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

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

Broiler chicks, 3 to 4 wk of age, were inoculated with either Eimeria acervulina or E. mitis, and mucosal dry weights, brush border enzyme activities, and carotenoid contents as well as plasma carotenoid levels were measured at 3, 5, and 7 days postinoculation (PI). At 5 and 7 days PI mucosal dry weights, brush border enzyme activities, and carotenoid contents were significantly decreased at primary sites of infection (duodenum, E. acervulina; lower small intestine, E. mitis). In contrast, at sites remote from infection, mucosal dry weights and brush border enzyme activities were significantly increased above control values. However, mucosal carotenoid contents were significantly decreased. Between 5 and 7 days PI mucosal renewal as signalled by increases in dry weight was accompanied by increases in brush border enzyme activities. However, mucosal carotenoid contents were further decreased. High correlations were found between plasma carotenoid levels and total mucosal carotenoids in control and coccidia-infected chicks, but not in 48-h-starved chicks. Infection with coccidia increased this correlation, and the increase with E. acervulina infection was significant. These data indicate that hyperplastic and renewing mucosal tissue is defective in absorbing carotenoids, and further, that there is no direct relationship between mucosal carotenoid content and brush border enzyme activities. Apparently carotenoids are not mobilized from body depots during the first week of coccidial infections as they are during 48-h starvation.
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PMID:Physiological responses of chicken gut tissue to coccidial infection: comparative effects of Eimeria acervulina and Eimeria mitis on mucosal mass, carotenoid content, and brush border enzyme activity. 368 53

The leucine auxotroph Escherichia coli 2961 exhibited stringent control of net ribonucleic acid (RNA) synthesis during amino acid starvation. After leucine was exhausted from the medium, the rate of uracil incorporation into RNA rapidly decreased to 2 to 4% of the prestarvation value. Infection of the starved cells with T2 phage stimulated uracil incorporation to a level equivalent to that of unstarved, T2-infected cells. The RNA synthesized during leucine starvation of the T2-infected cells consisted of T2 and E. coli messenger RNA, but stable ribosomal RNA (23S and 16S) did not appear to be synthesized. It is concluded that one or more T2-specific proteins are required to shut off host messenger RNA synthesis. Furthermore, transcription of E. coli and T2 deoxyribonucleic acid is not necessarily coupled to the translation of messenger RNA during stringent control of net RNA synthesis.
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PMID:Ribonucleic acid synthesis in T2-infected Escherichia coli during "stringent" control. 487

The target site for bacteriophage Mu integration in a lytic cycle of infection was investigated. DNA synthesis in five Hfr strains of Escherichia coli K-12 was synchronized by amino acid starvation and was allowed to proceed for 0, 8, or 15 min before infection. The Hfr cells were then infected with Mu and were subsequently mated with nonimmune F- recipient cells. Mating was interrupted mechanically at 5-min intervals and samples were assayed for infective centers. Conjugal transfer of Mu was delayed in Hfr strains that have transfer origins 15 map units or more from the E. coli replication origin, and the delays increased as the distance between an Hfr point of origin and the replication origin increased. When a gene A mutant of Mu was used for the infection, no infective centers were generated. Infection with a gene B mutant resulted in infective center formation only after long periods of mating. These data are most consistent with a model in which infecting Mu DNA or its progeny integrate at host chromosomal replication forks.
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PMID:Integration of bacteriophage Mu at host chromosomal replication forks during lytic development. 644 18

We used two-dimensional gel electrophoresis to quantitate the changes in rates of synthesis that follow phage lambda infection for 21 Escherichia coli proteins, including groE and dnaK proteins. Although total protein synthesis and the rates of synthesis of most individual E. coli proteins decreased after infection, some proteins, including groE protein, dnaK protein, and stringent starvation protein, showed increases to rates substantially above their preinfection rates. Infection by lambda Q- affected host synthesis in the same way as infection by gamma+, whereas infection by lambda N- showed no detectable effect on host synthesis. Deletion of the early genes between att and N abolished the effect, and shorter deletions in this region gave intermediate effects. By this sort of deletion mapping, we show that a large part, though not all, of the effect of lambda infection on host protein synthesis can be ascribed to the early region that contains phage genes Ea10 and ral. We compared the changes in protein synthesis after infection with the changes that occur in uninfected cells upon heat shock or amino acid starvation. The spectrum of changes that occurred on infection was very different from that seen after heat shock but quite similar to that seen during amino acid starvation. Despite this similarity of the effects of lambda infection and starvation, we did not detect any increase in the level of guanosine tetraphosphate during infection. We show that the groE protein is the same protein as B56.5 of Lemaux et al. (Cell 13:427-434, 1978) and A protein of Subramanian et al. (Eur. J. Biochem. 67:591-601, 1976).
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PMID:Effect of bacteriophage lambda infection on synthesis of groE protein and other Escherichia coli proteins. 646 Jul 50

Infection-induced malnutrition, the most common form of cytokine-induced malnutrition, results from the actions of proinflammatory cytokines, ie, tumor necrosis factor (TNF) and interleukins 1,6, and 8 (IL-1, IL-6, and IL-8). During acute generalized infections, these cytokines initiate the acute-phase reaction. This reaction is quite stereotyped, and includes fever, malaise, myalgia, headaches, cellular hypermetabolism, and multiple endocrine and enzyme responses. In addition, there is heightened catabolism of muscle proteins and many amino acids; flux of free amino acids into the liver; hepatic synthesis of acute-phase plasma proteins; sequestration of iron and zinc; gluconeo-genesis; insulin resistance; impaired cellular uptake of fatty acids from plasma triglycerides; sizable losses of body nitrogen, potassium, magnesium, phosphate, and zinc; retention of body salt and water; heightened metabolic degradation and/or loss of vitamins; and an activation of the immune system. The pathogenesis of cytokine-induced malnutrition is thus vastly different from the malnutrition caused by uncomplicated starvation. Cytokine-induced malnutrition can have a devastating effect on the immune system and its functions. Although proinflammatory cytokines are found in mucosal fluids, where they contribute to the pathogenesis of inflammatory bowel diseases, it is not known whether cytokines play a role in toxigenic, secretory diarrheas such as cholera, which cause huge losses of body water, electrolytes, and bicarbonate while exhibiting no systemic manifestations of an acute-phase reaction.
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PMID:Herman Award Lecture, 1995: infection-induced malnutrition--from cholera to cytokines. 757 15

Infection with mucoid, alginate-producing strains of Pseudomonas aeruginosa is the leading cause of mortality among patients with cystic fibrosis. Alginate production by P. aeruginosa is not constitutive but is triggered by stresses such as starvation. The algR2 (also termed algQ) gene has been previously identified as being necessary for mucoidy; an algR2 mutant strain is unable to produce alginate when grown at 37 degrees C. We show here that the levels of phosphorylated succinyl coenzyme A synthetase (Scs) and nucleoside diphosphate kinase (Ndk), which form a complex in P. aeruginosa, are reduced in the algR2 mutant. We were able to correlate the lower level of phosphorylated Scs with a decrease in Scs activity. Western blots (immunoblots) also showed a decreased level of Ndk in the algR2 mutant, but the presence of another kinase activity sensitive to Tween 20 provides the missing Ndk function. The effect of AlgR2 on tricarboxylic acid (TCA) cycle enzymes appears to be specific for Scs, since none of the other TCA cycle enzymes measured showed a significant decrease in activity. Furthermore, the ability of the algR2 mutant to grow on TCA cycle intermediates, but not glucose, is impaired. These data indicate that AlgR2 is responsible for maintaining proper operation of the TCA cycle and energy metabolism.
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PMID:Energy metabolism and alginate biosynthesis in Pseudomonas aeruginosa: role of the tricarboxylic acid cycle. 792 63

Infection with Ad5dl520EIB-, an adenovirus producing only the 243 residue E1A protein and lacking the E1B region, caused apoptosis in normal rat kidney (NRK) cells as judged by the production of nucleosomal DNA fragments. Apoptosis occurred only when the cells were growth-inhibited by cell-cell contacts in confluent cultures or by serum starvation and not when they were actively growing. In uninfected cultures, apoptosis also occurred at confluency, but more slowly than after infection. Studies with E1A deletion mutants of dl520E1B- showed that the regions of the E1A protein essential for induction of apoptosis were those in exon 1 required for binding to the cellular proteins p300 and pRb. Mutants defective at inducing apoptosis were previously found to be defective at inducing baby rat kidney cells to synthesize cellular DNA. In our experiments, cells underwent apoptosis when stimulated by E1A to proliferate under conditions where proliferation was blocked. It is possible that it was the proliferation block opposing the induction of proliferation that led directly to apoptosis. Circumstances leading to induction of apoptosis by c-myc (Evan et al., 1992) are similar and can be interpreted in a similar way.
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PMID:Induction of apoptosis by adenovirus type 5 E1A in rat cells requires a proliferation block. 813 21

The probing and salivation behaviour on a warm slide of three tsetse fly species or subspecies (glossina morsitans morsitans, Glossina palpalis gambiensis, Glossina tachinoides) was examined with respect to various parameters (species, sex, age, starvation period, trypanosome infection, quality of support). Each fly was given the opportunity to probe the warm slide (38 degrees C) for 5 minutes (we mean by probing an attempt to touch the glass slide by the proboscis in a biting position). G.m morsitans is by far the most efficient at probing (70.50%) when compared with G. tachinoides (50.50%) and G. palpalis gambiensis (45.80%). Globally, males (61.30%) are more active than females (52%) and those of the morsitans group are more active than those of the palpalis group. Teneral flies probe more easily than non-teneral flies, with an increased advantage in G. m. morsitans. The starvation period increases the probing behaviour, but at 48 h. G. m. morsitans probed as much as G. palpalis gambiensis and G. tachinoides at 72 h. The males of G. m. morsitans and G. palpalis gambiensis are more precocious than females, but the inverse is observed in G. tachinoides. Infection by T. congolense (EATRO 325 strain) does not affect the probing behaviour of males of all 3 species but seems to lower that of females in the palpalis group. Addition of a drop of PSG or blood improves the probing behaviour of infected G. m. morsitans females (the only ones tested). The results are discussed in relation to biological data and knowledge of the receptor systems of tsetse flies.
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PMID:[Improving the salivation technic in the tsetse fly for the detection of infective metatripanosomes: study of the effect of biologic and non-biologic factors in the probing behavior of the tsetse fly]. 855 46

"Septic autocannabalism" been coined to describe the metabolic response that follows severe sepsis in humans. The normal protein- and energy-conserving mechanisms evoked during simple starvation are not observed following the onset of sepsis. The metabolic response to sepsis entails rapid breakdown of the body's reserves of protein, carbohydrate, and fat. Hyperglycemia with insulin resistance, profound negative nitrogen balance, and diversion of protein from skeletal muscle to splanchnic tissues are prominent features. These responses are believed to be mediated in large part by inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha), interleukin 1beta (IL-1beta), and IL-6. Secondary induction of catecholamines, cortisol, and glucagon by cytokines is likely to be another important effector mechanism. Infection and inflammation elicit a complex network of interwoven responses, and no single mediator alone accounts for the responses observed. Sepsis also commonly involves alterations in cardiovascular function with altered flow to key metabolic sites, hypoxia, damage to the gut's mucosal barrier, secondary organ failure, and alterations in capillary permeability. These structural and functional alterations also strongly influence the metabolic profile during infection. If these catabolic responses persist for more than a few days, severe malnutrition results and is likely to be an important risk factor for mortality in these patients. The altered metabolic milieu during sepsis prevents effective use of exogeneously delivered glucose and protein; at best, administration of these agents ameliorates but does not prevent the persistence of catabolism. Delivery of agents that antagonize cytokines and other moieties such as glutamine and growth hormone may, in the future, help to restore nitrogen balance during sepsis.
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PMID:Metabolism of sepsis and multiple organ failure. 866 35

We have shown that a deletion mutant form of Bcr [Bcr(64-413)] is a strong inhibitor of the tyrosine kinase of Bcr-Abl in vitro and also inhibits its oncogenic growth effects (Liu et al., Cancer Res., 56: 5120-5124, 1996). To determine the effects of this Bcr-Abl kinase inhibitor on chronic myelogenous leukemia (CML) cells, we cloned BCR(64-413) into a recombinant, replication-defective adenovirus to express useful quantities of Bcr(64-413) in a wide variety of cells in culture. Infection of Cos1 cells with plaque-purified virus at a multiplicity of infection of 20-40 induced high expression of Bcr(64-413) as detected by Western blotting. Infection of hematopoietic cells at modest multiplicities of infection (20-40) required special conditions involving shifting cycling cells to a nongrowing condition involving serum starvation and cell crowding. Under these conditions, both Bcr-Abl-positive and -negative hematopoietic cells can be efficiently infected by adenovirus, as demonstrated by 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside staining of cells infected by beta-galactosidase (beta-GAL) adenovirus. We found that expression of Bcr(64-413) in Bcr-Abl-positive K562 and BV-173 cells, but not Bcr-Abl-negative SMS-SB cells, increased cell-cell clumping and inhibited cell growth. In contrast to the effects of the Bcr(64-413) adenovirus, the beta-GAL adenovirus, despite infecting both types of cells, did not block growth or increase cell-cell clumping of Bcr-Abl-positive and -negative hematopoietic cells. Expression of Bcr(64-413) protein in primary cultures of cells from CML patients with active disease interfered with cell growth, induced apoptosis (as measured by annexin staining), and increased cell-cell clumping, whereas the beta-GAL adenovirus and mock-infected cells lacked these effects. In contrast, normal marrow cells did not exhibit these effects on infection with Bcr(64-413) adenovirus. We conclude from these findings that Bcr(64-413) interferes with the oncogenic effects of Bcr-Abl and therefore has the potential for use in therapy of CML.
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PMID:Expression of a truncated first exon BCR sequence in chronic myelogenous leukemia cells blocks cell growth and induces cell death. 1119 51


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