Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anorexia, net proteolysis of skeletal muscle and consumption of body fat are hallmarks of the cachexia syndrome associated with chronic disease states. While inanition contributes to cachexia, this wasting diathesis has little in common with simple starvation. The cachexia syndrome is characterized by progressive weight loss and depletion of lean body mass in excess to that resulting from comparable caloric restriction. Accelerated mobilization and consumption of host protein stores from peripheral tissues occurs to support gluconeogenesis and acute phase protein synthesis [1, 2]. In contrast, simple starvation is associated with a relative sparing of lean tissue with the preferential consumption of fat. While the clinical manifestations of cachexia are readily apparent, identification of the specific mechanisms responsible for the development of cachexia remains an enigma. In recent years, interest has focused on the role that the immune system plays in the development of cachexia. Investigators initially hypothesized that the chronic production of two inflammatory cytokines, tumour necrosis factor alpha (TNF alpha) and/or interleukin-1 (IL-1), could explain the host non-specific responses resulting in cachexia [3-5]. Other pro-inflammatory cytokines, including interleukin-6 (IL-6) [6, 7] and interferon-gamma [8, 9], have been more recently proposed to be involved in this complex process. Although no consensus exists for the exclusive role of any one cytokine in the pathogenesis of cachexia, there is growing acceptance that the progression of cachexia results in part from the inappropriate release of one or more pro-inflammatory cytokines [10, 11]. In the present review, the current role of TNF alpha as a mediator of cachexia is examined.
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PMID:Tumor necrosis factor and cachexia: a current perspective. 788 18

The use of liquid protein products for treatment of obesity in the United States in the 1960s and '70s was associated with an increased risk of sudden cardiac death. The latter was related to long QT interval occurring in the absence of structural abnormalities of the heart. In an attempt to increase understanding of this phenomenon, the authors examined the possible role of diet-related circumstances. No evidence of increased incidence of sudden cardiac death or significant lengthening of QT interval in obesity, weight loss, starvation and dieting by methods other than liquid protein intake were found. It was concluded that sudden cardiac death during use of liquid protein products remains an enigma, but that other methods of properly medically supervised dieting appear to be safe.
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PMID:The enigma of sudden cardiac death related to dieting. 788 41

While the lore of anticholinesterases (antiChEs), particularly physostigmine and its natural source, the Calabar bean, is a subject of ethnomedicine and predates our scientific era, the pharmacological development of physostigmine analogues and related agents and of the antiChEs of the organophosphorus (OP) type, is a matter of the last two centuries; this development has reached an exponential character in the last fifty years. This explosion relates to certain uses and misuses of these drugs and this aspect of antiChEs is the main focus of this article. Firstly, there is the matter of Senile Dementia of Alzheimer's Type (SDAT); while there are several clinical applications of antiChEs, their employment in the treatment of SDAT is the last and most intense foray in their medical history and this article will focus on the uses and misuses of antiChEs in this area. Secondly, the applied use of antiChEs as insecticides which coincided with the historical development of OP antiChEs was and is, of major significance for the agricultural economy of both advanced and underdeveloped countries, as this employment may mean the difference between life and starvation. However, there are notable dangers with this application of OP drugs, as will be emphasized in this article. Thirdly, there is the significant and tragic development of the OP drugs as warfare agents and tools for terrorists and rogue states and this article will discuss the several types of toxicity of OP agents and their mechanisms, the enigma of the Persian Gulf War Syndrome being particularly stressed. Altogether, the immense range of antiChE topics includes areas of great basic interest and of practical applications that are of significant benefit to mankind as well as of potential danger.
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PMID:Invited review: Anticholinesterases: dramatic aspects of their use and misuse. 967 38

Upon starvation and growth arrest, Escherichia coli cells gradually lose their ability to reproduce. These apparently sterile/nonculturable cells initially remain intact and metabolically active and the underlying molecular mechanism behind this sterility is something of an enigma in bacteriology. Three different models have been proposed to explain this phenomenon. The first theory suggests that starving cells become nonculturable due to cellular deterioration, are moribund, and show some of the same signs of senescence as aging organisms. The two other theories suggest that genetically programmed pathways, rather than stochastic deterioration, trigger nonculturability. One "program" theory suggests that nonculturability is the culmination of an adaptive pathway generating dormant survival forms, similar to spore formation in differentiating bacteria. The other "program" theory states that starved cells lose viability due to activation of genetic modules mediating programmed cell death. The different models will be reviewed and evaluated in light of recent data on the physiology and molecular biology of growth-arrested E. coli cells.
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PMID:Nonculturable bacteria: programmed survival forms or cells at death's door? 1259 24

Despite its water-soluble chlorophyll-binding protein (WSCP) function, the putative trypsin inhibitor (TI) activity of the Brassica napus drought 22 kD (BnD22) protein and its physiological function in young leaves during leaf nitrogen (N) remobilization promoted by stressful conditions remains an enigma. Therefore, our objectives were to determine (1) if BnD22 is related to the 19-kD TI previously detected in B. napus young leaves, and (2) if the levels of BnD22 transcripts, BnD22 protein, and TI activity in young leaves are associated with plant responses to stress conditions (N starvation and methyl jasmonate [MeJA] treatments) that are able to modulate leaf senescence. Compared to control, N starvation delayed initiation of senescence and induced 19-kD TI activity in the young leaves. After 3 d with MeJA, the 19-kD TI activity was 7-fold higher than the control. Using two-dimensional electrophoresis gel, TI activity, and electrospray ionization liquid chromatography tandem mass spectrometry analysis, it was demonstrated that two 19-kD proteins with isoelectric points 5.0 and 5.1 harboring TI activity correspond to BnD22 perfectly. BnD22 gene expression, TI activities, and BnD22 protein presented similar patterns. Using polyclonal anti-WSCP antibodies of Brassica oleracea, six polypeptides separated by two-dimensional electrophoresis were detected in young leaves treated with MeJA. Electrospray ionization liquid chromatography tandem mass spectrometry analysis of six polypeptides confirms their homologies with WSCP. Results suggest that BnD22 possesses dual functions (WSCP and TI) that lead to the protection of younger tissues from adverse conditions by maintaining metabolism (protein integrity and photosynthesis). By sustaining sink growth of stressed plants, BnD22 may contribute to a better utilization of recycling N from sources, a physiological trait that improves N-use efficiency.
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PMID:A proteomic profiling approach to reveal a novel role of Brassica napus drought 22 kD/water-soluble chlorophyll-binding protein in young leaves during nitrogen remobilization induced by stressful conditions. 1855 35

Intracellular protein degradation is an essential process in all life domains. While in all eukaryotes regulated protein degradation involves ubiquitin tagging and the 26S-proteasome, bacterial prokaryotic ubiquitin-like protein (Pup) tagging and proteasomes are conserved only in species belonging to the phyla Actinobacteria and Nitrospira. In Mycobacterium tuberculosis, the Pup-proteasome system (PPS) is important for virulence, yet its physiological role in non-pathogenic species has remained an enigma. We now report, using Mycobacterium smegmatis as a model organism, that the PPS is essential for survival under starvation. Upon nitrogen limitation, PPS activity is induced, leading to accelerated tagging and degradation of many cytoplasmic proteins. We suggest a model in which the PPS functions to recycle amino acids under nitrogen starvation, thereby enabling the cell to maintain basal metabolic activities. We also find that the PPS auto-regulates its own activity via pupylation and degradation of its components in a manner that promotes the oscillatory expression of PPS components. As such, the destructive activity of the PPS is carefully balanced to maintain cellular functions during starvation.
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PMID:Survival of mycobacteria depends on proteasome-mediated amino acid recycling under nutrient limitation. 2498 81