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S Sugimoto

Publications and source records attributed to S Sugimoto.

At least 163 records · Page 9Linked to original sources
PubMed1988

Complement profiles in acute post-streptococcal glomerulonephritis.

It is well known that the hypocomplementemia of acute post-streptococcal glomerulonephritis (APSGN) is characterized by markedly reduced serum concentrations of C3 and moderately reduced levels of C5 and properdin (P). However, the extent of the activation of the classical pathway is not well defined and only limited data are available concerning serum concentrations of terminal components other than C5. In serial serum specimens from 14 children with APSGN, the presence and extent of C4 activation was directly assessed by measurement by rocket immunoelectrophoresis for C4 and C4 (C4d/C4 ratio). Elevated values for this ratio, indicating C4 activation, were found in 8 of 14 of the initial serum specimens, and in some patients the ratio remained elevated for several weeks. In contrast, the serum C4 level was low in only 1 specimen (the specimen with the highest C4d/C4 ratio). However, in 10 patients C4 concentrations within the normal range rose in serial serum specimens. Serum C2 concentrations were depressed in the initial specimens from 5 patients. The concentrations of 13 other complement component and control proteins were also measured in these specimens. Levels of terminal components, other than C5, in the initial serum specimens were normal except for depressed C8 in 3 of 13 patients and depressed C6 in 1 of 14. Of these 4 individuals, 3 had the lowest C3 levels in the study. It is concluded that the classical complement pathway is frequently activated in patients with APSGN early in the condition and that subtle abnormalities in C6 and C8 levels occasionally occur.

Adolescent↗
PubMed1987

Complement activation in IgA nephropathy.

Activation of alternative complement pathway is presumed to be important pathogenically in IgA nephropathy since renal biopsies usually exhibit glomerular deposition of C3 and P (properdin). Surprisingly, little is known about plasma complement activation in this disease, and the plasma C3 and C4 concentrations are usually normal or increased. We quantitated C3 activation in 202 plasmas from 81 patients with IgA nephropathy using a sensitive new assay that detects a neoantigen [iC3b-C3d neoantigen) which appears when C3b is inactivated to iC3b, C3dg, or C3d. This assay accurately quantitates small amounts of in vivo C3 activation. The concentration of iC3b-C3d neoantigen in plasma was significantly increased, indicating C3 activation in 37% of the pediatric and 57% of the adult plasmas assayed. When data from serial determinations in the patients were analyzed, 75% of the adult and 57% of the pediatric patients had C3 activation on at least one occasion. Classical pathway activation, quantitated by C4 activation was found in 20% of the adult and 5% of the pediatric plasmas. No association was found between elevated iC3b-C3d neoantigen concentration and history of macroscopic hematuria, chronic renal insufficiency or degree of proteinuria. These studies show that complement activation can frequently be detected in the plasma of IgA nephropathy patients. However, the pathophysiologic significance of this complement activation remains to be determined.

Adult↗
PubMed1987

[Different severity of brain ischemia between spontaneously hypertensive rats and Wistar-Kyoto rats induced by internal carotid infusion of arachidonic acid].

Arachidonic acid (AA) is a potent stimulator of platelet aggrgation and is known to induce endothelial cell damage and edema in the brain. An ischemic cerebral infarction model can be produced in rats by an internal carotid infusion of AA. In this study, water content, ATP and lactate in the brain and plasma prostaglandins (thromboxane B2; TXB2 and 6-keto-prostaglandin F1 alpha; 6-keto-PGF1 alpha) were measured and histological observations were made after an internal carotid infusion of AA in two strains of rats; stroke-resistant spontaneously hypertensive rat (SHRSR) and normotensive Wistar-Kyoto (WKY) rats. It is known that the blood pressure of the SHRSR begins to rise at about 8 weeks old. Throughout the study, AA was administered into the internal carotid artery under 2% fluothane anesthesia. In the first study, AA (1.7 mg/kg BW) was administered to 8- and 16-week-old rats and the length of survival was observed. In the second study, water content, ATP and lactate in the brain and plasma TXB2 and 6-keto-PGF1 alpha were measured 3 hours after AA (0.85 mg/kg BW) administration. In the third study, rats were perfusion-fixed 3 hours after the AA (1.7 mg/kg BW) infusion and cerebral arteries were observed by scanning electron microscopy (SEM). During the 6 hour observation period, there was no difference between the two groups in the number of 8-week-old rats which survived. However, the figure became significantly lower in the SHRSR at 16 weeks old. The water content in the bilateral cerebral hemispheres was significantly larger in the SHRSR than in the WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

[Effect of brovincamine fumarate on cerebral ischemia acutely induced by BLCL in SHRSR].

The present study was designed to clarify the effect of brovincamine fumarate (BV 26-723: BV) on the degree of cerebral ischemia acutely induced by bilateral common carotid artery ligation (BLCL) in stroke-resistant spontaneously hypertensive rats (SHRSR). BV was administered to SHRSR by intraperitoneal infusion (I.P.) of 30 mg/kg (BV 30 mg/kg group), 60 mg/kg (BV 60 mg/kg group) and 0.9% saline was similarly injected to SHRSR (control group) before and immediately after BLCL. Cerebral blood flow (rCBF) in the thalamus was measured by hydrogen clearance technique before and until 3 hr of BLCL periodically. The brain metabolites (ATP, lactate, pyruvate) were determined by the enzymatic method and the brain water content was measured by freeze-dry method 3 hr after BLCL. The histopathological changes in brain vessels were observed by scanning electron microscopy (SEM) 3 hr after BLCL. The rCBF of three groups were identical before BLCL. However, the rCBF of BV 30 mg/kg group was statistically higher than in control group until 2 hr after BLCL, and that of BV 60 mg/kg group was significantly higher even 3 hr after BLCL. In measurements of the brain metabolites after BLCL, ATP and pyruvate levels in both the BV 30 mg/kg and 60 mg/kg groups were statistically higher than the control group. And brain lactate concentrations in both the BV 30 mg/kg and 60 mg/kg groups were significantly lower than the control group. The brain water content of BV 30 mg/kg and 60 mg/kg groups were significantly lower then the control group after BLCL.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1987

[Involvement of arachidonic acid cascade in brain edema and cerebral energy metabolism after reperfusion].

The involvements of arachidonic acid metabolites in the development of ischemic brain edema and cerebral energy metabolism were investigated on the experimental ischemia and reperfusion model. The level of arachidonic acid in brain tissue increases especially on the ischemic insult, which is rapidly converted to prostaglandins and leukotrienes after the reperfusion. The drugs which modify the arachidonic acid metabolism were administrated to clarify the effect on ischemic brain edema and cerebral energy metabolism. Male stroke resistant spontaneously hypertensive rats (SHRSR) were subjected to incomplete ischemia for two hours by occlusion of both common carotid arteries with vascular clips, and reperfused for two hours. The drugs used are dexamethasone, indomethacin, trapidil and OKY-046. Indomethacin inhibits cyclooxygenase. Dexamethasone inhibits phospholipases by the production of lipocortin. OKY-046 inhibits thromboxane A2 synthetase. Trapidil inhibits thromboxane A2 synthetase and increases the level of 6-keto-PGF1 alpha. These drugs were administered 18 hours before, just after clipping on (1/2) and off (1/2). Brain water content, cerebral ATP and lactic acid levels were examined. In the saline treated group, the cerebral water content was increased after the reperfusion and reached its maximal level after two hours of the reperfusion. The development of brain edema was prevented by the administration of dexamethasone or trapidil, but not by indomethacin and OKY-046. Administration of trapidil or dexamethasone was found to prevent the decrease in ATP and the increase of lactic acid. In the indomethacin administrated group, only the increase of lactic acid was prevented. 6-keto-PGF1 alpha was high in the trapidil administrated group and low in the indomethacin administrated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

[Influence of long-term antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR--protective effect of nicardipine hydrochloride].

We have already reported that the long-term antihypertensive treatment reduced the degree of cerebral ischemia induced by bilateral common carotid artery ligation (BLCL) in stoke-resistant spontaneously hypertensive rats (SHRSR). This antihypertensive treatment was achieved by the combination of captopril and hydroflumethiazide. In this study, nicardipine hydrochloride which is one of the Ca2+ antagonist was similarly administrated to SHRSR for 8-10 weeks (T-SHR). The effect of long-term antihypertensive treatment by this agent on cerebral ischemia induce by BLCL was investigated and compared with untreated SHRSR (U-SHR). The degree of cerebral ischemia 4 hr after BLCL was estimated by the levels of brain energy metabolites (ATP, lactate, c-AMP) and brain water content. The brain metabolites and water content were measured in the forebrain and hindbrain of each hemisphere. And also the histopathological study on brain vessels 3 hr after BLCL was achieved by using scanning electron microscopy (SEM). The blood pressure of T-SHR gradually declined from 185 +/- 10 mmHg (mean +/- S.D.) to 154 +/- 8 mmHg after 8-10 weeks of antihypertensive treatment. However the blood pressure of U-SHR spontaneously changed from 185 +/- 8 mmHg to 206 +/- 12 mmHg after 8-10 weeks. The blood pressure of T-SHR after the treatment was significantly lower than that of U-SHR. The levels of ATP and c-AMP in T-SHR after BLCL were statistically higher than those in U-SHR, and the lactate levels in T-SHR were significantly lower than in U-SHR in the both fore- and hindbrain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The value of rocket immunoelectrophoresis for C4 activation in the evaluation of patients with angioedema or C1-inhibitor deficiency.

The correct diagnosis and characterization of C1-inhibitor deficiency depends on both clinical observations and laboratory evaluation of complement in plasma. Rocket immunoelectrophoresis for C4d is a sensitive assay for C4 activation in plasma. We have evaluated the value of this assay in identifying patients with C1-inhibitor deficiency. C4 activation was assessed in the plasmas of 15 patients with hereditary angioedema, five patients with variant form of hereditary angioedema, and four patients with acquired C1-inhibitor deficiency. Control groups consisted of 27 patients with chronic idiopathic urticaria and/or angioedema and seven normal volunteers. C4 activation was detected in all 52 plasma samples collected from the 24 patients with C1-inhibitor deficiency. The degree of C4 activation increased during attacks of angioedema and decreased (but remained elevated) during treatment with attenuated androgens. The concentrations of C4, C2, and C1 inhibitor were also measured; however, none of these measurements identified all of the patients with C1-inhibitor deficiency. Thus, we conclude that the measurement of C4 activation is one of the best tests available to evaluate a patient for C1-inhibitor deficiency, and a normal result will exclude the diagnosis of C1-inhibitor deficiency.

Androgens↗
PubMed1986

Multiple unit activity of prefrontal cortex and dorsomedial thalamus during delayed go/no-go alternation in the rat.

While the rat was performing a go/no-go alternation task with a 10-s delay period, neuronal activity was recorded from electrodes chronically implanted in the prefrontal cortex (PFC) and the dorsomedial thalamus (DMT). In both PFC and DMT, neuronal activity during the delay period prior to a 'go' response was different from that prior to a 'no-go' response. The results suggest that during the delay period the PFC and DMT maintain a memory for the generation of the response. Furthermore, it was found that DMT neuronal activity in the delay period was different between correct and error trials. Therefore, the DMT may be primarily important in performing the alternation behavior.

Animals↗