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Biomedical subjects

M Matsuda

Publications and source records attributed to M Matsuda.

At least 415 records · Page 23Linked to original sources
PubMed1996

A possible role of the nestin protein in the developing central nervous system in rat embryos.

Rat embryos at the head-hold stage (Slc:SD strain; 9.5 days of gestation) were cultured for 48 h in rat serum with the anti-nestin peptide antiserum. The antiserum identified a single band in Western blots of the tissue extracts from rat embryos and stained the cells from the neural tube, migrating neural crest, and somites immunohistochemically. The antiserum-treated embryos appeared to develop normally for the most part. However, histological observation disclosed that the ventral portion of the neural tube was deformed. The cells in the deformed portion did not show the elongated shape but were round. These round cells tended to crowd near the ventricular surface, and a gap was observed between the original pial surface and cells arranged in the most pialward region. The penetration of the anti-nestin peptide antibody into the embryos from the culture medium was confirmed by visualization of the penetrated antibody using biotinylated anti-rabbit IgG antibody raised in goats and Texas red-conjugated streptavidin. These results indicate that the nestin protein plays an important role in the organization or the maintenance of neuroepithelial cells of the elongated shape spanning the neural tube from the luminar to the pial side.

Animals↗
PubMed1996

A gamma Gly-268 to Glu substitution is responsible for impaired fibrin assembly in a homozygous dysfibrinogen Kurashiki I.

A new type of gamma Gly-268 (GGA) to Glu (GAA) substitution has been identified in a homozygous dysfibrinogen by analyses of the affected polypeptide and its encoding gene derived from a 58 year-old man manifesting no major bleeding or thrombosis. The functional abnormality was characterized by impaired fibrin assembly most likely due to failure to construct properly aligned double-stranded fibrin protofibrils. This presumption was deduced from the following findings: (1) Factor XIIIa-catalyzed cross-linking of the fibrin gamma-chains progressed in a normal fashion, indicating that the contact between the central E domain of one fibrin monomer and the D domain of another took place normally; (2) Nevertheless, factor XIIIa-catalyzed cross-linking of the fibrinogen gamma-chains was obviously delayed, suggesting that longitudinal association of D domains of different fibrin monomers, ie, D:D association was perturbed; (3) Plasminogen activation catalyzed by tissue-type plasminogen activator was not as efficiently facilitated by polymerizing fibrin monomer derived from the patient as by the normal counterpart. Therefore, gamma Gly-268 would not be involved in the 'a' site residing in the D domain, which functions as a complementary binding site with the thrombin-activated 'A' site in the central E domain, but would be rather involved in the D:D self association sites recently proposed for human fibrinogen. Thus, the gamma Glu-268 substitution newly identified in this homozygous dysfibrinogen seems to impair proper alignment of adjacent D domains of neighboring fibrin molecules in the double-stranded fibrin protofibril, resulting in delayed fibrin gel formation.

Afibrinogenemia↗
PubMed1996

Abnormalities in the mitochondrial permeability transition in diabetic rats.

Evidence of mitochondrial dysfunction in diabetes led us to examine whether diabetes altered the nature of the mitochondrial permeability transition. Our data reveal three diabetes-associated abnormalities in PT function: consistently delayed induction with calcium-phosphate, a variable delay with calcium-t-butyl-hydroperoxide (t-BuOOH), and an enhanced magnitude of response. The consistently delayed induction in calcium and phosphate is correlated with serum glucose levels, and is consistent with known changes in calcium uniporter function in diabetics. These data expand our knowledge of diabetes-associated abnormalities in mitochondrial function, represent the first evidence that the PT is altered by chronic disease, and provide potential partial mechanistic explanations for the previously observed resistance of diabetic tissues to ischemia-reperfusion injury and the altered Ca2+ homeostasis in diabetics.

Animals↗
PubMed1996

The ultrastructure of fibrinogen Caracas II molecules, fibers, and clots.

Fibrinogen Caracas II is an abnormal fibrinogen involving the mutation of A alpha serine 434 to N-glycosylated asparagine. Some effects of this mutation on the ultrastructure of fibrinogen Caracas II molecules, fibers, and clots were investigated by electron microscopy. Electron microscopy of rotary shadowed individual molecules indicated that most of the alphaC domains of fibrinogen Caracas II do not interact with each other or with the central domain, in contrast to control fibrinogen. Negatively contrasted Caracas II fibers were thinner and less ordered than control fibers, and many free fiber ends were observed. Scanning electron microscopy of whole clots revealed the presence of large pores bounded by local fiber networks made up of thin fibers. Permeation experiments also indicated that the average pore diameter was larger than that of control clots. The viscoelastic properties of the Caracas II clot, as measured by a torsion pendulum, were similar to those of control clots. Both the normal stiffness and increased permeability of the Caracas II clots are consistent with the observation that subjects with this dysfibrinogenemia are asymptomatic.

Asparagine↗
PubMed1996

Progression in gastric carcinoma relative to the ratio of CD44 epithelial variant transcript to CD44 hematopoietic variant transcript.

BACKGROUND: It has been suggested that CD44 splice variants play a role in the progression of certain epithelial cancers and non-Hodgkin's lymphoma. In this study, we investigated the epithelial variant/hematopoietic variant (E/H) ratio (the amount of the CD44 epithelial variant transcript relative to the CD44 hematopoietic variant transcript) in human gastric carcinoma compared with normal gastric mucosa. METHODS: The ratio was determined for tumors and adjacent noncancerous mucosa from 30 gastric carcinoma patients using reverse transcription-polymerase chain reaction and Southern blotting. We also determined the tumor (T)E/H--noncancerous mucosa (N)E/H (the difference between E/H ratios of tumor tissue and adjacent noncancerous mucosa) and examined these measurements for correlations with the pathologic features of gastric carcinoma, as well as for their usefulness as an indicator of tumor progression. RESULTS: The E/H ratio in tumor tissue was significantly higher than in adjacent noncancerous mucosa (P < 0.01). The TE/H--NE/H in patients with lymph node metastases was 0.16 +/- 0.11, compared with 0.07 +/- 0.08 in cases without lymph node metastases (P < 0.05). Significant correlations also were observed between the TE/H--NE/H and the depth of invasion, blood vessel invasion, and lymphatic vessel invasion (P < 0.03, P < 0.03, and P < 0.01, respectively). CONCLUSIONS: Our results suggest that increases in the E/H ratio may be a useful indicator of progression in gastric carcinoma.

Adult↗
PubMed1996

Hypertrophic neuritis due to chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): a postmortem pathological study.

A postmortem pathological study of a 65-year-old woman with hypertrophic neuritis associated with hand tremor and limb ataxia is described. There were many onion bulbs and loss of myelinated nerve fibers in the peripheral nerves, including the facial and subserosal visceral nerves. The hypertrophic neuritis was caused by chronic inflammatory demyelinating neuropathy (CIDP), in which interstitial amorphous substances in the endoneurium and onion bulb formation might contribute to nerve swelling. We speculate that visceral autonomic nerves as well as somatic peripheral nerves are involved in patients with a long clinical CIDP course and that peripheral nerve pathology in this disorder shows more heterogeneous changes than previously recognized.

Aged↗
PubMed1996

Mechanism of left atrial enlargement related to ventricular diastolic impairment in hypertension.

BACKGROUND AND HYPOTHESIS: Systemic hypertension is the leading cause of left ventricular (LV) hypertrophy. The present study aimed to investigate the mechanism of left atrial (LA) enlargement in patients with hypertensive heart disease during cardiac catheterization. METHODS: Data were obtained from eight control subjects and seven patients with hypertensive heart disease. Left atrial and LV pressures from catheter-tip micromanometer, and LA and LV volumes from biplane cineangiograms were analyzed during the same cardiac cycle. RESULTS: Left atrial maximal volume were 93 +/- 26 ml in patients with hypertensive heart disease and 63 +/- 12 ml in control subjects (p < 0.05). In patients with hypertensive heart disease, time constant of LV relaxation was significantly greater than that in controls (54 +/- 18 vs. 31 +/- 16 ms, respectively; p < 0.01). Left atrial maximal volume correlated with time constant of LV relaxation (r = 0.86, p < 0.01). The ratio of LV filling volume before LA contraction to LV stroke volume in patients with hypertensive heart disease was significantly lower than that in control subjects (65 +/- 13 vs. 76 +/- 7%, respectively; p < 0.05). On the other hand, the ratio of LV filling volume during LA contraction to stroke volume in patients with hypertensive heart disease was significantly higher than that in controls (35 +/- 13 vs. 24 +/- 7%, respectively; p < 0.05). Left atrial volume before LA contraction in patients with hypertensive heart disease was significantly larger than that in controls (74 +/- 22 vs. 47 +/- 10 ml, respectively, p < 0.01). During LA contraction, LA work was significantly increased in patients with hypertensive heart disease compared with that in controls (274 +/- 101 vs. 94 +/- 42 mmHg. ml, respectively; p < 0.001). Left atrial work showed significant correlation with LA volume before LA contraction (r = 0.75, p < 0.01). CONCLUSION: Left ventricular diastolic filling was impaired in patients with hypertensive heart disease. Enlargement of left atrium might be attributed to the impairment of blood flow from left atrium to left ventricle due to the increased LV stiffness.

Adult↗
PubMed1996

Potential doubling time and tumour doubling time in meningiomas and neurinomas.

Cell kinetic study plays an important role in treatment planning of brain tumour patients. MIB-1 antibody has recently become available, which detects Ki-67 antigen even in the formalin-fixed paraffin-embedded specimens. We performed MIB-1 immunostaining in 50 meningiomas and 50 neurinomas, and estimated the cell cycle time (tc) and potential doubling time (Tpot) from MIB-1 staining index (MIB-1 SI) and mitotic index (MI). MIB-1 SI logarithmically correlated with MI in both meningiomas and neurinomas. The tc and the Tpot were expressed as a function of the mitosis time (tm), while the tm is known to be around one hour and not exceeding two hours. When the tm was assumed to be one hour, the average tcs of meningiomas and neurinomas were 6.53 +/- 3.56 days and 7.67 +/- 3.27 days, respectively. The Tpots were 447 X (MIB-1 SI)-1.29 X tm in meningiomas, and 490 X (MIB-1 SI)-0.98 X tm in neurinomas. The tumour doubling times (Tds) were calculated from serial imaging studies in 22 neurinomas and 15 meningiomas. The Tds were formulated as 794 X (MIB-1 SI)-0.83 in meningiomas and 1380 X (MIB-1 SI)-0.97 in neurinomas. Most of the Tds correlated well with the Tpots in meningiomas and neurinomas, and exceeded values of the Tpot when the tm is assumed to be one hour, although a few tumours showed unexpectedly longer Tds. The Tpot and the to estimated from MIB-1 SI and MI are clinically useful parameters for predicting the growth potential of meningiomas and neurinomas where no other simple methods are available.

Adolescent↗
PubMed1996

Insulin resistance and coronary artery disease.

The purpose of the present study was to quantitate insulin-mediated glucose disposal in normal glucose tolerant patients with angiographically documented coronary artery disease (CAD) and to define the pathways responsible for the insulin resistance. We studied 13 healthy, normal weight, normotensive subjects with angiographically documented CAD and 10 age-, weight-matched control subjects with an oral glucose tolerance test and a 2-h euglycaemic insulin (40 mU.m-2.min-1) clamp with tritiated glucose and indirect calorimetry. Lean body mass was measured with tritiated water. All CAD and control subjects had a normal oral glucose tolerance test. Fasting plasma insulin concentration (66 +/- 6 vs 42 +/- 6 pmol/l, p < 0.05) and area under the plasma insulin curve following glucose ingestion (498 +/- 54 vs 348 +/- 42 pmol.l-1.min-1, p < 0.001) were increased in CAD vs control subjects. Insulin-mediated whole body glucose disposal (27.8 +/- 3.9 vs 38.3 +/- 4.4 mumol.kg fat free mass (FFM)-1.min-1, p < 0.01) was significantly decreased in CAD subjects and this was entirely due to diminished non-oxidative glucose disposal (8.9 +/- 2.8 vs 20.0 +/- 3.3 mumol.kg FFM-1.min-1, p < 0.001). The magnitude of insulin resistance was positively correlated with the severity of CAD (r = 0.480, p < 0.05). In the CAD subjects basal and insulin-mediated rates of glucose and lipid oxidation were normal and insulin caused a normal suppression of hepatic glucose production. In conclusion, subjects with angiographically documented CAD are characterized by moderate-severe insulin resistance and hyperinsulinaemia and should be included in the metabolic and cardiovascular cluster of disorders that comprise the insulin resistance syndrome or "syndrome X'.

Blood Glucose↗
PubMed1996

Chronic effect of hyperprolactinemia on blood glucose and lipid levels in mice.

We studied the chronic effects of hyperprolactinemia, induced by ectopic pituitary grafting, on blood glucose and lipid levels in adult male mice. For one year after pituitary grafting, we measured the blood levels of prolactin, growth hormone (GH), insulin, glucose and free fatty acid (FFA) at various intervals. The graft caused consistent hyperprolactinemia without changes in the serum GH levels. Hypoglycemia developed at 1 and 3 months after grafting but was not accompanied by any changes of the serum insulin levels. Thereafter, the blood glucose and serum insulin levels began to increase in the pituitary-grafted (PG) mice, and at 12 months after the operation, both levels became significantly higher in PG mice than controls. The serum FFA levels and the weight of epididymal fat bodies were significantly lower in PG mice than controls from 3-12 months after the grafting. Thus, hyperprolactinemia leads to persistent hypolipidemia and biphasic changes in the blood glucose level.

Adipose Tissue↗
PubMed1996

Plasma endothelin-1 level in athletes after exercise in a hot environment: exercise-induced dehydration contributes to increases in plasma endothelin-1.

We investigated whether dehydration due to exercise contributes to the increase in plasma endothelin-1 (ET-1) concentration. We measured the plasma concentration of ET-1 before and after exercise in a hot environment (about 30 degrees C). Five male intercollegiate Kendo (Japanese fencing) players entered the present study. Each athlete participated in 15 min of Kendo fighting, followed by 5 min of rest and another 15 min of Kendo fighting (i.e., total exercise 30 min), with or without oral intake of 700 ml of water. Body weight and left atrial diameter, a parameter that reflects changes in circulating plasma volume, were significantly decreased after exercise under both conditions. However, the decreases in both values were significantly greater after exercise without water intake than after exercise with water intake, indicating that dehydration and decreased circulating plasma volume were more marked after exercise without water intake. The extent of the increase in plasma ET-1 concentration appeared to be closely related to the extent of exercise-induced dehydration; the greater the dehydration, the greater the increase in plasma ET-1 concentration. These findings suggest that exercise-induced dehydration may contribute to increases in plasma ET-1 concentrations.

Adult↗
PubMed1996

Plasma protein-bound sulfhydryl group oxidation in humans following a full marathon race.

Physical exercise can induce oxidative stress in humans. We studied the influence of aerobic exercise on the status of plasma protein-bound sulfhydryl groups in seven moderately-trained male college students who participated in a full marathon race. The plasma protein-bound sulfhydryl group values were significantly declined immediately after the race (-22%, p < 0.01), and 24 h (-12%, p < 0.01) and 48 h (-13%, p < 0.01) after the race, as compared to the baseline value. The plasma concentrations of thiobarbituric acid reactive substances were unchanged following the race, while the activities of plasma creatine kinase were significantly increased, indicating skeletal muscle damage. These results suggested that prolonged exercise may cause the oxidation of plasma proteins.

Adult↗
PubMed1996

Acute focal cerebral ischemia in rats studied by diffusion-weighted magnetic resonance imaging--an experimental study.

BACKGROUND: Temporary occlusion of the cerebral artery is occasionally repeated during neurosurgical operations, but the safety of such a procedure remains to be studied further. METHOD: We studied early changes and reversibility of focal cerebral ischemia and the cumulative effects of repeated ischemic insults in rats using magnetic resonance imaging (MRI). RESULTS: Diffusion-weighted magnetic resonance images (DWI) and determination of signal intensity ratio (SIR) proved to be a valuable measure of studying early changes and reversibility of transient focal cerebral ischemia and cumulative adverse effects of repeated ischemic insults. DWIs showed marked intensity changes shortly after focal cerebral ischemia, while T2-weighted images failed to show hyperintensities until 2.5 hours after the onset of permanent ischemia. The critical period of ischemia in this model was 60 minutes. However, 20 minutes ischemia, when repeated twice with 60 minutes reperfusion in between, showed irreversible damage. CONCLUSION: Repeated insults of focal regional cerebral ischemia may cause irreversible tissue damage even if each ischemic period is less than the critical one.

Animals↗
PubMed1996

Emerging components of the Crk oncogene product: the first identified adaptor protein.

v-Crk, identified as an oncogene product of the CT10 retrovirus, became the first example of an adaptor protein. It consists mostly of the Src homology 2 (SH2) and Src homology 3 (SH3) domains. Two of the three major proteins bound to Crk SH2 have been identified as paxillin and p130Cas. Both paxillin and p130Cas are phosphorylated upon stimulation by integrin, suggesting that Crk transduces signals from integrin. The cloning of the complementary DNA of two major proteins bound to Crk SH3 was recently completed. Both cDNAs encoded novel proteins: C3G, a guanine nucleotide exchange protein for Rap1, and DOCK180, an SH3-containing protein of unknown function. The SH3 domain of Crk also binds to Sos, Abl, and Eps15. The variety of the proteins bound to Crk SH3 implies that Crk provides a set of effector proteins that are triggered together. Alternatively, other domains of the SH3-binding proteins enable Crk to specifically activate each of the SH3-binding proteins according to the particular form of stimulation.

Animals↗
PubMed1996

The structure-function relationship of hereditary dysfibrinogens.

Fibrinogen is a 340-kDa multi-subunit glycoprotein present in plasma and tissues of all classes of vertebrates. Fibrinogen exerts a variety of physiologically important functions, and most of them, if not all, are assigned to certain structures of fibrin including double-stranded fibrin protofibrils and highly crosslinked fibrin networks. Fibrin formation is indeed a series of highly ordered molecular interactions. The mechanisms underlying these molecular interactions have been extensively studied in the last 40 years, but there still remain many enigmas. In this mini-review, the structure-function relationships of hereditary dysfibrinogens are discussed.

Afibrinogenemia↗