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Transforming growth factor beta 2 inhibits cerebrovascular changes and brain edema formation in the tumor necrosis factor alpha-independent early phase of experimental pneumococcal meningitis.

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Prijava / prijava

Macrophages and granulocytes seem to play a key role in the pathogenesis of bacterial meningitis. Transforming growth factor beta (TGF-beta) leads to macrophage deactivation, as well as to inhibition of cytokine production and of endothelial granulocyte adhesion. We have investigated the influence

Tumor necrosis factor-alpha is expressed by monocytes/macrophages following cardiac microembolization and is antagonized by cyclosporine.

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Prijava / prijava

The time course of expression of TNF-alpha in myocardial wound healing following ischemic injury was investigated in the porcine heart. Microembolization was used to induce focal ischemia and necrosis in hearts of 39 adult pigs. The animals were sacrificed after 3, 6, 12, 24 h, 3 and 7 days, and

Furosemide enhancement of experimental gentamicin nephrotoxicity: comparison of functional and morphological changes with activities of urinary enzymes.

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Prijava / prijava

Dogs were given gentamicin (10 mg/kg) intramuscularly every 8 hr for 10 days. Levels of serum creatinine rose by day 6 (0.91 +/- 0.08 vs. 0.75 +/- 0.02 mg/dl for controls, P less than 0.05) and of blood urea nitrogen by day 8 (24.3 +/- 4.80 vs. 16.1 +/- 0.90 mg/dl for controls, P less than 0.05).

Uncommon cases of immature-type CD56+ natural killer (NK)-cell neoplasms, characterized by expression of myeloid antigen of blastic NK-cell lymphoma.

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Prijava / prijava

Immature-type CD56(+) natural killer (NK)-cell neoplasms are classified as either myeloid/NK-cell precursor acute leukemia or blastic NK-cell lymphoma. We identified two cases of immature-type CD56(+) NK-cell neoplasms that were not categorizable as either of these entities. The first case involved

Immunohistochemical findings in rheumatoid nodules.

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Prijava / prijava

Eighteen nodules from patients with rheumatoid disease were studied histologically and immunohistochemically. A continuum of microscopic changes was observed with varying degrees of fibrinoid necrosis, mononuclear cell infiltration and healing by fibrous scarring. In two cases there was focal

Organ injury and cytokine release caused by peptidoglycan are dependent on the structural integrity of the glycan chain.

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Prijava / prijava

Several studies have implicated a role of peptidoglycan (PepG) as a pathogenicity factor in sepsis and organ injury, in part by initiating the release of inflammatory mediators. We wanted to elucidate the structural requirements of PepG to trigger inflammatory responses and organ injury. Injection

Staphylococcus aureus peptidoglycan is a toll-like receptor 2 activator: a reevaluation.

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Prijava / prijava

Since the ability of peptidoglycan (PGN) to activate Toll-like receptor 2 (TLR2) was recently questioned, we reevaluated activation of TLR2 by PGN. Polymeric soluble or insoluble Staphylococcus aureus PGN, repurified by sodium dodecyl sulfate or phenol extraction, activated TLR2 at 0.1 to 1 or 10

Giant-cell myocarditis in a newborn with congenital herpes simplex virus (HSV) infection: an immunohistochemical study on the origin of the giant cells.

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Prijava / prijava

Giant-cell myocarditis is a rare inflammatory disorder characterized by degeneration and necrosis of myocardial fibers and presence of chronic inflammatory infiltrates associated with multinucleated giant cells forming a granulomatous inflammatory reaction. The etiology of giant-cell myocarditis is

Insulin reverses the protection given by diabetes against gentamicin nephrotoxicity in the rat.

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Prijava / prijava

Rats with untreated diabetes mellitus are protected from gentamicin-induced nephrotoxicity. In order to evaluate the role of hyperglycemia, glycosuria, and polyuria in this phenomenon, miniosmotic pumps filled with insulin were implanted for 15 days in seven female Sprague-Dawley rats with

Digestion of Streptococcus pneumoniae cell walls with its major peptidoglycan hydrolase releases branched stem peptides carrying proinflammatory activity.

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Prijava / prijava

The peptidoglycan of Gram-positive bacteria is known to trigger cytokine release from peripheral blood mononuclear cells (PBMCs). However, it requires 100-1000 times more Gram-positive peptidoglycan than Gram-negative lipopolysaccharide to release the same amounts of cytokines from target cells.

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Herbal & Natural Medicine

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