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Biomedical subjects

H Takano

Publications and source records attributed to H Takano.

At least 307 records · Page 17Linked to original sources
PubMed1995

Intracortical facilitation and inhibition after paired magnetic stimulation in humans under anesthesia.

The evoked spinal cord potential (ESCP) and the evoked compound muscle action potential (ECMAP) after paired transcranial magnetic stimulation were recorded simultaneously in eight subjects undergoing spine surgery. The ESCP was composed of a short-latency initial wave (D-wave) followed by later waves (I-waves). The mean conduction velocity of each wave was approximately 60 m/s. The interstimulus interval (ISI) affected the amplitude of both ESCP and ECMAP; the amplitude was inhibited at short ISIs (2 ms and 5 ms), was facilitated at ISI of 10 ms, and was inhibited again at longer ISIs (50 ms, 100 ms and 200 ms). The changes in later I-waves were prominent compared to the stable D-wave. These results suggest that transcranial magnetic stimulation alters the excitability of the motor cortex by affecting synaptic transmission in corticomotor (CM) neurons. The inhibition of the motor cortex at longer ISIs may contribute to a silent period following transcranial magnetic stimulation.

Aged↗
PubMed1995

Magnetic-evoked compound muscle action potential neuromonitoring in spine surgery.

STUDY DESIGN: Muscle action potentials elicited by paired transcranial magnetic stimulation were recorded during spine surgery in 34 patients. Anesthesia was based on ketamine and fentanyl. OBJECTIVES: To evaluate the optimal anesthetic regimen to be used for transcranial magnetic stimulation, and to determine the clinical import of magnetic-evoked compound muscle action potentials. SUMMARY OF BACKGROUND DATA: Muscle action potential by transcranial magnetic stimulation has been difficult to record under general anesthesia. Ketamine is known to not suppress the muscle responses, although no conclusive clinical study has been reported. METHODS: Paired transcranial magnetic stimulation was delivered as muscle action potentials were recorded from the limb musculature. RESULTS: Neuromonitoring was reliable in 56% of total cases and in 82% of the recent cases after reducing fentanyl dosage. Paired magnetic stimulation was an excellent facilitation technique for reliable monitoring. At higher dosages, fentanyl and ketamine decreased the reproducibility of the responses. CONCLUSIONS: Magnetic-evoked compound muscle action potential neuromonitoring is a sensitive and selective motor pathway monitoring method that covers the entire motor pathway, including the white and gray matter of the spinal cord. Ketamine-based anesthesia is a good choice for this purpose.

Action Potentials↗
PubMed1995

Left ventricular contractility predicts how the end-diastolic pressure-volume relation shifts during pacing-induced ischemia in dogs.

BACKGROUND: Two types of ischemia, pacing-induced and coronary occlusion-induced, have different effects on left ventricular diastolic properties. During pacing-induced ischemia, the diastolic pressure-volume relation is said to shift upward, whereas during coronary occlusion, it is said to shift rightward or downward. However, recent studies have shown that the relation can shift in any direction during both types of ischemia. The purpose of this study was to identify determinants of the shift of the end-diastolic pressure-volume relation (EDPVR) during pacing-induced ischemia. METHODS AND RESULTS: We retrospectively analyzed 46 pacing-induced ischemia experiments performed in 15 open-pericardium anesthetized dogs. Pacing ischemia was induced by constricting left anterior descending and left circumflex coronary arteries and pacing the left atrium at 150 to 180 beats per minute for 3 minutes. Left ventricular volume was measured with a conductance catheter. Hemodynamics were recorded during baseline, coronary stenosis, rapid pacing, and pacing-induced ischemia (immediately after rapid pacing). For each condition, hemodynamics were recorded in steady state and then during a brief inferior vena caval occlusion (except for during rapid pacing) to obtain left ventricular end-diastolic and end-systolic pressure-volume relations. The shift of the EDPVR from coronary stenosis to pacing-induced ischemia was assessed by an upward shift index (end-diastolic pressure during pacing-induced ischemia minus the pressure during coronary stenosis at the largest end-diastolic volume common to both conditions, SI-S) and a rightward shift index (the largest end-diastolic volume during pacing-induced ischemia minus the largest volume during coronary stenosis, delta EDVI-S). The index of left ventricular contractility, the end-systolic elastance (Ees), or the slope of the dP/dtmax-end-diastolic volume relation (dE/dtmax) during pacing-induced ischemia was the strongest determinant of the magnitude of SI-S and delta EDVI-S and thus of the shift of the EDPVR. As Ees or dE/dtmax decreased, SI-S decreased and delta EDVI-S increased. CONCLUSIONS: Our results suggest that left ventricular contractility is the best determinant of the shift of the EDPVR during pacing-induced ischemia. The more left ventricular contractility decreases, the more the EDPVR shifts downward and rightward.

Animals↗
PubMed1995

Gadolinium attenuates the upward shift of the left ventricular diastolic pressure-volume relation during pacing-induced ischemia in dogs.

BACKGROUND: The mechanism of the reversible upward shift of the left ventricular diastolic pressure-volume relation during demand ischemia is controversial. To assess the possibility that cation influx through stretch-activation channels may contribute to the upward shift, we asked whether gadolinium, a blocker of the stretch-activated channels, attenuates the upward shift of the diastolic pressure-volume relation during pacing-induced ischemia in 5 dogs. METHODS AND RESULTS: To produce pacing-induced ischemia, we constricted the left anterior descending and circumflex coronary arteries to reduce their flows by approximately 30% and paced the left atrium at 150 to 180 beats per minute for 3 minutes. We measured left ventricular pressure, volume, and two segment lengths with micromanometers, a conductance catheter, and ultrasonic crystals, respectively. We recorded these variables during baseline, coronary stenosis, and pacing-induced ischemia (immediately after rapid pacing). After injecting 20 mg/kg (76 mumol/kg) gadolinium, we repeated the measurements during coronary stenosis (gadolinium experiment) and pacing-induced ischemia (pacing-induced ischemia plus gadolinium experiment). For each measurement, we recorded the variables in steady state to obtain diastolic pressure-volume and pressure-segment length loops and then during a brief (within 25 seconds) inferior vena caval occlusion to obtain the left ventricular end-diastolic pressure-volume relation. We found that left ventricular diastolic pressure-volume and pressure-segment length loops in steady-state beats shifted upward from coronary stenosis to pacing-induced ischemia. After injection of gadolinium, the upward shift from gadolinium to pacing-induced ischemia plus gadolinium was smaller than the shift from coronary stenosis to pacing-induced ischemia. Similarly, the left ventricular end-diastolic pressure-volume relation obtained during vena caval occlusion shifted upward (by 2.2 +/- 0.6 [SE] mm Hg) from coronary stenosis to pacing-induced ischemia. After injection of gadolinium, the upward shift from gadolinium to pacing-induced ischemia plus gadolinium was smaller (by -2.1 +/- 0.4 mm Hg). CONCLUSIONS: These results indicate that gadolinium, a blocker of stretch-activated channels, attenuates the upward shift of the diastolic pressure-volume relation during pacing-induced ischemia, suggesting that the cation influx through stretch-activated channels may contribute to this upward shift.

Animals↗
PubMed1995

Regional myocardial sympathetic dysinnervation in patients with coronary vasospasm.

The purpose of this study was to assess the presence and location of impaired myocardial sympathetic innervation by using 123I metaiodobenzylguanidine (123I MIBG) in 15 patients with coronary vasospasm induced by intracoronary acetylcholine. The results were compared with those using thallium-201 (Tl-201). We also examined 14 patients with severe coronary stenosis (> 90%) and 8 control subjects without significant coronary stenosis (< 50%) and provokable coronary vasospasm. Regional myocardial sympathetic dysinnervation was detected by 123I MIBG single-photon emission computed tomography (SPECT) in all patients with coronary vasospasm, despite normal uptake during Tl-201 SPECT. This regional uptake-mismatch between 123I MIBG and Tl-201 Spect occurred specifically in the vasospasm group (p < 0.001 vs stenosis and control groups). Moreover, regional myocardial sympathetic dysinnervation was located in the distribution of perfusion in 25 of the 27 vasospasm-induced vessels. Normal uptake of 123I MIBG was observed in the perfused areas in 16 of the 18 non-vasospasm-induced vessels. The sensitivity ans specificity of 123I MIBG for detection of coronary vasospasm were 92% and 88% respectively. In patients with coronary vasospasm, we found regional myocardial sympathetic dysinnervation to be present. Furthermore, we were able to distinguish these patients from patients with critical coronary stenosis by 123I MIBG and Tl-201 SPECT.

3-Iodobenzylguanidine↗
PubMed1995

Proliferation and differentiation of myelodysplastic CD34+ cells: phenotypic subpopulations of marrow CD34+ cells.

In a search for a mechanism to explain the impaired growth of progenitor cells in patients with myelodysplastic syndromes (MDS), marrow CD34+ cells were purified up to 94.9% +/- 4.2% for normal individuals and 88.1% +/- 17.6% for MDS patients, using monoclonal antibodies and immunomagnetic microspheres (MDS CD34+ cells). Phenotypic subpopulations of these CD34+ cells were analyzed for CD38, HLA-DR, CD33, CD13, CD14, CD41 and CD3 plus CD19, in association with proliferative and differentiative capacities. The 15 studies performed included 12 MDS patients. Coexpression rate of CD13 significantly increased in the MDS CD34+ cell population with a value of 91.4% +/- 11.6% and ranging from 60.3% to 100%, and exceeded 99% in four studies, whereas that of normal CD34+ cells was 49.9% +/- 15.8%, ranging from 28.2% to 70.1% (P < .001). Coexpression rate of CD38, HLA-DR, CD33, CD14, and CD3 plus CD19 in MDS CD34+ cells did not significantly differ from that of normal CD34+ cells. The total number of colonies and clusters grown from 100 normal marrow CD34+ cells was 40.4 +/- 8.6, the range being from 27.2 to 50.3; this varied in MDS marrow CD34+ cells with a value of 34.0 +/- 28.7, the range being 0 to 95.9. The lineage of colonies and clusters promoted by MDS marrow CD34+ cells was predominantly committed to nonerythroid with impaired differentiation in 13 of 15 studies (87%). CD13 is first expressed during hematopoiesis by colony-forming unit granulocyte-macrophage and is absent in erythroid progenitors. Therefore, this study provides direct evidence for the lineage commitment of MDS CD34+ cells to nonerythroid with impaired differentiation and explains the mechanism of nil or low colony expression of MDS progenitor cells to erythroid lineage.

Aged↗
PubMed1995

Flow cytometric analysis of nuclear DNA content in tissues of colon cancer using endoscopic biopsy specimens.

Flow cytometric assay of nuclear DNA in endoscopic biopsy specimens was evaluated in colon cancer patients. When the cells were divided into diploid cells and aneuploid cells, aneuploidy was observed in 63% (58 of 92) of the colon cancer patients. However, no clear relation was observed between the frequency of aneuploidy and the invasive depth, size, or histological type of colon cancer. Noncancerous portions of the colon tissues including colon adenoma or normal mucosa were mostly (96%, 87 of 91) diploid. Nuclear DNA content could be analyzed in the fresh biopsy specimens of colon cancer tissues and such investigation might be possibly valuable for further biological characterization of colon cancer in the usual procedure of clinical diagnosis for colonic malignancy before surgical operation or other treatment.

Adenoma↗
PubMed1995

Isolation, characterization and chromosomal mapping of an actin gene from the primitive red alga Cyanidioschyzon merolae.

Based on the results of cytological studies, it has been assumed that Cyanidioschyzon merolae does not contain actin genes. However, Southern hybridization of C. merolae cell-nuclear DNA with a yeast actin-gene probe has been suggested the presence of an actin gene in the C. merolae genome. In the present study, an actin gene was isolated from a C. merolae genomic library using a yeast actin-gene probe. The C. merolae actin gene has no intron. The predicted actin is composed of 377 amino acids and has an estimated molecular mass of 42 003 Da. Southern hybridization indicated that the C. merolae genome contains only one actin gene. This gene is transcribed at a size of 2.4 kb. When Southern hybridization was performed with C. merolae chromosomes separated by pulsed-field gel electrophoresis, a band appeared on unseparated chromosomes XI and XII. A phylogenetic tree based on known eucaryote actin-gene sequences revealed that C. merolae diverged after the division of Protozoa, but before the division of Fungi, Animalia and Chlorophyta.

Actins↗
PubMed1995

Sexuality of mitochondria: fusion, recombination, and plasmids.

Mitochondrial fusion, recombination, and mobile genetic elements, which are essential for mitochondrial sexuality, are well established in various organisms. The recombination of mitochondrial DNA (mtDNA) depends upon fusion between parental mitochondria, and between their mtDNA-containing areas (mt-nuclei), to allow pairing between the parental mtDNAs. Such mitochondrial fusion followed by recombination may be called "mitochondrial sex." We have identified a novel mitochondrial plasmid named mF. This plasmid is apparently responsible for promoting mitochondrial fusion and crosses over with mtDNA in successive sexual crosses with mF- strains. Only in mF+ strains carrying the mF plasmid did small spherical mitochondria fuse which subsequently underwent fusion between the mt-nuclei that contained the mtDNA derived from individual mitochondria. Several successive mitochondrial divisions followed, accompanied by mt-nuclear divisions. The resulting mitochondria contained recombinant mtDNA with the mF plasmid. Such features remind us also of the bacterial conjugative plasmids such as F plasmid. Therefore, in the final part of this chapter, we discuss the origin of sex and its relationship to the sexuality of mitochondria.

Animals↗
PubMed1995

Identification of a novel phospholipase C family gene at chromosome 2q33 that is homozygously deleted in human small cell lung carcinoma.

Since a considerably high incidence of allelic loss on chromosome 2q was detected in lung carcinoma and a homozygous deletion at chromosome 2q33 was detected in a small cell lung carcinoma cell line, NCI-H82, a novel tumor suppressor gene has been suggested to be present in this chromosomal region. In the present study, we constructed a cosmid contig map covering the homozygous deleted region, which was estimated as being 220 kbp in size, and identified a gene from the deleted region. All of the coding exons of this gene were homozygously deleted in this cell line, while a 5'-non-coding exons was retained. Since the gene encodes a protein with striking similarity to several members of a family of phospholipase C, we designated this gene as PLC-L (phospholipase C-deleted in lung carcinoma). The PLC-L gene was expressed in a variety of fetal and adult organs including the lung. However, its expression was greatly reduced in seven of 13 (53.8%) of small cell lung carcinoma and 13 of 15 (86.7%) of non-small cell lung carcinoma cell lines. Since its homology to phospholipase C genes suggests the involvement of the PLC-L gene in inositol phospholipid-based intracellular signaling cascade, it is possible that aberrant expression of the PLC-L gene contributes to the genesis or progression of human lung carcinoma.

Amino Acid Sequence↗
PubMed1995

Flow cytometric analysis of nuclear DNA content in the endoscopic biopsy tissues of gastric cancer.

The nuclear DNA content was measured by flow cytometry in gastric cancer patients using endoscopically biopsied tissue specimens. When the specimens were classified into diploid and aneuploid according to the DNA histogram, 56% (65/117) of the specimens were aneuploid, and advanced cancer was clearly more often aneuploid than early cancer. The frequency of aneuploidy appeared to be higher as the histologic depth of cancer was greater. Noncancerous tissues of the stomach were mostly diploid. The nuclear DNA ploidy pattern in gastric cancer cells could be analyzed by using endoscopic biopsy samples and this flow cytometric investigation would be possibly contributive to further characterization of gastric cancer in the diagnostic procedure of malignancy.

Adult↗
PubMed1995

Angiotensin II partly mediates mechanical stress-induced cardiac hypertrophy.

We have previously shown that mechanical stress induces activation of protein kinases and increases in specific gene expression and protein synthesis in cardiac myocytes, all of which are similar to those evoked by humoral factors such as growth factors and hormones. Many lines of evidence have suggested that angiotensin II (Ang II) plays a vital role in cardiac hypertrophy, and it has been reported that secretion of Ang II from cultured cardiac myocytes was induced by mechanical stretch. To examine the role of Ang II in mechanical stress-induced cardiac hypertrophy, we stretched neonatal rat cardiac myocytes in the absence or presence of the Ang II receptor antagonists saralasin (an antagonist of both type 1 and type 2 receptors), CV-11974 (a type 1 receptor-specific antagonist), and PD123319 (a type 2 receptor-specific antagonist). Stretching cardiac myocytes by 20% using deformable silicone dishes rapidly increased the activities of mitogen-activated protein (MAP) kinase kinase activators and MAP kinases. Both saralasin and CV-11974 partially inhibited the stretch-induced increases in the activities of both kinases, whereas PD123319 showed no inhibitory effects. Stretching cardiac myocytes increased amino acid incorporation, which was also inhibited by approximately 70% with the pretreatment by saralasin or CV-11974. When the culture medium conditioned by stretching cardiocytes was transferred to nonstretched cardiac myocytes, the increase in MAP kinase activity was observed, and this increase was completely suppressed by saralasin or CV-11974. These results suggest that Ang II plays an important role in mechanical stress-induced cardiac hypertrophy and that there are also other (possibly nonsecretory) factors to induce hypertrophic responses.

Angiotensin II↗
PubMed1995

Mechanical stress activates protein kinase cascade of phosphorylation in neonatal rat cardiac myocytes.

We have previously shown that stretching cardiac myocytes evokes activation of protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and 90-kD ribosomal S6 kinase (p90rsk). To clarify the signal transduction pathways from external mechanical stress to nuclear gene expression in stretch-induced cardiac hypertrophy, we have elucidated protein kinase cascade of phosphorylation by examining the time course of activation of MAP kinase kinase kinases (MAPKKKs), MAP kinase kinase (MAPKK), MAPKs, and p90rsk in neonatal rat cardiac myocytes. Mechanical stretch transiently increased the activity of MAPKKKs. An increase in MAPKKKs activity was first detected at 1 min and maximal activation was observed at 2 min after stretch. The activity of MAPKK was increased by stretch from 1-2 min, with a peak at 5 min after stretch. In addition, MAPKs and p90rsk were maximally activated at 8 min and at 10 approximately 30 min after stretch, respectively. Raf-1 kinase (Raf-1) and (MAPK/extracellular signal-regulated kinase) kinase kinase (MEKK), both of which have MAPKKK activity, were also activated by stretching cardiac myocytes for 2 min. The angiotensin II receptor antagonist partially suppressed activation of Raf-1 and MAPKs by stretch. The stretch-induced hypertrophic responses such as activation of Raf-1 and MAPKs and an increase in amino acid uptake was partially dependent on PKC, while a PKC inhibitor completely abolished MAPK activation by angiotensin II. These results suggest that mechanical stress activates the protein kinase cascade of phosphorylation in cardiac myocytes in the order of Raf-1 and MEKK, MAPKK, MAPKs and p90rsk, and that angiotensin II, which may be secreted from stretched myocytes, may be partly involved in stretch-induced hypertrophic responses by activating PKC.

Amino Acid Sequence↗
PubMed1995

Simultaneous intraperitoneal administration of OK-432 and serum enhances superoxide generation from migrated polymorphonuclear leukocytes, with special emphasis on the role of complements.

Superoxide and its derived active oxygen species are responsible for the polymorphonuclear leukocyte (PMN)-mediated tumoricidal activity which is typically shown in the intraperitoneal administration of OK-432, a biological response modifier, for cancer ascites. We examined the effects of intraperitoneal administration of OK-432 with or without syngeneic serum on superoxide generation from PMNs which migrated in the peritoneal cavity using the new method of Cypridina luciferin analog-dependent chemiluminescence for the detection of superoxide. PMNs harvested from rat peritoneal cavity 6 h after the intraperitoneal administration of OK-432 (0.25KE/kg, or 2.5KE/kg) generated larger amounts of superoxide than those harvested after intraperitoneal injection of oyster glycogen (75mg/kg) when stimulated by opsonized zymosan or phorbol myristate acetate. Simultaneous intraperitoneal administration of OK-432 and syngeneic serum induced a greater increase in PMN superoxide generation than OK-432 alone, which was reversed by a complement activation inhibitor (MX-1). Simultaneous injection of OK-432 and heat-inactivated syngeneic serum did not exhibit a significant increase in PMN superoxide generation as compared with OK-432 alone. These results provide pharmacological evidence to the satisfactory therapeutic effects of the intraperitoneal administration of OK-432 with or without serum for patients with cancer ascites, and indicate that complements, in particular C5a, are involved in this enhanced PMN-derived superoxide generation induced by the simultaneous injection of OK-432 and serum.

Animals↗
PubMed1995

Atrophic nerve fibers in regions of reduced MIBG uptake in doxorubicin cardiomyopathy.

A myocardial MIBG-SPECT examination was conducted 2 wk after doxorubicin chemotherapy on a 52-yr-old woman without cardiac symptoms. Despite normal 201TI scintigraphy, reduced MIBG uptake was detected in the apical anterior, inferior and lateral segments of the left ventricle. The patient died of congestive heart failure due to doxorubicin-induced cardiomyopathy 10 mo later. At necropsy, the left ventricle was markedly dilated and the apical anterior, inferior and lateral walls were thin, stiff and whitish. Nerve fibers in the apical inferior wall were atrophic and markedly fibrotic where MIBG uptake was most reduced. Nerve fibers in the septum were normal where MIBG uptake had remained normal. The histologic findings correspond with the findings on the MIBG image. MIBG imaging may detect cardiac sympathetic denervation in doxorubicin-induced cardiomyopathy before cardiac symptoms are manifest and cardiac function deteriorates.

3-Iodobenzylguanidine↗
PubMed1995

Molecular cloning of a full-length cDNA for dentatorubral-pallidoluysian atrophy and regional expressions of the expanded alleles in the CNS.

Dentatorubral-pallidoluysian atrophy (DRPLA) is an autosomal dominant neurodegenerative disorder characterized by genetic anticipation and variable combinations of symptoms including myoclonus, epilepsy, cerebellar ataxia, choreoathetosis, and dementia. Recently, we discovered that DRPLA is caused by unstable expansion of a CAG repeat of a gene on the short arm of chromosome 12. We determined the consensus DRPLA cDNA sequence containing the complete coding region for 1,185 amino acids. The CAG repeat, which is expanded in DRPLA, is located 1,462 bp downstream from the putative methionine initiation codon and encodes a poly-glutamine tract. Although poly-serine and proline tracts exist near the CAG repeats, these polyserine or proline tracts did not show any polymorphisms, which is in strong contrast to the high heterogeneity in the length of the CAG repeat. Northern blot analysis revealed a 4.7-kb transcript that is widely expressed in various tissues including heart, lung, kidney, placenta, skeletal muscle, and brain. Reverse transcription-PCR analysis revealed that the expanded alleles are transcribed to levels comparable to those of normal alleles. These results indicate that there is no difference in transcriptional efficiency between expanded and normal alleles. Furthermore, mRNA from cerebellar hemispheres of DRPLA patients showed smaller sizes of CAG repeats compared with other regions of the brain, which reflects somatic mosaicism of the expanded alleles of the DRPLA gene.

Alleles↗