Search PubMed⌕ Search

Biomedical subjects

H Sugimoto

Publications and source records attributed to H Sugimoto.

At least 199 records · Page 11Linked to original sources
PubMed1996

Early-stage rheumatoid arthritis: diagnostic accuracy of MR imaging.

PURPOSE: To investigate the role of magnetic resonance (MR) imaging in diagnosing early rheumatoid arthritis (RA). MATERIALS AND METHODS: Twenty patients (three men, 17 women; age range, 21-72 years) with clinically and radiologically proved RA underwent evaluation to define an MR imaging criterion for diagnosing synovial inflammation due to RA. Twenty-seven patients (16 with RA, 11 without RA [control patients]; three men, 24 women; age range, 19-75 years) suspected to have early RA but without radiographic abnormalities underwent evaluation to test the accuracy of using the criterion to diagnose RA. In each patient, coronal, fat-suppressed, and gadolinium contrast material-enhanced, T1-weighted images of both hands were obtained. RESULTS: The MR imaging criterion was periarticular contrast material enhancement of the wrists or the metacarpophalangeal and/or proximal interphalangeal joints in both hands. In the diagnosis of early RA, sensitivity and negative predictive value were both 100%, specificity was 73%, and accuracy was 89%. CONCLUSION: MR imaging is extremely useful in diagnosing early RA.

Adult↗
PubMed1996

Increased gene expression of insulin-like growth factor-i receptor in experimental diabetic rat glomeruli.

Renal hypertrophy is a characteristic and early manifestation of diabetes in humans and experimental animals. We examined the precise distribution of insulin-like growth factor-I (IGF-I) mRNA and IGF-I receptor mRNA in the experimental diabetic rat kidney using a nonradioactive in situ hybridization technique. No significant difference in the distribution of IGF-I mRNA was found between the diabetic and control rats. IGF-I mRNA-positive cells were found in the collecting ducts and in scattered single cells in the distal tubules. The number of IGF-I mRNA-positive cells was very low in the glomeruli. Expression of IGF-I receptor mRNA was rarely seen in the glomeruli of control rats. IGF-I receptor mRNA was detected after induction of diabetes in glomerular mesangial, visceral epithelial, and parietal epithelial cells. The number of IGF-I receptor mRNA-positive cells in a glomerulus increased significantly, peaking at 4 weeks as compared with the control rats. Overexpression of IGF-I receptor in glomerular cells, especially mesangial and visceral epithelial cells, may contribute to glomerular hypertrophy in diabetic nephropathy.

Animals↗
PubMed1996

A variant alkaline phosphatase detected in a patient with lung cancer.

A variant alkaline phosphatase (ALP), with heat-sensitivity characteristics similar to that of the bone type, was found in the serum of a patient suffering from lung cancer. In disc polyacrylamide gel electrophoretic studies most of this enzyme had migrated to the region corresponding to liver ALP, with the remainder affecting bone ALP. Like kidney ALP, this ALP was markedly inhibited by 0.5 mmol/l L-cysteine. The K(m) of this ALP for p-nitrophenylphosphate was 0.39 mmol/l, similar to that of kidney ALP. The sugar moiety of this enzyme bore greater resemblance to that of kidney ALP than liver or bone ALP. However, immunoprecipitation of this particular ALP was strong with a monoclonal antibody against liver ALP and moderate with an antibody against bone ALP.

Aged↗
PubMed1996

Inhibitory effect of the NMDA receptor antagonist, dizocilpine (MK-801), on the development of morphine dependence.

We investigated the effect of a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imin ehydrogen maleate (dizocilpine, MK-801), on hippocampal norepinephrine release in morphine-treated rats in order to clarify the relationship between NMDA receptors and the development of morphine dependence. Naloxone hydrochloride injected subcutaneously (s.c.) into morphine-dependent rats, induced an immediate increase in hippocampal norepinephrine release, which was associated with a typical morphine withdrawal syndrome. The increased norepinephrine levels persisted for at least 2 hr, even after the disappearance of the behavioral withdrawal syndrome. This striking effect of naloxone on hippocampal norepinephrine release was dependent on the duration of the intracerebroventricular (i.c.v.) morphine infusion. Pretreatment with dizocilpine (s.c.) before naloxone challenge reduce the rate of the rise in hippocampal norepinephrine release induced by naloxone in morphine-treated rats. Concurrent infusion (i.c.v.) of dizocilpine and morphine decreased the level of hippocampal norepinephrine release after a naloxone challenge. Both pretreatment with dizocilpine (s.c.) before naxolone injection and infusion (i.c.v.) of dizocilpine suppressed rearing and teeth-chattering signs, but not wet-dog shakes in morphine-treated rats. These results suggest that dizocilpine attenuates the development of morphine dependence through NMDA receptors, and thus that interaction between opioid receptors and NMDA receptors may be involved in the development of morphine dependence.

Analysis of Variance↗
PubMed1996

[Urinary proteins (focusing on alkaline phosphatases)].

In order to gain a fuller understanding of sports-related stress markers, we studied urinary alkaline phosphatase (ALP) levels and isozyme patterns before and after strenuous exercise. ALP activity-peaks were seen 5 approximately 15 minutes or 1 hour after running. While levels of ALP of higher molecular mass were observed to increase slightly, following intense exercise, neither the intensity nor the duration of the exercise appeared to have an overly significant effect on them. After buthanol extraction, a distinct band of ALP activity was observed in the polyacrylamide gel, having the same degree of mobility as those of the renal cortex and medulla. A portion of post-exercise urinary ALP was considered to have originated from the kidney. As ALP is now understood to be one of the markers of bone metabolism, urinary ALP will most certainly come under ever more intense scrutiny, as regards its connection to sports-related stress and osteoporosis.

Adult↗
PubMed1996

Glomerular expression of macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor in patients with various forms of glomerulonephritis.

Macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) are major mediators for the differentiation, proliferation, and activation of the macrophage. Recently, M-CSF was documented to play a pivotal role in the development of nephritis via macrophage activation in MRL-lpr mice. The macrophage is also considered to be an important component in the development of human glomerulonephritis. The expression and function of colony-stimulating factors (CSF) in the human kidney have not yet been defined. This study was undertaken to elucidate the various roles of CSF in the development of glomerulonephritis in humans. We examined the glomerular expression of M-CSF and GM-CSF in patients with various forms of glomerulonephritis and in normal subjects using immunohistochemical methods and nonradioisotopic in situ hybridization. The expression of CSF at both the protein and mRNA level in the glomeruli was compared with the degree of mesangial proliferation; the number of macrophages, Ki67-positive cells, and HLA-DR-positive cells; and the degree of alpha-smooth muscle actin-positive area in the glomerulus and clinical data. M-CSF and GM-CSF were expressed mainly on the mesangial cells in the glomerulus. Intraglomerular expressions of CSF at the protein level were increased in cases of IgA nephropathy and lupus nephritis. There was a positive correlation among the M-CSF protein expression and glomerular proliferation, macrophage infiltration, and the degree of proteinuria. M-CSF mRNA expression also was increased in the cases of IgA nephropathy and lupus nephritis. The number of Ki67-positive cells and HLA-DR-positive cells and alpha-smooth muscle actin-positive area in the glomerulus were increased in the cases with enhanced M-CSF expression. These results suggest that the glomerular secretion of M-CSF promotes macrophage infiltration into the glomerulus and activates resident and extraneous macrophages in the mesangial proliferative glomerulonephritis. M-CSF is considered to be a major mediator in the development of mesangial proliferative glomerulonephritis in humans.

Adult↗
PubMed1996

[The clinical significance of the measurement of serum soluble interleukin-2 receptors in various diseases].

We measured the serum levels of soluble interleukin-2 receptor (sIL-2R) in patients with collagen disease, viral hepatitis, and chronic renal failure on hemodialysis (HD) by enzyme immunoassay. sIL-2R levels were significantly higher in patients with collagen diseases (rheumatoid arthritis (RA), 843 +/- 509; systemic lupus erythematosus (SLE), 774 +/- 308; Sjögren's syndrome (SjS), 760 +/- 288; progressive systemic sclerosis (PSS), 649 +/- 198U/ml), with the viral markers of hepatitis B or C (HBsAg positives, 911 +/- 589; anti-HCV positives, 664 +/- 455U/ml) or with chronic renal failure on HD(1,431 +/- 406U/ml) than in the controls (302 +/- 57U/ml). In RA patients, there was a significant positive correlation between sIL-2R level and Lansbury's Indice or serum rheumatoid factor level. Patients with viral hepatitis showed a significantly positive correlation between the sIL-2R level and the level of ZTT or TTT. There was a significant difference between the HD patients with the anti-HCV antibody and those without, and between those with the anti human T lymphotrophic virus-I (HTLV-I) antibody and those without. In addition, there was a significant positive correlation between the sIL-2R level and duration of HD. These findings suggest that sIL-2R is a useful marker for disease activity in collagen diseases, especially in RA, and chronic viral infection such as HBV, HCV or HTLV-I in HD patients.

Autoimmune Diseases↗
PubMed1996

[A study of relation between pulmonary function and bronchial hypersensitivity in severe asthmatic children].

We studied 198 acetylcholine inhalation tests in 31 subjects and 260 exercise loading tests in 43 subjects, who were severe asthmatic children received institutional therapy. Respiratory threshold to acetylcholine (RT-Ach) were significantly lower when %V50 or %MMF were less than 60%. %V50 were significantly lower when EIB (maximum %fall in FEV1.0 after exercise) were more than 15%. These results suggest that in bronchial hypersensitivity tests, %V50 and %MMF which are indexes of peripheral airway obstruction should be examined.

Acetylcholine↗
PubMed1996

[A quantitative of serum biotin with microplate-assay using affinity streptavidin].

We modified Bayer's method of micro-plate assay for quantitation of biotin concentration. Biotin concentration in the solution and serum which cannot be quantitated directly by a microorganism assay (bio-assay), was easily determined by this method, which showed a high affinity of streptavidin for biotin this method and had a wide measurement range (0.9-60,000 pg/ml). We measured the concentration of biotin in 150 sera from 44 patients (21 males and 23 females) with active hepatitis (high level of both GOT and GPT, over 100 IU/l), 15 patients (7 males and 8 females) with inactive hepatitis (positive HCV-Ab but within normal limits of both GOT and GPT level), 17 patients (8 males and 9 females) with hepatoma and liver cirrhosis and 71 healthy persons (34 males and 37 females). The biotin concentration of sera in the healthy persons was 243.5 +/- 184.6 pg/ml, there being no sex difference. The biotin concentration in sera was higher in the patients than in healthy persons. It was high in the hepatoma and cirrhosis group (4,394.0 +/- 6,176.3), the active hepatitis group (2,397.4 +/- 2,785.5), and the inactive hepatitis group (1,873.2 +/- 1,523.7). These findings suggest that the biotin concentration is not significantly correlated with an escape enzyme such as GOT and GPT. These findings suggest that a high biotin concentration reflects other mechanisms such as escape from damaged liver cells.

Adult↗
PubMed1996

[Energy substrate metabolism during stress].

Energy substrate metabolism during stress is characterized by increased REE (resting energy expenditure), hyperglycemia, hyperlactatemia and protein catabolism. This stress-induced hypermetabolic responses are closely related to increased secretion of neurohormonal and cytokine mediators. The insulin resistance hyperglycemia has been called "stress diabetes" or "surgical diabetes". Glucose disposal has been thought to be impaired in this condition. However, glucose uptake in most tissue is non-insulin mediated. Recent studies showed glucose uptake elevated in sepsis or TNF infusion. Insulin-regulatable glucose transporter (GLUT4) is present only in muscle, heart and adipose tissues. It was demonstrated that insulin binding to membrane receptors in these tissues was intact. This hyperglycemia in stress diabetes results from a postreceptor mechanism. Stress hyperlactatemia is thought to be caused by decreased pyruvate dehydrogenase activity rather than tissue hypoperfusion. Hyperlactatemia may promote gluconeogenesis. Glucose is a essential energy substrate in some tissues such as brain, erythrocyte and leukocyte. Hyperglycemia may be viewed as a beneficial response during stress.

Biological Transport↗
PubMed1996

[Effect of recombinant human basic fibroblast growth factor (bFGF) on the growth of human tumor cell lines].

Effect of bFGF on the growth of 24 human tumor cells (established cell lines of epithelium series, mesenchymal series, muscle cell series, and nervous system series) was investigated in vitro. Of 24 cell lines examined, bFGF accelerated the growth of 6 cell lines including[A431(epidermoid carcinoma), KB (epidermoid carcinoma), HuH28 (bile duct carcinoma), YMB-1 (breast carcinoma), SW1353 (chondrosarcoma) and SKN(leiomyosarcoma)]. Epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha), utilized as control growth factors, also accelerated the growth of HuH28, SW1353 and SKN, and HuH28 and SKN, respectively. On the other hand, transforming growth factor beta 1(TGF beta 1), inhibited the growth of variety of cell lines and acceleration on cell growth was not recognized. These findings demonstrate the bFGF, as well as other growth factors, was found to promote the growth of a few cell lines investigated and that further experiments including in vivo studies will be needed. In conclusion, majority of the cell lines examined in this study seem to proliferate by their own endogenous growth factor(s) but not by exogenous bFGF.

Cell Count↗
PubMed1995

Synthesis and structure-activity relationships of acetylcholinesterase inhibitors: 1-benzyl-4-[(5,6-dimethoxy-1-oxoindan-2-yl)methyl]piperidine hydrochloride and related compounds.

Following the discovery of a new series of anti-acetylcholinesterase (anti-AChE) inhibitors such as 1-benzyl-4-[2-(N-benzoylamino)ethyl]piperidine (1), we reported that its rigid analogue, 1-benzyl-4-(2-isoindolin-2-ylethyl)piperidine (5), had more potent activity. We have extended the structure-activity relationship (SAR) study for the rigid analogue and found that the 2-isoindoline moiety in compound 5 can be replaced with a indanone moiety (8) without a major loss in potency. Among the indanone derivatives, 1-benzyl-4-[(5,6-dimethoxy-1-oxoindan-2-yl)methyl]piperidine (13e) (E2020) (IC50 = 5.7 nM) was found to be one of the most potent anti-AChE inhibitors. Compound 13e showed a selective affinity 1250 times greater for AChE than for butyrylcholinesterase. In vivo studies demonstrated that 13e has a longer duration of action than physostigmine at a dose of 5 mg/kg (po) and produced a marked and significant increase in acetylcholine content in rat cerebral cortex. We report the synthesis, SAR, and a proposed hypothetical binding site of 13e (E2020).

Animals↗
PubMed1995

Purification and properties of lysophospholipase isoenzymes from pig gastric mucosa.

Two lysophospholipases, named gastric lysophospholipases I and II (enzymes I and II), were purified 3730- and 2680-fold from pig gastric mucosa. The preparations showed 22 and 23 kDa single protein bands on SDS/PAGE respectively. Both enzymes lacked transacylase activity and appeared to exist as monomers. Their activities were not affected by Ca2+, Mg2+ or EDTA. Enzyme I was most active at pH 8.5 and hydrolysed a variety of lysophospholipids including acidic lysophospholipids and the acyl analogue of platelet-activating factor, whereas enzyme II was most active at pH 8 and its activity was confined to lysophosphatidylcholine and lysophosphatidylethanolamine. When 1-palmitoylglycerophosphocholine was used as substrate, enzymes I and II showed half-maximal activities at 11 and 12 microM respectively. The enzymes exhibited no phospholipase B, lipase or general esterase activity. Enzyme II was significantly inhibited by lysophosphatidic acid whereas enzyme I was only moderately inhibited. Peptide mapping with V8 protease and papain revealed structural dissimilarity between the two enzymes. Antiserum raised against enzyme I did not recognize enzyme II, but did recognize the small-sized lysophospholipase purified from rat liver. Anti-(enzyme II) consistently did not cross-react with enzyme I or the liver enzyme. These antisera specifically recognized neither the 60 kDa lysophospholipase transacylase purified from liver nor any peritoneal macrophage protein. Thus gastric mucosa contains two different small-sized lysophospholipases: one is closely related to the small-sized lysophospholipase of liver, but the other appears to be a novel isoform.

Animals↗
PubMed1995

Effect of biotin on ammonia intoxication in rats and mice.

The effects of biotin on ammonia concentration in blood and brain were evaluated in hyperammonemic rats and mice. Rats were injected with 5 mmol/kg BW of ammonium acetate, and mice were injected with 10 mmol/kg BW. Increases in blood ammonia levels in rats 15-30 min after ammonia loading were prevented by treatment with 0.2 ml/100 g BW of biotin or 0.04 ml/100 g BW of arginine-glutamate with statistical significance. Blood ammonia levels after ammonia loading were lower, although not significantly, in the arginine glutamate-treated rats than in the biotin-treated animals. In mice also, increases in blood and brain ammonia levels after ammonia loading were prevented by the administration of biotin. The decrease in brain glutamate and aspartate after ammonia loading was lower and the brain glutamine level was higher in biotin-treated mice than in the controls. These findings indicate the protective effect of biotin against ammonia intoxication.

Acetates↗
PubMed1995

Racemization of aspartic acid in human cementum with age.

This study explored the application of the racemization reaction to forensic dental medicine in relation to estimation of age from tooth cementum. Cementum from the cervical two-thirds and the apical one-third of 16 upper incisor teeth gave ratios of D-/L-aspartic acid that correlated highly with actual age, the correlation coefficients being r = 0.993-0.996. For whole cementum from lower central and lateral incisors, first and second premolars (n = 8) the correlation coefficients were r = 0.984-0.997. Incisors gave more reliable results than premolars. The study was extended to compare cementum, enamel and dentine from first premolar teeth of the same individuals. The correlation of the ratio of D-/L-aspartic acids with actual age was highest for dentine (r = 0.992), followed by cementum (r = 0.988) and enamel (r = 0.961). These results indicate that the racemization reaction in cementum proceeds in a constant manner, and confirm that cementum remains stable throughout the individual's life. Accurate estimation of age is thus possible when cementum is subjected to the amino-acid racemization method.

Adolescent↗
PubMed1995

A simple and rapid method for preliminary evaluation of in vivo efficacy of anti-HIV compounds in mice.

In vivo efficacy of anti-HIV compounds is affected by various factors such as bioavailability, metabolism, clearance, and toxicity. Here we report a simple and rapid method that might be useful for preliminary evaluation of in vivo efficacy of anti-HIV compounds. MT-4 cells carrying proviral HTLV-1 were infected with HIV-1 in vitro and injected into the peritoneal cavity of SCID mice or BALB/c mice. Inoculated cells survive for 1-2 days, and support one to two cycles of viral replication which can be monitored by RT activity or p24 content in the supernatants of peritoneal wash fluids. Test compounds were administered either orally or subcutaneously. AZT, DDC and DDI, the nucleoside-type RT inhibitors currently in clinical use, all showed potent anti-HIV-1 activities in this mouse/MT-4 assay. HEPT (E-EBUdM), a non-nucleoside RT inhibitor, also showed potent anti-HIV-1 activity in vivo, whereas TIBO (R82913), another non-nucleoside RT inhibitor, was less active. In protease inhibitors KNI-272 and Ro 31-8959 showed good in vivo activities, while KNI-144, a compound closely related to KNI-272, showed poor in vivo activity. This mouse/MT-4 assay, although having a number of shortcomings as an animal model for HIV-1 infection, may be of some practical utility for preliminary evaluation of in vivo efficacy of potential anti-HIV compounds.

Animals↗
PubMed1995

Ultrastructure of nonenzymatically glycated mesangial matrix in diabetic nephropathy.

Advanced protein glycation has been proposed as a major factor in the development of diabetic nephropathy. Advanced glycation end products (AGEs) have altered the structure of extracellular matrix component and impaired self association in vitro. To elucidate the role of AGEs in the progression of diabetic nephropathy, the present study was undertaken to localize glomerular AGEs immunohistochemically. Ultrastructural changes of the mesangial matrix were analyzed with high resolution scanning electron microscopy. No glomerular AGEs staining was noted in normal control kidney specimens, or in tissue from glomerulonephritis patients without diabetes mellitus. The mesangium showed a positive AGEs staining in advanced stages of diabetic nephropathy, and the most characteristic finding was the strong AGEs staining in nodular lesions. By high resolution scanning electron microscopy, control and diabetic mesangial matrices revealed a meshwork structure composed of fine fibrils (10 nm in width) and numerous pores (12 to 13 nm in diameter). In the nodular lesions, however, loosening of the meshwork was significant, and the diameter of the pores was enlarged (approximately 24 nm). This study provides the first immunohistochemical evidence that AGEs are localized in diabetic glomeruli, most notably to nodular lesions. Advanced glycation might play a role in the progression of diabetic nephropathy through impairment of the assembly of matrix proteins in vivo.

Adult↗