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Y Koda

Publications and source records attributed to Y Koda.

At least 91 records · Page 5Linked to original sources
PubMed1991

Early mesangiolysis and monocyte influx observed in diabetic glomerulosclerosis: relation to nodule formation.

Lytic changes to the mesangium and subendothelial area in diabetic glomerulosclerosis were studied by electron microscopy with an emphasis on the mechanism of nodule formation. Renal biopsy specimens were obtained from 30 diabetics (11 males, 19 females; 27 NIDDM, 3 IDDM; mean age, 52.2 years) with renal involvement. Evaluations were made of the glomerular lesions, particularly the ultra-structural findings contributing to nodule formation, mainly by electron microscopy. Varying degrees of lytic change, such as a loose and edematous mesangial matrix, widening of the subendothelial space, followed by endothelial detachment, and destruction of anchor points, were observed in close association with progression of the diffuse lesions. Plasma proteins were found to infiltrate into the widened subendothelial space. Mesangial cells also protruded into the same space and encroached around the whole capillary wall. The interposed mesangial cells were occasionally separated from the basement membrane. Monocytes identified from their ultrastructure were frequently present noticed in the lytic areas, suggesting a reaction to lytic changes. These processes may occur repeatedly with direct expansion of the mesangial matrix, subsequently revealing a nodular appearance.

Adult↗
PubMed1990

Purification and characterization of calmodulin-dependent multifunctional protein kinase from smooth muscle: isolation of caldesmon kinase.

Previously, it was reported that smooth muscle caldesmon is a protein kinase and is autophosphorylated [Scott-Woo, G.C., & Walsh, M.P. (1988) Biochem. J. 252, 463-472]. We separated a Ca2+/calmodulin-dependent protein kinase from caldesmon in the presence of 15 mM MgCl2. The Ca2+/calmodulin-dependent caldesmon kinase was purified by using a series of liquid chromatography steps and was characterized. The subunit molecular weight (MW) of the kinase was 56K by SDS gel electrophoresis and was autophosphorylated. After the autophosphorylation, the kinase became active even in the absence of Ca2+/calmodulin. The substrate specificity of caldesmon kinase was similar to the rat brain calmodulin-dependent multifunctional protein kinase II (CaM PK-II) and phosphorylated brain synapsin and smooth muscle 20-kDa myosin light chain. The purified kinase bound to caldesmon, and the binding was abolished in the presence of high MgCl2. Enzymological parameters were measured for smooth muscle caldesmon kinase, and these were KCaM = 32 nM, KATP = 12 microM, Kcaldesmon = 4.9 microM, and KMg2+ = 1.1 mM. Optimum pH was 7.5-9.5. The observed properties were similar to brain CaM PK-II, and, therefore, it was concluded that smooth muscle caldesmon kinase is the isozyme of CaM PK-II in smooth muscle.

Animals↗
PubMed1990

Protein kinase C subtypes in tissues derived from neural crest.

Subtypes of protein kinase C were determined in tissues derived from neural crest. The bovine adrenal medulla and rat superior cervical ganglia contained type III enzyme as the major subtype with a small amount of type II enzyme. In PC12 cells, treated with or without nerve growth factor, type III was the major subtype but a minor peak which is distinct from types II and III was observed. These results show that the type III enzyme is prevalent in various differentiation stages of neural crest and suggest that the enzyme relevant to the regulation of catecholamine synthesis and release in these cells is type III.

Adrenal Gland Neoplasms↗
PubMed1990

Two types of glomerular lesion in non-amyloid immunoglobulin deposition disease: a case report of IgD-lambda myeloma.

A 60-year-old man with nephrotic syndrome and renal failure was found to have a IgD-lambda myeloma. Autopsy revealed advanced nodular glomerulopathy with codeposition of delta heavy and lambda light chains. Glomerular nodules were of two types: One (type I lesion) is caused by nodular expansion of the mesangium by deposition of abnormal immunoglobulin. The second type (type II lesion) is peripherally lamellated and is ascribed to repeated local mesangiolysis superimposed upon type I lesion. These type I and type II lesions correspond to the two types of nodules in diabetic glomerulosclerosis.

Diabetic Nephropathies↗
PubMed1989

Veratridine-induced phosphorylation and activation of tyrosine hydroxylase, and synthesis of catecholamines in cultured bovine adrenal medullary cells.

The mechanism of the synthesis of catecholamines by veratridine was studied in cultured bovine adrenal medullary cells. (1) Veratridine increased the phosphorylation and activity of tyrosine hydroxylase as well as the synthesis of [14C]catecholamines from [14C]tyrosine, all of which were inhibited by tetrodotoxin. Veratridine-induced activation of tyrosine hydroxylase and synthesis of [14C]catecholamines were reduced in 20 mmol/l extracellular Na+ or in Ca2+-free medium. (2) 12-O-Tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, increased the synthesis of [14C]catecholamines. In the presence of TPA, veratridine did not produce any additional increase in [14C]catecholamine synthesis. In protein kinase C-deficient cells which were prepared by pretreatment with 1 mumol/l TPA for 24 h, TPA failed to increase [14C]catecholamine synthesis and veratridine-induced [14C]catecholamine synthesis was suppressed by 50%. (3) Polymyxin B, an inhibitor of protein kinase C and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), an inhibitor of calmodulin, inhibited veratridine-stimulated synthesis of [14C]catecholamines as well as veratridine-induced influx of 22Na+ and 45Ca2+ with similar potencies. (4) In digitonin-permeabilized cells, polymyxin B attenuated the activation of tyrosine hydroxylase caused by Ca2+. These results suggest that veratridine-induced synthesis of catecholamines and activation of tyrosine hydroxylase were mediated by Ca2+-dependent phosphorylation of this enzyme, and protein kinase C may be responsible, at least in part, for this process.

Adrenal Medulla↗
PubMed1989

cis-unsaturated fatty acids stimulate catecholamine secretion, tyrosine hydroxylase and protein kinase C in adrenal medullary cells.

In digitonin-permeabilized bovine adrenal medullary cells, arachidonic acid and oleic acid, the cis-unsaturated fatty acids, enhanced Ca2+-induced secretion of catecholamines, whereas elaidic acid, a trans-unsaturated fatty acid and stearic acid, a saturated fatty acid, had no effect. Indomethacin, an inhibitor of cyclooxygenase and nordihydroguaiaretic acid, an inhibitor of lipoxygenase, failed to inhibit the stimulatory effect of arachidonic acid. Stimulation of catecholamine secretion by arachidonic acid was abolished by the removal of adenosine 5'-triphosphate and Mg2+ from the incubation medium. Pretreatment of the cells with phorbol 12-myristate 13-acetate, an activator of protein kinase C, enhanced Ca2+-induced catecholamine secretion. In cells pretreated with phorbol 12-myristate 13-acetate, the stimulatory effect of arachidonic acid on Ca2+-induced catecholamine secretion was greatly reduced. In digitonin-permeabilized cells, arachidonic acid and oleic acid enhanced Ca2+-induced activation of tyrosine hydroxylase in the presence of adenosine 5'-triphosphate and Mg2+, whereas elaidic acid and stearic acid did not activate the enzyme. In a soluble fraction of adrenal medullary cells, 32P incorporation to histone by protein kinase C was increased by arachidonic acid and oleic acid, but not by elaidic acid and stearic acid. These results suggest that cis-unsaturated fatty acids modulate Ca2+-induced catecholamine secretion and tyrosine hydroxylase activity by activation of protein kinase C in adrenal medullary cells.

Adenosine Triphosphate↗
PubMed1988

Gastrointestinal involvement of dialysis-related amyloidosis.

Beta-2 microglobulin-related amyloids were found in gastric biopsy specimens from 3 of 11 patients who had been on hemodialysis more than 10 years and examined. The deposits were found not only in arteriolar walls but also in lamina propria and muscle tissue. In another patient who was on hemodialysis for 8 years, beta 2-microglobulin-related amyloids were found in the muscle layer of operatively resected colon. These four patients also had the same substance deposited in the osteoarticular system. The results suggest the systemic involvement of beta 2-microglobulin-related amyloidosis in patients on long-term hemodialysis.

Amyloid↗
PubMed1987

Activation of tyrosine hydroxylase by micromolar concentrations of calcium in digitonin-permeabilized adrenal medullary cells.

In digitonin-permeabilized bovine adrenal medullary cells, Ca2+ (0.1-1.0 microM) caused an activation of tyrosine hydroxylase which was dependent on the presence of ATP. This Ca2+-induced activation of the enzyme was observed even in the presence of optimal concentration of either cyclic AMP or 12-O-tetradecanoylphorbol-13-acetate (TPA) which by itself increased the enzyme activity. Calmodulin inhibitors, trifluoperazine (TFP) and N-(6-aminohexyl)-5-chloro-1-naphtalenesulfonamide (W-7), had little effect on the Ca2+-evoked activation of enzyme. These results suggest that micromolar concentrations of Ca2+ activate the activity of tyrosine hydroxylase probably through a Ca2+-dependent phosphorylation in digitonin-permeabilized adrenal medullary cells although the protein kinase(s) responsible for it still remains to be determined.

Adenosine Triphosphate↗
PubMed1986

Sclerotic lesions in the glomeruli of Buffalo/Mna rats.

Spontaneously developing focal and segmental glomerulosclerosis (FGS) in Buffalo/Mna rats was studied. There were no differences in the occurrence of the disease between male and female rats. Plasma macromolecules were detected in the urine samples of 2-month-old rats using sodium dodecyl sulphate polyacrylamide gel electrophoresis. All 4-month-old animals had proteinuria in excess of 30 mg/24 h. At the age of 4 months, sclerotic glomeruli were rarely observed. At the age of 6 months, all animals had a few sclerotic glomeruli in every kidney section examined. Animals which were 22 months old had sclerotic lesions in 37.8-52.1% of the glomeruli. Ultrastructural examination revealed that alterations in epithelial cells, such as effacement of foot processes, vacuolization, and a podocytic membrane-like structure, were found at the age of 2 months. The animals examined were neither uremic nor hypertensive. Our present study showed that female as well as male Buffalo/Mna rats had an earlier onset of the disease than the other strains of rats and that alterations in glomerular epithelial cells were first detected in the early stage of the disease.

Aging↗
PubMed1984

Restoration of antigenicity of tissue antigens, cell-bound immunoglobulins and immune deposits in paraffin-embedded tissue. The influence of fixation and proteolytic enzymatic digestion.

The possibility of preservation and restoration of antigenicity of some antigens in paraffin-embedded tissue was evaluated by direct immunofluorescent technique on deparaffinized sections. Fixation with 96% ethanol-1% acetic acid, 10% neutral buffered formalin and p-formaldehyde was useful for the preservation of tissue antigens and immune deposits, whose antigenicity could be easily restored by trypsin digestion. Neutral buffered formalin was also a satisfactory fixative in immunofluorescent staining on lymphocyte/plasma cell-bound immunoglobulins. Fixation with alcohol-Bouin's fluid showed contrast results; feasible for staining of cell-bound immunoglobulins, but poor for that of glomerular immune deposits. After papain digestion, BSA and lysozyme, antigens of immune complexes, were easily detected in experimental chronic serum sickness glomerulonephritis. Pepsin was more efficient than trypsin in restoring the antigenicity of renal tissue antigens such as fibronectin and polyantigenic basement membrane, but the brush border antigen of the proximal renal tubules was frail to the pepsin digestion. In general, the enzymatic digestion time necessary for the restoration of antigenicity was in parallel with fixation time. Results obtained have shown that deparaffinized sections could be used as satisfactory substrate for immunohistochemistry when proper fixation and efficient proteolytic enzymatic pretreatments were performed.

Animals↗
PubMed1983

Alteration of glomerular anionic sites by the development of subepithelial deposits in experimental glomerulonephritis in the rat.

Using highly cationic polyethleneimine, alteration of glomerular anionic sites were evaluated ultrastructurally in two types of rat glomerulonephritis (GN); chronic serum sickness GN and heterologous (passive) or autologous (active) Heymann's GN. Daily i.v. injections of egg white lysozyme in physiologic saline into presensitized rats led to the formation of numerous mesangial and subepithelial deposits. In the non-proteinuric period in which immune deposits were localized predominantly in the mesangium, anionic sites of the laminae rarae and the epithelial cell coat were clearly observed. In the subsequent proteinuric period in which numerous subepithelial deposits were superimposed, a broad loss of anionic sites in the epithelial cell coat was seen. Splitting and focal loss of anionic sites on the lamina rara externa adjacent to the subepithelial deposits were commonly observed both in passive and active Heymann's GN and in lysozyme GN. These findings indicate that the subepithelial deposits are closely involved in the development of proteinuria by injuring the anionic sites, especially those on lamina rare externa of the glomerular basement membrane.

Animals↗