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)

The repair processes of incised wounds depend, in part, on fibroplasia induced by soluble mediators from monocytic macrophages. Two topical antimicrobials were evaluated, each of which effectively controlled wound sepsis and yet each had widely different effects on fibroplasia and wound strength. Paired-incision dermal wounds on the flanks of guinea pigs were treated with a substance containing reactive chlorine (Alcide) or with a compound that is a mixture of two surfactants. One side of each guinea pig was treated with one of the antimicrobials (treated wounds); the opposite side was treated with isotonic saline solution (control wounds). At 7, 10, and 16 days after surgery, tensiometric measurements of C31G (a surfactant)-treated wounds were 99%, 139%, and 195% of control wound values, respectively. Alcide-treated wounds were 76%, 58%, and 88% of control wounds, respectively. Wounds treated with chlorhexidine had reduced strength at 7 days (73%) and at 10 days (78%), but by 14 days, they were similar to control wounds (94%). The main difference between the wounds was the amount of collagen formation. Alcide-treated wounds incorporated less than 50% of the amount of 14C-proline than did the wounds treated with C31G. However, Alcide-treated wounds epithelialized as rapidly as did control wounds, and had minimal scar formation. Microscopic evaluations indicated greatly reduced inflammatory infiltrates in Alcide-treated wounds, indicating that reduced wound strength may be associated with lack of fibroblast-stimulating activity by monocytes.
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PMID:Controlled wound repair in guinea pigs, using antimicrobials that alter fibroplasia. 394 14

Intravenous infusion of live. E. coli bacteria in cats did not induce microscopic damage to the gastric mucosa within 3 hours. However, if the cats before the induction of bacteremia were given 80 mM HCl and 0.6 ml gallbladder bile/kg b.w. microscopic mucosal damage developed regularly in the corpus-fundus area of the stomach. The gastric mucosal damage was not associated with significant decrease of total gastric blood flow as measured continuously electromagnetically or decreased gastric mucosal blood flow measured early and late during sepsis using radioactively labelled microspheres. Neither was the development of gastric mucosal damage associated with reduced gastric wall collagen concentration nor in RNA, DNA concentrations or RNA/DNA ratio in the gastric mucosa.
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PMID:Acute gastric mucosal ulceration in septic shock. An experimental study on pathogenic mechanisms. 608 89

Fibronectin (FN) is a glycoprotein (disulfite-bonded dimer of 200 to 220 Kd submits) found in a soluble form in blood (concentration 250--500 microg/ml), it can be removed from it by cryoprecipitation and affinity chromatography on gelatin or heparin-agarose. It is also found in an insoluble fibrillar form as a component of connective tissue matrix like collagen, proteoglycans... FN fundamentally forms molecular complexes with collagen, fibrinogen or fibrin, heparin, activated factor XIII, bacteria, cellular membranes..., these various proteins binding with now well known functional "domains" on subunits. Thus FN mediates adhesion of cells to cells as well to biomaterials or tissue, cell migration and chemotactic activity, tissue stromal organization... The transformed cultured cells in presence of oncogen virus loose ability to secrete FN which contribute to their invasive tendency. FN also interacts with hemostatic and fibrinolytic systems, as component of the subendothelium (secreted, like Willbrand factor, by endothelial cells) and of platelet alpha-granules released by stimulated platelets. FN could then provoke platelet spreading on the subendothelium surface after collagen-platelet adhesion, triggered by Willebrand factor, has happened. FN is a part of the fibrinous clot. It participates in anchorage of the clot to subendothelium and mediates its colonisation by fibroblasts, first step to wound reparation. Lastly FN probably has an important role in organism defence. It acts as a non-immunological opsonin, promoting phagocytosis by RES macrophages of bacteria, cellular or fibrin fragments, immune complexes... present in blood. Plasmatic FN concentration is strongly decreased in several ill patients following major trauma, extensive burns, shock, sepsis, with or not evidence of DIVC, of respiratory distress... SABA and various other authors have obtained good results after injections of FN (as cryoprecipitates or concentrated fractions). It is yet necessary to confirm therapeutic role of FN.
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PMID:[Plasma fibronectin]. 641

Circulating immune complexes were studied using 3.5% polyethyleneglycol precipitation in 312 children with various diseases whose ages ranged from 1 month to 14 years. One hundred and one patients (32.6%) were positive and the groups with the highest percentage were those with viral hepatitis (90%), sepsis (80.7%), collagen diseases (76.4%) and Schonlein-Henoch purpura (57.1%). We found immune complexes less frequently in idiopathic thrombocytopenic purpura than in published series of adult cases, possibly due to the fact that the diseases in children is due to a different pathogenetic mechanism. The composition of the immune complexes was tested by 1% agarose immunodiffusion against a panel of antisera. IgG and IgM were found most frequently, and IgA was very uncommon except in some cases of hepatitis. C4 was the most frequently found complement component, followed by C3. Important differences between the various diseases studied were noted. Our results are very similar to those previously published by other authors. Whereas serum autoantibodies and autoimmune diseases are less common in children than in adults, circulating immune complexes seem to have a similar frequency in children to that already reported for adults. It is difficult to assess the significance of circulating immune complexes. They might be (a) a mere "marker" of no pathogenic significance (b) a mechanism of tissue damage by intravascular deposition, or (c) they might interfere with the cell membrane receptors of macrophages, producing a defect in phagocytosis. However, we were unable to demonstrate an increased number of infections in these patients.
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PMID:[Incidence of circulating immune complexes in pediatric diseases. Comparative study with adults]. 645 Nov 57

A new inherited neuromuscular disease was identified in 4 patients (1 male, 3 females), offspring of consanguineous marriages, belonging to the same kindred. The proband was a 24-year-old female with history of ptosis and ophthalmoplegia since childhood and progressive intestinal pseudo-obstruction for the last 4 years of her life. A sural nerve biopsy showed axonal and demyelinating neuropathy. Muscle biopsies of pectoral and gastrocnemius revealed myopathic alterations with marked variation in muscle fiber size, atrophy of both fiber types and normal mitochondria. An upper gastrointestinal study showed barium in the stomach after 8 h and jejunal diverticula. Tests for absorption of fat, protein, carbohydrate, folic acid and vitamin B12 were normal. Serum levels of vitamin A and lipoproteins were also normal. The patient underwent partial gastrectomy and gastrojejunostomy. Postoperatively, she developed severe pancreatitis, sepsis, peritonitis and expired. Tissue samples from the proband and from her brother, revealed normal mucosa, but degeneration of smooth muscle of the stomach and small intestine. The myenteric plexus and vagus nerves were normal. The biochemical studies of contractile proteins (myosin, actin, tropomyosin) in the fresh and cultured smooth muscle cells of the proband obtained at the time of gastrectomy showed a 50-75% decrease in the synthesis of different contractile proteins. Turnover of contractile proteins and synthesis and turnover of collagen showed normal values. The reduction in synthesis of contractile proteins may account for the weak peristalsis and be a factor in the pathogenesis of the intestinal pseudo-obstruction.
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PMID:Inherited ophthalmoplegia with intestinal pseudo-obstruction. 668 98

Delayed hypersensitivity skin testing was performed in 129 critically ill patients. Six intradermal antigens were used: tuberculin, candidin, varidase, epidermophytin, trichophytin and CCB (a polyvalent microbial vaccine from the Pasteur Institute). The response was judged as positive when one test or more were positive. Patients were devided in four groups: group A (40 cases): non-infected patients, a priori without immunodeficiency; group B (14 cases); suspected of immunodeficiency (cancers, hemopathies, collagen diseases receiving corticosteroids); group C (24 cases): decompensated chronic respiratory insufficienceis; group D (50 cases): overwhelming sepsis (septicaemias, septic acute respiratory distress syndromes, thoracic empyemas, purulent meningitis, peritonitis, mediastinitis). A significant diminution of delayed hypersensitivity was observed in groups B, C and D. No relation was found between delayed hypertensitivity and prognosis in groups C and D.
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PMID:[Cell-mediated immunity study by skin testing in 129 critically ill patients (author's transl)]. 698 93

Hyperbilirubinemia in the newborn results not only in visible yellow discoloration of the skin but, in high concentration, may cause bilirubin encephalopathy. Such damage to the central nervous system may be subtle and not apparent for several years, as with visual-motor perceptive defects; or it may cause severe neurologic damage (Kernicterus)--even death. Sick and immature infants are the most vulnerable to bilirubin toxicity. Although this condition affects nearly half of all newborns to some degree, only about 10% require treatment. Two methods of treatment are really effective in correcting hyperbilirubinemia, exchange blood transfusions, and/or phototherapy with light radiation in the blue part of the visible spectrum. If the rate of production of bilirubin is excessive or an infant's capacity to conjugate and excrete the pigment is deficient, bilirubin will accumulate in plasma, and will be taken up by other lipid-containing tissues, collagen, and (unless firmly bound to albumin) brain tissue. Many factors combine to raise plasma levels of bilirubin to toxic levels; for example, acidosis, sepsis, hypoxia, hemolysis, hypoalbuminemia, and certain competitive albumin binders. Bilirubin is photolabile in vivo, and if the whole body is irradiated with visible light in the absorption band (450-490 nm) of bilirubin, the pigment will undergo photocatabolism. Under phototherapy bilirubin undergoes photoisomerization at the meso double-bond to conformations less lipophyllic. It is now known that the major photo products of bilirubin IX-alpha are an unresolved mixture of its E, Z and Z, E isomers, easily excreted by the liver. Thus, phototherapy will reduce the accumulation of bilirubin in skin and other tissues and in circulating plasma.
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PMID:Molecular basis of hyperbilirubinemia and phototherapy. 725 51

Previously asymptomatic aneurysms in ten patients ruptured within 36 days (mean, ten days) of a prior laparotomy. The laparotomy and associated intra-abdominal disease may have precipitated rupture of the unresected abdominal aneurysms by reduction of the collagen content of the aneurysm wall, thus making the wall weaker. The scar-like collagen fibers of an aneurysm wall provide the strength that permits the wall to resist rupture. There is a dynamic equilibrium between synthesis and lysis of this collagen. Lysis of collagen is enhanced by injury, such as laparotomy, and by nutritional depletion and local inflammation. Collagen lysis is greatest in the area adjacent to the injury, but also occurs at remote sites as well. Lysis is greatest during the first postoperative week, after which, in the absence of sepsis or starvation, synthesis exceeds lysis and the equilibrium is restored. A thin aneurysm wall may be weakened enough during this period of negative collagen balance to allow rupture.
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PMID:Laparotomy as a precipitating factor in the rupture of intra-abdominal aneurysms. 735 84

Recent studies in our laboratories have shown how microwave (MW) irradiation can accelerate a number of tissue-processing techniques, especially staining, to aid in the preparation of single specimens on glass microscope slides or coverslips for examination by light microscopy (and electron microscopy, if required) for diagnostic purposes. Techniques have been developed, which give permanently stained preparations, that can be studied initially by light microscopy, their areas of interest mapped, and computer-automated image analysis performed to obtain quantitative information. This is readily performed after MW-accelerated staining with silver methenamine by the Giammara-Hanker PATS or PATS-TS reaction. This variation of the PAS reaction gives excellent markers for specific infectious agents such as lipopolysaccharides for gram-negative bacteria or mannans for fungi. It is also an excellent stain for glycogen and basement membranes and an excellent marker for type III collagen or reticulin in the endoneurium or perineurium of peripheral nerve or in the capillary walls. Our improved MW-accelerated Feulgen reaction with silver methenamine for nuclear DNA is useful to show the nuclei of bacteria and fungi as well as of cells they are infecting. Improved coating and penetration of tissue surfaces by thiocarbohydrazide bridging of ruthenium red, applied under MW-acceleration, render biologic specimens sufficiently conductive for SEM so that sputter coating with gold is unnecessary. The specimens treated with these highly visible electron-opaque stains can be screened with the light microscope after mounting in polyethylene glycol (PEG) and the structures or areas selected for EM study are mapped with a Micro-Locator slide. After removal of the water soluble PEG the specimens are remounted in the usual EM media for scanning electron microscopy (SEM) or transmission electron microscopy (TEM) study of the mapped areas. By comparing duplicate smears from areas of infection, such as two coverslips of buffy coat smears of blood from a patient with septicemia, the microorganisms responsible can occasionally be classified for antimicrobial therapy long before culture results are available; gram-negative bacteria are positive with the Giammara-Hanker PATS-TS stain, and gram-positive bacteria are positive with the SIGMA HT40 Gram stain. The gram-positive as well as gram-negative bacteria are both initially stained by the crystal violet component of the Gram stain. The crystal violet stain is readily removed from the gram-negative (but not the gram-positive) bacteria when the specimens are rinsed with alcohol/acetone. If this rinse step is omitted, the crystal violet remains attached to both gram-negative and gram-positive bacteria. It can then be rendered insoluble, electron-opaque, and conductive by treatment with silver methenamine solution under MW-irradiation. This metallized crystal violet is a more effective silver stain than the PATS-TS stain for a number of gram-negative spirochetes such as Treponema pallidum, the microbe that causes syphilis.
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PMID:Microwave-accelerated cytochemical stains for the image analysis and the electron microscopic examination of light microscopy diagnostic slides. 750 80

Inflammatory myofibroblastic tumor (IMT) or inflammatory pseudotumor is a spindle cell proliferation of disputed nosology, with a distinctive fibroinflammatory and even pseudosarcomatous appearance. Although the lung is the best known and most common site, inflammatory myofibroblastic tumor occurs in diverse extrapulmonary locations. We report our experience with 84 cases occurring in the soft tissues and viscera of 48 female patients and 36 male patients between the ages of 3 months and 46 years (mean, 9.7 years; median, 9 years). A mass, fever, weight loss, pain, and site-specific symptoms were the presenting complaints. Laboratory abnormalities included anemia, thrombocytosis, polyclonal hypergammaglobulinemia, and elevated erythrocyte sedimentation rate. Sites of involvement included abdomen, retroperitoneum, or pelvis (61 cases); head and neck, including upper respiratory tract (12 cases); trunk (8 cases); and extremities (3 cases). The lesions ranged in size from 1 to 17 cm (mean, 6.4; median, 6.0). Excision was performed in 69 cases. Eight had biopsy only. Five patients received chemotherapy or radiation in addition to undergoing biopsy or resection as initial treatment. Sixteen patients had multinodular masses involving one region. Clinical follow-up in 53 cases revealed that 44 patients were alive with no evidence of disease, four were alive with IMT, and five were dead. Thirteen patients had one or more recurrences at intervals of 1-24 months (mean, 6 months; median, 10 months). No distant metastases were documented. The five patients who died had complications either due to the location of the lesion (heart, peritoneum, retroperitoneum, or mesentery) or related to treatment (lymphoproliferative disorder following hepatic transplantation; sepsis following wound infection). The abdominal masses were the largest. All tumors were firm and white with infiltrative borders and focal myxoid change. Three basic histologic patterns were recognized: (a) myxoid, vascular, and inflammatory areas resembling nodular fasciitis; (b) compact spindle cells with intermingled inflammatory cells (lymphocytes, plasma cells, and eosinophils) resembling fibrous histiocytoma; and (c) dense plate-like collagen resembling a desmoid or scar. Immunohistochemistry demonstrated positivity for vimentin, muscle-specific actin, smooth muscle actin, and cytokeratin consistent with myofibroblasts. Based on this series, inflammatory myofibroblastic tumor is a benign, nonmetastasizing proliferation of myofibroblasts with a potential for recurrence and persistent local growth, similar in some respects to the fibromatoses.
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PMID:Extrapulmonary inflammatory myofibroblastic tumor (inflammatory pseudotumor). A clinicopathologic and immunohistochemical study of 84 cases. 866 41


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