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

Several studies demonstrated that previous heat shock treatment caused expression of heat shock proteins (HSPs) and reduced organ dysfunction and mortality in experimentally induced severe sepsis. However, the protective mechanism on platelet function remains unclear. The aim of this study was to investigate the effect of heat shock treatment on platelet aggregation ex vivo in endotoxin-induced rats with sepsis. Rats of the heated group were heated by whole-body hyperthermia 18 h before lipopolysaccharide (LPS) injection. Blood samples were obtained from the carotid artery 90 min after LPS injection. Platelet aggregation ability was measured by aggregometer. Results revealed that platelet aggregation ex vivo was significantly inhibited in LPS-induced rats in a manner of dose dependence. Previous heat shock treatment caused overexpression of HSPs and significantly attenuated the LPS-induced platelet hyporesponsiveness. This attenuation disappeared in accordance with absence of HSP72 at 7 days after heat shock treatment. Aggregation of normal platelets was also inhibited by incubating with plasma obtained from endotoxemic rats but not from preheated endotoxemic rats. Furthermore, no significant hyporesponsiveness was found in endotoxemic platelets in addition to preheated endotoxemic plasma. The addition of H2O2 scavenger catalase diminished the platelet hyporesponsiveness significantly only in nonheated endotoxemic rats. Moreover, the plasma nitrite and nitrate levels were significantly attenuated in preheated endotoxemic rats. These results revealed that previous heat shock treatment might attenuate LPS-induced hyporesponsiveness of platelets by changing the plasma components possibly through altering H2O2 and nitric oxide concentrations.
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PMID:Previous heat shock treatment attenuates lipopolysaccharide-induced hyporesponsiveness of platelets in rats. 1613 63

Chronic granulomatous disease (CGD) is a rare immunodeficiency disorder. The inability of phagocytic cells to kill catalase-positive organisms, such as Staphylococcus and Aspergillus species, causes recurrent infections, persistent inflammation, and granuloma formation. The imaging findings in nine cases of CGD were studied. Recurrent pulmonary infection was the most common abnormality (seven cases). Its complications included pulmonary abscesses, bronchiectasis, mediastinal abscesses, osteomyelitis, sepsis, and brain abscesses. Suppurative cervical adenitis was the second most common abnormality (four cases) and was also the presenting abnormality in the youngest patient (aged 31 days). Abdominal manifestations included hepatosplenomegaly, recurrent hepatic and splenic abscesses, necrotic mesenteric adenopathy, and gastric outlet obstruction. Osteomyelitis occurred in two cases secondary to hematogenous spread or spread of contiguous infection from the lung. Persistent infections led to formation of chronic inflammatory masses and granulomas in five cases. With improvements in therapy, the prognosis of CGD patients has improved and the general consensus is that most patients will survive into adulthood. Hence, radiologists are more likely to encounter the complications of CGD and should familiarize themselves with the spectrum of imaging findings.
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PMID:Imaging of chronic granulomatous disease in children. 1616 Jan 5

The antioxidant N-acetylcysteine (NAC) prevented sepsis-induced diaphragmatic dysfunction. As an indirect antioxidant NAC was shown to induce superoxide dismutase (SOD) activity in immune cells from endotoxaemic mice. The aim of this study was to assess whether NAC acts as an indirect antioxidant by inducing manganese (Mn)-SOD activity in the diaphragms of endotoxaemic rats, while preventing muscle dysfunction. A controlled study was conducted, in which protein carbonylation, Mn-SOD, catalase, and 3-nitrotyrosine immunoreactivity were detected using immunoblotting and immunohistochemistry in rat diaphragms. Six groups were studied for 24 h after a saline (control) or lipopolysaccharide (LPS; 20 mg.kg-1) i.p. injection in the absence and presence of NAC pre-treatment (either 1.5 or 3 mmol.kg(-1).24 h-1 for 7 days, oral administration). Diaphragm mitochondrial Mn-SOD activity and respiratory muscle function were also determined. Within 24 h, LPS induced maximal inspiratory pressure reduction, increasing diaphragmatic protein carbonylation and nitration. Pre-treatment with 3 mmol.kg-1 NAC clearly increased muscle Mn-SOD protein content and activity in both LPS- and saline-injected animals, while reducing protein carbonylation and nitration, and partially preventing the LPS-induced respiratory muscle dysfunction. Data produced from this study indicate that high doses of N-acetylcysteine induces manganese superoxide dismutase, as well as preserves its activity, possibly by preventing nitration of critical tyrosine residues of the enzyme.
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PMID:N-acetylcysteine increases manganese superoxide dismutase activity in septic rat diaphragms. 1631 32

Streptococcus agalactiae can cause severe pneumonia, sepsis and meningitis in neonates and remains one of the most prevalent causes of invasive neonatal infections. Maternal transmission of S. agalactiae during delivery can be prevented by prenatal screening and peripartal antibiotic prophylaxis. Implementation of CDC guidelines for group B streptococci (GBS) disease prevention resulted in a significant decline of invasive neonatal S. agalactiae infections in the USA. Similar national guidelines were issued in 2000 for Germany. However, the epidemiology of S. agalactiae colonization in Germany has not been investigated for more than 15 years and the impact these guidelines will have is therefore unknown. To assess colonization rates in Germany, we cultured vaginal and rectal swabs for S. agalactiae from pregnant and non-pregnant adult patients in the region of Aachen and Munich. Swabs were cultivated in selective broth medium for 24h and subsequently plated on blood agar plates according to the CDC recommendations. Colonies negative for catalase and pyrrolidonyl aminopeptidase were further differentiated by the CAMP test and a DNA probe specific for S. agalactiae. Rectal or vaginal colonization of S. agalactiae was found in 34 (16%) of 210 pregnant patients and in 41 (16%) of 250 non-pregnant women. S. agalactiae was found only in rectal swabs in 4% of pregnant and non-pregnant patients. For further characterization of the strains capsular serotypes and major surface protein antigens were determined by Ouchterlony immunodiffusion and PCR. Among the 75 different patient isolates serotype III was the most prevalent with 21 (28%) isolates, followed by 16 (21%) isolates of serotype II, 13 (17%) isolates of serotype Ia, 12 (16%) of serotype V, 11 (15%) of serotype Ib and only 2 (3%) isolates of serotype IV. The vast majority of all strains harbored genes for the major surface protein antigens, the alpha-C-protein or alpha-C-protein like antigens like Alp2-4, epsilon and Rib. These data show that S. agalactiae colonization is common in Germany and strict adherence to the guidelines for the preventions of GBS disease will result in peripartal antibiotic prophylaxis in up to 20% of all deliveries.
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PMID:Epidemiology of Streptococcus agalactiae colonization in Germany. 1636 Nov 13

This study investigates the association of oxidative stress with the function of the phrenic nerve and inquires whether N-acetylcysteine (NAC) may counteract the possible detrimental effects. Thirty rats were divided into three groups: sham, cecal ligation and puncture (CLP), and CLP plus NAC treatment. Sepsis was produced by the CLP procedure. NAC was administered at 70 mg/day for 7 days. Electrophysiology was evaluated by the needle electromyography of the diaphragm and phrenic nerve conduction study. Oxidative stress was evaluated by malondialdehyde (MDA), nitrite/nitrate (NN), and reduced-glutathione (ReGSH) levels and myeloperoxidase (MPO) and catalase (CAT) activities in the phrenic nerve. In the CLP group, ReGSH and CAT were decreased (P = 0.0001, P = 0.07, respectively); and MDA, MPO, and NN were increased (P = 0.02, P = 0.0001, P = 0.043, respectively), compared with the sham group. NAC administration increased the ReGSH (P = 0.036) and decreased the MDA, MPO, and NN (P = 0.008, P = 0.01, P = 0.032, respectively), compared with the CLP group. In the CLP group, electrophysiology revealed reductions in the number of motor unit action potentials (P = 0.0001) and prolongations in the latency of the compound nerve action potential (P = 0.0001), indicating phrenic nerve neuropathy. NAC administration significantly ameliorated these electrophysiological alterations (P = 0.011, P = 0.0001, respectively), compared with the CLP group. The present results showed that intraabdominal sepsis is closely associated with phrenic nerve neuropathy. In addition, NAC administration protects the rats against the detrimental events of sepsis.
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PMID:N-acetylcysteine protects the rats against phrenic nerve dysfunction in sepsis. 1636 83

Pulmonary oxidant stress plays an important pathogenetic role in disease conditions including acute lung injury/adult respiratory distress syndrome (ALI/ARDS), hyperoxia, ischemia-reperfusion, sepsis, radiation injury, lung transplantation, COPD, and inflammation. Reactive oxygen species (ROS), released from activated macrophages and leukocytes or formed in the pulmonary epithelial and endothelial cells, damage the lungs and initiate cascades of pro-inflammatory reactions propagating pulmonary and systemic stress. Diverse molecules including small organic compounds (e.g. gluthatione, tocopherol (vitamin E), flavonoids) serve as natural antioxidants that reduce oxidized cellular components, decompose ROS and detoxify toxic oxidation products. Antioxidant enzymes can either facilitate these antioxidant reactions (e.g. peroxidases using glutathione as a reducing agent) or directly decompose ROS (e.g. superoxide dismutases [SOD] and catalase). Many antioxidant agents are being tested for treatment of pulmonary oxidant stress. The administration of small antioxidants via the oral, intratracheal and vascular routes for the treatment of short- and long-term oxidant stress showed rather modest protective effects in animal and human studies. Intratracheal and intravascular administration of antioxidant enzymes are being currently tested for the treatment of acute oxidant stress. For example, intratracheal administration of recombinant human SOD is protective in premature infants exposed to hyperoxia. However, animal and human studies show that more effective delivery of drugs to cells experiencing oxidant stress is needed to improve protection. Diverse delivery systems for antioxidants including liposomes, chemical modifications (e.g. attachment of masking pegylated [PEG]-groups) and coupling to affinity carriers (e.g. antibodies against cellular adhesion molecules) are being employed and currently tested, mostly in animal and, to a limited extent, in humans, for the treatment of oxidant stress. Further studies are needed, however, in order to develop and establish effective applications of pulmonary antioxidant interventions useful in clinical practice. Although beyond the scope of this review, antioxidant gene therapies may eventually provide a strategy for the management of subacute and chronic pulmonary oxidant stress.
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PMID:Antioxidant strategies in respiratory medicine. 1640 15

Most bacteria require iron for growth. However, as it may not be directly available under aerobic conditions, bacteria may use iron-sequestering molecules, such as bacterially encoded siderophores, or heme, which is the major iron source in the animal host. Bacteria may also assimilate heme for purposes other than as an iron source. Once internalised, heme can activate, for example, a heme-dependent catalase and a cytochrome oxidase. In bacterial pathogen Streptococcus agalactiae, heme, in association with exogenous menaquinone, activates a respiratory chain. Respiration has radical effects on carbon metabolism. GBS respiration-grown cells display improved survival in an aerobic environment and greater virulence in a murine septicemia model. GBS might benefit from its ecological niches to capture heme and menaquinone, i.e., from other bacteria when it colonizes host mucosa, or from blood-containing organs during septicemia.
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PMID:Roles of environmental heme, and menaquinone, in streptococcus agalactiae. 1671 5

Although comprising less than 0.01% of the normal human gastrointestinal microbiota, Bilophila wadsworthia is the third most common anaerobe recovered from clinical material obtained from patients with perforated and gangrenous appendicitis. Since its discovery in 1988, B. wadsworthia has been recovered from clinical specimens associated with a variety of infections, including sepsis, liver abscesses, cholecystitis, Fournier's gangrene, soft tissue abscesses, empyema, osteomyelitis, Bartholinitis, and hidradenitis suppurativa. In addition, it has been found in the saliva and vaginal fluids of asymptomatic adults and even in the periodontal pockets of dogs. The organism is a saccharolytic, fastidious, and is easily recognized by its strong catalase reaction with 15% H2O2, production of hydrogen sulfide, and growth stimulation by bile (oxgall) and pyruvate. Approximately 75% of strains are urease positive. When grown on pyruvate-containing media, > 85% of strains demonstrate beta-lactamase production. Ribosomal RNA-based phylogenetic studies show Bilophila to be a homogeneous species, most closely related to Desulfovibrio species. Both adherence to human cells and endotoxin have been observed, and preliminary work suggests that environmental iron has a role in expression of outer membrane proteins. Penicillin-binding proteins appear to mediate the organism's susceptibility to at least some beta-lactam agents, which induce spheroplast formation that results in a haze of growth on agar dilution susceptibility test plates which is difficult to interpret. Bilophilastrains are inhibited in vitro by most antibiotics.
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PMID:Bilophila wadsworthia: a unique Gram-negative anaerobic rod. 1688 67

The application of a copper IUD can perforate completely the uterus and involve adjacent organs such as the bladder, small bowel, colon, rectum or appendix. Once the diagnosis is established, complete extraction must follow. We present a case report of a 33 year-old patient in which a copper IUD was placed in a medical office, three months after a third cesarean, without history of sepsis. Ninety days after placement, the patient complained of menstrual irregularities (opsomenhorrea) without any other symptoms. On physical examination with speculum, the IUD's guide strings were not visible; a transvaginal USG was performed without visualization of the IUD in the uterine cavity. An abdominal CAT scan showed the presence of the IUD outside the uterus. Hysteroscopy-laparoscopy was performed with transoperatory fluoroscopy, which revealed the copper IUD inside the yeyunum, a complete extraction followed with entero-entero anastomosis. This case will show that IUD placement is not innocuous and that adjacent organ damage must always be considered and resolved immediately.
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PMID:[Uterine and jejunum perforation due to intrauterine device. A report of a case and literature review]. 1703 4

Four bacterial isolates were recovered from the blood cultures of four patients, two of whom were from Hong Kong and two of whom were from Canada. The two Hong Kong strains were isolated from a 48-year-old man with intestinal obstruction and secondary sepsis (strain HKU16T) and from a 39-year-old man with acute appendicitis (strain HKU17), while the two Canadian strains were isolated from a 74-year-old man with biliary sepsis (strain CA1) and from a 66-year-old woman with metastatic carcinoma and sepsis (strain CA2). While the first three patients survived, the last patient died 2 weeks after the episode of bacteremia. All four isolates are strictly anaerobic, nonsporulating, gram-positive coccobacilli that were unidentified by conventional phenotypic tests and commercial identification systems. They grow on sheep blood agar as nonhemolytic pinpoint colonies after 48 h of incubation at 37 degrees C in an anaerobic environment. All are catalase positive and motile, with flagella. They produce acid from arabinose, glucose, mannose, and xylose. They do not produce indole or reduce nitrate. They are sensitive to penicillin, vancomycin, and metronidazole but resistant to cefotaxime. 16S rRNA gene sequence analysis showed 16.0%, 16.8%, and 21.0% base differences from Clostridium propionicum, Clostridium neopropionicum, and Atopobium minutum, respectively. The G+C content of strain HKU16T is 40.2% +/- 2.2%. Based on their phylogenetic affiliation, unique G+C content, and phenotypic characteristics, we propose a new genus and species, Catabacter hongkongensis gen. nov., sp. nov., to describe the bacterium, for which HKU16 is the type strain, and suggest that it be assigned to a new family, Catabacteriaceae. The gastrointestinal tract was probably the source of the bacterium for at least three of the four patients. The isolation of a catalase-positive, motile, nonsporulating, anaerobic gram-positive bacillus in clinical laboratories should raise the possibility of C. hongkongensis. Further studies should be performed to ascertain the epidemiology and other disease associations of this bacterium.
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PMID:Catabacter hongkongensis gen. nov., sp. nov., isolated from blood cultures of patients from Hong Kong and Canada. 1712 22


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