Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004623 (bacterial infection)
 15,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infusion of cycloheximide i.v., an antibiotic known to inhibit synthesis of protein, at a rate of 0.2 mg/kg/hr, reliably caused lysis of fever in 15 chronically febrile patients with Hodgkin's disease who did not have detectable bacterial, fungal, or viral infection. Antipyretic effects were also seen in some patients with reticulum cell sarcoma, lymphosarcoma, acute leukemia, histiocytic medullary reticulosis, plasma cell myeloma, carcinoma of the lung, and carcinoma of the cervix. The drug failed to produce defervescence in four patients with normal granulocyte reserves, who were febrile due to bacterial infection. When infused at a rate of 0.2 mg/kg/hr, the drug apparently caused an acute alteration of protein metabolism in man in that plasma amino acid nitrogen rose acutely while plasma levels of muramidase and ribonuclease fell during the period of the infusion. The data suggest that continuing synthesis of protein may be involved in nonbacterial fever of neoplastic disease. Mammalian granulocytes and monocytes are known to elaborate a pyrogenic protein following appropriate stimulation; it is suggested that in some types of neoplastic disease, particularly Hodgkin's disease, tumor cells may produce and release a pyrogenic protein and that drug-induced inhibition of its synthesis is responsible for the observed lysis of fever.
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PMID:Antipyretic effect of cycloheximide, and inhibitor of protein synthesis, in patients with Hodgkin's disease or other malignant neoplasms. 109 49

Metabolic changes in six severely affected tetanus patients suffering from characteristic labile hypertension (maximum systolic blood pressure greater than 200 mmHG, maximum diurnal change in systolic pressure greater than 100 mmHg) were investigated. Daily urinary excretion of urea nitrogen increased gradually from the onset of opisthotonus, reached a peak value (10.4 to 15.4 g/m2) in 8 to 20 days, and decreased subsequently. Average cumulative excretion in 30 days reached 239.6 +/- 32.7 g/m2. Urine catecholamine excretion was elevated in each patient and remained elevated during this period. Plasma cortisol and glucagon concentrations were not increased markedly except in a case complicated other systemic bacterial infection. Increased protein catabolism in these patients could not be explained by the metabolic effects of 'stressed hormones' alone, and neurologic factors must be considered.
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PMID:Metabolic changes in patients severely affected by tetanus. 198 40

The scientific literature suggests that ambient levels of nitrogen dioxide increase susceptibility to respiratory infections. However, this association has not been conclusively demonstrated. The epidemiologic data regarding this relationship are inconclusive because these studies have used parameters of "acute respiratory illness" that are not necessarily related to infectious episodes. Previous animal studies have used either mortality after bacterial infection with virulent bacteria or decreased rate of intrapulmonary killing of bacteria with low virulence. Studies using appropriate bacterial and viral challenge organisms, with morbidity as an endpoint, provide a better basis for extrapolation to humans. The investigations in animals suggest a relationship between nitrogen dioxide and increased susceptibility to respiratory infection, but studies in which functional parameters of host resistance to such infections have been used are few. The aim of this work was to determine the threshold level of acute nitrogen dioxide exposure that would induce increased susceptibility to, and increased severity of, viral and bacterial infections. Physiologic parameters of host resistance to respiratory infections were used as endpoints. A composite picture was developed of dose-response relationships between nitrogen dioxide and the impairment of a spectrum of defense parameters in the murine respiratory tract against viral and bacterial challenges. The salient findings of this study are as follows: (1) the intrapulmonary killing of Staphylococcus aureus was impaired at 5 ppm of nitrogen dioxide; (2) this effect was found at 2.5 ppm or less when nitrogen dioxide exposure was superimposed on lungs predisposed to lowered resistance through immunosuppression with corticosteroids; (3) the adverse effect of nitrogen dioxide occurred at lower concentrations when exposure followed bacterial challenge; and (4) during the course of murine Sendai virus infection, exposure to nitrogen dioxide for four hours per day did not alter the infection in the lungs, but rather it enhanced lung pathology. The implications of these findings are that the antibacterial defenses of the lungs are susceptible to the inhibiting effects of short acute exposures of lower concentrations of nitrogen dioxide when the lungs are predisposed by bacteria present or, even more so, by immunosuppression. The alveolar macrophage phagocytic system is the defense component of the lungs that is most susceptible to the adverse effects of nitrogen dioxide. The finding that nitrogen dioxide increases virus-associated lung damage suggests that the increased severity of the disease process results from the proliferation of the virus to high titers, rather than from alterations of the infective process.
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PMID:Modulation of pulmonary defense mechanisms against viral and bacterial infections by acute exposures to nitrogen dioxide. 285 73

In the presence of bacterial infection during the first week of life a catabolic state evolves more rapidly than in the later life. Hyperaminoacidaemia and subsequent hyperaminoaciduria, elevated urea concentrations in serum, and increased renal nitrogen losses are the most important metabolic changes. These findings correlate with the clinical course of the disease and refer to the primary disturbance of cell metabolism as the cause of the metabolic changes observed. While no relation could be observed between metabolic response and bacterial species, there is a significant dependence on the time interval from the occurrence of first clinical symptoms at the beginning of antibiotic treatment. If this period is longer than 8 h, serious metabolic disturbances will usually be found. Due to the limited amino acids utilization, especially by the liver, an adequate energy intake should be the primary aim of nutrition, whereas a protein intake of more than 2.0 to 2.5 g/kg X day may further aggravate the metabolic imbalance.
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PMID:Effects of bacterial sepsis on protein metabolism in infants during the first week. 309 15

Effects of human urinary trypsin inhibitor (MTI) against operative stress were investigated. Laparotomy in a mouse caused suppression of immunological functions such as phagocytic activity and antibody formation, followed by loss of resistivity to bacterial infection and acceleration of growth of concealed tumor. The operation also caused damages to the body such as enhancement of protein catabolism and suppression of renal function, followed by increase of blood urea nitrogen, increase of protease activity in skeletal muscle and suppression of PSP clearance. Since MTI wholly ameliorated these undesirable conditions of the body caused by operative stress, it was suggested that MTI has an effect on maintaining the homeostasis of the living body as well as the ability to inhibit trypsin.
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PMID:[Effects of human urinary trypsin inhibitor against operative stress]. 398 64

Markedly increased synthesis of alpha(2) and beta globulins and alpha(1), alpha(2), and beta glycoglobulins occurs during pneumococcal sepsis in the rat simultaneously with decreased albumin formation, diminished tritiated leucine incorporation into muscle protein, and enhanced excretion of nitrogen. This augmented synthesis of specific serum proteins does not become evident until fever and bacteremia develop, and it appears to be a fundamental aspect of host response to a proliferating bacterial infection in that it occurs even in rats fed a protein-deficient (6% protein) diet after weaning and before exposure to Diplococcus pneumoniae. Although amino acid catabolism, in general, appears to be increased during infection, tryptophan degradation via the kynurenine pathway, as assessed by measuring diazotizable urinary metabolites, changes little or is, at times, significantly less than in control animals. Coincidentally, functional tryptophan oxygenase activity decreases at 16 hr after exposure. Total tryptophan oxygenase activity, however, is unchanged.
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PMID:Nitrogen metabolism and protein synthesis during pneumococcal sepsis in rats. 440 82

Gas compositions in the middle ear cavities of patients with a perforated tympanic membrane, and in normal subjects, were analyzed by mass spectrometry. The results showed that the gas in normal subjects consisted of nitrogen (83.7%), oxygen (9.2%) and carbon dioxide (6.2%). (The volume concentration of the various gases was expressed as a percentage of 713 mm Hg.) Thus, the concentrations of the various gases in the middle ear cavity differed greatly from those in the atmosphere. The low concentration of oxygen is suitable for microaerophilic bacteria and acts as a physiological barrier against bacterial infection. It was also found that the gas in patients with exudative otitis media consisted of nitrogen (77.9%), oxygen (15.6%) and carbon dioxide (5.5%), and in patients with chronic perforated otitis media, of nitrogen (77.8%), oxygen (16.9%) and carbon dioxide (4.4%). The concentration of oxygen in the middle ear cavity with perforated tympanic membrane is higher than that in the normal state because of diffusion of atmospheric gas into the middle ear cavity. In other words, perforation of the tympanic membrane exposes the middle ear cavity to a nonphysiological gaseous condition. The diffusion of atmospheric gas was simulated using small cylinders. Simulated results revealed that the atmospheric gas diffused rapidly. The change in the gas concentration during diffusion was approximated by an exponential function and a constant, and reproduced by a mathematical model. The change in the gas concentration in the middle ear cavity was usually approximated by two exponential functions and a constant. The constant represents the estimated final value of the gas concentration from which the effect of the diffusion is excluded. The final values were estimated for normal subjects and patients with perforated tympanic membrane. The final values in the normal subjects were almost equal to the measured values. The final value of carbon dioxide in the patients was greater than the measured value and nearly equal to the final value in the normal subjects. The final oxygen value in the patients was smaller than the measured value, but still greater than the final value in the normal subjects. The high oxygen concentration in the patients suggests enhanced oxygen metabolism.
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PMID:[Analysis of middle ear cavity gas composition by mass spectrometry]. 806 3

Both trauma and infection cause a rise in body temperature, white blood cell count, acute phase proteins, fluid and sodium retention and negative nitrogen balance. This phenomenon is often described as "acute phase response" or "systemic inflammatory response syndrome" to denote a coordinated systemic response to significant tissue injury and/or microbial invasion. It is generally agreed that the acute phase response is mediated through the interaction of cytokine and neuroendocrine pathways. Tumor Necrosis Factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are two of the major key cytokines involved in the generation of acute phase response. Interleukin-6 are consistently found in septic, trauma and post-operative patients and correlated well with the severity of sepsis or injury. IL-6 is responsible for the fever and metabolic changes in the acute phase. In addition to IL-6, TNF-alpha was proved to be the mediator that orchestrates the hemodynamic and tissue injury in septic shock. TNF-alpha destroys endothelial cells and induces disseminated intravascular coagulation, fluid shift, shock, multiple organ system failure and death. On many clinical occasions, both infection and trauma may happen simultaneously on the same patient. Our study demonstrated that operation on the infected patients would cause a synergistic effect on both TNF-alpha and IL-6 levels. The pulse increase in TNF-alpha and the persistent elevation of IL-6 were responsible for the post-operative unstable clinical condition in the infected patients. Should we block the cytokine signal and inflammatory response that appear to be harmful? Animal studies have shown that the septic shock to endotoxin challenge can be prevented by pretreatment with monoclonal antibody against TNF-alpha. The transcription of TNF-alpha can be blocked with corticosteroid in vivo. The post-operative increase in IL-6 and its related inflammation can be attenuated with corticosteroid, epidural anesthesia and narcotics. However, although blocking the inflammatory response has a beneficial effect of stress free it also eliminates our ability to fight with bacterial infection by lowering our immune response. How to manipulate these cytokines is a question of art more than science.
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PMID:[Similarity and synergy of trauma and sepsis: role of tumor necrosis factor-alpha and interleukin-6]. 908 32

Cachexia and a decreased immune function are negative prognostic factors for cancer patients. While the decreased immunity results in a greater susceptibility to bacterial infection, the response of the host to the resulting infection is not clear. The experiments reported here were designed to evaluate the toxicity of endotoxin to rats with a transplantable Ward colon tumor (WCT) and to evaluate the mechanism of the observed increase in lethal toxicity. The lethal toxicity of endotoxin (lipopolysaccharide, LPS) at 5 mg/kg, i.p. was evaluated in the first of two experiments. Rats received LPS and were observed for morbidity and weight loss for a period of 11 days. A second experiment was done to evaluate the effect of LPS on the plasma nitrate/nitrite concentrations and plasma indicators of host tissue dysfunction. LPS was administered as previously described but blood and tissues were collected 5 h after LPS administration. LPS resulted in the death of 1 of 12 nontumor-bearing (NTB) rats and a transient weight loss in the survivors. This same dose of LPS, however, resulted in death for 10 of 12 WCT rats with tumor burdens less than 4% of body weight. The response of WCT rats 5 h after LPS was then compared with that of age-matched NTB rats. Plasma albumin concentrations were not affected by LPS in NTB rats but were significantly decreased in WCT rats. Peripheral blood gases were not consistently affected by LPS in either group. Peripheral blood white cell counts, except monocytes, were significantly decreased by LPS in both groups. Monocyte counts in peripheral blood were further reduced in WCT rats compared with NTB rats receiving LPS. The presence of the WCT significantly enhanced the LPS-associated increase in spleen weight. Liver weights were lower in LPS rats but there was no effect of the presence of WCT. The LPS-associated increase in plasma nitrate/nitrite concentration was enhanced by the WCT. The plasma arginine and citrulline concentrations were altered in a manner consistent with an increase in nitric oxide synthesis. An increase in plasma ornithine concentration suggests an increase in arginine metabolism by arginase. The plasma concentration of alanine aminotransferase was significantly elevated when WCT rats received LPS, suggesting enhanced hepatic dysfunction. The plasma blood urea nitrogen concentration was elevated by LPS to a greater extent in the WCT rats than in the NTB controls, indicating increased renal dysfunction. These results demonstrate that the Ward colon tumor increases the host lethal response to the endotoxin, a toxic product of bacterial infections. The mechanisms of lethality may include an increased nitric oxide synthesis in WCT rats and enhanced liver and renal toxicity.
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PMID:Influence of the Ward colon tumor on the host response to endotoxin. 917 90

When mice previously cured of a Plasmodium vinckei infection were subsequently infected with Salmonella enteritidis the course of bacterial infection was significantly retarded, showing increased survival duration as compared with control infections in naive mice. Moreover, on stimulation with lipopolysaccharide and/or interferon-gamma, spleen cells from malaria-cured mice showed an increased capacity to produce tumor necrosis factor, interleukin 6, and reactive nitrogen intermediates as compared with spleen cells from naive mice. However, no significant variation in the capacity of spleen cells to release reactive oxygen intermediates was observed between previously malarious and naive mice. The most significant increases were observed in the capacity for reactive nitrogen intermediate production after P. vinckei malaria. These results suggest that the observed protection of mice against salmonellosis in the convalescent phase after malaria may be mediated by nitric oxides.
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PMID:Protection of mice previously infected with Plasmodium vinckei against subsequent Salmonella enteritidis infection is associated with nitric oxide production capacity. 949 29


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