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H Sugimoto

Publications and source records attributed to H Sugimoto.

At least 145 records · Page 8Linked to original sources
PubMed1998

Profiles of circulating inflammatory- and anti-inflammatory cytokines in patients with hemolytic uremic syndrome due to E. coli O157 infection.

The systemic inflammatory response to Escherichia coli O157 infection was studied from the profiles of circulating inflammatory and anti-inflammatory cytokines. Twelve patients transferred sequentially to our hospital for the intensive care with acute illness due to Escherichia coli O157 infection and the possible form of haemolytic uraemic syndrome were included in this study. Increased circulating concentrations of tumour necrosis factor, interleukin 6, interleukin 8, granulocyte colony-stimulating factor, and interleukin 10 were found in patients with various stages of this infection and haemolytic uraemic syndrome. Especially, the degree of the increase of circulating interleukin 10 in those who had a typical signs of haemolytic uraemic syndrome was higher than those of other inflammatory cytokines. Two groups of E. coli infection could be classified into one with a typical haemolytic uraemic syndrome and the other with atypically bacteremic state over haemolytic uraemic syndrome according to these cytokine levels.

Adult↗
PubMed1998

Increased expression of selectins in kidneys of patients with diabetic nephropathy.

In diabetic nephropathy leukocytes, mainly composed of monocytes/macrophages, which accumulate in the glomeruli and the interstitium, play an important part in the progression of glomerulosclerosis. The infiltration of leukocytes into inflammatory tissues or atherosclerotic lesions is mediated by adhesion molecules, which are expressed on the vascular endothelial cells, although little is known about the mechanism of leukocyte infiltration into diabetic renal tissues. P- and E-selectin are leukocyte adhesion molecules, which are expressed on the vascular endothelial cells and promote the adhesion of leukocytes to the endothelium. We investigated the expression of P- and E-selectin in the kidney tissue of patients with diabetic nephropathy and compared it with that of patients with other glomerular diseases (minimal change nephrotic syndrome, membranous nephropathy, IgA nephropathy, mesangioproliferative glomerulonephritis, and lupus nephritis). Expression of P- and E-selectin were both significantly increased in the glomeruli and the interstitium of patients with diabetic nephropathy as compared with those with other glomerular diseases. P- and E-selectin were both expressed along the glomerular capillaries and the peritubular capillaries in the interstitium. Neither P- nor E-selectin were correlated with the number of infiltrated leukocytes in the glomeruli, however, interestingly the E-selectin expression on peritubular capillaries was correlated with the number of infiltrated CD14 positive cells in the interstitium. These results suggest that E-selectin may play a key role in leukocyte infiltration into the renal interstitium in patients with diabetic nephropathy.

Adolescent↗
PubMed1998

Increased expression of endothelial cell nitric oxide synthase (ecNOS) in afferent and glomerular endothelial cells is involved in glomerular hyperfiltration of diabetic nephropathy.

The overproduction of nitric oxide (NO) is reported in the diabetic kidney and considered to be involved in glomerular hyperfiltration. The precise mechanism of NO production in the diabetic kidney is, however, not known. In this report, we compare the localization of endothelial cell nitric oxide synthase (ecNOS) isoform expression in the kidney tissue of streptozotocin (STZ)-induced diabetic rats and 5/6 nephrectomized rats and clarify the pivotal role of ecNOS for the glomerular hyperfiltration in the early stages of diabetic nephropathy. In diabetic rats, the diameters of afferent arterioles, the glomerular volume, creatinine clearance, and urinary NO2/NO3 were increased after the induction of diabetes. Efferent arterioles were, however, not altered. Insulin or L-NAME treatment returned the diameters of afferent arterioles, glomerular volume, creatinine clearance, and urinary NO2/NO3 to normal. The expression of ecNOS in afferent arterioles and glomeruli of diabetic rats increased during the early stages of the disease, but was not altered in efferent arterioles. Treatment with either insulin or L-NAME decreased ecNOS expression in afferent arterioles and in glomeruli. In contrast, the ecNOS expression was upregulated in both afferent and efferent arterioles and in the glomeruli of 5/6 nephrectomized rats, where the dilatation of afferent and efferent arterioles and glomerular enlargement were observed. Treatment with L-NAME ameliorated the ecNOS expression and dilatation of arterioles. We conclude that enhanced NO synthesis by ecNOS in afferent arterioles and glomerular endothelial cells in response to the hyperglycaemic state could cause preferential dilatation of afferent arterioles, which ultimately induces glomerular enlargement and glomerular hyperfiltration.

Animals↗
PubMed1998

The SAPHO syndrome: defining the radiologic spectrum of diseases comprising the syndrome.

The objective of our study was to clarify the radiologic spectrum of disease entities belonging to the SAPHO syndrome (SAPHO being an acronym for synovitis, acne, pustulosis, hyperostosis, and osteitis). A retrospective analysis of radiologic data was undertaken to determine the relationship of the osteoarthritic changes seen in palmoplantar pustulosis (PPP, n = 179), acne (n = 3), psoriasis vulgaris (PsV, n = 355), generalized pustular psoriasis (GPP, n = 25), and chronic recurrent multifocal osteomyelitis (CRMO, n = 4). Osseous changes of PPP, acne, and CRMO overlap each other; 7 PPP, 2 acne, and 3 CRMO patients manifested stenocostoclavicular hyperostosis as well as hyperostosis of the spine, pelvis, and/or femur. These findings were not seen in either PsV or GPP patients. Thirteen PsV and 4 GPP patients had peripheral arthritis and/or symmetrical sacroiliitis, which were not observed in the PPP, acne, and CRMO patients. The PPP, acne, and CRMO patients may be grouped as belonging to the single disease entity, namely SAPHO syndrome. Our findings do not support the inclusion of PsV and GPP in the spectrum of this syndrome.

Acne Vulgaris↗
PubMed1998

A unique method of closure for an aortocaval fistula in association with a ruptured abdominal aortic aneurysm: report of a case.

We report herein the case of a 78-year-old man in whom an aortocaval fistula caused by spontaneous rupture of an abdominal aortic aneurysm (AAA) was successfully treated by a unique surgical technique. The aortocaval fistula had been revealed by an aortography after the patient presented with high-output heart failure. During the operation, massive bleeding from the fistula was evident. The fistula measured 2 cm in diameter, and was located between the right posterior wall of the AAA and the inferior vena cava (IVC). Direct suturing of the defect in the IVC failed to close the fistula because the tissue around it would not hold together due to degeneration. However, the bleeding was finally able to be controlled by plugging the fistula with isolated and properly trimmed omentum packed within the excluded aneurysmal sac. Unfortunately, the patient died due to respiratory failure on the 201st postoperative day. A pathological autopsy revealed that the aortocaval fistula had been closed by fibrous tissue and that the IVC was patent. Although such a drastic operative measure to repair an aortocaval fistula has never before been reported, it could be an alternative when direct closure proves unsuccessful.

Aged↗
PubMed1998

Therapeutic effects of prostacyclin analog on crescentic glomerulonephritis of rat.

Prostacyclin (PGI2) is known to have a relaxative action on vascular smooth muscle, an inhibitory action against platelet activation and neutrophil function. Previous studies showed the preventive effects of PGI2 on lupus nephritis and Thy-1 nephritis, although the mechanism has not been clarified. Glomerular endothelial expression of intercellular adhesion molecule-1 (ICAM-1) is up-regulated in experimental and human glomerular diseases, and is known to facilitate leukocyte infiltration into the glomeruli, which ultimately induces the various glomerular injuries. In the present study, we evaluated the therapeutic effects of PGI2 on a rat model for crescentic glomerulonephritis and investigated its putative mechanism in relation to ICAM-1-mediated leukocyte recruitment. Wistar-Kyoto (WKY) rats were injected with nephrotoxic serum and received continuous intraperitoneal infusion of PGI2. PGI2 dramatically decreased proteinuria (123.0 +/- 18.8 vs. 31.6 +/- 4.5), crescent formation and deposition of fibrinogen in the glomeruli, while the deposition of rabbit IgG, rat IgG and rat C3 along the capillary walls was not changed. Furthermore, intraglomerular expression of ICAM-1 and infiltration of macrophages were significantly suppressed by administration with PGI2. In contrast, influx of CD4 or CD8 positive cells was not altered. The present results suggest that PGI2 shows the preventive effects on experimental crescentic glomerulonephritis by inhibiting intraglomerular coagulation and ICAM-1-mediated macrophage-glomerular endothelial cell adhesive pathway.

Animals↗
PubMed1998

Assessment of disease activity in rheumatoid arthritis using magnetic resonance imaging: quantification of pannus volume in the hands.

We attempted to assess whether pannus volume measured by magnetic resonance imaging (MRI) can be used as an indicator of disease activity in rheumatoid arthritis (RA). Eleven women (mean age 46 yr) with uncontrolled RA were studied for 1 yr. Pannus formation in both hands was quantified using MRI at the start of the study, and at 6 and 12 months thereafter. The volume of enhancing pannus (VEP) was compared with changes in the radiological scores, grip strength, joint tenderness counts, joint swelling counts, erythrocyte sedimentation rate (ESR), and serum C-reactive protein (CRP). Patients were classified into three groups based on VEP changes between 0 and 12 months: unchanged (n = 2), decreased (n = 6) and increased (n = 3). VEP at 6 months and at 12 months differed significantly between the three groups. No statistically significant differences were found between the groups in radiographic scores, physical parameters or laboratory parameters despite the fact that some of these parameters changed in the direction indicated by the changes in VEP. VEP can be used as a new indicator to assess disease activity in individual RA patients and, using this parameter, treatment outcome can be assessed in fewer subjects than with traditional measures.

Adult↗
PubMed1998

Recombinant human granulocyte colony-stimulating factor attenuates inflammatory responses in septic patients with neutropenia.

OBJECTIVE: The objective of this study was to determine the effects of recombinant human granulocyte colony-stimulating factor (rhG-CSF) administration in septic patients with neutropenia. METHODS: Twenty consecutive septic patients were administered rhG-CSF subcutaneously (2 microg x kg(-1) x d(-1)) for 5 days (group G). They were compared with 14 septic patients treated earlier without rhG-CSF (group N). All patients in both groups met the criteria of total leukocyte count (TLC) less than 5,000/mm3 and C-reactive protein (CRP) more than 10 mg/dL. Changes in TLC, absolute neutrophil count (ANC), CRP, respiratory index (RI), Acute Physiology and Chronic Health Evaluation (APACHE) II score, and Goris's Multiple Organ Failure (MOF) index were evaluated. In addition, nucleated cell count (NCC), differentiation in bone marrow aspiration, neutrophil phagocytic and bactericidal activity, serum concentrations of interleukin-6 (IL-6) and IL-8 as inflammatory markers, and plasma concentration of leukocyte elastase (LE) as an indicator of the tissue injury were evaluated in group G. RESULTS: In group G, TLC, ANC, NCC, and neutrophil functions increased significantly, whereas CRP, IL-6, and IL-8 decreased reciprocally. There was no deterioration of LE and RI. Consequently, the APACHE II score and MOF index improved. In group N, however, CRP showed no change concomitant with the APACHE II score and MOF index. CONCLUSION: Administration of rhG-CSF attenuates inflammatory responses without inducing tissue injury in septic patients with neutropenia.

APACHE↗
PubMed1998

S-1153 inhibits replication of known drug-resistant strains of human immunodeficiency virus type 1.

S-1153 is a new imidazole compound that inhibits human immunodeficiency virus (HIV) type 1 (HIV-1) replication by acting as a nonnucleoside reverse transcriptase inhibitor (NNRTI). This compound inhibits replication of HIV-1 strains that are resistant to nucleoside and nonnucleoside reverse transcriptase inhibitors. S-1153 has a 50% effective concentration in the range of 0.3 to 7 ng/ml for strains with single amino acid substitutions that cause NNRTI resistance, including the Y181C mutant, and also has potent activity against clinical isolates. The emergence of S-1153-resistant variants is slower than that for nevirapine, and S-1153-resistant variants contained at least two amino acid substitutions, including F227L or L234I. S-1153-resistant variants are still sensitive to the nucleoside reverse transcriptase inhibitors zidovudine (AZT) and lamivudine. In a mouse and MT-4 (human T-cell line) in vivo HIV replication model, S-1153 and AZT administered orally showed a marked synergy for the inhibition of HIV-1 replication. S-1153 shows a significant accumulation in lymph nodes, where most HIV-1 infection is thought to occur. S-1153 may be an appropriate candidate for two-to three-drug combination therapy for HIV infection.

Animals↗
PubMed1998

Pentoxifylline attenuates reperfusion injury in skeletal muscle after partial ischemia.

Leukocytes have been shown to contribute to ischemia-reperfusion injury in skeletal muscle. Pentoxifylline (PTXF), a xanthine-derived phosphodiesterase inhibitor, has received recent attention because of its action on leukocytes. To clarify the effects of PTXF in reperfusion injury, we measured the resting transmembrane potential difference (Em) and evaluated postcapillary venule microcirculation using intravital microscopy in rat skeletal muscle during ischemia and reperfusion. The infrarenal aorta was clamped for 90 min and then reperfused for 60 min. Persistent depolarization of the resting Em was observed in an ischemia-reperfusion (IR) group and was significantly repolarized in a PTXF group during the reperfusion period. The tissue water content was significantly reduced in the PTXF group, although no difference was noted in the tissue lactate content. Flowing erythrocyte velocity and wall shear rate in the PTXF group were significantly higher than in the IR group during the reperfusion period but without significant differences in vessel diameter and hemoglobin oxygenation. Blood flow measured by laser-Doppler flowmeter was also significantly improved in the PTXF group. Furthermore, the adherent leukocyte count was significantly reduced in the PTXF group during this same period. These results indicate that PTXF attenuated reperfusion-associated membrane injury and tissue edema and that PTXF suppressed leukocyte adhesion and improved hindlimb blood flow during the reperfusion period.

Animals↗
PubMed1998

Intercellular adhesion molecule 1 mediates mononuclear cell infiltration into rat glomeruli after renal ablation.

Mononuclear cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. Intercellular adhesion molecule 1 (ICAM-1) is expressed on the vascular endothelium and mediates the infiltration of leukocytes into the site of inflammation. Although the expression of ICAM-1 can be induced by the stimulation of inflammatory cytokine, ICAM-1 expression can also be induced by such nonimmune mechanisms as shear stress. Glomerular hyperfiltration is a major mechanism that contributes to the progression of the glomerular sclerosis that results from the loss of functioning nephrons. In the present study, we examined the role of ICAM-1 for mononuclear cell infiltration in the glomeruli of the five-sixth nephrectomized rat as a model of glomerular hyperfiltration. The fluorescence intensity score of the staining for ICAM-1 in the glomeruli of the five-sixth nephrectomized rats was significantly increased as compared with that in the control (sham-operated) rats at 1 week (1.51 +/- 0.15 vs. 0.61 +/- 0.13; p < 0.01) and 2 weeks (1.31 +/- 0.17 vs. 0.51 +/- 0.09; p < 0.01). The number of leukocytes present in the glomeruli was significantly increased in the five-sixth nephrectomized rats compared with control (sham-operated) rats at 1 week (3.44 +/- 0.16 vs. 0.99 +/- 0.08; p < 0.01) and 2 weeks (3.14 +/- 0.14 vs. 0.89 +/- 0.07; p < 0.01). Leukocytes mainly consisted of macrophages in the five-sixth nephrectomized rats at 1 week (2.39 +/- 0.19) and 2 weeks (1.46 +/- 0.11). Anti-ICAM-1 monoclonal antibody effectively prevented the infiltration of macrophages into the glomeruli following nephrectomy. These results indicate that glomerular hyperfiltration may be involved in the induction of the expression of ICAM-1 and the infiltration of macrophages into the renal glomeruli following glomerular injury.

Animals↗
PubMed1998

Accumulation of Nsigma-(carboxy-methyl)lysine and changes in glomerular extracellular matrix components in Otsuka Long-Evans Tokushima fatty rat: a model of spontaneous NIDDM.

Increases in extracellular matrix (ECM) and changes in its components have been documented in the glomeruli of diabetic nephropathy. Advanced glycation end products formed by glycoxidation have been shown to induce the synthesis of ECM components and transforming growth factor beta (TGF-beta), suggesting that advanced glycation end products may be involved in the etiology of imbalance of ECM components in diabetic glomerulosclerosis. The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an inbred strain that spontaneously develops non-insulin-dependent diabetes mellitus which progresses to diabetic glomerulosclerosis. Nepsilon-(carboxymethyl)lysine (CML) is known to be formed by glycoxidation. To clarify the involvement of glycoxidation in diabetic nephropathy, we examined the localization of CML, ECM components, and TGF-beta1 in the glomeruli of OLETF rats. The amounts of alpha3(IV) collagen, type VI collagen, and fibronectin were significantly increased in the glomeruli of OLETF rats, whereas the heparan sulfate proteoglycan levels were decreased. After 6 months of age, CML levels were significantly increased in the mesangial area of the glomeruli in these animals. The overexpression of TGF-beta1 preceded the increase in glomerular ECM components. The present study demonstrated that the accumulation of CML precedes the changes of glomerular ECM components in the glomeruli during the course of diabetic nephropathy, suggesting that glycoxidation may be one of the major causes of diabetic glomerulosclerosis.

Animals↗
PubMed1998

Deposition of mannan binding protein and mannan binding protein-mediated complement activation in the glomeruli of patients with IgA nephropathy.

Mannan binding protein (MBP) is a C-type lectin and has a high affinity to mannose and N-acetyl glucosamine. It is also known to activate C4 and C2 without C1 component, which is called 'lectin pathway'. We now report the presence of MBP and MBP-mediated complement activation in renal glomeruli of IgA nephropathy patients using an immunohistochemical method. In 7 of 42 cases with IgA nephropathy, MBP was detected in the glomerular mesangial area and colocalized with IgA1. In 19 cases with other types of IC-mediated glomerulonephritis including lupus nephritis and membranous nephropathy or without nephritis, MBP was not detected in the glomerulus. The C2- and/or C4-positive rate was 87.5% in the MBP-positive group and 20% in the MBP-negative group of IgA nephropathy. In addition, MBP-positive cases showed marked mesangial cell proliferation, lower creatinine clearance (53.4 +/- 10.0 vs. 77. 8 +/- 4.7 ml/min) and higher urinary protein excretion (2.5 +/- 0.9 vs. 0.9 +/- 0.2 g/day) compared with MBP-negative cases. These findings suggested that MBP was involved in glomerular complement activation through the lectin pathway and thus induced glomerular injury of IgA nephropathy. Since oligosaccharide chain alterations such as reduced sialic acid and galactose of IgA1 molecule have been reported in IgA nephropathy patients, MBP might bind to the IgA1 molecule via interaction between MBP and sugar chain.

Adult↗
PubMed1998

[Effects of KB-R7943, a novel Na+/Ca2+ exchange inhibitor, on myocardial ischemia/reperfusion injury].

The effects of KB-R7943 (2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea methanesulfonate) on major ion transporters were studied in canine cardiac sarcolemmal and sarcoplasmic reticular vesicles. KB-R7943 inhibited the Na+/Ca2+ exchange more potently than the Na+/H+ exchange, the Na+/K(+)-ATPase and the Ca2(+)-ATPase. The effects of KB-R7943 on ischemia/reperfusion-induced injury were studied in isolated rat perfused hearts in comparison with those of diltiazem and lidocaine. In normal hearts, diltiazem (10 microM) and lidocaine (100 microM) markedly reduced contractile function, but KB-R7943 (1, 10 microM) had no such effect. In the hearts subjected to 25-min ischemia and 30-min reperfusion, KB-R7943 concentration-dependently and significantly improved post-ischemic recovery of left ventricular developed pressure, left ventricular dP/dtmax and left ventricular end-diastolic pressure by pre-ischemic treatment (5 min) or post-ischemic treatment (10 min). Diltiazem and lidocaine showed similar improvement of recovery by pre-ischemic treatment, but they had no effect by post-ischemic treatment. Furthermore, the effect of KB-R7943 on arrhythmia was studied in anesthetized rats subjected to 5-min cardiac ischmeia and 10-min reperfusion. KB-R7943 (1, 10 mg/kg, i.v.) dose-dependently reduced the incidence and the duration of ventricular fibrillation. These results indicate that KB-R7943, a selective Na+/Ca2+ exchange inhibitor, has beneficial effects against myocardial ischemia/reperfusion injury and suggest that activation of the Na+/Ca2+ exchange mainly occurs immediately after reperfusion in the pathophysiological process of myocardial ischemia/reperfusion injury.

Animals↗
PubMed1998

Serum levels of soluble interleukin-2 receptor in patients with various renal diseases.

To clarify the serum levels of soluble interleukin-2 receptor (sIL-2R) in patients with renal diseases, we examined 281 patients without various renal diseases with or without systemic disease (including 197 patients without systemic diseases and 84 patients with systemic diseases). The sIL-2R level was significantly higher in patients with renal diseases, than in healthy volunteers. In the group of renal diseases, the sIL-2R level in patients with rapidly progressive nephritic syndrome was especially higher than in patients with other renal diseases. In patients without systemic diseases, the serum level of sIL-2R was significantly and positively correlated with the urinary excretion of protein, and the serum levels of creatinine and uric acid, and was negatively correlated with the glomerular filtration rate (GFR). In the patients with systemic diseases, the correlation between the serum levels of sIL-2R and the serum levels of creatinine or GFR were not as strong as observed in the patients without systemic diseases. The serum level of sIL-2R was outside the normal range in patients with systemic diseases with a serum level of creatinine above 2.0 mg/100 ml. These findings suggest that the serum levels of sIL-2R in patients with renal disease may increase and correlate with the impaired renal function, that he increased sIL-2R levels in patients with systemic diseases may be dependent on the activity of systemic disease, and that it may be not useful indicator of diseases activity in patients with systemic diseases when the serum level of creatinine was above 2.0 mg/100 ml.

Adult↗
PubMed1998

Selection of severely head injured patients for mild hypothermia therapy.

OBJECT: The authors have analyzed the efficacy of inducing mild hypothermia (34 degrees C) in 62 severely head injured patients to control fulminant intracranial hypertension. METHODS: All 62 patients fulfilled the following criteria: 1)persistent intracranial pressure (ICP) greater than 20 mm Hg despite fluid restriction, hyperventilation, and high-dose barbiturate therapy; 2) an ICP lower than the mean arterial pressure; and 3) a Glasgow Coma Scale (GCS) score of 8 or less on admission. The patients were divided into three groups based on computerized tomography findings: extracerebral hematoma (34 patients with subdural and/or epidural hematoma), focal cerebral lesion (20 patients with localized brain contusion and/or intracerebral hematoma), and diffuse swelling (eight patients with no focal mass lesion). Mild hypothermia prevented ICP elevation in 35 (56.5%) of the 62 patients whose ICP was greater than 20 mm Hg despite conventional therapies. Among those 35 patients whose ICP was controlled by mild hypothermia, 12 (34.3%) achieved functional recovery (good outcome or moderate disability). However, functional recovery was observed in only five (10.9%) of the 46 patients whose ICP was greater than 40 mm Hg after conventional therapies. Of 40 patients with an admission GCS score of 5 to 8, there were 11 (27.5%) who achieved functional recovery. On the contrary, mild hypothermia was not effective in 22 patients with an admission GCS score of 3 or 4. In the patients with focal cerebral lesions, ICP was controlled by mild hypothermia in 17 patients (85%) and patient outcome was intimately related to the extent of the damage. Among 18 patients with extracerebral hematoma who had a midline shift of 9 to 12 mm, raised ICP could be successfully controlled by mild hypothermia in 16 patients (88.9%) and three (16.7%) achieved functional recovery. However, ICP could not be controlled in patients with extracerebral hematoma who had a midline shift of 13 mm or more. In patients with diffuse swelling, ICP elevation could not be prevented at all by mild hypothermia. CONCLUSIONS: The authors conclude that mild hypothermia is effective for preventing ICP elevation in patients without diffuse brain swelling in whom ICP remains higher than 20 mm Hg but less than 40 mm Hg after conventional therapies.

Adolescent↗