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)

Nutritional depletion is a common problem seen in critically ill patients with cancer and is associated with increased morbidity and mortality. Infection and injury activate a cascade of metabolic events that leads to a poor nutritional state and wasteful energy consumption. The goals of nutritional support entail minimizing starvation, preventing nutrient deficiencies, supporting or improving immune function, and facilitating tissue repair and wound healing. Further understanding of the metabolic changes of illness will improve effective regulation of the inflammatory events occurring in critically ill patients. Multiple clinical parameters are available to assess the nutritional status in critically ill patients, but no standard recommendations can be made at this time. The use of these parameters can be appropriate, provided that their limitations are understood clearly. The development and standardization of objective parameters to identify patients at risk or with subclinical malnutrition are needed. Enteral and parenteral feedings are safe and effective methods to deliver nutrients to critically ill patients with cancer who are unable to ingest adequate amounts orally. Early nutritional support should be instituted in the appropriate clinical setting. Specialized nutritional solutions and supplements require careful consideration in patients with renal, hepatic, cardiac, or pulmonary disorders. The unselective use of nutritional support is not indicated in well-nourished patients with cancer undergoing surgery, chemotherapy, or radiotherapy in whom adequate oral intake is anticipated. Nutritional support remains an important adjunctive therapy in the overall management of critically ill patients. Continued clinical investigations in nutrition are necessary to identify other groups of patients who can benefit from nutritional interventions.
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PMID:Nutritional support in critically ill patients with cancer. 1152 56

Mice were deprived of food for a period of 72 h at varying times relative to the time of infection with Paracoccidioides brasiliensis. Host resistance was diminished profoundly when the period of food deprivation was from 48 h before to 24 h after infection (group B). When food deprivation was initiated immediately after infection (group C), host resistance was reduced less profoundly. When food deprivation was initiated at 24 and 48 h post-infection, reductions in host resistance were only moderate or not observed respectively. These results suggest that the earlier in the course of infection starvation occurs, the more profoundly host resistance is impaired. When food deprivation was initiated 72 h before infection, finishing at the time of infection (group A), the reduction in host resistance was considerably less profound compared with group B mice, suggesting that refeeding initiated immediately after infection is responsible for rapid restoration of the antifungal resistance in starved mice. Infection-induced responses of corticosterone and interferon-gamma were changed according to the timing of food deprivation. Group A mice, similar to non-fasted controls, showed an infection-induced increase in serum corticosterone concentration, while groups B and C did not. Group C mice showed a substantially greater infection-induced increase in serum interferon-gamma compared with the other fasted and non-fasted control groups.
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PMID:Effect of timing of food deprivation on host resistance to fungal infection in mice. 1214 18

Hypoxia-inducible factor-1 (HIF-1) mediates transcriptional activation of vascular endothelial growth factor (VEGF) and other hypoxia-responsive genes. Transgenic expression of a constitutively stable HIF-1alpha mutant increases the number of vascular vessels without vascular leakage, tissue edema, or inflammation. This study aimed to investigate the molecular basis by which HIF-1 mediates the angiogenic response to hypoxia. In primary human endothelial cells, hypoxia, desferrioxamine, or infection with Ad2/HIF-1alpha/VP16, an adenoviral vector encoding a constitutively stable hybrid form of HIF-1alpha, increased the mRNA and protein levels of VEGF, angiopoietin-2 (Ang-2), and angiopoietin-4 (Ang-4). Infection with Ad2/CMVEV (a control vector expressing no transgene) had no effect. Angiopoietin-1 (Ang-1) expression was not detected in human endothelial cells. Ang-4 was also induced by hypoxia or Ad2/HIF-1alpha/VP16 in human cardiac cells, whereas Ang-1 expression remained unchanged. Recombinant Ang-4 protein protected endothelial cells against serum starvation-induced apoptosis and increased cultured endothelial cell migration and tube formation. Ad2/HIF-1alpha/VP16 stimulated endothelial cell proliferation and tube formation. Hypoxia- or Ad2/HIF-1alpha/VP16-induced tube formation was significantly reduced by a Tie-2 inhibitor. These results suggest that HIF-1 mediates the angiogenic response to hypoxia by upregulating the expression of multiple angiogenic factors. Ang-4 can function similarly as Ang-1 and substitute for Ang-1 to participate in hypoxia-induced angiogenesis. Activation of the angiopoietin/Tie-2 system may play a role in the ability of HIF-1 to induce hypervascularity without excessive permeability.
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PMID:Hypoxia-inducible factor-1 mediates activation of cultured vascular endothelial cells by inducing multiple angiogenic factors. 1295 44

During an expressed sequence tag sequencing project, a gene encoding a methylglyoxal lyase (glyoxalase I) was identified, cloned and characterised from the necrotrophic wheat pathogen Stagonospora nodorum. Sequence analysis identified the gene, named Gox1, as having reasonable identity to GLO1 from yeast and hypothetical proteins identified in fungal genome sequencing projects. Expression analysis in vitro revealed Gox1 to be up-regulated in the presence of methylglyoxal and salt but not affected by starvation conditions. Analysis of Gox1 transcription in planta showed its highest expression was in ungerminated spores and during sporulation, suggesting a role for the glycolytic bypass pathway in sporulation. The gene was inactivated by homologous recombination, resulting in a S. nodorum strain with no detectable glyoxalase I activity. The gox1 mutants exhibited no discernable phenotype, with the exception of being more sensitive to the presence of methylglyoxal. Infection assays demonstrated the mutants retained full pathogenicity and sporulation was unaffected. This is the first report describing the characterisation of a glyoxalase I from a pathogen of any description. The gene has been sequenced, functionally characterised and shown not to be required for the infection of wheat by S. nodorum.
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PMID:Functional characterisation of glyoxalase I from the fungal wheat pathogen Stagonospora nodorum. 1520 12

Infection with the apicomplexan parasite Toxoplasma gondii results in a significant alteration of the host-cell transcriptional profile. We have previously shown that the transferrin receptor (TfR) is specifically up-regulated in T. gondii-infected human fibroblasts but not in host cells infected with the bacterial pathogens Salmonella Typhimurium and Chlamydia trachomatis. In this report, we describe the prerequisites and physiological conditions that are associated with this pathogen-specific gene induction. Band-shift assays revealed that T. gondii infection resulted in increased activity in the iron response protein IRP1, which, in this state, stabilizes TfR mRNA from degradation. Although T. gondii depends on host-cell iron as demonstrated by sensitivity to deferoxamine, a parasite-induced iron starvation is not responsible for TfR up-regulation. The increased iron availability due to treatment with holotransferrin and FeNTA did not prevent TfR induction nor was the transferrin-independent iron-transporter NRAMP2 up-regulated in infected host cells. In addition, inhibition of parasite replication by drug treatment did not prevent TfR up-regulation. Instead, TfR induction was sensitive to cycloheximide and could be induced by treatment with conditioned media from infected human fibroblasts. Together our findings suggest that the T. gondii-specific TfR up-regulation is not due to a direct interaction of parasitic factors with the iron-uptake machinery of the host cell but is instead mediated indirectly as a result of secreted host cell- or parasite-derived factors.
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PMID:Transferrin receptor induction in Toxoplasma gondii-infected HFF is associated with increased iron-responsive protein 1 activity and is mediated by secreted factors. 1534 72

Chinese hamster ovary (CHO) cells are traditionally regarded as nonpermissive cells for herpes simplex virus type 1 (HSV-1) infection as they lack the specific entry receptors, and modified CHO cells have been instrumental in the identification of HSV-1 receptors in numerous studies. In this report we demonstrate that the HSV-1 strain 17+ variant HSV1716 is able to infect unmodified CHO cells but only if the virus is propagated in baby hamster kidney (BHK) cells. Infection of CHO cells by BHK-propagated HSV1716 results in expression of immediate-early, early, and late viral genes, and infectious progeny virions are produced. In normally cultured CHO cells, up to a maximum of 50% of cells were permissive for BHK-propagated HSV1716 infection, with 24 h of serum starvation increasing this to 100% of CHO cells, suggesting that the mechanism used by BHK-propagated virus to infect CHO cells was cell cycle dependent. The altered tropism of HSV1716 was also evident in another nonpermissive mouse melanoma cell line and is an exclusive property resulting from propagation of the virus using BHK cells, as viruses propagated on Vero, C8161 (a human melanoma cell line), or indeed, CHO cells were completely unable to infect either CHO or mouse melanoma cells.
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PMID:Herpes simplex virus type 1 strain HSV1716 grown in baby hamster kidney cells has altered tropism for nonpermissive Chinese hamster ovary cells compared to HSV1716 grown in vero cells. 1601 57

Chlamydia trachomatis, an intracellular pathogen, is the leading cause of preventable blindness and sexually transmitted infections in the world. Infection of epithelial cells with Chlamydia results in the production of antigen-specific IFN-gamma -secreting CD4+ and CD8+ T cells. IFN-gamma activates indoleamine 2,3-dioxygenase (IDO), an enzyme that degrades tryptophan in the host cell. This IDO mediated tryptophan starvation is known to activate genes for persistence in the Chlamydia, which renders antibiotics ineffectiveness against it. Tryptophan supplementation causes reactivation of Chlamydia from persistent into metabolically active forms and then the antibiotics easily eradicate these active forms of Chlamydia. Therefore treating the chronic Chlamydia infection with antibiotics and tryptophan together may lead to better clearance of Chlamydia infection, and may be a better therapeutic approach in the future.
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PMID:Role of Tryptophan supplementation in the treatment of Chlamydia. 1704 16

Infection of keratinocytes with high risk human Papilloma virus causes immortalization, and when followed by further mutations, leads to cervical cancer and other anogenital tumors. Here we monitor the progressive loss of robustness in an in vitro model of the early stages of transformation that comprises normal keratinocytes and progressive passages of HPV16 immortalized cells. As transformation progresses, the cells acquire higher proliferation rates and gain the ability to grow in soft agar. Concurrently, the cells lose robustness, becoming more sensitive to serum starvation and DNA damage by Cisplatin. Loss of robustness in the course of transformation correlates with significant reductions in the activities of the anti-apoptotic proteins PKB/Akt, Erk, Jnk and p38 both under normal growth conditions and upon stress. In parallel, loss of robustness is manifested by the shrinkage of the number of growth factors that can rescue starving cells from apoptosis, with the emergence of dependence solely on IGF1. Treatment with IGF1 activates PKB/Akt and Jnk and through them inhibits p53, rescuing the cells from starvation. We conclude that transformation in this model induces higher susceptibility of cells to stress due to reduced anti-apoptotic signaling and hyper-activation of p53 upon stress.
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PMID:Loss of robustness and addiction to IGF1 during early keratinocyte transformation by human Papilloma virus 16. 1762 50

Infection with the malaria parasite Plasmodium falciparum leads to widely different clinical conditions in children, ranging from mild flu-like symptoms to coma and death. Despite the immense medical implications, the genetic and molecular basis of this diversity remains largely unknown. Studies of in vitro gene expression have found few transcriptional differences between different parasite strains. Here we present a large study of in vivo expression profiles of parasites derived directly from blood samples from infected patients. The in vivo expression profiles define three distinct transcriptional states. The biological basis of these states can be interpreted by comparison with an extensive compendium of expression data in the yeast Saccharomyces cerevisiae. The three states in vivo closely resemble, first, active growth based on glycolytic metabolism, second, a starvation response accompanied by metabolism of alternative carbon sources, and third, an environmental stress response. The glycolytic state is highly similar to the known profile of the ring stage in vitro, but the other states have not been observed in vitro. The results reveal a previously unknown physiological diversity in the in vivo biology of the malaria parasite, in particular evidence for a functional mitochondrion in the asexual-stage parasite, and indicate in vivo and in vitro studies to determine how this variation may affect disease manifestations and treatment.
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PMID:Distinct physiological states of Plasmodium falciparum in malaria-infected patients. 1807 67

The infection-related expression of a Heterobasidion annosum (Fr.) Bref. sensu lato (s.l.) putative cytochrome P450 gene (CPM2) was analysed with realtime quantitative PCR. CPM2 was highly expressed after 20 days of growth in bark of living spruce trees, and up-regulated by nitrogen starvation on artificial media. Infection of pine seedlings in the presence of high-carbon medium results in low expression levels of CPM2, thus indicating that starvation is the primary regulatory factor for induction of this gene. The predicted cpm2 protein contains 507 amino acids with an estimated molecular mass of 56.1 kDa, and display all conserved amino acids of the cytochrome P450 protein family. The protein has a high similarity to the ord1/ordA O-methylsterigmatocystin oxidoreductases from Aspergillus flavus/A. parasiticus, responsible for catalysing the final step in aflatoxin biosynthesis. Results indicate that cpm2 is potentially important for pathogenicity in H. annosum s.l.
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PMID:A fungal cytochrome P450 is expressed during the interaction between the fungal pathogen Heterobasidion annosum sensu lato and conifer trees. 1829 2


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