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Biomedical subjects

I Kihara

Publications and source records attributed to I Kihara.

At least 91 records · Page 5Linked to original sources

Culture of isolated glomeruli from normal and nephritic rabbits. II. Kinetics of outgrowing cells.

In the autologous phase of nephrotoxic nephritis in the rabbit, many round (Type III) cells appeared in the glomerular outgrowth. They had receptors for Fc and C3 and a pronounced phagocytic capacity for carbon. The number of Type III cells in the glomerular outgrowth from rabbits 8 days after injection of nephrotoxic serum (NTS-8) was higher than that of NTS-10 or -15. In contrast, they were rarely observed in the outgrowth of glomeruli from normal and NTS-3 rabbits. The Type II (fusiform) cell, a type of intrinsic glomerular cell, was also increased earlier and more markedly in NTS-8, -10, and -15 than in normal and NTS-3 rabbits.

Animals↗

Role of divalent cations in binding polymorphonuclear leucocytes to glomeruli with immune complexes.

The binding of polymorphonuclear leucocytes (PMN) to the glomeruli of rats in which glomerulonephritis had been induced by bovine serum albumin, suggested a biological activity of the immune complexes localized in the glomeruli. To evaluate divalent cations or serum factors which may be involved, a two-step method for PMN binding was introduced. PMN were suspended in serum-free media and incubated with cryostat kidney sections pretreated with divalent cation-chelated or fresh sera. An appropriate concentration of Mg++ was found to be essential for maximal PMN binding; however, Ca++ may represent a partial substitute for Mg++. Immune complexes localized in the glomeruli fix and activate the complement system via both the classical and the alternative pathways.

Animals↗

Attachment of polymorphonuclear leukocytes to glomeruli with immune deposits.

A method for quantitative evaluation of a biological activity of immune complexes deposited in glomeruli is described. The activity reflects the activation of complement and is represented by the number of PMN attached to a glomerulus. It is possible to compare data from different individuals or different phases of glomerulonephritis. The complement component concerned is considered to be C3, activated through the classical or alternate pathway.

Animals↗

Accelerated immune complex nephritis due to mesangial overloading in spontaneous hypertensive (SHR) rats.

Immune complex nephritis induced by bovine serum albumin (BSA) and horseradish peroxidase (HRP) was superimposed upon spontaneous hypertensive rats (SHR rats) which were pretreated with polyvinyl alcohol (PVA). PVA accumulated predominantly in the mesangium, and the superimposed nephritis developed more accelerated glomerular damage with marked capillary deposition of immune complexes than control animals which were not pretreated with PVA.

Animals↗

Immunoassay with fluorescein-labelled antigens--device of a method and its clinical application.

A simple, sensitive, highly reproducible method for assay of antibodies using fluorescein-labelled antigens according to the method by Farr is described. We measured titers of anti-BSA antibodies and antigen binding capacity of sera in BSA immunized rabbits by fluorometric assay with fluorescein isothiocyanate (FITC) labelled BSA, and obtained highly reproducible and quantitative results. The resultd times more sensitive than the results from single radial immunodiffusion. FITC-labelled double or single stranded calf thymus DNA was incubated with sera of patients with systemic lupus erythematosus and New Zealand Black mice. Both anti-double and single stranded DNA antibodies were detected in sera of systemic lupus erythematosus, but only anti-single stranded DNA antibodies in sera of New Zealand Black mice.

Animals↗

Bovine serum albumin (BSA) nephritis in rats. I. Experimental model.

Proliferative glomerulonephritis with proteinuria was induced in Wistar rats by bovine serum albumin (BSA). Rats were first immunized with 1 mg or 2.5 mg of BSA and complete Freund's adjuvant (CFA) and eight weeks later 1 mg of BSA were given intravenously six times a week for four weeks. Immunofluorescence revealed granular deposits of IgG, C3, and BSA in the mesangial area with or without deposition of the same components along the capillary wall. Evaluation of the circulating antibody disclosed an apparent correlation between the level of antibody and histological findings. Rats with an intermediate amount of antibody production developed mesangial widening with mesangial immune deposits and no proteinuria. Rats with a low response developed proliferative glomerulonephritis with immune deposits along the capillary wall as well as in the mesangial area and proteinuria.

Animals↗

Participation of blood born cells in rat Masugi nephritis.

Participation of blood born cells in rat Masugi nephritis was investigated with ultrastructural demonstration of peroxidase, in addition to conventional light and electron microscopies. Polymorphonuclear leukocytes appear immediately and transiently after injection of nephrotoxic serum. Hypercellularity in the early stage of the disease is consisted mainly of monocyte-macrophage. Proteinuria and infiltration of few monocytes are persistent through the course up to 124 days and focal sclerosis with hyaline material appears in the later stage.

Animals↗

Fibrous long spacing type collagen fibrils in the glomeruli of experimental amyloidosis in rabbit.

Fibrous long spacing type collagen fibrils were observed in the glomeruli of experimental amyloidosis induced by either injections of casein or prolonged sensitization of Arthus type tissue antigens in the rabbit. These fibrous long spacing type fibrils were admixed with amyloid fibrils which accumulated both in nodular and diffuse deposition, but they were observed also in irregularly thickened capillary basement membranes and mesangial areas, where amyloid did not deposit. The periodicity of these fibrous long spacing fibrils was approximately 1200 , and nine symmetrical intraperiodic bands were obviously discerned within each period.

Amyloid↗