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Biomedical subjects

S Kiyama

Publications and source records attributed to S Kiyama.

At least 37 records · Page 2Linked to original sources
PubMed1995

Developmental expression of renal angiotensin II receptor genes in the mouse.

The cellular distribution of angiotensin II type 1 (AT1) and type 2 (AT2) receptor mRNA was examined in mouse kidneys at several embryonic stages (12 to 18 days; 19 days = full term) and up to three weeks after birth by in situ hybridization. The expression of both AT1 and AT2 mRNAs appeared simultaneously at 14 days of gestation. However, their distributions were contrasting: AT1 mRNA was expressed in mature glomeruli and maturing S-shaped bodies throughout the stages examined. AT1 expression was also detected at 16 days of gestation in the proximal and distal tubules and peaked at the end of gestation. Both the temporal and spatial expression of AT1 coincide with the differentiation and proliferation of glomerular mesangial and tubular cells during nephrogenesis. In contrast, AT2 mRNA was present only in the mesenchymal cells adjacent to the stalk of the ureter bud at early developmental stages, and, later, extended to the mesenchymal cells located near, but outside, the nephrogenic area of superficial cortex and also the cells between collecting ducts. AT2 expression in these regions decreased markedly within three weeks after birth. Temporally and spatially, AT2 mRNA expression coincides with the epithelial-mesenchymal interactions that take place during early phases of nephrogenesis. The site of AT2 expression also overlaps closely with that of a specific group of cells which undergo apoptosis following nephrogenesis. Thus, contrary to current belief, the activation of AT1 and AT2 genes takes place in different cell types of the kidney during embryonic development, and thereby conceivably contributes to the ontogeny of those specific renal cells.

Angiotensin II↗
PubMed1995

Strategic locus for the activation of the superoxide dismutase gene in the nephron.

Upon exposure to a transient ischemia, the distal tubule of the kidney often escapes the severe damage which afflicts the proximal tubule. To ascertain whether this feature of the distal tubule is attributable to its intrinsic cellular properties, we focused on two pairs of unique tubule segments; distal versus proximal convoluted tubules in the superficial cortex and distal versus proximal straight tubules in the outer stripe of the outer medulla. These tubules were chosen because, firstly, they can be identified by morphology and immunostaining, and secondly, each pair has the same anatomical relationship to the circulation. Detailed morphometric analyses were performed six hours following unilateral transient ischemia in adult rats to semiquantitate the local tissue damage in these specific nephron segments. The architecture of the distal convoluted and straight tubules was remarkably well preserved, contrasting to the moderate to extensive necrotic changes seen in the proximal tubules. In search of the potential intrinsic cellular mechanism that underlies the observed difference, we examined the segmental distribution along the nephron of manganese superoxide dismutase gene transcripts by in situ hybridization. This antioxidant enzyme gene was expressed primarily in the distal tubules with contrastingly low levels of expression in the proximal tubules. Moreover, following ischemia-reperfusion, this distal tubule-dominant pattern was further accentuated immediately following reperfusion. The study indicates that the marked difference between the proximal and distal tubules in their susceptibility to injury in vivo is attributable to their intrinsic cellular properties, which include the local level of antioxidants.

Animals↗
PubMed1995

[One-year experience as a clinical anaesthetist in England].

Current practice of British clinical anaesthesia is introduced, including anaesthesia in the operating theatre as well as obstetric analgesia in the labour ward. Although many people feel that British National Health Service has been affected by their chronic economic recession, the author's general impression is that the standard of anaesthetic care is kept at a quite high level despite financial difficulties. It is still valuable to experience clinical anaesthesia in the United Kingdom and the author encourages young Japanese anaesthetists to get an opportunity to work in British hospitals.

Anesthesia, Obstetrical↗
PubMed1994

Inhibitory effects of antihypertensive drugs on mesangial cell proliferation after anti-thymocyte serum (ATS)-induced mesangiolysis in spontaneously hypertensive rats.

The effects of antihypertensive drugs on mesangial cell proliferation were studied in spontaneously hypertensive rats (SHR) with anti-thymocyte serum (ATS)-induced glomerulo-nephritis. Rats were treated with either enalapril (Group 1), nifedipine (Group 2), or reserpine + hydrochlorothiazide + hydralazine (Group 3), or were untreated (Group 4). The animals were sacrificed 2, 4 and 7 days after ATS injection and the glomerular cell number and degree of mesangial area expansion were examined. A marked, similar decrease in glomerular nuclear cell number (NC) due to severe mesangiolysis was observed in all of the groups on day 2. Thereafter, an increase in NC reflecting mesangial cell proliferation after mesangiolysis occurred in Group 4 on days 4 and 7. In Group 1 and 2, the NC was significantly smaller than that in Group 4 on days 4 and 7, indicating suppression of mesangial cell proliferation. In Group 3, however, the number of NCs did not differ from that in Group 4 on days 4 and 7, indicating a lack of such suppression by conventional antihypertensive drugs. The degree of mesangial area expansion (MS) showed the same pattern as mesangial cell proliferation. That is, the rapid increases in MS seen in Group 4 on days 4 and 7 were apparently suppressed in Groups 1 and 2, but not in Group 3. Our in vivo observations that both an angiotensin converting enzyme (ACE) inhibitor and a calcium channel blocker suppress mesangial cell proliferation and mesangial area expansion suggest that these agents have practical implications in the treatment of mesangial proliferative glomerular diseases through the suppression of excess mesangial cell proliferation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Effects of endothelin and angiotensin II on renal hemodynamics in experimental mesangial proliferative nephritis.

The renal hemodynamic response to pressor substances in the diseased kidney has been suggested to be different from that in the normal kidney. The aim of this study was to investigate the effects of endothelin and angiotensin II on renal hemodynamics in experimental nephritis induced by the administration of antithymocyte serum in Wistar rats. This model showed mesangiolytic lesions in the glomeruli on day 2 and hypercellular lesions on day 8. Prior to the injection of either endothelin or angiotensin II, the glomerular filtration rate and renal plasma flow were significantly lower in model rats on day 2 or day 8 than in the control rats. The basal glomerular filtration rate and renal plasma flow on day 8 were negatively correlated with the mesangium cell number. The injection of endothelin (0.5 ng/kg BW) led to a decrease in both renal plasma flow and glomerular filtration rate in rats on day 8 which was significantly greater than that in the control rats. Similarly, angiotensin II infusion (0.2 micrograms/kg BW) reduced both renal plasma flow and glomerular filtration rate in the rats on day 8 and the reductions were significantly greater than those in the control rats. In conclusion, renal hemodynamics in rats with mesangial proliferation of the kidney were more sensitive to both endothelin and angiotensin II than those in the normal kidney.

Angiotensin II↗
PubMed1991

Antithrombotic mechanisms of urokinase immobilized polyurethane.

Urokinase immobilized polymer is highly antithrombotic, which cannot be explained only by fibrinolysis. We immobilized 10 IU/cm2 of urokinase to polyurethane by using maleic anhydride methylvinyl ether copolymer as a carrier. Then we incubated blood in circular tubes made of this material, measured the clotting factors and observed the surface of the tubes after incubation by scanning electronmicroscopy and immunofluorescence microscopy. After 5 min incubation, the relative activities of factors V, VIII, IX, X and XII, fibrinogen, plasminogen and alpha 2 plasmin inhibitor decreased, but the activity of factor VII increased. No platelet adhesion to the surface of the urokinase immobilized polyurethane was observed and there was no significant adsorption of serum proteins, including fibrinogen, fibronectin and vWF antigen, on the surface. Urokinase-immobilized polyurethane catalyzed the digestion of clotting factors as well as fibrinolysis and also inhibited platelet adhesion on its surface probably by inhibiting protein adsorption and its clinical application including vessel prosthesis should be developed further.

Blood Coagulation Factors↗
PubMed1991

Renal disease in an adult with type 1 glycogen storage disease.

The renal disease in an adult woman with Type 1 glycogen storage disease (GSD) is reported. Since she was 15 years old, several episodes of gouty arthritis had developed. At the age of 18, proteinuria was pointed out. Hepatomegaly, renomegaly out of proportion to the impairment of renal function, hyperuricemia, hyperlipidemia, fasting hypoglycemia and lactic acidemia were observed. The diagnosis of GSD was established on the basis of a glucose tolerance test, glucagon test and liver biopsy. The findings of renal biopsies performed at the ages of 24 and 27 years old suggested that glomerular damage might have preceded the tubulo-interstitial lesion.

Adult↗
PubMed1990

Subacute nephrotoxicity of germanium dioxide in the experimental animal.

Germanium (Ge; atomic number 32, atomic weight 72.6) belongs to IVb group of the Periodic Table and is found as a trace metal in soil, rocks, plants, and animals. It is widely used in industry because of its semiconductive nature. Some biological activities have been shown in Ge derivatives. Recently, patients with persistent renal damage after chronic ingestion of germanium dioxide (GeO2)-containing compounds have been reported in Japan. This study aimed to investigate subacute nephrotoxicity of GeO2 in Lewis male rats. The rats were treated orally with GeO2 for 13 weeks (GeO2 group) and were compared with those treated with GeO2 for only the first 4 weeks (GeO2-4-week group) and with untreated controls. Renal dysfunction was demonstrated by the increased serum creatinine, BUN, and serum phosphate and decreased creatinine clearance. Liver dysfunction was observed as demonstrated by the increased GOT and GPT, and hypoproteinemia by the decreased total protein and albumin in the GeO2 group. However, daily urinary protein excretion or urinalysis did not differ among the groups. Kidney weight and Ge content of tissues were significantly elevated in the GeO2 group. With the light microscope, vacuoles and the depositions of PAS-stained particles, which correspond to electron-microscopic dense granules in the swollen mitochondria, were predominantly observed in distal tubular epithelium in the GeO2 group. Even in the GeO2-4-week group of rats, serum creatinine was increased and the above-mentioned histological abnormalities were observed, but were less intense.

Acute Kidney Injury↗
PubMed1990

IgA nephritis associated with plasminogen abnormalities.

Two patients with IgA nephritis associated with hereditary plasminogen abnormalities are described. One patient had dysplasminogenemia and the other had plasminogen deficiency. In both patients, renal biopsy specimens showed significant arteriosclerotic changes in addition to mesangial proliferation. Increased fibrinopeptide A concentration in their plasma suggested increased thrombin generation. In one patient, no systemic arteriosclerosis coexisted, judging from normal optic fundi and the absence of neurological and cardiac abnormalities. In IgA nephritis, renal vascular hyalinosis is often observed, probably resulting from vascular injury. Thus, it was suggested that the decreased fibrinolysis and renal vascular injury of these patients synergistically induced more fibrin thrombi and accelerated arteriosclerosis of the kidney. These cases imply the important role of fibrinolytic disorders in the progression of IgA nephritis.

Adult↗