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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients treated for obesity by total starvation were followed up after a period ranging from 7 to 60 months. Starvation treatment had been carried out 12 times in women and 7 times in men. Weight regain was less than 33% of weight loss in 5 women and 5 men and the regain was 40% in 1 man. Weight increase was higher than 50% of weight loss in 7 women and 1 man. The weight of one of these women exceeded the prestarvation weight. In view of these poor long-term results, therapeutic starvation should be carried out only in selected cases. Our experience indicates a better prognosis for men than for women. There is some indication that long-term results of therapeutic starvation are more favorable in patients with previous myocardial infarction or with somatic conditions which may improve after weight reduction.
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PMID:[Late results after zero calorie diet therapy in adiposity]. 125 Nov 49

A new developmental mutant of Myxococcus xanthus has been isolated by screening TnV insertion mutants for AMI-dependent development in submerged culture. This mutant (ER304) aggregated and sporulated on agar surfaces but required at least 3.8 micrograms of autocide AMI per ml for development in submerged cultures. Spore rescue of ER304 was obtained with the saturated, monounsaturated, and diunsaturated fatty acid fractions of AMI, with specific activities of 68, 115, and 700 U/mg, respectively. In addition, several model fatty acids were capable of rescuing sporulation of ER304; however, there was no correlation between specific lytic activity observed in vegetative cultures and specific rescue activity. Rescue of ER304 was effected during the first ca. 12 h after the initiation of starvation conditions; after this time, addition of AMI or model fatty acids killed the cells. Supernatant fluids of ER304 rescued development in dsg mutants (e.g., DK3260) in submerged cultures, but dsg mutant supernatant fluids were incapable of rescuing ER304 development. The data presented in this article support the idea that the primary mechanism of rescue by AMI is not via lysis, although developmental lysis may be an indirect result of the rescue event. A membrane permeability model is presented to explain the role of autocides in early developmental events in wild-type strains and in the aggregation and sporulation rescue of developmental mutants ER304 and DK3260.
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PMID:Role of autocide AMI in development of Myxococcus xanthus. 216 74

Obesity, a well-known phenomenon in Western society, is frequently associated with cardiovascular and endocrine disease. Strokes, myocardial infarction, diabetes and hyperlipidemia are classical reasons for the high mortality and morbidity of overweight people. For this reason, intensive weight-reduction programs have been proposed: low-calorie diets, total starvation, drugs and even surgery. Total starvation and some low-calorie diets are, however, also associated with sudden death, most probably of cardiac origin. Experimental data from our laboratory show that total starvation is accompanied by a severe depletion of magnesium in myocardial tissue. Protein-sparing modified low-calorie diets, however, can protect against this mineral loss even if magnesium supplementation alone cannot obtain this goal. Applying these principles in overweight man show weight reduction without mineral loss or cardiac disturbance. Surgery with 'ileal bypass' procedures gives rise to severe hypomagnesemia and hypocalcemia with tetany and spasmophilia. New procedures, derived from experimental surgery, are 'gastric bypass' and 'gastroplasty'. These methods, only applied in very obese patients (body mass index greater than 40, normal 23-27) show no change in mineral concentrations of calcium and magnesium and no clinical symptoms suggestive for mineral loss. A good, controlled weight-reduction program under strict medical surveillance can, in this way, offer new perspectives in the treatment of one of our most frequent 'culture-induced' diseases.
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PMID:Magnesium and obesity: effects of treatment on magnesium and other parameters. 382 Nov 74

Diseases in other organs may impair the male reproductive system. Acute critical conditions such as severe trauma, surgery, myocardial infarction, burns, liver failure, intoxication, or starvation are associated with suppression of gonadotropin secretion and secondary hypogonadism. With chronic illnesses, a primary testicular disorder with elevated gonadotropin levels may occur. This may be associated with increased peripheral conversion of androgens to estrogens, resulting in clinical presentation of combined androgen deficiency and estrogen excess. The association of hypogonadism and feminization with cirrhosis of the liver is a classic example. Types of hypogonadism that may occur with chronic anemia, chronic renal failure, chronic spinal cord injury, thyroid diseases, Cushing's syndrome, diabetes mellitus, obesity, HIV infection, neoplasia, and other chronic illnesses are also described. Numerous drugs have side effects on the reproductive system.
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PMID:Reproductive effects of nontesticular illness. 992 10

Clinical heart failure results from the cumulative loss of functioning myocardium from any cause. At the cellular level, cardiac myocytes die from three causes, individually or in combination: Necrosis occurs when external conditions are not sufficient to sustain minimal cellular functions, as with ischemia, and there is a general and unorganized breakdown of cell organelles, engendering an inflammatory response that may have harmful collateral tissue effects. Apoptosis, or cell suicide, occurs when specific external or internal conditions provoke a highly structured sequence of events to shut down cellular functions and remove the cell, with minimal consequences to surrounding tissue. Autophagy is a normal response to cell starvation that is induced under conditions of chronic metabolic or other stress. Current therapeutics, such as early myocardial revascularization after myocardial infarction, are focused exclusively upon minimizing cardiac myocyte necrosis and may even contribute to secondary apoptosis and autophagy. This review explores possible approaches to bring cardiac myocytes that are destined to die, back to life, i.e., cellular resuscitation. Two pro-apoptotic proteins in particular, Bnip3 and Nix, are transcriptionally upregulated specifically in response to myocardial ischemia and pathological hypertrophy and have been examined as therapeutic targets. In Bnip3 and Nix genetic mouse models, prevention of cardiac myocyte apoptosis in ischemic and hemodynamically overloaded hearts salvaged myocardium, minimized late ventricular remodeling, and enhanced ventricular performance. Cardiomyocyte resuscitation by preventing programmed cell death shows promise as an additive approach to minimizing necrosis for long-term prevention of heart failure.
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PMID:The rationale for cardiomyocyte resuscitation in myocardial salvage. 1856 79

Autophagy, a highly conserved cellular mechanism wherein various cellular components are broken down and recycled through lysosomes, occurs constitutively in the heart and may serve as a cardioprotective mechanism in some situations. It has been implicated in the development of heart failure and is up-regulated following ischemia-reperfusion injury. Autophagic flux, a measure of autophagic vesicle formation and clearance, is an important measurement in evaluating the efficacy of the pathway, however, tools to measure flux in vivo have been limited. Here, we describe the use of monodansylcadaverine (MDC) and the lysosomotropic drug chloroquine to measure autophagic flux in in vivo model systems, specifically focusing on its use in the myocardium. This method allows determination of flux as a more precise measure of autophagic activity in vivo much in the same way that Bafilomycin A(1) is used to measure flux in cell culture. MDC injected 1 h before sacrifice, colocalizes with mCherry-LC3 puncta, validating its use as a marker of autophagosomes. This chapter provides a method to measure autophagic flux in vivo in both transgenic and nontransgenic animals, using MDC and chloroquine, and in addition describes the mCherry-LC3 mouse and the advantages of this animal model in the study of cardiac autophagy. Additionally, we review several methods for inducing autophagy in the myocardium under pathological conditions such as myocardial infarction, ischemia/ reperfusion, pressure overloading, and nutrient starvation.
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PMID:Novel methods for measuring cardiac autophagy in vivo. 1921 14

Acute myocardial infarction represents the leading cause of morbidity and mortality in the western societies. Importantly, both apoptosis and necrosis of cardiomyocytes have been implicated in the pathomechanism of myocardial infarction. The simplest way to analyze apoptosis in cardiac cells is the application of isolated neonatal primary cardiac myocytes, in which ischemia/reperfusion can be mimicked in vitro by exposing them to hypoxia and serum starvation, followed by restored oxygen and serum conditions, referred to as hypoxia/reoxygenation. In this chapter, we describe protocols routinely applied in our lab for investigating cardiomyocyte apoptosis. In summary, a better understanding of the apoptotic pathways and their regulation in the heart will potentially yield novel therapeutic targets for cardiac infarction.
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PMID:Analysis of apoptosis in isolated primary cardiac myocytes. 1960 65

Transplantation of autologous skeletal myoblasts (SMBs) is a potential therapeutic approach for myocardial infarction. However, their clinical efficacy and safety is still controversial. Electrical coupling through gap junction between SMBs and host myocardium is essential for synchronized contraction and electrical stability. Here, we investigated the effect of heart beat-simulating environment, oscillating pressure, on the expression of connexin43 in two types of SMBs from rat and mouse. We found that connexin43 is markedly decreased under ischemia-mimicking conditions such as serum starvation and hypoxia (1% O(2)) in rat primary cultured SMBs and mouse C2C12 SMB cell line. Interestingly, the decrease of connexin43 expression under serum starvation was attenuated by oscillating pressure. Oscillating pressure treatment increased the expression of connexin43 twofold through AP-1 stimulation, which was blocked by PD98059, ERK inhibitor. In coculture of cardiomyocytes and C2C12, pressure-treated C2C12 and cardiomyocytes were able to form functional gap junction, which was demonstrated by both calcein-AM dye transfer assay and measurement of simultaneous contraction. In rat myocardial infarction model, transplantation of SMBs pretreated with oscillating pressure resulted in lesser ventricular dilatation and better systolic function than transplantation of untreated SMBs and control group. These results suggested that application of oscillating pressure on SMBs before transplantation may be useful to promote therapeutic efficacy for myocardial infarction by enhancing gap junction formation between transplanted and host cells.
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PMID:Oscillating pressure treatment upregulates connexin43 expression in skeletal myoblasts and enhances therapeutic efficacy for myocardial infarction. 1965 Sep 69

Autophagic activity increases in the heart in response to a variety of stresses including hypertension, ischemia and neonatal starvation. Constitutive autophagy plays an important role in the maintenance of cellular homeostasis in the heart, whereas unrestrained autophagic activity accentuates the maladaptive cardiac remodeling response to stress (e.g., hypertension) and may contribute to the pathogenesis of heart failure. A detailed understanding of the molecular mechanisms governing autophagy induction and autophagosome maturation is evolving, but little is currently known about the extra- and intracellular cues that trigger autophagic induction in the heart. The renin-angiotensin system (RAS) is implicated in the pathogenesis of a number of cardiovascular conditions including hypertension, cardiac hypertrophy, myocardial infarction and heart failure. We now provide the first link between angiotensin II (AngII) and autophagy regulation in the heart. We demonstrate that AngII increases autophagosome formation via the AngII type I (AT1) receptor and that this response is constitutively antagonized by co-expression of the AngII type 2 (AT2) receptor in neonatal cardiomyocytes.
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PMID:Cardiomyocyte autophagy is regulated by angiotensin II type 1 and type 2 receptors. 1995 53

Finding more than one body in the place of residence brings suspicion of poisoning or action of a third party. The authors present a case of two bodies--a handicapped mother and her son--found in their own house. The son was last seen by their neighbours three days before the bodies were revealed. There was a stove in the house which was cold with no signs of penetration. No indication of a third party action was found on the corpses. The autopsy on the son revealed a heart attack with subsequent rupture and tamponade which resulted in death. The cause of the mother's death was assumed to be total starvation of the handicapped person deprived of care. In the presented case autopsy findings contributed to the assessment of the factual cause and sequence of the deaths.
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PMID:[Sole guardian's death as a cause of his handicapped mother's death--a case report]. 2014 84


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