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Biomedical subjects

T Murase

Publications and source records attributed to T Murase.

At least 217 records · Page 12Linked to original sources
PubMed1994

Magnetic stimulation of biceps after intercostal cross-innervation for brachial plexus palsy. A study of motor evoked potentials in 25 patients.

We studied the motor evoked potentials (MEP) in the biceps of 25 patients with traumatic brachial plexus palsy from root avulsion after cross-innervation by intercostal nerves. We used transcranial, transcervical and transthoracic magnetic stimulation at 8 to 235 months (mean 51) after transfer of intercostal nerves to the musculocutaneous nerve. Biceps strength recovered to MRC grade 2 in eight patients, grade 3 in three and grade 4 in 14. The mean latency of the MEP in the normal biceps on transcranial stimulation was 12.5 +/- 1.3 ms and on transcervical stimulation 6.3 +/- 1.1 ms. After intercostal reinnervation the mean latency on transcranial stimulation was 21.7 +/- 4.5 ms and on transthoracic stimulation 11.6 +/- 3.8 ms. The latency of the biceps MEP after reinnervation by intercostal nerves on transcranial and transthoracic magnetic stimulation correlated well with the duration of follow-up and the latency of the MEP on transthoracic magnetic stimulation correlated significantly with muscle power.

Adolescent↗
PubMed1994

Exocrine pancreatic ductograms in insulin-dependent diabetes mellitus.

OBJECTIVES: To examine the prevalence of abnormal pancreatic ductograms in patients with insulin-dependent diabetes mellitus (IDDM) and to determine the clinical characteristics of those patients. METHODS: Pancreatic exocrine morphology was studied by endoscopic retrograde pancreatography (ERP) in 43 patients with IDDM, 12 patients with islet cell antibody (ICA)-positive non-insulin-dependent diabetes mellitus (NIDDM), and 22 patients with ICA-negative NIDDM. RESULTS: ERP revealed a significantly higher prevalence of abnormal pancreatic ducts (dilation and stenosis, tortuosity, obstruction, and intraductal calculi) in the patients with IDDM (17/43, 40%) than in the patients with ICA-negative NIDDM (2/22, 9%, p = 0.018). IDDM patients who slowly progressed to insulin dependency more than 13 months after the onset of diabetes had a higher frequency of abnormal pancreatic ducts (13/22, 59%) than those who needed insulin therapy within 12 months after the onset (4/21, 19%, p = 0.016). There was no difference in duration of diabetes between the two groups. ICA-positive NIDDM patients also had a higher frequency of abnormal pancreatic ducts (7/12, 58%) than ICA-negative NIDDM patients (2/22, 9%, p = 0.0074). CONCLUSIONS: These results indicate that a high proportion of IDDM patients who have prolonged histories of non-insulin dependency with ICA suffer pancreatic exocrine impairment. A similarity between IDDM with a slowly progressive clinical course and fibrocalculous pancreatic diabetes seen in tropical countries also was suggested.

Autoantibodies↗
PubMed1993

Mitochondrial gene mutation in islet-cell-antibody-positive patients who were initially non-insulin-dependent diabetics.

Autoimmunity is thought to lead to islet-cell-antibody (ICA) formation in diabetes mellitus. However, we found a mitochondrial gene mutation at nucleotide pair 3243 in 3 of 27 Japanese ICA-positive, initially non-insulin-dependent diabetic patients. All 3 progressed to insulin-dependency within 13-31 months, whereas 5 of the other 24 are non-insulin-dependent after 54-90 months. ICA, at least in these 3 patients, may follow gradual beta-cell destruction due to mitochondrial gene mutation, although the possibility of beta-cells with the mutation being susceptible to autoimmune destruction cannot be excluded.

Adolescent↗
PubMed1993

Direct evidence for preferential multiplication of Babesia gibsoni in young erythrocytes.

To clarify the effect of the age of host erythrocytes on the multiplication of Babesia parasites, B. gibsoni was cultured together with reticulocytes, immature erythrocytes, or mature erythrocytes from dogs. Parasitemia reached peak levels (34.1% +/- 15.8%) at cultivation day 8 in immature-erythrocyte culture, whereas the highest parasitemia attained in mature-cell culture was only 3.6% +/- 2.2% at day 5. These results clearly demonstrate that B. gibsoni parasites preferentially invade and multiply in young erythrocytes rather than in mature cells.

Animals↗
PubMed1993

Secretory component and lactoferrin in pure pancreatic juice in chronic pancreatitis.

To evaluate pathophysiological roles of proteins in pancreatic secretion, immunoreactive lactoferrin (LF) and secretory component (SC) were measured in the first fraction of the pure pancreatic juice obtained endoscopically from 17 control, 21 suspected (SCP), 14 noncalcified (NCP), and 14 calcified chronic pancreatitis (CCP) subjects. The protein and amylase tended to decrease both in concentration and output from control to CCP. LF concentration was elevated in CCP (18.0 +/- 4.9 micrograms/ml) when compared with controls (2.3 +/- 0.2 micrograms/ml), and LF output in NCP (12.3 +/- 3.8 micrograms/min) was increased from controls (3.8 +/- 0.6 micrograms/min). The combination of high LF concentration with low protein output was observed in 10/14 in CCP but 0/14 in NCP and can be a biochemical discriminator of CCP from NCP. SC concentrations were also elevated in NCP (8.5 +/- 2.0 micrograms/ml) and CCP (5.6 +/- 1.6 micrograms/ml) from controls (1.2 +/- 0.2 micrograms/ml). SC outputs in SCP (9.8 +/- 3.1 micrograms/min) and NCP (21.1 +/- 4.8 micrograms/min) were increased from controls (1.7 +/- 0.3 micrograms/min), but there was no further increase in CCP. Hypersecretion of LF and SC in chronic pancreatitis is different, especially in CCP, although the mechanisms for hypersecretion are unknown.

Adult↗
PubMed1993

Relationships among residual beta cells, exocrine pancreas, and islet cell antibodies in insulin-dependent diabetes mellitus.

Quantitative analysis was performed using computerized morphometry on the relationships between residual beta cells, pancreatic exocrine glands, and islet cell antibodies (ICA) in 14 pancreata of insulin-dependent diabetic (IDDM) patients. Both pancreatic exocrine glands and beta cells were markedly reduced in weight in IDDM patients compared with non-insulin-dependent diabetic (NIDDM) patients or nondiabetic controls. beta cells were preserved in six cases and were completely abolished in eight cases. In nine IDDM pancreata weighed at autopsy, the weights of pancreatic exocrine glands in six patients with either no or virtually no residual beta cells (32.3 +/- 1.6 g) were greater than those in three patients with residual beta cells (23.1 +/- 2.5 g, P < .05). Infiltration of lymphocytes positive for leukocyte common antigen (LCA) around the islet was observed in only one case with ICA and residual beta cells. Infiltration of LCA-positive lymphocytes around pancreatic acinar cells was observed in 50% (six of 12) of patients examined. The weight of pancreatic exocrine glands in patients with LCA-positive lymphocyte infiltration (26.2 +/- 2.3 g) was lower than that in patients without this condition (33.2 +/- 2.4 g, P < .05). Pancreatic cytokeratin autoantibodies (PKA) were detected in four of 10 patients examined. In addition, all four ICA-positive patients had residual beta cells, while only one of seven ICA-negative patients had residual beta cells (P = .03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Serum lipoprotein(a) levels differ in different phenotypes of primary hyperlipoproteinemia.

Previous studies have indicated that serum lipoprotein(a) [Lp(a)] levels are mostly under genetic control. We have attempted to determine whether serum Lp(a) levels differ in different phenotypes of primary hyperlipoproteinemia (HL). A total of 129 subjects with HL (three with type I, 43 with familial hypercholesterolemia [FH], 17 with type IIa [non-FH], 11 with type IIb, six with type III [E2/2], 44 with type IV, and five with type V) and 18 normolipidemic controls were included in the study. Thirty-two FH subjects were being treated with hypolipidemic agents, but none of the other subjects were receiving any medication. Fasting blood samples were collected for determination of both serum lipid and Lp(a) levels. Lp(a) level was measured by enzyme-linked immunosorbent assay. The 18 controls had serum Lp(a) concentrations of 18.0 +/- 14.5 mg/dL (mean +/- SD), and four of them had high serum Lp(a) levels (> or = 25 mg/dL). Serum Lp(a) concentrations in FH subjects tended to be higher than in the controls (30.5 +/- 25.0 mg/dL), and the incidence of high Lp(a) levels in FH subjects was significantly higher than in the controls (51% v 22%, P < .01). There was no difference between serum Lp(a) levels of FH subjects depending on whether they were receiving medication. In contrast, most of the subjects with selective hypertriglyceridemia had very low serum Lp(a) levels (1.5 +/- 0.7, 8.1 +/- 8.3, and 3.5 +/- 5.3 mg/dL in type I, IV, and V, respectively; P < .01 v controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Erythrocyte ALA-d activity in experimentally lead-poisoned ducks and its change during treatment with disodium calcium EDTA.

To determine useful procedures for the diagnosis and prognosis of lead poisoning in waterfowl caused by ingestion of lead pellets, erythrocyte delta-aminolevulinic acid dehydratase (ALA-d) was investigated in experimentally lead-poisoned ducks. A highly positive correlation was observed between the concentration of blood lead and the ALA-d activity ratio (the ratio of activated:non-activated enzyme activity) in those birds given seven lead pellets (3 mm diameter). The ALA-d activity ratio rapidly increased after the administration of lead pellets, but began to fall immediately after the initiation of disodium calcium ethylenediamine tetra-acetate (CaEDTA) therapy which resulted in a rapid decrease in the concentration of lead in the blood of these birds. In contrast, the ALA-d activity remained inhibited even after blood lead levels began to decrease following treatment. These results demonstrated that the ALA-d activity ratio is a very useful and sensitive indicator for the diagnosis and evaluation of therapeutic effects after lead poisoning in waterfowl.

Animals↗
PubMed1993

Effects of different protein supplements in fertilization medium on in vitro penetration of cumulus-intact and cumulus-free bovine oocytes matured in culture.

Bovine oocytes matured in culture were inseminated with frozen-thawed spermatozoa in BO medium containing 5 mM-caffeine, 10 mug/ml of heparin and different protein supplements at various concentrations. When cumulus-enclosed oocytes were inseminated, no significant differences were observed in the penetration rates (89 to 100%) between media with and without protein supplements and among the different concentrations of each protein supplement, except for 20% calf serum (CS), in which the penetration rate decreased drastically (43%). Notably higher incidences of polyspermy were obtained in medium with FCS (75 to 86%) than with either no supplement (25%) or with BSA (20 to 24%) and CS (13 to 49%). On the other hand, there was almost no penetration of cumulus-free oocytes in the nonsupplemented control medium. Concentration-dependent increases in penetration and polyspermy occurred with BSA, FCS and CS supplementation. A high concentration (5%) of FCS yielded a high incidence (97%) of polyspermy. A decrease in the penetration of cumulus-enclosed oocytes was observed when spermatozoa were capacitated with a high concentration (20%) of CS; difficulty of sperm penetration of cumulus-free oocytes occurred when the capacitation medium lacked protein supplementation; and an increased rate of polyspermy was observed following supplementation with FCS in both cumulus-enclosed and cumulus-free oocytes after insemination with spermatozoa from 5 different bulls.

Journal Article↗
PubMed1993

Ultrasonically guided follicular aspiration during a pregnancy with massive ovarian cysts following ovulation induction by gonadotropins.

In this report, the treatment by follicular aspiration was evaluated in a pregnant patient with severe ovarian cysts subsequent to ovulation induction with CC and gonadotropins. The patient had dramatic and immediate improvement of the symptoms and general condition as well as a significant shorter hospital stay. The procedure was, under meticulous US guidance, safe and effective, providing additional improvement or increased therapeutic confidence in the severe complications after ovulation induction, as an assisted option during pregnancy.

Adult↗
PubMed1993

Apolipoprotein E metabolism in sciatic nerves of diabetic rats. Implication for diabetic neuropathy.

Apolipoprotein (apo) E secreted by macrophages plays an important role in nerve injury and repair. We investigated the disturbance of neural apo E metabolism in diabetic rats and its relation to diabetic neuropathy. In BB/W rats, genetically diabetes prone rats, the secretion of apo E from sciatic nerves was 3-fold greater than that in control rats. Furthermore, a similar enhancement of apo E secretion was observed in injured nerves of STZ-induced diabetic rats (2-fold) as compared with those of nondiabetic rats, and this was reversible with insulin treatment. Histological examination of the nerves revealed more extensive infiltration of mononuclear cells in the injured nerves of STZ-induced diabetic rats than in those of non-diabetic rats. This is consistent with the findings that chemotactic activities for mononuclear cells, which were released from injured nerves, were greater in the STZ-induced diabetic rats than in the non-diabetic rats. From these results we conclude that the recruitment of monocyte/macrophages into injured nerves is enhanced in diabetes, thereby causing derangement of neural apo E metabolism. These abnormalities might contribute to the development of diabetic neuropathy.

Adult↗
PubMed1993

Enhancing effects of estrogens on endometrial carcinogenesis initiated by N-methyl-N-nitrosourea in ICR mice.

The present study was undertaken to examine the effects of estrogens, such as estrone (E1), 17 beta-estradiol (E2) and estriol (E3), on endometrial carcinogenesis initiated by N-methyl-N-nitrosourea (MNU) in mice. A total of 120 female ICR mice received MNU solution (1 mg/100 g body wt.) and normal saline at 10 weeks of age into their left and right uterine corpora, respectively. One week later, they were divided into four groups and treated as follows: Group 1 (30 mice) was given 25 ppm E1-containing diet; and Group 2 (30 mice) was fed 5 ppm E2-containing diet; Group 3 (30 mice) was given 25 ppm E3-containing diet; and Group 4 (30 mice) was fed the basal diet alone. At the termination of the experiment (Week 30), all surviving animals were autopsied and histopathological examinations revealed that endometrial adenocarcinomas had developed in all groups. The incidence of adenocarcinomas in the MNU-treated uterine corpus in Group 1 (25 ppm E1-feeding, 9/23, 39%) was significantly higher than that in Group 4 (basal diet, 3/26, 12%, P < 0.05). Also, the incidences of adenocarcinomas in the MNU-treated uterine corpus in Groups 2 (5 ppm E2-feeding, 8/24, 33%) and 3 (25 ppm E3-feeding, 7/26, 28%) were higher than in Group 4, but the difference was not statistically significant. Feeding of diet containing E1, E2 and E3 increased the incidences of the preneoplastic endometrial lesions (atypical, adenomatous or cystic glandular hyperplasia). In the uterine cervix, small numbers of squamous cell carcinomas, dysplasias or hyperplasias were occasionally found in all groups. These results indicate enhancing effects of the above three types of estrogens on the endometrial carcinogenesis induced by MNU in ICR mice.

Adenocarcinoma↗
PubMed1993

Determinants of fasting hypertriglyceridemia in ventromedial hypothalamic obesity in rats.

The present study investigated the mechanism of fasting hypertriglyceridemia in ventromedial hypothalamic (VMH) obesity by measurement of post-heparin plasma lipoprotein lipase (LPL) activity, triglyceride secretion rate (TGSR), and plasma insulin. One week after VMH lesions, when the lesioned rats were gaining weight rapidly (the dynamic phase), they showed normal plasma triglyceride levels with increased plasma LPL activity and TGSR. There was a positive correlation between hyperinsulinemia and elevated plasma LPL activity or TGSR in VMH-lesioned rats, while no correlation was observed in control rats. Ten weeks after VMH lesions, when the rats had become obese and reached a steady-state weight gain (the static phase), they showed hypertriglyceridemia with increased plasma LPL activity and TGSR. There was, again, a positive correlation between hyperinsulinemia and elevated plasma LPL activity or TGSR in VMH-lesioned rats. These results suggest a possible mechanism of fasting hypertriglyceridemia in these rats; in the dynamic phase adipose tissue adequately takes up circulating triglyceride because the tissue has sufficient take-up capacity and hence hypertriglyceridemia does not develop. In the static phase the tissue cannot adequately take up circulating triglyceride because of a limitation of its capacity, resulting in hypertriglycemia despite enhanced triglyceride secretion and increased LPL activity in both phases.

Animals↗
PubMed1993

Galanin as a physiological neurotransmitter in hemodynamic control of arginine vasopressin release in rats.

Previous neuroanatomical studies have revealed a localization of galanin in several nuclei in the brain stem which are involved in the hemodynamic control of arginine vasopressin (AVP) release. The present study, therefore, investigates the contribution of endogenous galanin to the plasma volume-mediated control of AVP release in conscious rats. Injection of synthetic rat galanin (12.5-50 pmol/rat) into the cisterna magna (i.c.s.) suppressed plasma AVP increased by polyethylene glycol-induced hypovolemia (2.45 +/- 0.24 pg/ml at 50 pmol/rat vs. the vehicle group 5.72 +/- 0.69 pg/ml, p < 0.01). In contrast, when plasma AVP was suppressed by isotonic plasma volume expansion, immunoneutralization of endogenous galanin by antigalanin-antibody i.c.s. significantly reversed the suppression (1.02 +/- 0.07 pg/ml vs. vehicle group 0.63 +/- 0.05 pg/ml, p < 0.01) without altering the mean arterial blood pressure. These results suggest that endogenous galanin is physiologically involved in the plasma volume-mediated control of AVP release through an inhibitory action on this pathway.

Animals↗
PubMed1993

Pituitary adenylate cyclase-activating polypeptide stimulates arginine vasopressin release in conscious rats.

The effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on arginine vasopressin (AVP) release was investigated in conscious rats. Intracerebroventricular (i.c.v.) administration of PACAP raised the plasma AVP concentration in a dose-dependent manner (50-500 pmol/rat), and the maximum effect was obtained at 5 min after the administration. This AVP-releasing effect was not due to a fall of blood pressure, increase of plasma Na or decrease of plasma volume, all of which are known to stimulate AVP release. PACAP had little effect on blood pressure at a low dose, but at higher doses increased it. Vasoactive intestinal peptide (VIP), which is homologous to PACAP, also raised the plasma AVP concentration by i.c.v. injection. An antagonist for VIP receptor, [Lys, Pro, Arg, Tyr]-VIP inhibited the VIP-induced increase of plasma AVP, but had little effect on PACAP-induced increase of plasma AVP. These results suggest that PACAP stimulates AVP release, via specific receptors which are distinct from VIP receptors.

Animals↗
PubMed1993

Possible involvement of inefficient cleavage of preprovasopressin by signal peptidase as a cause for familial central diabetes insipidus.

A transition of G to A at nucleotide position 279 in exon 1 of the vasopressin gene has been identified in patients with familial central diabetes insipidus. The mutation predicts an amino acid substitution of Thr (ACG) for Ala (GCG) at the COOH terminus of the signal peptide in preprovasopression (preproVP). Translation in vitro of wild-type and mutant mRNAs produced 19-kD preproVPs. When translated in the presence of canine pancreatic rough microsomes, wild-type preproVP was converted to a 21-kD protein, whereas the mutant mRNA produced proteins of 21 kD and 23 kD. NH2-terminal amino acid sequence analysis revealed that the 21-kD proteins from the wild-type and the mutants were proVPs generated by the proteolytic cleavage of the 19-residue signal peptide and the addition of carbohydrate. Accordingly, mutant preproVP was cleaved at the correct site after Thr-19, but the efficiency of cleavage by signal peptidase was < 25% that observed for the wild-type preproVP, resulting in the formation of a predominant glycosylated but uncleaved 23-kD product. These data suggest that inefficient processing of preproVP produced by the mutant allele is possibly involved in the pathogenesis of diabetes insipidus in the affected individuals.

Amino Acid Sequence↗