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Update on the diagnosis and treatment of Pneumocystis pneumonia.

Ther Adv Respir Dis

February 2011

Thoracic Diseases Research Unit and the Division of Pulmonary and Critical Care and Internal Medicine, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, MN 55905, USA.

Pneumocystis is an opportunistic fungal pathogen that causes an often-lethal pneumonia in immunocompromised hosts. Although the organism was discovered in the early 1900s, the first cases of Pneumocystis pneumonia in humans were initially recognized in Central Europe after the Second World War in premature and malnourished infants. This unusual lung infection was known as plasma cellular interstitial pneumonitis of the newborn, and was characterized by severe respiratory distress and cyanosis with little or no fever and no pathognomic physical signs.

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Strong LFA-1 and VCAM-1 expression in histological type II of rheumatoid arthritis.

Cell Mol Biol (Noisy-le-grand)

September 2003

Institute of Pathology, University Leipzig, Liebigstrasse 26, 04103 Leipzig, Germany.

With an own histological classification of rheumatoid arthritis (RA) in synovial membranes (SM) of two main types: type I (B-lymphocytic and plasma cellular, local non-destructive, better prognosis); type II (T-lymphocytic, macrophacytic, local destructive, worse prognosis) and type III as a mixed one we examined whether there is a relation between special adhesion molecules and any of this histological types. 32 fresh cryo-conserved RA-SM (type I, II, III; n = 9, 11, 12, respectively) were investigated immunohistochemically using the APAAP method in order to obtain the expression of LFA-1, VCAM-1, CD44 and E-selectin. Positive cells were counted morphometrically within six histological areas: lining layer, subintimal, perivascular, lymphatic follicles, perifollicular and interstitial.

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[Acute interstitial nephritis following piperacillin].

Klin Wochenschr

July 1989

Medizinische Klinik A, Landeshauptstadt Wiesbaden.

A 75-year-old woman developed fever, exanthema and nonoliguric renal failure 16 days after the beginning of Piperacillin treatment. Renal biopsy revealed lympho-plasma-cellular acute interstitial nephritis (AIN). A lymphocyte-transformation-test showed significant stimulation of patient's lymphocytes by Piperacillin.

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A concept of the pathogenesis of tubular interstitial nephritis (TIN) is presented, based on histologic, immunohistologic and electromicroscopic investigations on 61 patients with glomerulonephritis, lupus erythematodes and rheumatoid arthritis. The pathogenic model is a hypersensitivity reaction which leads to alterations in the tubular basement membrane (TBM) and results in changes in the TBM and secondary damage to stroma, vessels and tubular cells. The findings change depending on the stage, reflecting the transition from an acute to a chronic process.

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