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PubMed2006

Control of AIF-mediated cell death by the functional interplay of SIRT1 and PARP-1 in response to DNA damage.

Cell survival after genotoxic stress is determined by a counterbalance of pro- and anti-death factors. Sirtuins (SIRTs) are deacetylases that promote cell survival whereas poly(ADP-ribose) polymerases (PARPs) can act both as survival and death inducing factor and the two protein families are strictly dependent on NAD(+) for their activities. Here we report that SIRT1 modulates PARP-1 activity upon DNA damage. Activation of SIRT1 by resveratrol leads to reduced PARP-1 activity and there is a drastic increase in PAR synthesis in sirt1-null cells. The unbalanced regulation of PARP-1 in the absence of SIRT1 results in AIF (apoptosis inducing factor)-mediated cell death. Our findings establish a functional link between the two NAD+-dependent enzyme systems and provide a physiological interpretation for the mechanism of death in cells lacking SIRT1.

Animals↗
PubMedDate not supplied

Health and behavior: the interplay of biological, behavioral, and social influences: summary of an Institute of Medicine report.

An Institute of Medicine committee was convened to explore the links between biological, psychosocial, and behavioral factors and health and to review effective applications of behavioral interventions. Based on the evidence about interactions of the physiological responses to stress, behavioral choices, and social influences, the committee encouraged additional research efforts to explore the integration of these variables and to evaluate their mechanisms. An understanding of the social factors influencing behavior is growing and should be considered in programs and policies for public health, in addition to individual behavior and physiological status. Interventions to change behaviors have been directed toward individuals, communities, and society. Many intervention trials have documented the capacity of interventions to modify risk factors. However, more trials that include measures of morbidity and mortality to determine if the strategy has the desired health effects are needed. Behavior can be changed and new behaviors can be taught. Maintaining behavior changes is a greater challenge. Although short-term changes in behavior following interventions are encouraging, long-duration efforts are needed to improve health outcomes and to provide long-term assessments of effectiveness. Interventions aimed at any level can influence behavior change; however, existing research suggests that concurrent interventions at multiple levels are most likely to sustain behavior change and should be encouraged.

Behavior Therapy↗
PubMedDate not supplied

Racial/ethnic disparities in health: the interplay between discrimination and socioeconomic status.

In the past decade, racial/ethnic discrepancy in health status has drawn increased attention from academicians, policy makers and planners, service providers, and community advocates. While the field has witnessed a growth in research projects and intervention programs, the gap in health status among racial/ethnic groups persists, which suggests that future research should incorporate a focus on one neglected area, ie, the health implications of discrimination. Using the National Survey of Functional Health (N=1,659), a nationally representative sample of English-speaking persons 18 years of age and older living in non-institutional arrangements within the United States, we analyzed how self-perceived unfairness (discrimination due to racial identity or to low socioeconomic status [SES]) was linked to self-assessed health status. The study found that racial and class discrimination were rather pervasive in the United States. Experiences of discrimination tended to have a strong negative association with health and accounted for some racial/ethnic differences in health status. The study also revealed a complex relationship between experiences of discrimination and social class, suggesting that future research should focus on specifying the social distribution of discrimination and assessing its subsequent association with health.

Adult↗
PubMed1999

Aspects of secretion and actions of amylin: interplay between amylin and other hormones.

Amylin is a second beta-cell hormone, co-localized and co-secreted with insulin in response to nutrient stimuli. Amylin is released in a pulsatile pattern similar to insulin. It is mostly expressed in pancreatic islet cells but smaller amounts are present elsewhere, e.g. in the central nervous system. Apparently amylin (and amylin analogues) has actions capable of modifying glucose homeostasis. It suppresses arginine-stimulated and postprandial glucagon secretion, inhibits insulin secretion and slows gastric emptying. Furthermore, amylin seems to be a satiety agent. In vitro and in vivo studies in animals have demonstrated that amylin may induce insulin resistance. However, it exerts no effect on insulin sensitivity in humans. The literature on the possible actions of amylin/amylin analogues on secretion of growth hormone (GH) is limited. Hypothetically, amylin treatment could be of relevance to improve glycemic control in diabetes mellitus. Muticenter trials with an amylin analogue are ongoing and results are being awaited with interest.

Amyloid↗
PubMed1999

Antagonistic interplay between antimitotic and G1-S arresting agents observed in experimental combination therapy.

Paclitaxel is a naturally occurring antimitotic agent that has been shown to stabilize microtubules, induce mitotic arrest, and ultimately induce apoptotic cell death. The favorable clinical activity of paclitaxel has prompted considerable interest in combining paclitaxel with numerous other antineoplastic agents. Our previous studies have suggested 5-fluorouracil (5-FU), an antineoplastic agent that usually arrests tumor cells at the G1-S phase of the cell cycle, in combination with paclitaxel significantly represses paclitaxel-induced mitotic arrest and apoptosis. In the present study, we have extended this investigation to include several other antimitotic agents (vinblastine, colchicine, and nocodazole) in various combination schedules with the G1-S arresting agents 5-FU and hydroxyurea (HU). We found 5-FU, as well as HU, could significantly interfere with the overall cytotoxicity as compared with treatment with antimitotic agents alone. It appeared that 5-FU or HU severely limited the antimitotic agents' cytotoxic effects on both mitotic arrest and apoptosis. No combination of a G1-S arresting agent with an antimitotic agent in any schedule produced an antitumor effect greater than that of the antimitotic agent alone. In addition, biochemical examination revealed that 5-FU and HU blocked the antimitotic agent-induced increase of p21WAF1/CIP1 protein levels, as well as prevented the hyperphosphorylation of the bcl-2 and c-raf-1 proteins. These findings suggest that careful considerations may be necessary when combining antineoplastic agents that exert their cytotoxic action at different phases of the cell cycle.

Antineoplastic Agents↗
PubMed1999

Sarcoglycan complex: a muscular supporter of dystroglycan-dystrophin interplay?

In striated muscle, the cytoskeletal protein dystrophin, the protein product of the Duchenne muscular dystrophy gene, is associated with a number of sarcolemmal glycoproteins to form a large oligomeric complex, the dystrophin-glycoprotein complex (DGC). Over the last 10 years, four of these sarcolemmal glycoproteins, alpha-, beta-, gamma- and delta-sarcoglycans, have been shown to form a distinct subcomplex, the sarcoglycan complex, in the DGC. Furthermore, the genetic defects of alpha-, beta-, gamma- and delta-sarcoglycans have been identified as the causes of four distinct forms of muscular dystrophies, which are now collectively called sarcoglycanopathy. Current studies are beginning to focus on the biological functions of the sarcoglycan complex and the molecular mechanism by which its dysfunction leads to muscle cell degeneration.

Animals↗
PubMed1999

[Helicobacter pylori infections and autoimmunity: the interplay in the pathogenesis of gastritis].

Recent studies suggest a significant association of Helicobacter pylori (H.p.) gastritis and antigastric autoimmunity. Sera of H.p. infected patients exhibit antigastric autoantibodies with high prevalence (over 50 percent of the cases) and with antiluminal and/or anticanalicular binding patterns on gastric mucosa. Models for the pathogenesis of this H.p. associated autoimmunity are antigenic mimicry or Th 1-induced expression of MHC class II and costimulatory molecules on gastric epithelial cells. The anticanalicular autoantibodies binding to gastric parietal cells show fine specificities for the alpha- and for the beta-subunit of the gastric H, K-ATPase, which correspond to the findings in classical autoimmune gastritis. They are significantly correlated with higher grades of corpus gastritis as well as morphologic and functional glandular atrophy of the corpus. The development of this antigastric autoimmunity apparently is a relevant pathogenic factor of the host reaction and might be crucial for the different types and outcomes of H.p. gastritis.

Autoantibodies↗
PubMed2000

[The interplay between embryo and endometrium is important for successful implantation. Increased knowledge can result in new contraceptive methods and better treatment of infertility].

It seems likely that local factors such as cytokines play an important role in synchronizing the development of the embryo and the gestational tract and in determining pregnancy outcome. Evaluation of the precise sequence of cytokines to which the embryo is exposed and responds during the critical periimplantation period may also make it possible to develop culture media which will improve embryo viability and hence increase implantation rates in IVF programs. In addition, an in vitro three-dimensional culture system is being developed which closely resembles endometrium in vivo. This system offers an opportunity to study the local molecular events involved in blastocyst adhesion and to elucidate the role played by local factors, such as cytokines, in producing a receptive luminal epithelium.

Blastocyst↗
PubMed2000

[Malnutrition and infections in children--a destructive interplay with global dimensions].

BACKGROUND: Seven out of ten deaths among the world's children are caused by infectious diseases. Malnutrition is a contributing cause in more than half of the children's deaths. At present, interventions against such diseases in children are the most cost-effective way of reducing the world's morbidity and mortality. MATERIAL AND METHODS: This paper discusses how nutritional status affects the immune defence, and vice versa. General protein and energy malnutrition and some specific nutrients are discussed. The paper is based on review of recent literature found in Medline, and key references in the papers identified. RESULTS: Malnutrition is the most common cause of acquired immune deficiency in children. Malnourished children are especially prone to develop persistent diarrhoea, which in turn aggravates the nutritional status. Iron deficiency may be caused or worsened by hookworm and a number of other gastrointestinal infections. There are indications that iron deficiency in itself reduces the immune defence. Vitamin A supplements have reduced the mortality of measles and other infectious diseases. Some studies have shown reduced vertical transmission of HIV when pregnant women get vitamin A supplements. Chronic diarrhoea may cause zinc deficiency which may aggravate the diarrhoea. In areas where the general population's zinc status is marginal, zinc supplementation has reduced the incidence and duration of persistent diarrhoea. INTERPRETATION: The interaction between malnutrition and common infections in children causes a considerable fraction of the global burden of disease, yet so far this is not reflected in research, which mainly targets the diseases of the rich.

Bacterial Infections↗
PubMed2000

Interplay between dietary inducers of GST and the GSTM-1 genotype in colon cancer.

The purpose of this study is to determine if cruciferous vegetables and coffee, two dietary inducers of glutatione-S-transferases, interact with GSTM-1 genotype to alter risk of colon cancer. Data were available on 1579 incident cases of adenocarcinoma of the colon and 1898 population-based controls. Intake of cruciferous vegetables, specific types of cruciferous vegetable, and coffee were not associated with colon cancer; GSTM-1 genotype did not modify these associations. However, age at diagnosis and cigarette smoking appeared to be important effect modifiers of the associations between GSTM-1, cruciferous vegetables and colon cancer. Among GSTM-1 null individuals, <55 years at diagnosis, we observed an inverse association between colon cancer and high levels of cruciferous vegetable intake relative to people who did not eat cruciferous vegetables (ORs 0.23 95% CI 0.10-0.54); broccoli was the cruciferous vegetable associated with the strongest inverse association (OR 0.30 95% CI 0.13-0.70). Among younger individuals who were GSTM-1 present (relative to those with GSTM-1 null), we observed an inverse association with colon cancer regardless of level of cruciferous vegetable intake (OR 0.74 95% CI 0.30-1.79 for no intake; OR 0.44 95% CI 0.21-0.92 for <4 servings/week; and OR 0. 44 95% CI 0.19-0.99 for >/=4 servings/week). These associations were further modified by cigarette smoking. People <65 years of age who smoked had a greater reduction in risk of colon cancer from consumption of cruciferous vegetables than non-smokers at the same age. In summary, although cruciferous vegetables do not appear to modify colon cancer risk in the total population, there are subgroups of the population for whom these vegetables may be important. These subgroups are defined mostly by age and smoking status.

Adenocarcinoma↗
PubMed2001

Pharmacogenetics of alcohol response and alcoholism: the interplay of genes and environmental factors in thresholds for alcoholism.

Recent advances in neuroscience and genetics have enabled a better understanding of genetically influenced differences in ethanol ("alcohol")-related responses and differential vulnerability to alcohol dependence at the cellular and molecular levels. Heritability studies reveal that the role of genetic factors in alcoholism is largely substance-specific, with the exception of nicotine. One focus of genetic research in alcoholism is the study of functional polymorphisms influencing alcohol metabolism, such as the aldehyde dehydrogenase type 2 Glu487Lys and alcohol dehydrogenase type 2 His47Arg polymorphisms, which affect vulnerability to alcoholism via pharmacokinetic mechanisms, and cross-population studies have begun to reveal important gene-environment interactions. The other focus is on functional genetic variants of proteins involved in the neuronal response to alcohol, including alcohol sensitivity, reward, tolerance, and withdrawal. Studies on the roles of GABA(A) alpha6-amino acid substitutions in rodents in alcohol and benzodiazepine sensitivity, and potential roles in human alcohol and benzodiazepine sensitivity are reviewed. These studies, together with recently developed knowledge on a GABA(A) receptor gene cluster at a quantitative trait loci for alcohol withdrawal on mouse chromosome 11, indicate that research investigation of variation at GABA(A) neurotransmission is a promising area in the pharmacodynamics of alcohol and in differential susceptibility to alcoholism. Genes for proteins involved in alcohol-mediated reward include genes for transporters and receptors for dopamine, serotonin, opioids, and GABA. These genes and their functional variants also represent important targets for understanding alcohol's effects in humans. Identification of genes for alcoholism vulnerability is important in the near future, not only for prevention, but also for development and targeting treatments.

Alcoholism↗