Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0038187 (
starvation
)
24,951
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
"Addiction modules" consist of two genes. In most of them the product of one is long lived and toxic while the product of the second is short lived and antagonizes the toxic effect; so far, they have been described mainly in a number of prokaryotic extrachromosomal elements responsible for the postsegregational killing effect. Here we show that the chromosomal genes mazE and mazF, located in the Escherichia coli rel operon, have all of the properties required for an
addiction
module. Furthermore, the expression of mazEF is regulated by the cellular level of guanosine [corrected] 3',5'-bispyrophosphate, the product of the RelA protein under amino acid
starvation
. These properties suggest that the mazEF system may be responsible for programmed cell death in E. coli and thus may have a role in the physiology of
starvation
.
...
PMID:An Escherichia coli chromosomal "addiction module" regulated by guanosine [corrected] 3',5'-bispyrophosphate: a model for programmed bacterial cell death. 865 Feb 19
The endogenous plasma alkaloids codeine and morphine were shown to be elevated in patients with anorexia nervosa and bulimia nervosa compared to control subjects. The role of these opioids in the pathophysiology of these eating disorders is discussed in relation to an auto-
addiction
opioid model. This model proposes that endogenous opioids are released during an initial period of dieting and reinforce a state of
starvation
dependence [1,2].
...
PMID:Endogenous codeine and morphine in anorexia and bulimia nervosa. 915 Apr 13
Antidote/toxin gene pairs known as "addiction modules" can maintain plasmids in bacterial populations by means of post-segregational killing. However, several chromosome-encoded
addiction
modules may provide an entirely distinct function in the programmed cell death of moribund subpopulations under
starvation
conditions. We now report a novel chromosomal bacteriolytic module of Escherichia coli called the entericidin locus, which is activated in stationary phase under high osmolarity conditions by sigmaS and simultaneously repressed by the osmoregulatory EnvZ/OmpR signal transduction pathway. The entericidin locus encodes tandem paralogous genes (ecnAB) and directs the synthesis of two small cell-envelope lipoproteins. An attenuator precedes ecnA and an ompR-sensitive sigmaS promoter governs expression of ecnB. The entericidin A lipoprotein is an antidote to the bacteriolytic lipoprotein entericidin B. The entericidins are predicted to adopt amphipathic alpha-helical structures and to reciprocally modulate membrane stability. The entericidin locus is not present on any known plasmids, but is conserved in the homologous region of the Citrobacter freundii chromosome. Although the cloned C. freundii entericidin locus is expressed in E. coli independently of ompR, it carries an additional ompR-like gene called ecnR. The organization of the entericidin locus as a chromosomal antidote/toxin gene pair, which is regulated by both positive and negative osmotic signals during
starvation
, is consistent with an emerging paradigm of programmed bacterial cell death.
...
PMID:The entericidin locus of Escherichia coli and its implications for programmed bacterial cell death. 967 90
A number of theories have been proposed to explain the substantial comorbidity between the eating disorders and the substance-related disorders. Among them is the claim that self-
starvation
--exacerbated by excessive exercising--is itself an
addiction
to the body's endogenous opioids. While efforts have also been made to identify an "addictive personality," attempts to establish whether eating-disordered patients share these characteristics have met with mixed success. The present study was designed to determine the degree to which anorexic and bulimic patients display addictive personality characteristics, and whether these traits are useful in predicting the severity of the patient's weight preoccupation and their degree of excessive exercising. Results confirmed that both anorexic and bulimic patients had high scores on the
Addiction
Scale of the Eysenck Personality Questionnaire, and that addictiveness and obsessive-compulsiveness were related simultaneously to weight preoccupation and excessive exercising in both patient groups. Findings are discussed within the framework of the auto-
addiction
opioid theory, and they highlight the similarities and differences in the personality structure of the eating-disorder subtypes.
...
PMID:The eating disorders as addiction: a psychobiological perspective. 969 75
In Escherichia coli, programmed cell death is mediated through "addiction modules" consisting of two genes; the product of one gene is long-lived and toxic, whereas the product of the other is short-lived and antagonizes the toxic effect. Here we show that the product of lambdarexB, one of the few genes expressed in the lysogenic state of bacteriophage lambda, prevents cell death directed by each of two
addiction
modules, phd-doc of plasmid prophage P1 and the rel mazEF of E. coli, which is induced by the signal molecule guanosine 3',5'-bispyrophosphate (ppGpp) and thus by amino acid
starvation
. lambdaRexB inhibits the degradation of the antitoxic labile components Phd and MazE of these systems, which are substrates of ClpP proteases. We present a model for this anti-cell death effect of lambdaRexB through its action on the ClpP proteolytic subunit. We also propose that the lambdarex operon has an additional function to the well known phenomenon of exclusion of other phages; it can prevent the death of lysogenized cells under conditions of nutrient
starvation
. Thus, the rex operon may be considered as the "survival operon" of phage lambda.
...
PMID:rexB of bacteriophage lambda is an anti-cell death gene. 986 Sep 94
In confluent human dermal fibroblasts brought to quiescence (G0) by serum
starvation
, the S phase peaked at 24 h after serum re-
addiction
and G2/M phase peaked at 36 h. This was confirmed by titration of h-gas1 mRNA (a marker of G0 phase) and histone H3 (a marker of S phase). Clusterin mRNA accumulation progressively increased in cells proceeding to confluence after seeding and to quiescence upon serum
starvation
, and peaked at around G0, in parallel with h-gas1 mRNA. At 6 h (roughly G1 phase) clusterin transcript formed a second peak, followed by a gradual decrease until 36 h. Correspondence of clusterin protein accumulation to its mRNA occurred solely with regard to the G0 peak but not to the second one. The possible meaning of the cell cycle related clusterin gene expression is discussed.
...
PMID:Clusterin (SGP-2) gene expression is cell cycle dependent in normal human dermal fibroblasts. 1021 96
Anorexia nervosa is an eating disorder defined by a symptomatic triad, anorexia, emaciation and amenorrhoea. This disease mainly affects young women. Besides these three symptoms, hyperactivity is often associated with anorexia nervosa. Hyperactivity can be considered as a strategy to lose weight, but studies on animal models have shown that it could be explained by more complicated mechanisms. Hyperactivity is defined by an excess of physical activity, which can induce social, professional and family consequences. Hyperactivity can take different forms, most striking is the restless one. Patients with anorexia nervosa are not all hyperactive. Brewerton et al. have compared patients with anorexia nervosa and hyperactivity to patients without hyperactivity. Hyperactive patients are more dissatisfied by their body image, they use less means of purging (laxatives, vomiting), and they start starving earlier than patients without hyperactivity. Many factors can promote the emergence and maintenance of hyperactivity, especially social and cultural requirements, sports environment, family influences. Various models can explain the links between excessive exercise and anorexia nervosa. Epling and Pierce have exposed a behavioural model which shows how hyperactivity can lead to
starvation
, creating a self-maintained cycle. Eisler and Le Grande have described four models to explain the links between hyperactivity and anorexia nervosa. First, excessive exercise can be considered as a symptom of anorexia nervosa. It can also promote the development of eating disorders. Anorexia nervosa and hyperactivity can be a manifestation of an other psychiatric disorder. At least, hyperactivity can be a variant of anorexia nervosa, which has the same effects, as weight loss. Hyperactivity can also be considered as a kind of obsessive compulsive disorder. Hyperactivity and obsessive compulsive disorders actually share some clinical and neurochemical characteristics. An other model consists in comparing excessive exercise in anorexia nervosa to an addictive behaviour. Self-
starvation
exacerbated by hyperactivity can be considered as an
addiction
to endogenous opioid. Few studies are carried out in order to estimate the prevalence of high level exercise in the eating disorders. Davis et al. have achieved a prevalence study. The results indicate that a large majority of patients with anorexia nervosa (80,8%) were exercising excessively during an acute phase of the disorder. Research on animals, specially on rats, brings us an interesting model explaining interactions between anorexia nervosa and hyperactivity. With animal models, we have noticed that, when rats with access to a running wheel, are restricted in their food intake, they become excessively active, and paradoxically reduce food consumption. Many searchers have tried to explain this phenomenon. Morse et al. have pointed from animal models that the level of hyperactivity was linked to the severity of food restriction. This result can be explained by a failure of a part of the brain involved in rest and activity regulation. Animal research brings us explanations about the effects of
starvation
on the endocrine system and the neurotransmitters. Broocks et al. have shown that corticosterone concentration in plasma was synergistically increased by semi
starvation
and exercise, and the reduction of triiodothyronine by semi
starvation
was significantly greater in the running wheel group. An other study of Broocks et al. has revealed an increased hypothalamic serotonin metabolism with the combined effect of hyperactivity and food restriction. Tryptophan, an amid acid involved in serotonin synthesis, can also play a role in the maintenance of anorexia nervosa. In
starvation
conditions, opioid releasing caused by physical exercise would decrease food intake. Exner's study and Adan's one have shown that leptin would be involved in semi
starvation
induced hyperactivity mechanisms. In spite of animal models can not be entirely generalized to human, they are useful to try to explain biological supports of hyperactivity. Hyperactivity is not only a strategy to lose weight, but also a specific symptom which completes the clinical triad. Animal studies have led to promising results; we might use medicine, such as serotonin reuptake inhibitors or opioid antagonists in the treatment of hyperactivity in anorexia nervosa.
...
PMID:[Hyperactivity and anorexia nervosa: behavioural and biological perspective]. 1562 53
We have previously reported that mazEF, the first regulatable chromosomal '
addiction
module' located on the Escherichia coli chromosome, downstream from the relA gene, plays a crucial role in the programmed cell death in bacteria under stressful conditions. It consists of a pair of genes encoding a stable toxin, MazF, and MazE, a labile antitoxin interacting with MazF to form a complex. The cellular target of MazF toxin was recently described to be cellular mRNA, which is degraded by this toxin. On the same operon, downstream to the mazEF genes, we found another open reading frame, which was called mazG. Recently, it was shown that the MazG protein has a nucleotide pyrophosphohydrolase activity. Here we show that mazG is being transcribed in the same polycistronic mRNA with mazEF. We also show that the enzymatic activity of MazG is inhibited by MazEF proteins. When the complex MazEF was added, the enzymatic activity of MazG was about 70% inhibited. We demonstrate that the enzymatic activity of MazG in vivo causes depletion of guanosine 3',5'-bispyrophosphate (ppGpp), synthesized by RelA under amino acid
starvation
conditions. Based on our results, we propose a model in which this third gene, which is unique for chromosomal
addiction
systems, has a function of limiting the deleterious activity of MazF toxin. In addition, MazG solves a frequently encountered biological problem: how to avoid the persistence of a toxic product beyond the time when its toxicity is useful to the survival of the population.
...
PMID:MazG -- a regulator of programmed cell death in Escherichia coli. 1639 Apr 52
Self-
starvation
as well as binge eating appears to be far more complex than the uniformity of eating disorders clinical features let us predict. One reason is that these "body-centred" behaviours generate severe biological effects, the complications playing a great part in the recovery process. Furthermore, these disorders which origins are likely to be multi-factorial seem to arise from physiological (ephebic modifications, gene pool...), family and sociocultural factors, psychological features predominating in a synergy always leading to a specificity that cannot be ignored. The progression towards mixed forms made the distinction between anorexia and bulimia nervosa, insufficiently accurate, leading to examine the addictive dimension these troubles have in common. Despite different theoretical surroundings, it has been suggested that an insecure style of attachment may be highly implicated in the disorders occurring. Moreover, a great number of surveys insisted on identity disturbance, and predisposition to intemperate dependency, resulting from the poor quality of internalized relationships. From that viewpoint, both fasting and binge eating appear as a form of
addiction
meant to mitigate the defense mechanisms failure and the flaws of the psychological organization. Impulsivity appears as a way to avoid processing affects, acting-out being here to balance the ego weakness deriving from the lack of inner security. The fluctuations in the sense of self lead them to self-damaging behaviours meant to vent their pervasive, chronic feeling of emptiness. Occurring whereas the subject still depends on his parents, puberty reactivates a vivid anguish of passivity, and generates attempts to take the control back. Therefore, these patients re-enact in their dealings with food and their body dissatisfaction the pattern of unstable relationships established with their kin, characterized by alternating between merging and rejection, engulfment and remoteness.
...
PMID:[Psychopathology in eating disorders: new trends]. 1836 Dec 75
In order to study the effect of heat stress on the antibacterial resistance and plasmid profile in Escherichia coli, thirty E. coli were isolated from sheep liver. Antibiotic susceptibility test were done by antibiotic disc diffusion method using filter paper disc on two 24 h cultures of each isolate which grown at 37 and 43 degrees C simultaneously in BHI Broth (Merck VM460193 531). The isolates which grown at 43 degrees C were under heat stress during their growth. Ten commonly used antibiotics, viz., ampicillin, erythromycin, neomycin, trimethoprim-sulfamethoxazol, lincospectine, tetracycline, gentamycin, flumequine, vancomycin and Tiamulin (Padtan Teb). The resistance level of all E. coli isolates against 10 antibacterial drugs compared statistically in 37 and 43 degrees C using MINITAB Version 14 program. Plasmid DNAs were extracted from each of the E. coli isolates which were grown at 37 and 43 degrees C overnight using alkali lysis method. In this study *lambdaDNA (EcoR1+Hind III digested) was used as marker DNA. According to the results of this study, the resistance rate of E. coli isolates have decreased against trimethoprim-sulfamethazol, lincospectine, tiamaulin, tetracyclin and gentamycin at 43 degrees C but only the difference between the resistance rate against gentamycin in 37 degrees C (83.3%) and 43 degrees C (60%) was significant Characterization of Plasmid DNAs by agarose gel electrophoresis showed that each of the thirty drug resistant E. coli harbored a single plasmid. There was no difference among the plasmid profiles of the thirty isolates in 37 and 43 degrees C. As the plasmid profile did not change in 43 degrees C (heat stress) so the resistance differences against antibacterial drugs were not significant except for gentamycine that its resistance may is chromosomal. According to the results of this study, In conclusion it can be said that heat stress could not be effective on antibacterial resistance and plasmid profile if the duration of the stress is short. The long duration of the heat stress plus other stress factors such as
starvation
will effect the plasmid replication and finally plasmid copy number of bacteria. Mechanism of this phenomenon remains unknown, though one might speculate that some bacterial
addiction
modules that are activated upon amino acid
starvation
, like mazEF could be involved.
...
PMID:The effect of heat stress on the antibacterial resistance and plasmid profile in Escherichia coli isolates. 1908 82
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