Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial failure is uniformly fatal when associated with post-traumatic sepsis and multisystem failure. Controversy exists as to whether endotoxin has a direct effect on the myocardium. A nonanoxic isolated arterially perfused rabbit interventricular septum was used in this study to evaluate the effects of endotoxin, live E. coli, and endotoxin/septic shock plasma on myocardial function and ultrastructure. Purified E. coli endotoxin and live E. coli bacteria did not have a significant direct effect on rabbit cardiac muscle function or ultrastructure. Perfusion of the rabbit septum with plasma from rabbits exsanguinated following a 2-hour septic or endotoxin shock insult, however, caused significant (p less than 0.02) myocardial depression when compared with control septa perfused with normal rabbit plasma. Septa perfused with shock plasma demonstrated ultrastructural alterations of mitochondria that were not noted in control preparations.
 ...
PMID:Myocardial depression in sepsis. 36 63

Severe injury, whether the result of a major accident, a large burn, or a complicated surgical operation, often results in sepsis. Under such conditions both specific and nonspecific host defense systems are affected. The individual facets of major concern are chemotaxis, phagocytosis, intracellular killing, complement depletion, and depression of humoral and cellular mediated immunity. The most profound changes occur in cell-mediated immunity. Within a few hours o injury, the number of circulating T cells becomes depleted, concomitantly thoracic duct lymphocytes are markedly reduced. This change is not only quantitative but functional. The clinical impact of these deficient host defense mechanisms lies in the fact that low virulent organisms may become a lethal threat to the injured patient. Currently, investigators are attempting to reverse thse deficiencies through the use of immunotherapy.
 ...
PMID:Natural host defense mechanisms. 39 70

The importance of adhesion in regulating locomotion and accumulation of polymorphonuclear leukocytes (PMN) has remained vague. We found that the chemotaxis of human PMN resuspended in heat-inactivated plasma was maximal toward 1-10 nM N-formyl-met-leu-phe (f-Met-Leu-Phe), but fell below random motility toward >/= 100 nM. This impressive decrease of motility was paralleled by increased cell adherence on Petri dishes being minimal at 1 nM and maximal at >10 nM f-Met-Leu-Phe (6+/-1 and 37+/-2% [SE] adherent cells, respectively). Checked by phase-contrast microscopy, cells under stimulated adhesion lost the typical bipolar shape of moving PMN and became immobilized and highly flattened. PMN, preexposed to 250 nM f-Met-Leu-Phe and tested after washing, retained increased adhesiveness and showed extremely low random and chemotactic motility. In contrast, preexposure to 1 nM f-Met-Leu-Phe had no effect on chemotaxis. Supporting the concept that immobilizing hyperadhesiveness does not correspond to a general functional hyporesponsiveness of PMN, no depression of the initial ingestion rate was observed in the presence of 250 nM f-Met-Leu-Phe. Moreover, a close correlation was found between the induction of PMN adhesiveness and the stimulation of the hexose monophosphate pathway activity as well as of lysomal enzyme release (r >/= 0.98). Thus, "chemotactic deactivation" and "high-dose inhibition of chemotaxis" by N-formyl peptides is the consequence of increased cell adhesiveness. This phenomenon provides a mechanism for cell trapping at the inflammatory site. Conversely, if operative in circulating blood, e.g., in septicemia, it may impair PMN emigration to such sites.
 ...
PMID:Modulating influence of chemotactic factor-induced cell adhesiveness on granulocyte function. 44 62

Sera from 103 fasting individuals 3 to 76 years of age and free of clinical infectious disease and sera from 183 patients with infectious disease were assayed for serum total non-esterfied fatty acids (tNEFA) and compared. Data were also separated into five groups according to age of donor: 3--7, 8--19, 20--35, 36--60, and 61--76 years. The mean group serum levels of tNEFA increased with age. Among patients with infectious diseases sixty-five were diagnosed as having hepatitis, 41 with infectious mononucleosis, 18 with cellulitis, 12 with pulmonary tuberculosis, 11 with non-pneumococcal pneumonia, 9 with pneumococcal pneumonia, 8 with pharyngitis, 6 with pyelonephritis, 6 with aseptic meningitis, 4 with Gram-negative sepsis, and 3 with encephalitis. The sera from 23 non-fasting patients with gonorrhea were also tested. The serum tNEFA levels were found to be altered, in fact depressed from normal group values, only in patients with pneumonia or tuberculosis. This depression may be related to aberrant pulmonary metabolism during pneumonia.
 ...
PMID:Reduced level of non-esterified fatty acids in sera from patients with infectious respiratory disease. 69 41

Sequential chemotherapeutic regimens, primarily used in the treatment of hematopoietic malignancies, and employing ara-C as a basic antineoplastic agent induce mucosal alterations in the entire gastrointestinal tract. These are characterized by surface and glandular epithelial atypia, immaturity, and necrosis. Glandular regeneration is characteristically delayed leading to a state of intestinal aproliferative cytopenia. Other toxic intestinal changes include telangiectasia of blood vessels and the formation of intramural hematomas. Intestinal infections develop frequently and are complicated by peritonitis, liver abscesses, pneumatosis cystoides in testinalis and sepsis. These intestinal lesions are accompanied by a predictable clinical syndrome which begins concomitantly with ara-C infusions and is characterized by diarrhea, ileus, abdominal pain, hematemesis and melena, severe hypokalemia, hypocalcemia and a protein-losing enteropathy. Additional toxic manifestations induced by ara-C include transient weight gains, fever elevations and severe bone marrow depression. The genesis of the intestinal lesions is linked to the three day dose schedule of ara-C infusions which insures both arrest of the cycling intestinal cells in the S-phase and a high cytotoxic index. The severity of these lesions is markedly augmented by prior treatment with ara-C and cyclophosphamide which causes synchronization and probable recruitment of intestinal stem cells, respectively.
 ...
PMID:Cytosine arabinoside induced gastrointestinal toxic alterations in sequential chemotherapeutic protocols: a clinical-pathologic study of 33 patients. 70 32

A study was made of some nonspecific immunity indices in staphylococcus sepsis and gastroenterocolitis during the infectious process in young children. Results of these investigations pointed to the depression of bactericidal and lysozyme activity of the blood serum and of the immunoadherence reaction at the acute period of the disease, and to some increase at the phase of recovery. There was also found an elevation of the phagocytic activity (of the phagocytolysis percentage) at the acute phase of the staphylococcus sepsis and gastroenterocolitis Antistaphylococcus gamma-globulin produced a positive effect on the lysozyme and bactericidal activity of the blood sera and promoted an increase of the blood phagocytic activity in the sick children.
 ...
PMID:[Several indices of non-specific immunity in staphylococcal sepsis and staphylococcal gastroenterocolitis in children of different ages]. 98 93

In preparation for the use of bovine thymosin, a thymic hormone, as a specific T cell stimulator in immunodepressed patients, we studied its effect on E rosette formation of peripheral lymphocytes from patients with (1) advanced malignancies, (2) extensive burns, and (3) septicemia. E rosette formation in vitro with and without thymosin was evaluated in 52 patients with carcinoma of the breast (25) or lung (27) in relation to adjuvant therapy and/or surgery. The depression of E rosettes in cancer patients was most striking when adjuvant therapy, irradiation, and/or chemotherapy were used; in 20 patients this was elevated by incubation with thymosin. There was a delay in recovery of depressed E rosette levels after radical mastectomies in four patients, recovery being accelerated by thymosin. In ten burn patients (40 to 80 percent of body surface area, second and third degree burns), the depression in E rosette levels occurred in the first week and was most marked in 3 to 4 weeks. In eight patients this was elevated by thymosin in vitro. In four septic patients, all undergoing operation, serial studies suggested that recovery from sepsis was accompanied by spontaneous rise in E rosette levels. This process was accelerated by thymosin in vitro. This study as well as previous experiments with animals suggest that thymosin may influence depressed host resistance favorably by increasing T-cell-mediated immunity.
 ...
PMID:In vitro effect of thymosin on T cells from immunodepressed surgical patients. 108 39

Two boys aged up to 2 weeks suffered from enterobacter-sepsis. In both cases osteomyelitis developed in spite of treatment with Gentamycin or Gentamycin combined with Chepazolin. Both children were, taking accont of the risks, then treated with Chloramphenicol (100 mg/kg body weight/24 hours) and the first patient also, for a short time, with tetracyclin. In the second patient we saw a marrow depression dependent on Chloramphenicol and its dosage which disappeared rapidly, when the drug was withheld.
 ...
PMID:[Enterobacter-osteomyelitis in two neonates (author's transl)]. 123 63

The covalent modification of receptor proteins via phosphorylation and dephosphorylation is one of the principal mechanisms controlling carbohydrate metabolism and is known to be regulated by various protein kinases. Recent studies indicated that many hormones may exert their effects on cellular metabolism by regulating intracellular c-AMP levels and by activating a c-AMP dependent protein kinase, i.e., protein kinase A. The metabolic disturbances during sepsis are characterized by an initial hyperglycemia followed by a progressive hypoglycemia and a depletion of hepatic glycogen content. The latter is coupled with a slowdown in glycogenesis, an accelerated glycogenolysis, and a depression in gluconeogenesis in the liver. Since the liver is the major organ that regulates the homeostatic level of blood glucose, it is conceivable that the sepsis-induced glucose dyshomeostasis might be mediated by changes in protein kinase activity and the kinetic characteristics of enzymes. The present experiment was designed to study the correlation between protein kinase A and the pathophysiology of hepatic glucose dyshomeostasis during sepsis. Sepsis was induced in rats by cecal ligation and puncture (CLP). Late sepsis occurred 18 hours after CLP. Protein kinase A was extracted from the rat livers by acid precipitation and ammonium sulfate fractionation, and then partially purified by DEAE-cellulose. The results show that in the late sepsis, type-I protein kinase A (eluted at low ionic strength) activity was significantly decreased by 34-52% (P < 0.01). The kinetic parameters such as Vmax's for ATP, histone, and c-AMP were also significantly decreased from the control values of 6.1 +/- 0.9, 5.4 +/- 0.8, and 5.1 +/- 1.9 nmoles/mg.min. to 3.6 +/- 0.5, 2.8 +/- 0.3, and 2.5 +/- 0.5 nmoles/mg.min., respectively. Analysis using Hill's equation indicates that the S0.5 and n (Hill coefficient) values of the various substrates and activators for type-I protein kinase A remained unchanged. In the case of type-II protein kinase A (eluted at high ionic strength), the Vmax, S0.5, and n values for ATP, histone, and c-AMP were unchanged during late sepsis. The results of the present study indicate that the activities and kinetic characteristics of type I protein kinase A in rat liver are modified during late sepsis. Since protein kinase A is known to regulate glucose metabolism through adrenergic receptor mediation, these findings may have a pathophysiological significance in the understanding of hepatic glucose dyshomeostasis during sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Kinetic studies of protein kinase A in rat liver during late sepsis]. 129 61

The most common cause of late death following trauma is sepsis. The traumatized patient has a significant increased risk of infection. Transfusion, hypotension, and prolonged ventilatory support are predictive of septic complications. In addition, the trauma patient has a higher predisposition to pneumonia than nontrauma patients (18% versus 3% incidence of pneumonia, P < .001). Additional risk factors include the degree of nutrition status and the type of medications used during surgery. Immunologic depression may be an additional risk factor. There is mounting evidence that trauma can result in host defense abnormalities. To prevent the significant mortality caused by sepsis, close surveillance must be maintained, nutritional status must be optimal, and liberal use of antibiotics should be discouraged. Their use should be guided by appropriate cultures and sensitivities.
 ...
PMID:Risk factors for infection in the trauma patient. 129 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>