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T Mashimo

Publications and source records attributed to T Mashimo.

At least 55 records · Page 3Linked to original sources
PubMed2000

Mapping of four simple sequence repeat (SSR) markers on rat chromosome 4.

We previously reported that several markers on rat chromosome (Chr) 4 cosegregated with the occurrence of cerebral stroke and brain edema in stroke-prone spontaneously hypertensive rats (SHRSP). To obtain insights into the positional candidate genes for stroke susceptibility in this region, we mapped four genes, Taurine transporter (Tau), tumor necrosis factor receptor (Tnfr), GABA transporter (Gat1) and glucose transporter-3 (Glut3) genes, using newly developed simple sequence repeat (SSR) markers on rat Chr 4. We isolated the SSRs for the genes either by screening a rat genomic library or by searching the GenBank database. By linkage analysis using two sets of backcrosses, Gat1 and Tnfr were mapped in the region associated with stroke, while Taut was located distant from the region. The Glut3 locus was also assigned to rat Chr 4 using a rat x mouse hybrid clone panel. These results indicated that the Tnfr, Gat1 and Glut3 genes were good positional candidates for the stroke susceptibility in SHRSP, suggesting that further evaluation of these genes by functional studies could prove useful.

Animals↗
PubMed2000

Performance of transport ventilator with patient-triggered ventilation.

OBJECTIVES: Transport ventilators with inspiratory triggering functions and pressure support-control modes have recently become commercially available. We evaluated these ventilators in comparison with a standard ICU ventilator. STUDY DESIGN: Laboratory study with a mechanical lung model. METHODS: We compared the performance of four transport ventilators (model 740, Mallinckrodt, Pleasanton, CA; TBird, Bird Products Corp, Palm Springs, CA; LTV1000, Pulmonetic Systems, Colton, CA; Esprit, Respironics, Vista, CA) with a standard ICU ventilator (model 7200ae; Mallinckrodt) using a test lung that simulated spontaneous breathing (compliance, 46.8 mL/cm H(2)O; resistance, 5 cm H(2)O/L/s). The settings of ventilators were positive end-expiratory pressure (PEEP) of 0 or 5 cm H(2)O, and pressure support (PS) of 0 or 10 cm H(2)O. The settings of the test lung were inspiratory time of 1 s, respiratory rate of 10/min, peak inspiratory flow of 40, 60, and 80 L/min. To evaluate inspiratory function at each setting, we measured the inspiratory delay time (DT), inspiratory trigger pressure (P-I), and the time for airway pressure to rise from the baseline pressure to 90% of the end-inspiratory pressure (T(90%)); for expiratory function, supraplateau expiratory pressure (P-E) and the time constant (taue) for pressure decrease during exhalation were evaluated. Oxygen requirement was assessed as the time required to empty a 3.5-L oxygen tank. RESULTS: For inspiratory triggering, four transport ventilators had DT < 100 ms, which is considered clinically satisfactory, in all the settings except for PS 0 cm H(2)O, PEEP 0 cm H(2)O, and inspiratory flow of 80 L/min with LTV1000. P-I increased only in LTV1000 when PEEP was increased from 0 to 5 cm H(2)O. taue for the transport ventilators was > 50% shorter than for the ICU ventilator except for PS 0 cm H(2)O and PEEP 5 cm H(2)O with TBird. Oxygen requirement was lowest for the Esprit, followed by the 740, LTV1000, and TBird. CONCLUSION: The newer Food and Drug Administration-approved transport ventilators have performance indexes comparable to the ventilator currently used in ICUs and can probably be recommended for clinical use.

Equipment Design↗
PubMed2000

Motor cortex stimulation for central and peripheral deafferentation pain. Report of eight cases.

The authors tested a modified motor cortex stimulation protocol for treatment of central and peripheral types of deafferentation pain. Four patients with thalamic pain and four with peripheral deafferentation pain were studied. Preoperative pharmacological tests of pain relief were performed using phentolamine, lidocaine, ketamine, thiopental, and placebo. In five patients we placed a 20- or 40-electrode grid in the subdural space to determine the best stimulation point for pain relief for a few weeks before definitive placement of a four-electrode array. In three patients, the four-electrode array was implanted in the interhemispheric fissure as a one-stage procedure to treat lower-extremity pain. In two patients with pain extending from the extremity to the trunk or hip, dual devices were implanted to drive two electrodes. Six of eight patients experienced pain reduction (two each with excellent, good, and fair relief) from motor cortex stimulation. No correlation was apparent between pharmacological test results and the effectiveness of motor cortex stimulation. Patients with peripheral deafferentation pain, including two with phantom-limb pain and two with brachial plexus injury, attained pain relief from motor cortex stimulation, with excellent results in two cases. Testing performed with a subdural multiple-electrode grid was helpful in locating the best stimulation point for pain relief. Motor cortex stimulation may be effective for treating peripheral as well as central deafferentation pain.

Aged↗
PubMed2000

[Intraoperative management of heart transplantation in Japan--report of two cases].

We experienced intraoperative anesthetic management of two cases of heart transplantation in Japan. Both patients were in the end stage of cardiac failure due to dilated cardiomyopathy. One patient had had implantation of left ventricular assist system, and another patient had had implantation of automated cardioveter defibrillator. Transesophageal echocardiography was useful for the monitoring of cardiac function during the operation. Anti-arrythmic therapy including heart pacing and protection of right heart failure are important for the circulatory management of heart transplantation. The anesthesiologist is needed not only for the management of respiration and circulation but also for the prevention of infection and control of the time schedule.

Adult↗
PubMed2000

[Anesthetic management of heart transplantation].

We anesthetized a 47-yr-old man with end-stage hypertrophic cardiomyopathy for heart transplantation. This is the first case of heart transplantation from a patient with brain death, since the organ transplantation law had become valid in Japan. Anesthesia was induced and maintained with fentanyl and diazepam. Aseptic technique was used in inserting and securing all catheters. The patient was assisted by left ventricular assist system, and hemodynamic suppression at anesthetic induction was trivial. Since complete AV block was present at the termination of cardiopulmonary bypass (CPB), VVI pacing and infusion of isoproterenol were started. In addition, nitroglycerin was given for pulmonary vasodilation. The cardiovascular support used for weaning from CPB included dobutamine, isoprote-renol, dopamine and milrinone. Following weaning from CPB sinus rhythm appeared spontaneously and function of the transplanted heart was satisfactory. When the patient was transported to ICU reduction in doses of catecholamines was possible, and dopamine and milrinone were infused. The patient was extubated 10 hours after admission to ICU.

Anesthesia, Inhalation↗
PubMed2000

[Successful weaning from mechanical ventilation in an infant with congenital tracheal stenosis and bronchial malacia using endobronchial stent, nasal CPAP and continuous sedation].

A 1.9 kg male infant who showed respiratory distress at his birth, was diagnosed by bronchoscopy as having congenital segmental stenosis of trachea with complete ring. Tracheoplasty was performed and the infant was admitted to ICU. After admission to ICU, we suspected the residual tracheal stenosis and the left main bronchial malacia by bronchoscopy. Although we tried to wean him from mechanical ventilation, but failed and re-intubated him four times because of marked respiratory acidosis after extubation. Bronchoscopy was performed repeatedly, and the residual tracheal stenosis and the left main bronchial malacia were apparent. After patch tracheoplasty of the costal cartilage to the residual tracheal stenosis and implantation of angioplastic expandable metallic stent to the left main bronchus, he was successfully extubated under continuous sedation. In addition, nasal CPAP was effective to reduce retraction and wheezing after extubation. He was discharged from ICU on the 183rd ICU day.

Bronchi↗
PubMed2000

[Comparison of propofol and isoflurane anesthesia on postoperative nausea, vomiting and pruritus induced by epidural morphine].

We compared propofol-nitrous oxide anesthesia (Group P) with isoflurane-nitrous oxide anesthesia (Group I) on the incidence of postoperative nausea, vomiting and pruritus induced by epidural morphine. Twenty-eight patients for thoracotomy for lung surgeries were randomly assigned either to Group P or Group I. All patients were administrated epidural morphine (4-7 mg.day-1) during and after the operation. The incidence of nausea, vomiting and pruritus was evaluated at the postoperative early (< 9 hour) and late (> 9 hour) periods. In the late postoperative period, in Group P the incidence of nausea and vomiting tended to be low compared with Group I, but the difference was not statistically significant. The incidence of pruritus was not different between the two groups in both early and late periods.

Aged↗
PubMed1999

The effects of a point mutation of the beta2 subunit of GABA(A) receptor on direct and modulatory actions of general anesthetics.

The gamma-aminobutyric acid type A receptor (GABA(A) receptor) sites involved in the direct and modulatory actions of general anesthetics remain to be elucidated. The mutation of tyrosine at position 157 in the beta2 GABA(A) receptor subunit was reported to reduce sensitivity to activation by GABA, but not pentobarbital. We examined whether this mutation of the beta2 subunit (Tyr157-->Phe) affects the direct and modulatory actions of other general anesthetics such as propofol and etomidate. Using the two-electrode voltage clamp method, we recorded Cl- current in Xenopus oocytes expressing alpha1beta2gamma2s and alpha1-mutated beta2gamma2s subunits. The mutation of the beta2 subunit reduced the apparent affinity for propofol. However, the mutation had no effect on both the direct actions of pentobarbital and etomidate or on the modulatory actions of pentobarbital, propofol and etomidate. These results suggest that unique loci may exist for the direct action of propofol and that the GABA binding site may not mediate the modulatory actions of general anesthetics at GABA(A) receptors.

Amino Acid Substitution↗
PubMed1999

Oral clonidine reduces the requirement of prostaglandin E1 for induced hypotension.

PURPOSE: To determine the effects of preanesthetic oral clonidine on the dose of prostaglandin EI (PGEI) required to produce hypotension during anesthesia. METHOD: Oral placebo, 75 microg or 150 microg clonidine were administered 60 min prior to induction of anesthesia. Anesthesia was maintained with O2:N2O (30:70) and isoflurane 1.0%. After hemodynamic stabilization, an infusion of prostaglandin EI was started (0.05 microg x kg(-1) x min(-1)) and the rate of infusion was adjusted to maintain mean arterial pressure (MAP) between 60-70 mm Hg during operation. RESULTS: Duration of hypotension in placebo, 75 microg and 150 microg preanesthetic oral clonidine treated groups were 132+/-46, 117+/-37 and 129+/-56 min, respectively. The PGEI requirement in each group were 1563+/-180 (28.6+/-3.2), 594+/-197 (10.8+/-3.6) and 283+/-30 (5.5+/-3.6) microg (microg x kg(-1)), respectively. In addition, blood loss in each group were 1461+/-389, 805+/-240 and 931+/-40 ml, respectively. CONCLUSION: Preanesthetic oral clonidine decreased the dose of PGEI required to produce hypotension, and decreased the blood loss during operation.

Administration, Oral↗
PubMed1999

Aging and salt-loading modulate blood pressure QTLs in rats.

To evaluate the effects of nongenetic factors, aging, and salt-loading on the quantitative trait loci (QTLs) for blood pressure (BP), we conducted a genome-wide linkage analysis using multiple sets of BP measurements in 125 male F2 generation cross derived from stroke-prone spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. The experiment was arranged in two stages. In the first stage, corresponding to the developing period of the rats, BP was measured repeatedly without loading of salt; this continued until the rats were 5 months of age. In the second stage, after the baseline BP leveled off, 1% salt water was given to the rats and BP was monitored for the subsequent 7 months. Genome scanning was performed using 201 markers. In the developing period, three QTLs were identified on chromosomes 1, 3, and 4 (logarithmic odds [LOD] scores of 5.6, 3.1, and 3.2, respectively), which had peaks at 8 or 10 weeks of age. In the latter salt-loading stage, QTLs for BP were detected on chromosomes 1 and 10 (LOD scores 4.6 and 4.5, respectively). When the BP increase during salt-loading was analyzed as a phenotype, however, only the region on chromosome 10 showed linkage at a suggestive level (LOD score 3.2). The present study provides experimental evidence that QTLs for BP could be modulated by nongenetic factors, such as aging and salt-loading.

Aging↗
PubMed1999

Analysis in spontaneously hypertensive rats.

1. Linkage analysis is performed between basal or salt-sensitive high blood pressure and several loci on chromosomes in F2 progenies obtained from crossing stroke-prone spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats. 2. Basal hypertensive genes are mapped to a region near the D1Mit2 locus on chromosome 1 and near the D3Mgh8 locus on chromosome 3 in the male and female F2 progenies. 3. Salt-sensitive hypertensive gene is mapped to a region near RR1023 locus on chromosome 10 in the male F2 progenies. 4. Salt-sensitive hypertensive gene is mapped to a region near D3Mgh12 locus on chromosome 3 in the female F2 progenies.

Animals↗
PubMed1999

Effects of crystalloid and colloid preload on blood volume in the parturient undergoing spinal anesthesia for elective Cesarean section.

BACKGROUND: The role of crystalloid preloading to prevent hypotension associated with spinal anesthesia in parturients during cesarean section has been challenged. Direct measurement of blood volume should provide insight regarding the volume-expanding effects. The aim of the current study was to clarify the effects of volume preload with either crystalloid or colloid solution on the changes in blood volume of parturients undergoing spinal anesthesia for cesarean section. METHODS: Thirty-six healthy parturients scheduled for elective cesarean section during spinal anesthesia were allocated randomly to one of three groups receiving 1.5 l lactated Ringer's solution (LR; n = 12), 0.5 l hydroxyethylstarch solution, 6% (0.5 l HES; n = 12), and 1.0 l hydroxyethylstarch solution, 6% (1.0 l HES; n = 12), respectively. Blood volume and cardiac output were measured before and after volume preloading with indocyanine green (ICG), and the indocyanine green blood concentrations were monitored by noninvasive pulse spectrophotometry. RESULTS: After volume preload, the blood volume significantly increased in all three groups (P < 0.01). The volume of infused solution remaining in the vascular space in the LR, 0.5-l HES, and 1.0-l HES groups were 0.43+/-0.20 l, 0.54+/-0.14 l, and 1.03+/-0.21 l, respectively, corresponding to 28% of lactated Ringer's solution and 100% of hydroxyethylstarch solution infused. Significant increases in cardiac output were observed in the 0.5-l and 1.0-l HES groups (P < 0.01). A significant correlation between the percentage increase in blood volume and that of cardiac output was observed by volume preloading (r2 = 0.838; P < 0.001). The incidence of hypotension was 75% for the LR group, 58% for the 0.5-l HES group, and 17% for the 1.0-l HES group, respectively. CONCLUSIONS: The incidence of hypotension developed in the 1.0-l HES group was significantly lower than that in the LR and 0.5-l HES groups, showing that greater volume expansion results in less hypotension. This result indicates that the augmentation of blood volume with preloading, regardless of the fluid used, must be large enough to result in a significant increase in cardiac output for effective prevention of hypotension.

Adult↗
PubMed1998

Binding of volatile anesthetics to purple membranes studied by X-ray diffraction.

Volatile anesthetics, diiodomethane and trifluoroethyl iodide, acted on the purple membrane of Halobacterium halobium in two different modes depending on the concentration. At low concentration, the absorption maximum of bacteriorhodopsin shifted from 561 to 558 nm (BR558) and the M-intermediate of the photocycle decayed faster than the native one. Higher concentration induced a species absorbing maximally at 480 nm (BR480) and the long-lived M-intermediates. The X-ray study suggested that anesthetics bound specifically to the protein-lipid interfacial region within a trimer near the surface of membrane in BR558 and entered into the hydrophobic domain of the membrane in BR480.

Anesthetics, Inhalation↗
PubMed1998

Human chromosome 16 suppresses metastasis but not tumorigenesis in rat prostatic tumor cells.

Genomic aberrations at the chromosome 16q arm are one of the most consistent abnormalities observed by loss of heterozygosity and comparative genomic hybridization analyses in human prostate cancer, suggesting that there are tumor suppressor or metastasis suppressor genes encoded by this chromosomal region. To functionally identify such suppressor genes, we have conducted microcell-mediated chromosome transfer to introduce human chromosome 16 into the highly metastatic Dunning rat prostatic cancer cell line, AT6.1. The metastatic ability of the resultant microcell hybrid clones was then tested in a standard spontaneous metastasis assay using SCID mice. When the microcell-mediated chromosome transfer hybrid cells containing whole human chromosome 16 were injected, the number of metastatic lesions in the lung was significantly reduced as much as 99% on average. Therefore, chromosome 16 has a strong activity to suppress the metastatic ability of AT6.1 cells while it did not affect the tumorigenesis and tumor growth rate. A PCR analysis of various microcell hybrid clones with sequence-tagged site markers indicates that the metastasis suppressor activity is located in the q24.2 region of chromosome 16. Our results are consistent with the previous finding that the region of human chromosome 16q has frequent loss of heterozygosity in prostate cancer patients and suggest that there is a metastasis suppressor gene in this region that may play an important role in the progression of prostate cancer.

Animals↗
PubMed1998

The expression of the KAI1 gene, a tumor metastasis suppressor, is directly activated by p53.

KAI1 is a tumor metastasis suppressor gene that is capable of inhibiting the metastatic process in animals. The expression of the KAI1 gene also is found to be down-regulated during the tumor progression of prostate, breast, lung, bladder, and pancreatic cancers in humans, and this down-regulation appears to be at or posttranscription level. We have found that the tumor suppressor gene p53 can directly activate the KAI1 gene by interacting with the 5' upstream region. The p53 responding region is located at approximately 860 bases upstream of the transcriptional initiation site, and it contains a typical tandem repeat of the p53 consensus-binding sequence. A gel-shift mobility analysis showed that this sequence indeed had the ability to bind to the purified p53 protein. Mutations of this sequence abolished the responsiveness to p53 and also the binding ability to the p53 protein. Furthermore, immunohistochemical analysis of 177 samples of human prostate tumors revealed that the expression of the KAI1 gene was correlated strongly to that of the p53 gene and that the loss of these two markers resulted in poor survivals of patients. Our data indicate a direct relationship between p53 and KAI1 genes and suggest that the loss of p53 function, which is commonly observed in many types of cancer, leads to the down-regulation of the KAI1 gene, which may result in the progression of metastasis.

Base Sequence↗
PubMed1998

Rapid development of nitric oxide-induced hyperalgesia depends on an alternate to the cGMP-mediated pathway in the rat neuropathic pain model.

Intrathecal injection of a nitric oxide releasing compound, NOC-18, was used to define the role of nitric oxide (NO) in the spinal mechanism of neuropathic pain caused by unilateral chronic constriction injury to rat sciatic nerves. Paw withdrawal latency was used to evaluate nociception induced by thermal stimuli before surgery and afterwards at 1, 3, and 6 h, and on days 1, 2, 3, 4, 5, 8, and 12 after the nerve ligature. In the sham-surgery control groups, intrathecal injection of 10 or 100 microg of NOC-18 did not produce any change in withdrawal latencies. In rats with unilateral nerve ligation, however, administration of 1 or 10 microg, but not 0.1 microg, of NOC-18 significantly shortened the time in which thermal hyperalgesia developed after nerve injury. Injection of 1 microg of NOC-18 decreased the onset time of thermal hyperalgesia from 2 days to 3 h and with 10 microg hyperalgesia developed within 1 h after the nerve injury. The effects of intrathecal injection of MK-801, a N-methyl-D-aspartate (NMDA) receptor antagonist, N-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, methylene blue (MB), a soluble guanylate cyclase inhibitor, and hemoglobin (Hb), a NO scavenger, on the development of thermal hyperalgesia after the sciatic nerve ligature were examined in the presence and absence of 1 and 10 microg of NOC-18. Acceleration of the development of thermal hyperalgesia induced by 1 and 10 microg NOC-18 was completely inhibited by Hb, but was not affected by either MK-801, L-NAME or MB. These findings indicate that NO plays an important role in the rapid development of thermal hyperalgesia after the nerve injury, but that facilitation of nociceptive processing in the spinal cord may entail an alternate to the NO-cyclic guanosine 3',5'-monophosphate (cGMP) pathway.

Animals↗