Biomedical subjects

H Tsuchimochi

Publications and source records attributed to H Tsuchimochi.

At least 19 recordsLinked to original sources

PubMed2002

Altered sarcoplasmic reticulum function in rat diaphragm after high-intensity exercise.

The present study examined the effects of acute high-intensity exercise on Ca(2+) uptake and release rates and Ca(2+)-adenosine triphosphatase (ATPase) activity of the sarcoplasmic reticulum (SR) from the costal diaphragm. The rats were run on a treadmill at an estimated requirement of 100% of maximal O2 consumption until fatigued (average time to exhaustion: 4.79 min). Muscle lactate and inorganic phosphate after exercise were increased by 65% (P < 0.05) and 35% (P < 0.05), respectively. With exercise, Ca(2+) uptake and release, which were detected in homogenates using the Ca(2+) fluorescent dye indo-1, were decreased by 24% (P < 0.05) and 22% (P < 0.05), respectively. The reduction in Ca(2+) uptake was paralleled by decreased activity of SR Ca(2+)-ATPase in both the absence and presence of Ca(2+) ionophore. These findings demonstrate that, in the diaphragm as well as in the locomotor muscles that have been explored in previous studies, the attenuations of the SR function is brought about by acute high-intensity exercise. These changes in the SR of the diaphragm may contribute, at least in part, to deteriorations in exercise tolerance and work productivity resulting from repetitive physical activities.

Animals↗

PubMed2001

Reflex responses in plasma catecholamines caused by static contraction of skeletal muscle.

To examine a hypothesis of whether static muscle contraction produces a release of catecholamines from the adrenal medulla via reflex stimulation of preganglionic adrenal sympathetic nerve activity induced by receptors in the contracting muscle, we compared the reflex responses in a concentration of epinephrine (Ep) and norepinephrine (NEp) in arterial plasma during static contraction and during a mechanical stretch of the hindlimb triceps surae muscle in anesthetized cats. Static contraction was evoked by electrically stimulating the peripheral ends of the cut L(7) and S(1) ventral roots at 20 or 40 Hz. Mean arterial pressure (MAP) and heart rate (HR) increased 23 +/- 3.1 mmHg and 19 +/- 4.3 beats/min during static contraction. Ep in arterial plasma increased 0.18 +/- 0.072 ng/ml over the control of 0.14 +/- 0.051 ng/ml within 1 min from the onset of static contraction, and NEp increased 0.47 +/- 0.087 ng/ml over the control of 0.71 +/- 0.108 ng/ml. Following a neuromuscular blockade, although the same ventral root stimulation failed to produce the cardiovascular and plasma catecholamine responses, the mechanical stretch of the muscle increased MAP, HR, and plasma Ep, but not plasma NEp. With bilateral adrenalectomy, the baseline Ep became negligible (0.012 +/- 0.001 ng/ml) and the baseline NEp was lowered to 0.52 +/- 0.109 ng/ml. Neither static contraction nor mechanical stretch produced significant responses in plasma Ep and NEp following the adrenalectomy. These results suggest that static muscle contraction augments preganglionic adrenal sympathetic nerve activity, which in turn secretes epinephrine from the adrenal medulla into plasma. A muscle mechanoreflex from the contracting muscle may play a role in stimulation of the adrenal sympathetic nerve activity.

Adrenal Medulla↗

PubMed2000

A case of papillary meningioma with a t(1;4)(q44;q21).

We report the results of cytogenetic analyses of three cases of meningiomas. The first case, a papillary meningioma, showed only one cytogenetic abnormality, 46,XX,t(1;4)(q44;q21). In contrast, the other two benign fibroblastic meningiomas showed loss of chromosome 22. Loss and/or rearrangement of chromosomes other than chromosome 22 appears to be associated with a more aggressive clinical course. It is suggested that a sole cytogenetic abnormality with a normal chromosome 22 indicates an atypical nature of meningioma.

Adult↗

PubMed1999

Assessment of long-distance running performance in elite male runners using onset of blood lactate accumulation.

The purpose of this study was to evaluate the relationship between onset of blood lactate accumulation (OBLA) and long-distance running performance in order to examine whether OBLA can be a good predictor of long-distance running performance even in elite male runners with similar performance levels. Eleven highly-trained male long-distance runners participated in this study. The average running velocities of the individuals' running performance were 5.918 +/- 0.084 m.s-1 and 5.672 +/- 0.095 m.s-1 for 5000 m (V5000) and 10,000 m (V10000), respectively. The blood lactate concentrations and heart rate responses were measured immediately after field running, and the average value of running velocity corresponding to OBLA (VOBLA) was 5.447 +/- 0.132 m.s-1. Variations of these three velocities expressed as a coefficient of variance (CV) ranged from 1.4 to 2.4%. A strong inverse relationship between heart rate corresponding to OBLA (HROBLA) and performance was observed (r = -0.709, p < 0.02 for V5000 and r = -0.830, p < 0.01 for V10000), while there was a lack of significant relationship between VOBLA and performance (r = 0.293, NS for V5000 and r = 0.130, NS for V10000). Furthermore, the average value of HROBLA obtained in this study (174.5 +/- 8.2 b.min-1) was quite similar to that of the heart rate threshold reported by some previous researchers. In conclusion, VOBLA alone could not explain the small variation of long-distance running performance, and HROBLA should be used in place of VOBLA for evaluating long-distance running performance in elite runners with quite similar performance levels.

Adult↗

PubMed1997

Phosphorylation-independent inhibition by intracellular cyclic nucleotides of brain inwardly rectifying K+ current expressed in Xenopus oocytes.

An inwardly rectifying K+ current, which was heterologously expressed in Xenopus oocytes, was inhibited by isoproterenol, a fadrenergic agonist. Poly(A)+ mRNA isolated from guinea-pig brain was injected into oocytes 2-3 days before experiments. Isoproterenol inhibition of the K+ current was time-and voltage-dependent: the inhibition became faster and more pronounced as the command voltage steps were applied to more negative potentials. This inhibition was prevented by propranolol. Dibutylyl cyclic (dB-c) AMP could mimic the effect of isoproterenol, while injection of the catalytic subunit of cAMP-dependent protein kinase into the oocytes did not affect the K+ current. Inhibitors of the protein kinases, WIPTIDE and H-8, did not prevent the inhibition by dB-cAMP. Furthermore, dB-cGMP also inhibited the K+ current in a similar time- and voltage-dependent manner. We propose that the phosphorylation-independent action of cyclic nucleotides mediates beta-adrenergic inhibition of brain inwardly rectifying K+ channels expressed in Xenopus oocytes.

Adrenergic beta-Agonists↗

PubMed1997

Role of the claustrum in convulsive evolution of visual afferent and partial nonconvulsive seizure in primates.

PURPOSE: We tested cross-species validity of the role of the claustrum in the convulsive evolution of the visual afferent and amygdaloid seizure and the specificity of the claustral lesioning effect. METHODS: In 7 Senegalese baboons, we examined the effect of unilateral claustral lesioning on generalized convulsive seizures either kindled from the amygdaloid nucleus (AM) and cingulate cortex (CG) or induced by intermittent photic stimulation (IPS) after systemic administration of D,L-allylglycine (AG). RESULTS: A lesioned area common to all animals was the anterior half of the left claustrum. Postoperative restimulation of the kindled left AM or CG evoked only nonconvulsive seizures. When few convulsive seizures emerged in 1 CG-kindled animal, they were mirror image of the kindled seizure and arose from the nonlesioned right hemisphere. Restimulation of the kindled right AM or CG reactivated kindled seizures. An IPS-induced generalized convulsive seizure was transformed into a secondarily generalized seizure arising from the nonlesioned right hemisphere. CONCLUSIONS: The primate claustrum regulates the convulsive evolution of partial seizures originating from nonmotor structures such as the AM and CG and also regulates the convulsive development that follows IPS. Our findings suggest that predisposed susceptibility expressed at the claustrum may be involved in the clinical variation with respect to convulsive evolution of nonmotor partial seizures and convulsive susceptibility to IPS in human primates.

Allylglycine↗

PubMed1995

Cingulate kindling in Senegalese baboons, Papio papio.

Kindling of the cingulate cortex in the Senegalese baboon Papio papio led to a protracted nonconvulsive seizure state characterized by immobile staring with (anterior cingulate, AC) or without (posterior cingulate, PC) widening of eyelids and neck flexion, followed by postictal visual searching behavior. Despite early bilateral spread of EEG discharges, ictal and interictal patterns remained persistently asymmetric. Secondary generalization was rapid and predictable once contralateral lower facial twitching associated with sustained adversion developed. After the primary site had been kindled, stimulation of the contralateral homotopic posterior cingulate cortex readily produced afterdischarge. However, it remained localized and kindling growth did not occur. The findings suggest that (a) the cingulate cortex can support nonconvulsive seizures; (b) cingulate seizures are accompanied by asymmetric convexity EEG discharges indicating its lateralized onset; (c) further evolution to convulsive seizures after kindling of cingulate cortex requires access to the ipsilateral frontocentral cortex responsible for facial twitching; and (d) the development of focal epileptogenesis at one cingulate site interferes with clinical seizure development at the homotopic contralateral site.

Adolescent↗

PubMed1994

Symptomatic Chiari malformation and associated pathophysiology in pediatric and adult patients without myelodysplasia.

The clinical characteristics of eight pediatric and five adult patients with Chiari malformation were evaluated. Six pediatric and five adult patients had associated syringomyelia. All patients initially underwent a suboccipital craniectomy with upper cervical (C-1 and/or C-2) laminectomy and duraplasty, and/or shunting procedures. The clinical characteristics of the pediatric and adult groups were compared. The mean interval between onset of symptoms and operation was shorter in the pediatric group (3 yrs 6 mos) than in the adult group (7 yrs 1 mo). Pediatric patients without syringomyelia had the shortest mean interval of 1 year 8 months. Preoperatively, the clinical features were more severe in the adult patients than in the pediatric patients. Postoperatively, seven of eight pediatric patients improved and one stabilized, while two of five adult patients improved, one stabilized, and in two the disease continued to progress despite multiple corrective procedures. Cine magnetic resonance imaging revealed correction of the abnormal cerebrospinal fluid (CSF) flow at the craniovertebral junction and decreased to-and-fro movement in the syrinx after posterior fossa decompression, which were closely correlated with the improvement of clinical features in pediatric patients. However, adult patients required further procedures because of the multifactorial nature of the disease. Evaluation of abnormal CSF pathways at the craniovertebral junction is important for investigating the pathogenesis of Chiari malformation and associated syringomyelia.

Adolescent↗

PubMed1992

Molecular cloning and characterization of the platelet-activating factor receptor gene expressed in the human heart.

PAF decreases cardiac contractility and blood pressure. To characterize the cardiac PAF receptor, we screened a human ventricular cDNA library in a low stringency condition, using a PCR product derived from guinea pig lung PAF receptor as a probe. Four clones were obtained and named HV1-4. In Xenopus oocytes injected with cRNA derived from HV3 or 4 but not from HV1 or 2, PAF elicited a Ca(2+)-activated Cl- current. HV3 and HV4 were duplicate clones, encoding a 342 amino-acid polypeptide which was identical to that of the human leukocyte PAF receptor. However, a portion of the 5' untranslated region of HV3 (or 4) was different from that of the leukocyte receptor cDNA. Northern blotting of human ventricles and atria using the HV3 insert showed a single band of approximately 4 kb. These results suggest a tissue-specific translational mechanism responsible for regulation of the expression of the PAF receptor mRNA in these tissues.

Amino Acid Sequence↗

PubMed1992

[Clinicopathological evaluation of EVAL embolization in arteriovenous malformations].

The clinical and pathological aspects of two large arteriovenous malformations which were removed totally after preoperative embolization using ethylene vinyl alcohol copolymer (EVAL) were studied. The material, which is not adhesive, is handled easily during the procedure of embolization. However, it involves some risks because it might migrate to and occlude the normal branches of the brain and pass through the nidus to the venous system. Histopathological study of AVM nidus which was removed showed embolic materials within the vessels and inflammatory reaction of the vessel wall and its surrounding tissue. There were patchy hemorrhages within the AVM nidus and its surrounding brain tissue. Recanalization was also found within the occluded vessels. These findings suggest that preoperative embolization has some risk of causing intracerebral hemorrhage after the embolization. AVM should be removed surgically as a radical treatment if the patient is able to tolerate the operation.

Adolescent↗

PubMed1991

cDNA cloning of a myosin heavy chain isoform in embryonic smooth muscle and its expression during vascular development and in arteriosclerosis.

Adult rabbit smooth muscles contain two types of myosin heavy chain (MHC) isoforms, SM1 and SM2 which are generated through alternative RNA splicing from a single gene (Nagai, R., Kuro-o, M., Babij, P. & Periasamy, M. (1989) J. Biol. Chem. 264, 9734-9737). We previously reported that the expression of SM1 and SM2 during vascular development is differentially regulated at the level of RNA splicing, whereby SM1 is constitutively expressed from early development but SM2 appear after birth (Kuro-o, M., Nagai, R., Tsuchimochi, H., Katoh, H., Yazaki, Y., Ohkubo, A. & Takaku, F. (1989) J. Biol. Chem. 264, 18272-18275). We also demonstrated that embryonic vascular smooth muscles contain a third type of MHC isoform, referred to as SMemb in this report, which comigrates on sodium dodecyl sulfate-polyacrylamide gel electrophoresis with SM2. In the present study we have isolated and characterized a cDNA clone (FSMHC34) for SMemb. FSMHC34 encodes the light meromyosin region including the carboxyl terminus and showed 70% amino acid sequence identity with SM1 or SM2. SMemb is a nonmuscle-type MHC and identical with brain MHC, but clearly distinct from 196-kDa nonmuscle MHC in cultured smooth muscle cells. The expression of SMemb was predominant in embryonic and perinatal aortas, but down-regulated with vascular development. Interestingly SMemb was reexpressed in proliferating smooth muscle cells of arteriosclerotic neointimas. These results suggest that smooth muscle proliferation is coupled to the expression of SMemb and that dedifferentiation of smooth muscles toward the embryonic phenotype is involved in the mechanisms underlying atherosclerosis.

Aging↗

PubMed1991

Surgical results of brain metastasis from lung cancer--prognostic factors.

Twenty-five patients receiving surgical treatment for brain metastasis from lung cancer were retrospectively studied to evaluate the prognostic factors for survival time. Twenty-two patients had died of respiratory distress by April, 1989. Favorable prognostic factors derived from the median survival time (MST) in these patients included; 1) resection of primary tumor (MST 10 months); 2) total or subtotal removal of metastatic tumor (MST 6.5 months); 3) adenocarcinoma (MST 13 months); 4) metachronous onset of brain metastasis (MST 12 months); 5) single metastasis (MST 8 months). These results suggest that therapy for the primary lung cancer is important before surgery for metastatic brain tumor.

Adenocarcinoma↗

PubMed1991

[Clinicopathological study of meningiomas of the tentorium and its surrounding structures].

We report the clinical features, radiological studies, operative procedures and results, and follow-up data in 29 patients with meningiomas of the tentorium and its surrounding structures. The cases represented 22.5% of all the intracranial meningiomas operated on in a 15 year period and were divided into three groups, depending on their main attachments, tentorial, cerebellopontine angle (dorsal aspect of the petrous ridge) and others. Tumor size was generally large and 13 cases were larger than 5 cm. The most common tumor site was along or near the superior petrosal sinus and transverse-sigmoid junction in cases involving the tentorium, and medial to the porus acousticus in cases involving the cerebellopontine angle. Different operative approaches to these tumors were carried out, depending on their location. The tumors in the lateral or medial petrous ridge were approached mainly with a suboccipital craniectomy using a retromastoid incision. Total removal was carried out in 80% of the tentorial cases, in 46.2% of cerebellopontine angle cases, and in the 83.3% in the others. Total operative mortality rate was zero. Follow-up periods ranged up to 5 years 5 months in the tentorial cases, 4 years 6 months in cerebellopontine angle cases, and 7 years 1 month in the others. Long-term results were good in 21 cases (72.4%), fair in 3 cases (10.3%) and poor in 2 (6.9%). Three patients died due to tumor recurrence. One of them suffered lung metastasis, and two of them suffered extensive local recurrences. We recommend the retromastoid approach combined with the petrosal approach, if the CPA tumor is large enough and extends to the retroclival region.

Adult↗

PubMed1990

Functional identification of the transcriptional regulatory elements within the promoter region of the human ventricular myosin alkali light chain gene.

We have identified and functionally characterized DNA sequences that regulate the expression of the human ventricular/slow twitch isoform of myosin alkali light chain (VLC1) gene. By using primer extension and S1 nuclease mapping techniques, we have shown that the VLC1 gene is transcribed from the identical site in the ventricular and slow twitch skeletal muscles. Comparison of the VLC1 sequences from +1 to -1296 in the genes for human and mouse showed that the 5'-proximal flanking region, up to about 220 nucleotides, was highly conserved (83% homology). To determine the location of sites that may be important for the function of the VLC1 promoter, a series of transient expression vectors containing progressive deletions of the VLC1 gene 5'-flanking sequence fused to the bacterial chloramphenicol acetyltransferase (CAT) gene was introduced into myogenic and nonmyogenic cells. Deletion mutagenesis of sequences between -357 and +40 revealed the presence of positive and negative activity in all the cells tested. We demonstrated that the minimal promoter sequence required to generate muscle cell-specific expression is the region between -94 to -64 upstream from the cap site and a sequence element located between -107 and -94 was found to have a positive effect in both myogenic cells and nonmyogenic cells. These two proximal regions located between -107 and -64 appear to act together to determine the cell type-specific high level expression of the VLC1 gene in muscle cells. Competition gel retardation assays revealed that the CArG sequence located between -96 and -87 interacts specifically with nuclear extracts from myogenic and nonmyogenic cells and compete for binding with the CArG sequence present in the human cardiac alpha-actin gene and with the serum response element of the c-fos gene. These results strongly suggested that similar, if not identical, the CArG box binding proteins interact with the functionally different promoter element in the VLC1, cardiac alpha-actin, and c-fos genes.

Animals↗

PubMed1990

Expression of major histocompatibility complex class I antigen in murine ventricular myocytes infected with Coxsackievirus B3.

Evidence has accumulated that T cell-mediated autoimmunity plays an important role in the pathogenesis of viral myocarditis. T lymphocytes are known to recognize antigen-presenting cells, such as virus-infected cells, being restricted by syngeneic major histocompatibility complex (MHC) antigens. To clarify in more detail the immunological mechanisms involved, we induced acute viral myocarditis in C3H/He mouse ventricles with coxsackievirus B3 (CVB3) and examined, by immunofluorescence, the expression of MHC class I and II antigens, previously reported not to be expressed by normal cardiac myocytes. Furthermore, to confirm the expression of MHC class I (H-2Kk) antigens at the cellular level, we treated cultured cardiac myocytes with interferon gamma and examined the antigen expression by immunofluorescence and Northern blot hybridization, using an antisense RNA probe for MHC messenger RNA. Our observations demonstrated 1) CVB3-induced myocarditis resulted in the enhanced expression of MHC class I (H-2Kk) gene product on the surface of cardiac myocytes but low or undetectable levels of MHC class II or H-2Dk gene products, and moderate focal transient (days 5-7) expression of both MHC class I (Kk + Dk) region gene products and MHC class II antigens were induced on capillary endothelial cells; 2) murine fetal cardiac myocytes cultured in vitro in the presence of interferon gamma similarly were shown to express marked levels of MHC class I (H-2Kk) but low to undetectable levels of the H-2Dk gene product; however, weak to moderate MHC Class II antigens were expressed by these cultured myocytes; and 3) the expression of MHC antigens in cardiac myocytes was modulated at the transcriptional level.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

The myosin gene switching in human cardiac hypertrophy.

Cardiac hypertrophy is associated with qualitative as well as quantitative changes in myocardial cells. To analyze the molecular basis of isozymic transitions of cardiac myosins in response to pressure overload, we have constructed and characterized two types of myosin heavy chain (MHC) cDNA clones, specifying alpha- and beta-MHCs, and two types of myosin alkali light chain cDNA clones, complementary to atrial type (ALC1) and ventricular type (VLC1) mRNAs from a human fetal heart cDNA library. Using the S1 nuclease mapping procedure, we showed that the MCH isozymic transitions from alpha- to beta-MHC in the pressure overloaded atria are produced by changes in the relative level of alpha- and beta-MHC gene expression. In addition, we observed that the expression of VLC1 gene is also induced in the atria subjected to severe pressure overload. Thus, it appears that the increased expression of VLC1 gene, together with the isogene switch from alpha- to beta-MHC gene, may participate in the adaptation of myocardium to new functional requirement. Then, to get a better understanding of the genetic mechanisms involved in the regulation of isogene expression, we have isolated and sequenced genomic clone for VLC1 isoform. Sequence analysis has identified multiple potential cis regulatory elements within a 686-bp upstream region. This region includes 28-bp alternating purine/pyrimidine sequences and two segment exhibiting homology to consensus sequence proposed for viral and cellular enhancer elements. In particular, a comparison of the VLC1 upstream gene sequence with those available for several muscle-specific genes revealed that CC(A + T-rich)6GG elements and CATTCCT sequence are conserved. These results suggested that CArG box (-96 to -87) has an important role in the positive regulation of the VLC1 gene and this element may be involved in the co-regulation of VLC1 and cardiac alpha-actin genes.

Adaptation, Physiological↗

PubMed1989

Developmentally regulated expression of vascular smooth muscle myosin heavy chain isoforms.

Two types of smooth muscle myosin heavy chain (MHC) isoforms, SM1 and SM2, were recently identified to have different carboxyl termini (Nagai, R., Kuro-o, M., Babij, P., and Periasamy, M. (1989) J. Biol. Chem. 264, 9734-9737). SM1 and SM2 are considered to be generated from a single gene through alternative RNA splicing. In this study we investigated expression of vascular MHC isoforms during development in rabbits at the mRNA, protein, and histological levels. In adults, all smooth muscle cells reacted with both anti-SM1 and anti-SM2 antibodies on immunofluorescence, suggesting the coexpression of SM1 and SM2 in a single cell. In fetal and perinatal rabbits, however, only anti-SM1 antibody consistently reacted with smooth muscles. Reactivity with anti-SM2 antibody was negative in the fetal and neonatal blood vessels and gradually increased during 30 days after birth. These developmental changes in SM1 and SM2 expression at the histological level coincided with mRNA expression of each MHC isoform as determined by S1 nuclease mapping, indicating that expression of SM1 and SM2 is controlled at the level of RNA splicing. However, sodium dodecyl sulfate-polyacrylamide gel electrophoresis of myosin from fetal and perinatal aortas revealed the presence of large amount of SM2. Interestingly, fetal SM2 did not cross-react with our anti-SM2 antibody on immunoblotting. We conclude that expression of SM1 and SM2 are differentially regulated during development and that a third type of MHC isoform may exist in embryonic and perinatal vascular smooth muscles.

Animals↗

PubMed1989

Molecular adaptation to pressure overload in human and rat hearts.

The process of enlargement of the heart due to overload involves a significant reconstitution of the organ including myocytes and intracellular constituents. We demonstrated the distribution of two types of cardiac myosin heavy chains (HC alpha and HC beta) in the human heart using monoclonal antibodies. The ventricle comprised mainly HC beta which has low ATPase activity, whereas the atrium was predominantly composed of HC alpha which has high ATPase activity. We also demonstrated isozymic transition of HC alpha to HC beta in the human atrium and ventricle by hemodynamic overload, regarded as a compensatory mechanism to meet an increased demand in work. To examine the molecular mechanism for the expression of these HCs, we have isolated human HC alpha and HC beta cDNA clones from a fetal heart cDNA library. Comparison of the nucleotide and amino acid sequences deduced from the DNA between these cDNA clones showed 91 and 96% homology, respectively. Using HC alpha and HC beta gene-specific sequences, we demonstrated that the transition of HC alpha to HC beta in the overloaded human heart was induced by the expression of HC beta-gene. To determine the role of cellular oncogenes in the process of cardiac growth and hypertrophy, we examined the expression pattern of eight cellular oncogenes during the developmental stage and pressure-overloaded hypertrophy of the rat heart by Northern blot analysis. c-fos, c-myc and c-Ha-ras were expressed in the heart in response to pressure overload and in a stage-specific manner, suggesting that these cellular oncogenes participate in the normal developmental process and hypertrophy of the heart. We also cloned the genes of which expression level was rapidly changed by pressure overload by differential hybridization technique. Our results suggest that clone 4 may be involved in the molecular mechanism for the development of cardiac hypertrophy due to overload.

Adaptation, Physiological↗