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Biomedical subjects

Y Kira

Publications and source records attributed to Y Kira.

At least 19 recordsLinked to original sources

Inducing peripheral sympathetic nerve activity by therapeutic electrical stimulation.

PURPOSE: To examine whether the activity of peripheral sympathetic nerves in animals with spinal cord injury can be controlled using therapeutic electrical stimulation. METHODS: The spinal cords of 6 Wistar rats were severed at T12/T13 disk level and were given continuous therapeutic electrical stimulation. Microneurography was used to record sympathetic nerve activity at 24, 48, and 72 hours after severing the spinal cord. RESULTS: Integrated values of muscle sympathetic nerve activity after 72 hours of therapeutic electrical stimulation revealed significantly larger potentials on the stimulated side than the non-stimulated side. Skin sympathetic nerve activity showed no difference between the 2 sides. CONCLUSION: Therapeutic electrical stimulation was found to have a facilitatory effect on the muscle sympathetic nerve activity, whereas regulatory function was activated by the sympathetic nerves.

Animals↗

Sympathetic skin response in patients with spinal cord injury.

PURPOSE: To assess the effectiveness of sympathetic skin response in evaluating peripheral sympathetic nerve activity of patients with spinal cord injury, and to report on the basic properties of sympathetic skin response. METHODS: Sympathetic skin response evoked by electrical stimulation was recorded from the palms and soles of healthy volunteers and patients with spinal cord injury. RESULTS: Sympathetic skin response was recorded in 17 healthy volunteers and 14 patients with spinal cord injury. Of the 4 waveforms, the shortest latency was obtained from the palm; the sympathetic skin response was 1.2 to 1.4 ms at all stimulated sites, 1.9 to 2.0 ms at the sole, with a difference of about 0.6 ms between the palm and the sole. None of the patients with spinal cord injury responded at either the upper or lower limbs. In patients with a thoracic cord injury, some responded at the upper limbs but none at the lower limbs; some responded at neither upper nor the lower limbs; and some responded at both upper and lower limbs. The conducting pathway of sympathetic skin response in the spinal cord for the upper limbs descends to the upper thoracic cord (T4-6), and the conducting pathway for the lower limbs departs from the spinal cord at the lower thoracic cord (T9-10). CONCLUSION: It appears that sympathetic skin response should be used for the evaluation and morbid investigation of the functional abnormalities of the sympathetic nervous system in patients with spinal cord lesions such as spinal cord injuries, cervical spondylosis, and spinal canal stenosis.

Adolescent↗

Diagnostic utility of waveform analysis of compound muscle action potentials for carpal tunnel syndrome.

PURPOSE: To determine the diagnostic utility of waveform analysis of compound muscle action potentials (CMAP) for carpal tunnel syndrome (CTS). METHODS: A total of 131 hands in 71 patients diagnosed with CTS (grouped according to severity) and 80 hands in 44 normal subjects were evaluated using nerve conduction test through the carpal tunnel combined with waveform analysis of CMAP. RESULTS: Compared to normal subjects, the sensory nerve conduction velocity and mean frequency of the CMAP waveform were significantly reduced in patients with CTS. Compared with distal motor latency and sensory nerve conduction velocity, the mean frequency of the CMAP decreased significantly with increasing clinical severity. CONCLUSION: This study suggests that waveform analysis of CMAP is of diagnostic value in CTS, and is also of value in objective evaluation of postoperative recovery of carpal median nerve dysfunction.

Action Potentials↗

The relationship between nerve conduction study and clinical grading of carpal tunnel syndrome.

PURPOSE: To conduct a median nerve conduction study on patients with carpal tunnel syndrome and investigate the relationship between nerve conduction study parameters and clinical grading. METHODS: A nerve conduction study was performed on 60 upper limbs of 37 patients with idiopathic carpal tunnel syndrome, and the relationship between the clinical grade and various study parameters was assessed. RESULTS: The amplitude of the sensory nerve action potential and the motor nerve action potential differed according to clinical grading, but this pattern was not seen for sensory nerve conduction velocity, motor nerve conduction velocity, or motor nerve terminal latency and clinical grading. CONCLUSION: The amplitude of the sensory nerve action potential and motor nerve action potential reflect the functional state of axons, and are useful parameters for assessing clinical grading based on nerve conduction velocity.

Action Potentials↗

Transmembrane TNF (pro-TNF) is palmitoylated.

Human transmembrane tumor necrosis factor (pro-TNF) was examined for protein acylation. The cDNA encoding pro-TNF was expressed in both COS-1 cells and Sf9 cells and metabolic labeling with [(3)H]myristic or [(3)H]palmitic acid was attempted. The 17 kDa mature TNF secreted from the transfected cells was not labeled, whereas the 26 kDa pro-TNF was specifically labeled with [(3)H]palmitic acid. The [(3)H]palmitic acid labeling of pro-TNF was eliminated by treatment with hydroxylamine, indicating that the labeling was due to palmitoylation of a cysteine residue via a thioester bond. Site-directed mutagenesis of the two cysteine residues residing in the leader sequence of pro-TNF demonstrated that palmitoylation of pro-TNF occurs solely at Cys-47, located at the boundary between the transmembrane and cytoplasmic domains of pro-TNF. Thus, pro-TNF interacts with the plasma membrane via both its proteinaceous transmembrane domain and a lipid anchor.

Acylation↗

Tributyltin interacts with mitochondria and induces cytochrome c release.

Although triorganotins are potent inducers of apoptosis in various cell types, the critical targets of these compounds and the mechanisms by which they lead to cell death remain to be elucidated. There are two major pathways by which apoptotic cell death occurs: one is triggered by a cytokine mediator and the other is by a mitochondrion-dependent mechanism. To elucidate the mechanism of triorganotin-induced apoptosis, we studied the effect of tributyltin on mitochondrial function. We found that moderately low doses of tributyltin decrease mitochondrial membrane potential and induce cytochrome c release by a mechanism inhibited by cyclosporine A and bongkrekic acid. Tributyltin-induced cytochrome c release is also prevented by dithiols such as dithiothreitol and 2,3-dimercaptopropanol but not by monothiols such as GSH, N-acetyl-L-cysteine, L-cysteine and 2-mercaptoethanol. Further studies with phenylarsine oxide agarose revealed that tributyltin interacts with the adenine nucleotide translocator, a functional constituent of the mitochondrial permeability transition pore, which is selectively inhibited by dithiothreitol. These results suggest that, at low doses, tributyltin interacts selectively with critical thiol residues in the adenine nucleotide translocator and opens the permeability transition pore, thereby decreasing membrane potential and releasing cytochrome c from mitochondria, a series of events consistent with established mechanistic models of apoptosis.

Animals↗

Ascitic fluid cytology of adenosarcoma of the ovary: a case report.

Extrauterine adenosarcoma is very rare and originates in the ovary, adnexa, or myometrium. Cytologic study of ascites is very important to determine clinical staging of malignant ovarian tumors and provide adequate therapy for recurrence. The cytomorphologic features of adenosarcoma have been only rarely described. A 77-yr-old woman visited a hospital with a complaint of lower abdominal pain for 1 mo. A tumor originating from the right adnexa in the pelvis, and involving the rectum, was found in surgery. In the ascitic fluid cytology, a few dispersed tumor cells with large cytoplasm and nuclei were oval-shaped, with nuclear invagination. The chromatin was finely granular; one or two nucleoli were conspicuous. To our knowledge, this is the fifteenth reported case of adenosarcoma of the ovary, and there have been no prior reports describing the cytological features of ascitic fluid cells in adenosarcoma of the ovary.

Adenosarcoma↗

Sympathetic skin response evoked by respiratory stimulation as a measure of sympathetic function.

OBJECTIVES: To compare respiratory and electrical methods of evoking a sympathetic skin response (SSR). METHODS: SSRs evoked by both electrical and respiratory stimulation were recorded from the palms of 47 healthy volunteers. Expiration and inspiration were used as separate stimuli. The correlation coefficients between the amplitude and latency of the SSR from the palm electrodes and the various components of heart rate variability were calculated. RESULTS: Waveform patterns of the SSRs obtained from electrical stimulation showed varied responses to and habituation to this type of stimulation. On the other hand, no subjects showed a phase change in SSR waveform patterns between the first and last expiratory stimuli. The potentials recorded after expiratory stimulation had significantly greater amplitudes than those recorded after electrical stimuli. The low frequency component of heart rate variability induced by expiratory stimulation was significantly greater than that induced by electrical stimulation. The SSR may also correlate strongly with the change of respiratory rate since a more rapid pressure change occurs during expiratory movement than during inspiratory movements. CONCLUSIONS: The SSR evoked by expiratory stimulation is more reliable than either electrical stimulation or inspiratory stimulation for determining sympathetic function.

Adult↗

Hypoxic induction of adrenomedullin in cultured human umbilical vein endothelial cells.

OBJECTIVES: The current study evaluated the hypoxic induction of adrenomedullin gene expression and secretion, and its mechanism in cultured human umbilical vein endothelial cells (HUVEC). METHODS: HUVEC were exposed to hypoxia or normoxia as controls for 1 to 24 h. Using Northern blot analysis and a radioimmunoassay, we evaluated adrenomedullin expression in HUVEC. The transcriptional component of adrenomedullin gene regulation was assessed by nuclear run-off experiments, and adrenomedullin mRNA half-life was measured by actinomycin D experiments. RESULTS: We found that hypoxic conditions (1-3% oxygen) significantly increased adrenomedullin mRNA and protein in HUVEC. This increase was inversely proportional to oxygen tension and was reversible upon re-exposure to a 21% oxygen environment Nuclear run-off experiments revealed the enhanced transcriptional rate of adrenomedullin gene. Next, actinomycin D experiments revealed the enhanced adrenomedullin mRNA stability. CONCLUSIONS: These results indicate that hypoxia increases adrenomedullin gene expression and secretion in HUVEC by transcriptional and post-transcriptional mechanisms. Hypoxic induction of adrenomedullin may play a pathophysiological role in the vascular systems.

Adrenomedullin↗

Identification of putative gene encoded on ORF16 of the 81 kb contig of Arabidopsis thaliana chromosome III as alpha-mannosidase.

We isolated cDNA corresponding to open reading frame (ORF) 16 of the 81 kb contig of Arabidopsis thaliana chromosome III [Quigley., Nucleic Acids Res., 24, 4313-4318 (1996)] and expressed alpha-mannosidase activity in tobacco suspension-cultured cells, which revealed that ORF16 encodes alpha-mannosidase. We also suggested that Arabidopsis harbors three genes encoding alpha-mannosidase by homology search against the database.

Journal Article↗

Localization of nitric oxide synthase activity in unfertilized oocytes and fertilized embryos during preimplantation development in mice.

Changes in the activities of nitric oxide synthase (NOS) during embryonic development, and the distribution of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) isoforms were examined in unfertilized mouse oocytes at the second meiotic metaphase (MII) stage and in fertilized mouse embryos during preimplantation development. In addition, the effects of NOS inhibitors on mouse preimplantation development in vitro were investigated. The activities of NOS in MII oocytes and fertilized embryos during the preimplantation period were determined by NADPH-diaphorase staining. Although NOS activity was detected in unfertilized MII oocytes, the intensity of staining was much weaker than that of fertilized embryos at the one-cell stage. There was a decrease in NOS activity in embryos from the four-cell to the eight-cell stage; however, NOS activity increased again in embryos at the morula stage, particularly in the inner cell population. In the expanded blastocysts, staining was confined to the inner cell mass. Immuno-cytochemical staining showed that eNOS and iNOS were expressed in the cytoplasm of oocytes and embryos during the preimplantation period, and eNOS was also distributed in the nuclei of the embryos. When one-cell embryos were treated with 1 mmol N(omega)-nitro-L-arginine methyl ester (L-NAME) l(-1), their development in vitro was arrested at the two-cell stage. This inhibition of development was overcome by the addition of 1 mmol L-arginine l(-1) to the medium. These observations indicate that nitric oxide plays an important role as a diffusible regulator of cell proliferation and differentiation, especially at the developmental transition from the two-cell to the four-cell stage during preimplantation development of mice.

Animals↗

Effect of Chlamydia pneumoniae infection on coronary flow reserve and intimal hyperplasia after stent implantation in patients with angina pectoris.

OBJECTIVES: Chlamydia pneumoniae (C. pneumoniae) has been detected in tissue from coronary atherosclerotic vascular lesions and may be involved in the pathogenesis of atherosclerosis. However, the effect of prior C. pneumoniae infection on coronary intimal hyperplasia after stent implantation and on coronary microvascular function is unknown. METHODS: Seventy-three patients with stable angina pectoris and a single de novo coronary lesion were studied prospectively. All patients underwent successful coronary angioplasty and stent implantation for the stenotic lesion. Blood samples were tested for prior C. pneumoniae infection before the procedure, and patients were divided into two groups: Seropositive and seronegative. Coronary flow reserve was measured in the non-stenotic coronary vessel before angioplasty, and quantitative coronary arteriography was performed at the stent implantation site before angioplasty and 6 months later in all patients. RESULTS: Coronary flow reserve in the non-stenotic vessel was significantly lower in the seropositive group than in the seronegative group (2.51 +/- 0.35 vs 2.76 +/- 0.43, p < 0.05). The minimum luminal diameter was smaller and late loss was greater in the seropositive group than in the seronegative group (minimum luminal diameter: 1.52 +/- 0.59 vs 1.91 +/- 0.79 mm, p < 0.05, late loss: 1.17 +/- 0.55 vs 0.76 +/- 0.67, p < 0.05). However, there was no significant difference in the restenosis rate or target lesion revascularization rate between the two groups. CONCLUSIONS: Prior C. pneumoniae infection may accelerate intimal hyperplasia after stent implantation and impair coronary microvascular function in the non-stenotic coronary vessels.

Aged↗

[Effect of long-term cilostazol administration on coronary flow velocity and coronary flow reserve].

Cilostazol, a novel potent inhibitor of phosphodiesterase, increases coronary flow. The effects of cilostazol on coronary flow velocity and coronary flow reserve were studied in 103 patients with coronary artery disease who underwent coronary angiography. Cilostazol 200 mg/day was administered for 3 months (31 patients) or 6 months (37 patients), and coronary flow reserve were measured before and after the cilostazol administration. Coronary flow reserve were measured twice at an interval of 6 months in the control group (35 patients). The Doppler guide wire was advanced into the coronary artery with no significant vessel stenosis. After obtaining continuous baseline coronary flow velocity, an intracoronary infusion of papaverine (10 mg) was performed to measure coronary flow reserve. There were no significant differences in coronary flow velocity just before intracoronary papaverine infusion between the initial and follow-up studies in any of the 3 groups. Coronary flow reserve increased significantly after cilostazol administration in the 3 months and 6 months groups compared with before administration (3 months group: 2.8 +/- 0.8 vs 2.4 +/- 0.9, p < 0.05; 6 months group: 2.8 +/- 1.0 vs 2.4 +/- 0.7, p < 0.01). However, there was no significant difference in coronary flow reserve in the control group between follow-up and initial studies (2.7 +/- 0.8 vs 2.5 +/- 0.8, NS). In conclusion, the long-term oral administration of cilostazol for 3 or 6 months improves coronary flow reserve.

Administration, Oral↗

Acute effects of nicotine content in cigarettes on coronary flow velocity and coronary flow reserve in men.

We investigated the acute effects of smoking on coronary flow reserve in terms of the nicotine content of cigarettes in 21 smokers. Coronary flow velocity was measured with a Doppler flow wire. Subjects smoked cigarettes containing >1 mg nicotine (n = 8, group 1) or <1 mg (n = 6, group 2). Subjects in the control group mimicked smoking without a cigarette (n = 7). Coronary flow reserve decreased after smoking in group 1, but not in group 2 or the control group. This reduction may have mediated nicotine or some other unknown substances influenced by smoking.

Adult↗

[Impaired coronary flow reserve due to long-term smoking recovers after quitting].

Cigarette smoking is a major risk factor for coronary artery disease. The present study examined whether impaired coronary flow reserve by smoking can be recovered by quitting. Coronary flow velocity was measured by Doppler guide wire during coronary angiography and coronary flow reserve was determined by injecting 10 mg intracoronary papaverine in 45 patients who were present or former smokers. Twenty-three patients were smoking more than 800 cigarettes/day x years and 22 patients less than 800, and 13 patients had smoked more than 800 but had quit smoking at least for 5 years. None of the patients had any significant coronary stenosis in the left anterior descending artery where the Doppler probe was positioned, nor any coronary risk factors except smoking. Twenty-six non-smokers served as control subjects. There was no difference in the coronary flow reserve between controls and light smokers (3.3 +/- 0.7 vs 3.3 +/- 1.0), but it was significantly reduced in heavy smokers (2.6 +/- 0.8) compared to controls or light smokers (p < 0.05, p < 0.05, respectively), There was no significant difference in coronary flow reserve between controls, light smokers and ex-smokers (3.3 +/- 1.2). These results suggest that the deteriorating effect on the coronary flow reserve by smoking is corrected after its cessation.

Aged↗

Inhibition of rat vascular smooth muscle proliferation in vitro and in vivo by bone morphogenetic protein-2.

Vascular proliferative disorders are characterized by the proliferation of vascular smooth muscle cells (SMCs) and excessive extracellular matrix synthesis. We found that bone morphogenetic protein-2 (BMP-2) inhibited serum-stimulated increases in DNA synthesis and cell number of cultured rat arterial SMCs in a fashion quite different from that in the case of transforming growth factor-beta1 (TGF-beta1). In addition, TGF-beta1 stimulated collagen synthesis in SMCs, whereas BMP-2 did not. In an in vivo rat carotid artery balloon injury model, the adenovirus-mediated transfer of the BMP-2 gene inhibited injury-induced intimal hyperplasia. These results indicate that BMP-2 has the ability to inhibit SMC proliferation without stimulating extracellular matrix synthesis, and suggest the possibility of therapeutic application of BMP-2 for the prevention of vascular proliferative disorders.

Adenoviridae↗

Effect of time interval between two balloon inflations on ischemic preconditioning during coronary angioplasty.

Ischemic preconditioning, defined as a reduction in myocardial ischemia caused by repeated brief episodes of coronary occlusions, is observed during percutaneous transluminal balloon angioplasty (PTCA). To elucidate the effects of the length of the interval between consecutive balloon inflations on ischemic preconditioning during PTCA, we examined 62 patients with chronic stable angina (48 males and 14 females; mean age 62 +/- 10 yr). PTCA was performed on the left anterior descending artery lacking in collateral vessels. A 2-min balloon inflation was performed twice and the extent of ST segment elevation in the electrocardiogram and the severity of chest pain (scored from 0 to 10) for each inflation were determined and compared. Patients were divided into three groups according to the interval between the two inflations: 1 min, Group 1; 2 min, Group 2; and 5 min, Group 5. In Groups 2 and 5, ST-segment elevation was significantly decreased during the second balloon inflation, as compared with that during the first inflation (P < 0.01, P < 0.001). A significant decrease was also observed in the severity of chest pain (P < 0.05, P < 0.01). However, Group 1 showed no significant decrease in ST-segment elevation or severity of chest pain between the first and second inflations. ST-segment elevation and chest pain were reduced to a greater extent in Group 5 than in Group 2. Results suggest that an interval of more than 2 min between balloon inflations is required to achieve ischemic preconditioning during PTCA.

Aged↗

Lysophosphatidylcholine transduces Ca2+ signaling via the platelet-activating factor receptor in macrophages.

To clarify the molecular mechanism underlying the lysophosphatidylcholine (LPC) signaling, we studied the effect of LPC on the intracellular free calcium concentration ([Ca2+]i) in murine peritoneal macrophages. LPC when added alone induced biphasic elevation of [Ca2+]i, which consisted of a rapid increase followed by sustained elevation. LPC, when added with equimolar cholesterol, induced only the rapid increase in [Ca2+]i, which was blocked by WEB-2086, a selective platelet-activating factor (PAF) receptor antagonist. These results suggest LPC exerts a specific Ca2+ signaling. The sustained elevation reflected the cell lysis. Furthermore, we confirmed its pathway in a more specific manner using cloned PAF receptors expressed in Chinese hamster ovary cells. LPC induced an elevation of [Ca2+]i in a concentration-dependent manner only when the PAF receptor had been expressed, and the elevation of [Ca2+]i was blocked by WEB-2086. Taken together, LPC transduces Ca2+ signaling via the PAF receptor. Activation of the PAF receptor by LPC may indicate its novel important role in the pathogenesis of atherosclerosis.

Animals↗