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

The histology and ultrastructure of the rat gastric mucosa were investigated during 168 hours of starvation. An increased desquamation of individual foveolar cells was found. In the preserved cells of the foveolae, the content of the PAS positive mucosubstances did not change during starvation, and no changes took place in the appearance and in the amount of the mucous granules at the electron microscopic investigation. The number of lipid droplets increased in the mucous foveolar cells within 24 and 48 hours. During starvation the mitochondria (mainly in the parietal cells) were enlarged and contained rare mitochondrial cristae. Some mitochondria were distintegrated and removed by lysosomes. The number of lysosomes (mainly cytosergresomes) was markedly increased n parietal cells. A collapse of the intracellular canaliculi occurred as well as a narrowing in the tubulovesicular profiles. In chief cells the profiles of the granular endoplasmic reticulum and Golgi apparatus were reduced. It was shown that the ultrastructural changes induced by starvation can be interpreted functionally in changed histochemical parameters of the gastric mucosa.
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PMID:Influence of starving on the rat gastric mucosa -- light and electron microscopical findings. 59 Apr 16

Total starvation is effective for acute weight reduction in obesity. However, in 200 patients, most of whom also had internal diseases, 8% exhibited sometimes severe complications, i.e. reversible cerebral ischemia in 3 hypertensive patients when the blood pressure was lowered to the normal range by natriuresis of fasting; breakdown of water and electrolyte homeostasis with circulatory collapse, vomiting and vertigo; acute crises of paroxysmal nocturnal hemoglobinuria and porphyria respectively and increase of transaminases up to 200 mu/ml, or cardiac arrhythmias. Relative (?) contraindications for total fasting appear to be clinical sings of arteriosclerosis such as vascular bruits, angina pectoris and intermittent claudication. In case of doubt, the method should only be used in hospital.
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PMID:[Complications in null-diet]. 91 86

This commentary by Maurice King questions the viability of current public health strategies. He advocates for an ecological approach that seeks to improve the health of the entire planet. He discusses the concept of the demographic trap. Being demographically trapped refers to a population being stuck in an "unsustainable state with a high birth rate and death rate, with an ever increasing pressure on its resources, and with a rapidly deteriorating environment". King points out that the possible outcomes are limited for a population that becomes trapped. Some of the possible outcomes include dying from starvation and disease; fleeing as ecological refugees; being destroyed by war or genocide; or being supported by food and other resources from elsewhere, first as emergency relief and then perhaps indefinitely. King believes that ecological collapse has already taken place in parts of Ethiopia and the process may have begun on a wider scale elsewhere. According to King, this ecological predicament can be found in both rural and urban areas in the developing world. This article also discusses the problem of high fertility. King believes that the widely held belief that the necessary and sufficient condition for reducing the birth rate is to reduce the child death rate is erroneous. He states that a causal relationship between the 2 rates is untenable, instead, it is more reasonable to say that both rates respond to other common factors. The author suggests that a fall in the birth rate requires the harnessing of social and economic gains to reduce poverty and promote socio-economic development. He also believes that the continued growth in the size of the world's population is due to declining efforts in family planning and declining child mortality not having its alleged effects on fertility. King also brings forth an ethical dilemma. He asks, "are there some programs which, although they are technically feasible, should not be initiated because of there long-term population-increasing consequences?" He suggests that other factors such as ecological deterioration, integrity of the ecosystem, and the welfare of future communities need to be taken into consideration. King presents a new global strategy based on the concept of "sustainability". He says that "sustainability should be the maintenance of the capacity of the ecosystem to support life in quantity and variety". Specifically, he advocates for consumption control in the industrial North with intensive energy conservation and recycling. In the South, he calls for renewed vigor in family planning efforts. Public health measures need to be understood in terms of their demographic and ecological implications. If measures are found to be desustaining, King says that complementary ecologically sustaining measures should be introduced with them. He also believes that desustaining measures, such as oral rehydration, should not be introduced on a public health scale if no adequately sustaining complementary measures are possible. He asserts that desustaining measures, without complementary interventions, can ultimately increase the man-years of human misery.
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PMID:Health is a sustainable state. 197 30

Patients requiring long term intensive care and/or prolonged ventilatory support, are frequently undergoing progressive malnutrition, occasionally complicated by a hypercatabolic state. Sepsis, fever and the requirements for postoperative healing will add further nutritional demands on such patients. In contrast to starvation, critically ill patients maintained on protein-free energy-deficient diet do not adapt to utilization of their lipid to provide energy needs. Mobilization of endogenous fat stores is reduced, and this reduction leads to increased gluconeogenesis from amino acids derived from muscle protein to meet the increased energy needs. Low serum albumin, possible low surfactant production, devitalization of the alveolo-capillary membrane and impaired immunocompetence could contribute to the development of pulmonary transudation, alveolar collapse, low compliance and pulmonary infection. Such sequelae of a protein-free energy-deficient diet would delay weaning patients off prolonged mechanical ventilation. Nutritional assessment, which may be determined serially, and means of nutritional support are outlined.
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PMID:Nutritional support in long term intensive care with special reference to ventilator patients: a review. 678 7

Few organ systems are spared the progressive deterioration seen in this disease. Most medical complications are the result of starvation and can be reversed with a well-planned refeeding program. A potentially catastrophic treatment complication is the refeeding syndrome, in which the demands that a repleted circulatory system places on a nutritionally depleted cardiac mass result in cardiovascular collapse.
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PMID:Eating disorders: 1. Anorexia nervosa. 859 83

The results of experiments with 50 volunteers are presented, exposed to conditions, similar to those of ship-wreck-on rafts and boats anchored in the sea and with restricted taking of food and water. Complex medical studies have been accomplished. The state of the cardio-vascular, nerve, respiratory and sensor systems and the metabolism of certain substances are followed up. The electrophysiological studies include: EKG, EEG, ENG, SPO, ZPO, SSEP, craniocorpography, computer analysis of the cardiac variability. A part of these have been monitored during the whole experiment using Holter records or by cable and telemetric way in special laboratories on the beach. The biochemical studies include indicators characterizing the metabolism of carbohydrates, lipids, proteins, mineral-electrolytes and biogenic amines. Some individual features in the course of sea-sickness are described according to the phenotype and the genotype characteristics of the adaptation processes. Special attention is paid to vestibular-vegetative, neurologic and psychic changes as well as on the manifestations of orthostatic collapse, sometimes ending by loss of consciousness or epi-fainting. It is considered that the orthostatic collapse is due to the combined influence of prolonged vestibular overstrain, hypokinesia, starvation, thirst and psycho-emotional stress. This is the possible main cause for the death of some saved ship-wreckers. An actualization of the instruction for saving of ship-wreckers is recommended with including of a special movement regime in the saving devices. Sibellium (flunarizin) is offered as a prophylactic and therapeutic agent against sea-sickness.
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PMID:[Complex biomedical studies of the body under conditions of extreme marine factors]. 919 Jun 1

Stress modifies all aspects of cellular physiology, including the targeting of macromolecules to the nucleus. To determine how distinct types of stress affect classical nuclear protein import, we followed the distribution of NLS-GFP, a reporter protein containing a classical nuclear localization sequence (NLS) fused to green fluorescent protein GFP. Nuclear accumulation of NLS-GFP requires import to be constitutively active; inhibition of import redistributes NLS-GFP throughout the nucleus and cytoplasm. In the yeast Saccharomyces cerevisiae, starvation, heat shock, ethanol and hydrogen peroxide rapidly inhibited classical nuclear import, whereas osmotic stress had no effect. To define the mechanisms underlying the inhibition of classical nuclear import, we located soluble components of the nuclear transport apparatus. Failure to accumulate NLS-GFP in the nucleus always correlated with a redistribution of the small GTPase Gsp1p. Whereas predominantly nuclear under normal conditions, Gsp1p equilibrated between nucleus and cytoplasm in cells exposed to starvation, heat, ethanol or hydrogen peroxide. Furthermore, analysis of yeast strains carrying mutations in different nuclear transport factors demonstrated a role for NTF2, PRP20 and MOG1 in establishing a Gsp1p gradient, as conditional lethal alleles of NTF2 and PRP20 or a deletion of MOG1 prevented Gsp1p nuclear accumulation. On the basis of these results, we now propose that certain types of stress release Gsp1p from its nuclear anchors, thereby promoting a collapse of the nucleocytoplasmic Gsp1p gradient and inhibiting classical nuclear protein import.
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PMID:Stress-mediated inhibition of the classical nuclear protein import pathway and nuclear accumulation of the small GTPase Gsp1p. 1102 3

The permeability transition pore (PTP) is a mitochondrial channel whose opening causes the mitochondrial membrane potential (deltapsi) collapse that leads to apoptosis. Some ubiquinone analogues have been demonstrated previously to modulate the PTP open-closed transition in isolated mitochondria and thought to act through a common PTP-binding site rather than through oxidation-reduction reactions. We have demonstrated recently both in vitro and in vivo that the ubiquitous free radical scavenger and respiratory chain coenzyme Q10 (CoQ10) prevents keratocyte apoptosis induced by excimer laser irradiation more efficiently than other antioxidants. On this basis, we hypothesized that the antiapoptotic property of CoQ10 could be independent of its free radical scavenging ability and related to direct inhibition of PTP opening. In this study, we have verified this hypothesis by evaluating the antiapoptotic effects of CoQ10 in response to apoptotic stimuli, serum starvation, antimycin A, and ceramide, which do not generate free radicals, in comparison to control, free radical-generating UVC irradiation. As hypothesized, CoQ10 dramatically reduced apoptotic cell death, attenuated ATP decrease, and hindered DNA fragmentation elicited by all apoptotic stimuli. This was accompanied by inhibition of mitochondrial depolarization, cytochrome c release, and caspase 9 activation. Because these events are consequent to mitochondrial PTP opening, we suggest that the antiapoptotic activity of CoQ10 could be related to its ability to prevent this phenomenon.
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PMID:Coenzyme q10 prevents apoptosis by inhibiting mitochondrial depolarization independently of its free radical scavenging property. 1273 73

Ovarian cell death is an essential process for the homeostasis of ovarian function in human and other mammalian species. It ensures the selection of the dominant follicle and the demise of excess follicles. In turn, this process minimizes the possibility of multiple embryo development during pregnancy and assures the development of few, but healthy embryos. Degeneration of the old corpora lutea in each estrus/menstrual cycle by programmed cell death is essential for maintaining the normal cyclicity of ovarian steroidogenesis. Although there are multiple pathways that can determine cell death or survival, crosstalk among endocrine, paracrine and autocrine factors, as well as among protooncogenes, tumor suppressor genes, survival genes and death genes, play an important role in determining the fate of ovarian somatic and germ cells. The establishment of immortalized rat and human steroidogenic granulosa cell lines and the investigation of pure populations of primary granulosa cells allows for systematic studies of the mechanisms that control steroidogenesis and apoptosis of granulosa cells. We have discovered that during initial stages of granulosa cell apoptosis progesterone production does not decrease. In contrast, we found that it is elevated for up to 24hr following the onset of the apoptotic stimuli exerted by starvation, cAMP, p53 or tumor necrosis factor alpha stimulation, before total cell collapse. These observations raise the possibility for an alternative unique apoptotic pathway, one that does not involve mitochondrial cytochrome C release associated with the destruction of mitochondrial structure and steroidogenic function. Using mRNA from apoptotic cells and Affymetrix DNA microarray we discovered that Granzyme B, a protease that normally resides in T cytotoxic lymphocytes and natural killer cells of the immune system is expressed and activated in granulosa cells, thereby allowing the apoptotic signals to bypass mitochondrial signals for apoptosis, which can preserve their steroidogenic activity until complete cell destruction. This unique apoptotic pathway assures the cyclicity of estradiol and progesterone release in the estrus/menstrus cycle even during the initial stage of apoptosis.
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PMID:Alternative pathways of ovarian apoptosis: death for life. 1455 9

We tested the effect of ACE inhibition on the survival of bovine retinal (REC) and choroidal (CEC) endothelial cells (EC) in culture. The ACE inhibitor captopril delayed the apoptotic tube collapse of REC on Matrigel for >15 days. Captopril treatment of confluent monolayers (2-8 weeks) followed by slow starvation (2-4 weeks) increased EC viability by approximately 200%. Two-week captopril exposures were sufficient to confer maximal protection. Only vehicle-treated EC demonstrated apoptotic features such as membrane blebbing and DNA laddering. By RT-PCR, the starvation marker p202 was upregulated only in starved cells. In REC, captopril upregulated the pro-survival proteins mortalin-2, uPA, and uPAR while downregulating the anti-growth sprouty-4 and tPA. In CEC, captopril also upregulated tPA and its inhibitor PAI-1. Amiloride (uPA inhibitor) blocked the captopril-induced increase in EC survival, secondary sprouting, and invasion in Matrigel. The pro-survival effects of captopril involve the reprogramming of genes involved in cell survival and immortalization.
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PMID:ACE inhibition actively promotes cell survival by altering gene expression. 1455 46


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