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At least 109 records · Page 6Linked to original sources
PubMed2001

Melanocyte and gonad activity as potential severity modifying factors in C3H/HeJ mouse alopecia areata.

Circumstantial evidence has previously suggested gonad derived steroid hormones and melanogenesis related antigens may modify human alopecia areata (AA). AA-like hair loss can be induced in C3H/HeJ mice after skin allografts from spontaneous AA-affected mice. This inducible model was used to evaluate hormones and hair follicle melanocyte presence as disease-severity modifiers. Ten females and 9 males were gonadectomized and received AA-affected allografts. All gonadectomized mice had 2-4 weeks delay in AA onset relative to non-gonadectomized controls. Two females and 4 males failed to develop any AA by 25 weeks after grafting. The experiment was repeated with gonadectomized female and male mice plus non-gonadectomized mice subcutaneously implanted with silastic capsules containing 80 microg 17beta estradiol or 10 mg 5alpha dihydrotestosterone, respectively. Five of 11 ovariectomized and 9 of 11 non-ovariectomized, estradiol supplemented females developed AA with extremely rapid progression. Three of 8 castrated, but none of 11 non-castrated, dihydrotestosterone-supplemented males expressed AA. In a separate study, 14 mice were freeze-branded, producing white hair on the dorsal lumbar region, and later received full-thickness allografts. Thirteen mice developed patchy pigmented and non-pigmented hair loss. One mouse developed diffuse, pigmented hair loss, but with white hair survival persisting 25 weeks after grafting. The results suggest that gonadal steroid hormones can modulate C3H/HeJ mouse AA where estradiol promoted rapid progression of AA while dihydrotestosterone increased resistance to AA onset. In general, both pigmented and non-pigmented C3H/HeJ mouse hair is susceptible to AA. Murine AA susceptibility and severity clearly involves an interplay between genetic and epigenetic factors.

Alopecia Areata↗
PubMed1991

Dietary calcium and blood pressure: modifying factors in specific populations.

Epidemiologic findings continue to add to the body of evidence supporting a relationship between calcium intake and blood pressure. These findings also indicate that there is a threshold of the potential protective effect of adequate calcium intake, below which the risk of hypertension increases at a greater rate. The set point of this threshold, estimated at 700-800 mg/d, may be modified by a variety of factors including dietary patterns and components, lifestyle, and genetics. This may explain, at least in part, the heterogeneous response observed in dietary-intervention studies. In animal models of hypertension it was shown that greater amounts of calcium must be given to cause a blood pressure change comparable with that in normal animals, suggesting that in high-risk human populations in which calcium metabolism may be disordered, calcium intake may have to be increased to amounts greater than 700-800 mg/d to demonstrate the blood-pressure-lowering effect. Calcium intake at or above the currently recommended daily allowance of 800 mg could be of potential benefit to certain racial groups, individuals ingesting excessive alcohol, and pregnant women, all of whom generally consume low amounts of calcium and who are at higher risk of developing hypertension.

Animals↗
PubMedDate not supplied

Developmental factors modify stress ulcer incidence in a stress-susceptible rat strain.

Our multifactor theory of stress ulcer assumes that environmental factors that operate during early growth stages influence the elaboration of stress ulcer in adult rats. The theory would predict that rats exposed to either neonatal handling, or raised in a stimulus enriched environment, would reveal differences in stress ulcer susceptibility. In study 1, some Wistar rats and ulcer-susceptible Wistar Kyoto (WKY) rats were handled daily from birth to day 21, whereas other rats from each strain were not disturbed. In study 2, Wistar and WKY rats were raised (3 months) in a large stimulus-dense enriched environment, whereas other rats from each strain were raised in standard rat cages where visual and auditory stimuli were minimized. At 3 months all rats were observed in the open field test (OFT), a test of emotionality, as well as the Porsolt forced swim test (FST), a test of behavioral depression, and subsequently exposed to the ulcerogenic water restraint procedure. Neonatal handling produced results suggesting increased wall climbing activity in the FST, reduced response latency in the OFT, increased body weight and reduced ulcer severity, but these differences were not significant. Rearing in an enriched environment produced similar results but these difference were more pronounced and significant in the Wistar rats as compared to the WKY rats. Thus early environmental manipulations can influence adult behavior and the elaboration of stress ulcer disease, but the impact of these manipulations is less salient in an organism with an endogenous susceptibility to the disease.

Animals↗
PubMed1995

[Which factors modify drug-compliance?].

Since the extent of medication noncompliance in schizophrenic patients ranges between 50 and 60%, evaluation of factors that are associated with noncompliance has become an important issue. 197 schizophrenic patients have been interviewed with regard to numerous issues: Form and type of medication; information about side effects; attitude of patients towards illness and medication. Our data suggest that information about benefits and side effects, as well as the attitude of patients towards illness and medication play an important role in the adherence to the treatment regimen.

Adult↗
PubMed1996

Local infusion of brain-derived neurotrophic factor modifies the firing pattern of dorsal raphé serotonergic neurons.

Previous studies have reported a neuromodulatory effect of brain-derived neurotrophic factor (BDNF) on serotonin neurons in the central nervous system. In the present study, we examined the effects of local infusion of BDNF on the electrophysiological activity of serotonergic neurons in the rat dorsal raphé nucleus with extracellular single unit recording in vivo. Compared with vehicle-infused rats, chronic administration of BDNF (10-14 days) caused serotonergic neurons to fire in a significantly less regular pattern, without altering the mean firing rate or other measures of electrical activity. These results suggest that the ability of similar infusions of BDNF to produce behavioral effects (i.e. analgesia and an antidepressant-like effect) associated with elevated serotonin turnover may be in part the result of more irregular firing patterns of dorsal raphé neurons.

Animals↗
PubMed1979

Effect of different factors modifying the activity of some enzyme systems of the endoplasmic reticulum on the sensitivity of cell organelles against the damaging action of chemical agents. II. Studies with chlorpromazine, 2,4-dinitrophenol, phenobarbital and DDT.

Further investigations on the effect of different stress factors on the stability of intracellular membranes were carried out. Large granule fractions derived from livers of sleep-deprived and dehydrated rats and subjected to preincubation at 37 degrees and pH 5 were shown to release latent acid phosphatase with a delayed rate indicating an increased lysosomal stability towards acid media conditioning. Lysosomes of such animals, however, were found to be more sensitive to mechanical treatments (homogenization procedure in this case) than that of controls, a conclusion made on the basis of enhanced "free" and nonsedimentable phosphatase activities in liver homogenates. The stress factors which previously were included in the group of modifiers of the activity of the endoplasmic reticulum-located enzymes caused some changes in the action of certain chemicals on membranes. Earlier such changes were elicited for carbon tetrachloride and only on low-temperature-conditioned rats for chlorpromazine. The present results show that stress factors studied result in deviations (different in extent and in direction) from the usual effects of chlorpromazine, 2,4-dinitrophenol, phenobarbital and DDT on liver lysosomes and peroxisomes.

Acid Phosphatase↗
PubMed2001

Polymorphisms of clotting factors modify the risk for primary intracranial hemorrhage.

Intracranial hemorrhage is the third most frequent cause of cerebrovascular disease, but few genetic risk factors have been associated with its development. Recently, it has been reported that some polymorphisms that affect clotting factors increase the risk for thrombosis. However, reports have analyzed the effect of polymorphisms influencing the hemostatic state in bleeding disorders insufficiently. A case-control study was conducted of 201 patients with spontaneous intracranial hemorrhage and 201 control subjects matched for age, race, sex, and selected risk factors (hypertension, smoking, and alcohol consumption). Genomic polymerase chain reaction was used to analyze the prevalence of 4 polymorphisms: factor V Leiden, prothrombin 20210A, factor VII-323 Del/Ins of a decanucleotide, and factor XIII V34L. Subjects with factor V Leiden had decreased risk for spontaneous intracranial hemorrhage (odds ratio, 0.19; 95% confidence interval, 0.03-0.95). The frequency of the prothrombin 20210A/G genotype was also lower among patients than controls (1.5% vs 3%, respectively). Moreover, carriers of the -323 Ins allele of factor VII had a 1.54-fold risk for intracranial hemorrhage (95% CI, 1.03-2.72). Finally, no significant differences were observed in the prevalence of factor XIII V34L polymorphism between patients and controls. Therefore, new genetic factors affecting the risk for spontaneous intracranial hemorrhage were identified. These data, together with the relevance of these polymorphisms in thrombotic diseases, support the idea that a polymorphism may play opposite roles in thrombosis and hemorrhage, suggesting an explanation for the high frequency of these polymorphisms in the general population.

Aged↗
PubMed1986

[Effect of levorin and its combination with a modifying factor on lipid peroxidation in Crithidia oncopelti].

It was shown earlier by the authors that in the presence of sodium acetate as a modifier of C. oncopelti reaction to levorin, a polyenic antibiotic sensitivity of this organism to the antibiotic increased. At the same time there were observed changes in the ratio of the lipids and fatty acids of the total lipid fraction of C. oncopelti. The changes in the lipid composition of the biological membranes influenced lipid peroxidation (LPO). The present paper deals with investigation of interrelation between increasing of C. oncopelti sensitivity to levorin in the presence of sodium acetate and LPO levels. Accumulation of the primary, secondary and final LPO products in C. oncopelti under the effect of sodium acetate, levorin (1 microgram/ml) added simultaneously with the modifier and levorin in a concentration of 10 micrograms/ml was investigated. It was shown that sodium acetate did not induce accumulation of LPO products as compared to the initial culture. Levorin added simultaneously with sodium acetate and levorin in a concentration of 10 micrograms/ml induced an increase in the content of LPO products in the C. oncopelti lipids. The causes of the LPO rate increase in the presence of the polyenic antibiotic are discussed.

Acetates↗
PubMed2005

A weighted cohort approach for analysing factors modifying disease risks in carriers of high-risk susceptibility genes.

The authors propose a novel approach to evaluate the effects of risk factors on disease risks in carriers of high-penetrance alleles in disease susceptibility genes. Most studies to date have utilised data collected on carriers identified through ongoing genetic testing programs. The advantage of this approach is that it allows relatively large numbers of affected and unaffected carriers to be identified rapidly. However, genetic testing is targeted at individuals with a strong family history of disease, so that the selection of carriers is not random with respect to disease status. Risk factors are often analysed by standard cohort analysis methods, but these can be biased in retrospective studies if subjects are selected on the basis of phenotype. To overcome this problem, a weighted cohort approach is proposed, under which individuals are weighted according to certain sampling probabilities in order to mimic a true cohort. The method is illustrated by analyses of data from the International BRCA1/2 Carrier Cohort Study (IBCCS). Simulations demonstrate that the method gives rate ratio estimates that are close to unbiased provided that the absolute disease risks are well estimated. The power to detect associations is, however, reduced compared with an unweighted approach.

Adult↗
PubMed1987

Neuroleptic treatment and other factors modifying cancer risk in schizophrenic patients.

In a Danish cohort of schizophrenics consisting of 6,168 patients followed during 1957-1980, the incidence of certain types of cancer has been shown to be significantly decreased (5). From this cohort 30 males with lung cancer, 21 males with bladder cancer, 17 females with cancer of the uterine cervix and 40 females with breast cancer, were each matched to two "healthy" schizophrenic controls from the same cohort. A range of social, demographic and nosocomial factors were registered from the individual case files, and statistical analysis was carried out, using Cox's regression model. Neuroleptic treatment with various drugs other than reserpine reduced the risk of developing all four cancer types studied. In contrast reserpine treatment increased the risk of developing cancer of the breast and uterine cervix. Furthermore, cancer risk was found to be modified by other well-known risk factors.

Antipsychotic Agents↗
PubMed1994

Pharmacological effects of recombinant human granulocyte colony-stimulating factor modified by polyethylene glycol on anticancer drug-induced neutropenia in mice.

1. To clarify the pharmacological effects of recombinant human granulocyte colony-stimulating factor (rhG-CSF) conjugated to polyethylene glycol (PEG), its effects on the number of circulating neutrophils in mice made neutropenic by cyclophosphamide (CPA) or 5-fluorouracil (5-FU) were compared with rhG-CSF lacking PEG. 2. In normal mice, PEG-conjugated rhG-CSF (PEG-rhG-CSF, 10 micrograms protein/kg) induced an increase in neutrophils which lasted for 72 h after injection whereas the effect of rhG-CSF (10 micrograms protein/kg) disappeared by 24 h after injection. 3. In CPA or 5-FU-induced neutropenic mice, PEG-rhG-CSF inhibited neutropenia or accelerated recovery from neutropenia and its potency was higher than that of rhG-CSF. 4. These results indicate that PEG-rhG-CSF has a longer duration of action than rhG-CSF and is more effective in the recovery from neutropenia.

Animals↗
PubMedDate not supplied

[Small doses of ionizing radiation as radiation modifying factor].

To investigate the biological effects of small dose ionizing radiation has been acquiring greater importance. The awareness of how and in what direction it show its modifying effects in small doses is an essential scientific basis for developing standards, living conditions under specific environmental conditions. Cultured Hela cells and DEF 4/21 fibroblasts were used to evaluate the biological effects of small-dose ionizing radiation, by examining the conditions under which it showed its modifying effect in small doses (0.1 Gy) in particular. Preexposure to small-dose radiation was shown to alter cell responses to subsequent radiation in large doses. The modifying effects of small-dose radiation turned out to depend on the interval of exposure to small and large doses. Sensitization was recorded at an interval of 2-3 min; an adaptive response was achieved when the interval increased up to 3-5 hours. Upon exposure, intercellular contacts contribute to the modifying effects of small-dose radiation. There was neither effect of sensitization nor adaptive response if single cells were exposed to radiation.

Cell Line↗
PubMed1997

[Do psychological factors modify survival of cancer patients? II: Results of an empirical study with bronchial carcinoma patients].

The present prospective test study of hypotheses addressed the question whether psychological factors are predictive of survival time in lung cancer patients. The hypotheses were: Emotional distress, depression and depressive coping are associated with shorter survival; hope and active coping with longer survival. The study was based on a sample of n = 103 patients who were investigated post-diagnosis and before the beginning of primary treatment. Emotional distress and hope were assessed by clinical scales (self-reports and interviewer ratings), depression by the Depression Scale of von Zerssen, depressive coping and active coping by the Freiburg Questionnaire on Coping with illness by Muthny. At follow-up, which took place three to five years later, n = 74 patients had died, for n = 29 patients the survival data are censored. The prediction of the survival time was performed applying multivariate analyses (Kaplan-Meier-method, Cox-Regression), adjusting for biological risk factors (histological classification, stage of the disease, type and amount of treatment, Karnofsky performance status, age). Results were as follows: Active coping and hope were associated with longer survival, emotional distress, depression and depressive coping with shorter survival, respectively. These associations were found consistently across assessment methods. The predictive effects of coping and distress were statistically independent of the influence of the somatic risk factors. The best psychological predictor was the interviewer rating of active coping. Its predictive power equalled that of the Karnofsky performance status. However, there was evidence that the effects of the psychological factors varied somewhat in interaction with treatment modalities. The findings are discussed from a methodological perspective. Possible causal models and mechanisms are presented which could account for interactions of psychological measures and the course of the disease: Thus, it can be conceived that psychological effects were mediated by patients' compliance with medical treatment. In addition, it cannot be ruled out that psychological factors themselves were influenced by the physical status of the patients at the time of entry to the study.

Adaptation, Psychological↗
PubMed1994

Human cytotrophoblast invasion is up-regulated by epidermal growth factor: evidence that paracrine factors modify this process.

Formation of the human placenta requires a subset of cytotrophoblast stem cells to acquire an invasive phenotype. We examined the effect on cytotrophoblast invasiveness of growth factors that control the differentiation of other cells. Exogenous TGF-beta 1, PDGF-AA, PDGF-BB, and TNF-alpha affected neither cell morphology nor the rate of cytotrophoblast invasion in vitro. In contrast, addition of EGF to first trimester cytotrophoblast cultures produced dramatic changes in morphology and a severalfold increase in invasive capacity. The effects of EGF on later gestation cytotrophoblasts, whose invasive capacity is diminished, were much less pronounced. Next we investigated whether cytotrophoblasts themselves produce ligands that interact with the EGF receptor. A radioimmunoassay and a radioreceptor assay failed to detect EGF receptor ligands in cytotrophoblast-conditioned medium. Likewise, by RT-PCR cytotrophoblasts expressed neither EGF nor TGF-alpha mRNA. In contrast, EGF receptor mRNA was expressed and its protein levels remained constant during the experiment. Immunolocalization using F(ab') fragments of an anti-human EGF antibody failed to detect this growth factor in the chorionic villus. We conclude that maternal ligands that interact with the EGF receptor could play an important role by up-regulating trophoblast invasion, particularly during the early stages of pregnancy.

Becaplermin↗
PubMedDate not supplied

[May the dialogue between genes and environmental factors modify the behavioural phenotype of Rett syndrome and others?].

Formation of a phenotype during development of the human being may result from a specific dialogue between genes and environmental factors. Expression of particular genes is controlled not only on the transcriptional level but also on the level of accessibility of genetic information through the influence for remodelling of chromatin. We characterized Rett syndrome and its molecular basis as an example of the relation between genes and environment and their influence on epigenetic processes determining the gene expression. Examples of importance of DNA methylation in psychiatric disorders were shown.

DNA Methylation↗
PubMed1985

Growth hormone-releasing factor modifies dopaminergic but not serotonergic activity in the arcuate nucleus of hypothalamus in the rat, as recorded in vivo by differential pulse voltammetry.

Parenteral (i.v.) injection of growth hormone-releasing factor (GRF) increases the height of the 3,4-dihydroxyphenylacetic acid oxidation peak (peak 2) but does not change 5-hydroxyindole extracellular content (peak 3) in the arcuate nucleus of the hypothalamus, both peaks being recorded by the differential pulse voltammetry technique using a single specifically pretreated monopyrolytic carbon fibre electrode. Conversely, no significant changes are observed in the peak 2 and peak 3 heights recorded in the medial or in the lateral nucleus of the hypothalamus. These data suggest a specific interaction between GRF and the dopaminergic system.

Animals↗
PubMed2006

Do breast cancer risk factors modify the association between hormone therapy and mammographic breast density? (United States).

OBJECTIVE: To evaluate whether the association between hormone therapy (HT) and breast density differs by levels of breast cancer risk factors. METHODS: We evaluated 80,867 screening mammograms from 39,296 postmenopausal women from Washington State. We estimated odds ratios and 95% confidence intervals for dense breasts (Breast Imaging Reporting and Data System categories 3 "heterogeneously dense" and 4 "extremely dense") compared to fatty breasts (categories 1 "almost entirely fat" and 2 "scattered fibroglandular") among HT users compared to never users. We separately examined former HT use and current HT use by type (estrogen plus progestin therapy (EPT) and estrogen-only therapy (ET)). We stratified the associations by age, BMI, race, family history, and reproductive and menopausal factors. RESULTS: Current EPT users had a 98% (1.87-2.09) greater odds of having dense breasts and current ET users had a 71% (1.56-1.87) greater odds compared to never users. Current HT users were more likely to have dense breasts if they were older, had more children, or younger at first birth compared to never users; these associations were stronger among EPT users than ET users. CONCLUSIONS: HT, particularly EPT, may reduce protective effects of older age, parity, and younger age at first birth on mammographic density.

Adult↗