-0.20; 95% CI: -0.25, -0.14) and women (-0.32; 95% CI: -0.40, -0.25) when adjusted for age. Among women, a weaker positive correlation was found for the unshared environmental effects contributing to the 2 traits (0.06; 95% CI: 0.02, 0.12). The same factors that affected the association between education and BMI in 1975 largely explained the association between education and weight change in 1981. CONCLUSION: The results suggest the possibility that common genetic factors affect educational attainment and body weight, which contribute to education-associated disparities in BMI in adulthood.

Adult↗
PubMed1978

[Genetic factors in the etiology of breast cancer (author's transl)].

A review of literature shows that, at present, genetic factors are difficult to distinguish from environmental factors. A number of studies have put into light relationships between factors tranmetted genetically and an increased risk of breast cancer in some women. This might be a reflect of the transmission of a certain susceptibility. However, one of these factors alone cannot explain the increase of the risk. Most likely, as for many types of cancers, the development of breast cancer is due both to a multigenic transmission of a certain susceptibility and to the action of environmental factors. Though, epidemiological studies make possible to identify a high risk population. A regular follow-up of this population would permit early diagnosis and possibly prophylactic measures concerning the known environmental factors, and in particular hormonal factors.

Adult↗
PubMed2000

[Field epidemiological and experimental study on relationship between genetic factor and nonresponse or hyporesponse to hepatitis B vaccine].

OBJECTIVE: To evaluate the role of genetic factor in the development of nonresponder or hyporesponder to hepatitis B vaccine in Chinese people from field epidemiology and experimental study. METHODS: Six hundred and thirty-four susceptible healthy students were vaccinated with three doses of plasma-derived hepatitis B vaccine. Twenty-nine non- or hypo-responders (subjects) and 30 hyperresponders (controls) as well as their 80 and 79 first degree relatives were determined and recruited in the study. The first degree relatives of subjects and controls were then immunized with hepatitis B vaccine and followed up. On the basis of the above results, alleles of HLA-A, B, C, DR and DQ locus were further detected in the two groups. RESULTS: The non- and hypo-response rate in immunized students was 4.6% (29/634). After administered with hepatitis B vaccine, the first degree relatives of the subjects displayed a 17.9% frequency of nonresponsiveness, higher than in the controls. The phenotype frequency of HLA-DR7 and B54 was 52.2% and 21.7% in subjects, 9.1% and 0.0% higher than in controls, respectively. The extended haplotype B54-DR7 was more frequent in the former (17.0%) than in the latter (0.0%) (P < 0.01). CONCLUSION: These results demonstrated that the genetic factor was likely associated with the non- and hypo-response to hepatitis B vaccine in Chinese people.

Adolescent↗