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T Nishikawa

Publications and source records attributed to T Nishikawa.

At least 235 records · Page 13Linked to original sources
PubMed1999

Four novel plectin gene mutations in Japanese patients with epidermolysis bullosa with muscular dystrophy disclosed by heteroduplex scanning and protein truncation tests.

Epidermolysis bullosa with muscular dystrophy (EB-MD) is a distinct variant of EB caused by mutations in the plectin gene (PLEC1). In this study, we have examined two Japanese patients with EB-MD using heteroduplex scanning or a protein truncation test for mutation detection analysis. The results revealed that both patients were compound heterozygotes for novel PLEC1 mutations (Q1936X/Q1053X and R2421X/12633ins4), which all caused premature termination of translation of the corresponding polypeptides. These cases, which demonstrate the utility of two complementary mutation detection strategies, add to the repertoire of plectin mutations in EB-MD.

Adult↗
PubMed1999

Human autoantibodies against HD1/plectin in paraneoplastic pemphigus.

Paraneoplastic pemphigus (PNP) is an autoimmune blistering disease that occurs in association with underlying neoplasms. PNP patients develop characteristic autoantibodies directed against multiple antigens, mostly identified as members of the plakin family of cytoplasmic proteins (desmoplakin I and II, bullous pemphigoid antigen I, envoplakin, and periplakin). HD1/plectin, another member of the plakin family, has not previously been detected in the characteristic PNP antigen complex, which may relate to practical difficulties associated with its large size (molecular weight approximately 500 kDa). In this study, a combination of immunoprecipitation and immunoblot is used to demonstrate that HD1/plectin is also recognized by sera from PNP patients. Thirteen of 16 PNP sera tested were positive for HD1/plectin compared with none of 43 control sera (11 pemphigus vulgaris, 11 pemphigus foliaceus, 11 bullous pemphigoid, and 10 normal individuals). Combined with our recent finding that desmoglein 3 and desmoglein 1 are cell surface target antigens in PNP, this demonstration of plectin/HD1 as another component of the antigen complex in PNP confirms that PNP is an autoimmune disease against desmoglein and plakin family molecules.

Autoantibodies↗
PubMed1999

Arterial baroreflex function in humans anaesthetized with sevoflurane.

Volatile anaesthetic agents attenuate arterial baroreflex function, while noxious stimuli may modify baroreflex-induced circulatory responses during anaesthesia. We have examined baroreflex control of heart rate during the entire course of sevoflurane anaesthesia in adult patients undergoing surgical procedures. Baroreflex sensitivity was assessed in nine healthy patients undergoing general anaesthesia with sevoflurane. After an 8-10-h fast and no premedication, measurements of R-R intervals were made at conscious baseline (awake), during 2% end-tidal sevoflurane and 67% nitrous oxide before incision (anaesthesia), during surgery at 2% end-tidal sevoflurane and 67% nitrous oxide (surgery) and 20 min after extubation (recovery). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine 50-100 micrograms and nitroprusside 100-200 micrograms to increase and decrease systolic arterial pressure by 20-30 mm Hg, respectively. Baroreflex sensitivities to both pressor and depressor tests were significantly depressed during anaesthesia, surgery and the recovery periods compared with awake values. Pressor test sensitivity during recovery increased significantly from that during surgery (mean 6.16 (SD 2.95) vs 4.42 (3.19) ms mm Hg-1; P < 0.05), but was still significantly less than the awake value (22.50 (17.02) ms mm Hg-1). No improvement in the depressor test sensitivity was seen during the recovery period.

Adult↗
PubMed1999

Propofol anaesthesia in mice is potentiated by muscimol and reversed by bicuculline.

We have examined the role of gamma-aminobutyric acid (GABA) neurones in propofol anaesthesia in mice using the righting reflex. Propofol i.p. increased the percentage of loss of the righting reflex in a dose-dependent manner with an ED50 value of 140 (95% confidence limits 123-160) mg kg-1 (n = 40; eight animals per dose, five doses per dose-response curve). The ED50 for propofol decreased significantly to 66 (58-75) mg kg-1 in the presence of the GABAA receptor agonist muscimol 1 mg kg-1 i.p. (n = 40) (P < 0.05). In contrast, the ED50 increased significantly to 240 (211-274) mg kg-1 in the presence of the antagonist bicuculline 5 mg kg-1 i.p. (n = 40) (P < 0.05). Our results suggest that propofol anaesthesia may be mediated, at least in part by GABA neurons.

Anesthetics, Local↗
PubMed1999

Aminoguanidine supplementation delays the onset of senescence in vitro in dermal fibroblast-like cells from senescence-accelerated mice.

The effects of aminoguanidine supplementation on senescence acceleration in vitro were examined in fibroblasts from the dorsal dermis of newborn SAMP11 (accelerated senescence-prone mice), and were compared to the effects in cell lines from SAMR1 (accelerated senescence-resistant) mice. Four millimolar aminoguanidine supplementation significantly delayed the senescence/crisis in cell lines from SAMP11 mice, but did not affect the senescence/crisis in cell lines from SAMR1 mice. Flow cytometric analysis of the DNA content of confluent cells revealed that aminoguanidine supplementation significantly decelerated the increase in the number of tetraploid cells until senescence/crisis. Although mean concentrations of lipid peroxides in the primary cultures did not differ significantly, considerably higher lipid peroxidation was observed in some SAMP11 cultures, and aminoguanidine supplementation reduced them to the levels in SAMRI cultures. These results strongly suggest that oxidative stress derived from polyamine catabolism may contribute to the senescence acceleration in vitro in cell lines from SAMP11 mice.

Animals↗
PubMed1999

Evaluating T-wave amplitude as a guide for detecting intravascular injection of a test dose in anesthetized children.

UNLABELLED: Previous reports have suggested that accidental intravascular injection of an epinephrine-containing test dose increases T-wave amplitude in anesthetized children. We designed this study to prospectively determine whether changes in T-wave amplitude could be a reliable indicator for detecting intravascular injection. We studied 32 ASA physical status I infants and children (3.4 +/- 1.7 yr) undergoing elective minor surgeries during 1.0 minimum alveolar anesthetic concentration of sevoflurane and 67% nitrous oxide in oxygen. After the i.v. administration of atropine 0.01 mg/kg, the patients were randomly assigned to receive either saline (n = 16) or a test dose consisting of 1% lidocaine (0.1 mL/kg) with 1:200,000 epinephrine (0.5 microg/kg, n = 16) via a peripheral vein to simulate the intravascular injection of the test dose. Heart rate (HR) and systolic blood pressure (SBP) were recorded every 20 and 30 s, respectively, and the T-wave amplitude of lead II was continuously recorded for subsequent analysis. Of the 16 children receiving the test dose, 16, 13, and 16 developed increases in HR, SBP, and T-wave amplitude > or = 10 bpm, > or = 15 mm Hg, and > or = 25%, occurring at 30 +/- 7, 70 +/- 31, and 20 +/- 5 s, respectively. Because no patient receiving saline met these criteria, sensitivity, specificity, and positive and negative predictive values were all 100% based on the criteria using the T-wave amplitude and the peak HR. Our results suggest that changes in T-wave amplitude are as effective as HR for detecting the intravascular injection of an epinephrine-containing test dose in sevoflurane-anesthetized children. IMPLICATIONS: To determine whether an epidurally administered local anesthetic is unintentionally injected into a blood vessel, a small dose of epinephrine is often added to a local anesthetic. We found that increases in T-wave amplitude by > or = 25% in lead II monitor electrocardiography are as effective as a heart rate increase > or = 10 bpm for detecting intravascular injection in sevoflurane-anesthetized children.

Anesthetics, Inhalation↗
PubMed1999

A comparative study of hemodynamic and T-wave criteria for detecting intravascular injection of the test dose (epinephrine) in sevoflurane-anesthetized adults.

UNLABELLED: This study was designed to determine the efficacy of heart rate (HR), systolic blood pressure (SBP), and changes in T-wave morphology in detecting intravascular injection of 15 microg of epinephrine (test dose) in sevoflurane-anesthetized adults. In addition, the testing threshold using the T-wave amplitude was derived. Ninety-six healthy patients were randomized to receive end-tidal sevoflurane 0.5%, 1%, or 2% and nitrous oxide 67% in oxygen (n = 32 for each sevoflurane concentration). Each group of patients was further randomized to receive 3 mL of 1.5% lidocaine plus 15 microg of epinephrine IV or 3 mL of saline IV (n = 16 each). HR, SBP, and T-wave amplitude were continuously monitored for 5 min after the IV injection of the study drug. None receiving IV saline and 15,15, and 14 patients receiving the IV test dose developed HR increases > or =10 bpm during 0.5%, 1%, and 2% sevoflurane, respectively. No patient receiving saline and all patients receiving the test dose developed SBP increases > or =15 mm Hg. T-wave amplitude decreased by >0.1 mV and by >25% in all patients receiving the IV test dose, and its magnitude was similar regardless of the sevoflurane concentrations. When 0.1-mV and 25% decreases in T-wave amplitude were considered as testing thresholds, 100% sensitivities and specificities were obtained. We conclude that a peak SBP increase > or =15 mm Hg and a decrease in T-wave amplitude > or =0.1 mV and > or =25% are more reliable than a HR increase > or =10 bpm for detecting intravascular injection of epinephrine-containing test dose during sevoflurane anesthesia. IMPLICATIONS: To determine whether an epidural catheter resides in a blood vessel, a standard test dose containing a local anesthetic and 15 microg of epinephrine is used. We found that, in sevoflurane-anesthetized adult patients, a systolic blood pressure increase > or =15 mm Hg and a decrease in T-wave amplitude > or =0.1 mV and > or =25% in lead II, but not a heart rate increase > or =10 bpm, are reliable indicators for detecting intravascular injection.

Adult↗
PubMed1999

Sevoflurane speeds recovery of baroreflex control of heart rate after minor surgical procedures compared with isoflurane.

UNLABELLED: Volatile anesthetics attenuate arterial baroreflex functions, whereas noxious stimuli may modify baroreflex-induced circulatory responses during anesthesia. We designed the present study to compare baroreflex control of heart rate during sevoflurane and isoflurane anesthesia in young healthy surgical patients. Baroreflex sensitivity was assessed in 24 patients randomized to receive either sevoflurane (n = 12) or isoflurane (n = 12) for general anesthesia. After an 8- to 10-h fast and no premedication, measurements of RR intervals obtained from electrocardiography and systolic blood pressure (SBP) measured through a radial artery catheter were made at conscious baseline (Awake), during end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide before incision (Anesth), during surgery at end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide (Surg), and 20 min after tracheal extubation (Recov). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine (100-150 micrograms) and nitroprusside (100-150 micrograms) to increase and decrease SBP by 15-30 mm Hg, respectively. The linear portions of the baroreflex curves relating RR intervals and SBP were determined to obtain baroreflex sensitivities. Baroreflex sensitivities to both pressor and depressor tests were significantly depressed during Anesth and Surg periods compared with Awake values in both anesthetic techniques. The pressor test sensitivity during the Recov period returned to the Awake value after sevoflurane (12.9 +/- 3.7 vs 11.0 +/- 8.7 ms/mm Hg [mean +/- SD]) but was still depressed after isoflurane anesthesia (13.9 +/- 8.0 vs 4.8 +/- 3.2 ms/mm Hg; P < 0.05). The depressor test sensitivities during the Recov period remained depressed after both anesthetic techniques. We conclude that both sevoflurane and isoflurane depress arterial baroreflex function during anesthesia and surgery, but the pressor test sensitivity was restored more quickly after sevoflurane than after isoflurane anesthesia. IMPLICATIONS: Arterial baroreflex function is an important neural control system for maintaining cardiovascular stability. We found that baroreflex control of heart rate due to hypertensive perturbation returned to the preanesthetic level more quickly after sevoflurane than after isoflurane anesthesia.

Adult↗
PubMed1999

The efficacy of a simulated intravascular test dose in sevoflurane-anesthetized children: a dose-response study.

UNLABELLED: A recent study demonstrated that changes in both heart rate (HR; positive if > or = 10bpm increase) and T-wave amplitude (positive if > or = 25% increase) reliably detect accidental intravascular injection when a full test dose containing epinephrine 0.5 microg/kg is injected intravascularly. We designed this study to prospectively determine whether a smaller dose of epinephrine would produce reliable HR and T-wave changes in sevoflurane-anesthetized children. We studied 80 ASA physical status I infants and children (6-72 mo) undergoing elective surgeries during 1.0 minimum alveolar anesthetic concentration sevoflurane and 67% nitrous oxide in oxygen. After the administration of i.v. atropine 0.01 mg/kg, the patients were randomly assigned to receive either i.v. saline (n = 20), an i.v. test dose (0.1 mL/kg) consisting of 1% lidocaine with 1:200,000 epinephrine (epinephrine 0.5 microg/kg group, n = 20), an i.v. test dose (0.05 mL/kg) (epinephrine 0.25 microg/kg group, n = 20), or an i.v. test dose (0.025 mL/kg) (epinephrine 0.125 microg/kg group, n = 20) via a peripheral vein to simulate the intravascular injection of the test dose. HR and systolic blood pressure were recorded every 20 and 30 s, respectively, and T-wave amplitude of lead II was continuously recorded for subsequent analysis. After the i.v. injection of the test dose, all children in the epinephrine 0.5 and 0.25 microg/kg groups developed positive responses based on the peak T-wave amplitude, whereas all children in the epinephrine 0.5 microg/kg group and 17 children (85%) in the epinephrine 0.25 microg/kg group elicited a positive response according to the peak HR criterion. No false-positive responses were observed with saline injections. Children in the epinephrine 0.125 microg/kg group showed clinically unacceptable efficacy based on either criterion. We conclude that the efficacies of detecting an intravascular injection of the test dose based on the hemodynamic and T-wave criteria are reduced with smaller doses of epinephrine and that HR and T-wave changes are still useful indicators in most patients if epinephrine 0.25 microg/kg is accidentally injected intravascularly. IMPLICATIONS: To determine whether an epidurally administered local anesthetic has been unintentionally injected into a blood vessel, a small dose of epinephrine is often added to a local anesthetic. We found that an increase in T-wave amplitude > or = 25% in lead II and a heart rate increase > or = 10 bpm are useful indicators for detecting the accidental intravascular injection of a small dose of epinephrine in sevoflurane-anesthetized children.

Anesthesia, Inhalation↗
PubMed1999

The effect of intravenous or subarachnoid lidocaine on glutamate accumulation during transient forebrain ischemia in rats.

UNLABELLED: We studied whether IV or subarachnoid (SA) lidocaine would influence the increase in extracellular glutamate concentration in the hippocampal CA1 and the cerebral cortex during transient forebrain ischemia in rats by using the dialysis electrode method. Fifty-four Sprague-Dawley rats were assigned to one of six treatment groups: IV lidocaine 5 mg/kg, IV lidocaine 10 mg/kg, IV 0.9% saline 0.5 mL/kg, SA lidocaine 5 mg/kg, SA lidocaine 10 mg/kg, and SA 0.9% saline 0.5 mL/kg (n = 9 in each group). Transient forebrain ischemia was induced by hemorrhagic hypotension and carotid artery occlusion, 15 min after administration of lidocaine or saline. The maximal values of glutamate concentration and the areas under glutamate concentration curves in the CA1 were significantly less in the IV lidocaine 10 mg/kg group than the IV saline group, whereas those in the CA1 and the cortex were significantly less in the SA lidocaine 5 and 10 mg/kg groups than the SA saline group. The accumulation of glutamate in the CA1 or the cortex during transient forebrain ischemia was attenuated by IV or SA lidocaine. We conclude that the neuroprotective effect of lidocaine against transient cerebral ischemia involves the suppression of the increase in extracellular glutamate concentration. IMPLICATIONS: IV or subarachnoid lidocaine was demonstrated to suppress glutamate accumulation in the hippocampus and the cortex during transient forebrain ischemia in rats by using the dialysis electrode method. Lidocaine can have a neuroprotective effect through the suppression of the increase in extracellular glutamate concentration.

Anesthetics, Local↗
PubMed1999

Oral clonidine premedication enhances postoperative analgesia by epidural morphine.

UNLABELLED: This study was designed to evaluate the effects of oral clonidine premedication on postoperative analgesia by epidural morphine in a prospective, randomized, double-blinded design. Sixty consenting patients, scheduled for total abdominal hysterectomy, were randomly assigned to one of three groups (n = 20 each); the clonidine-morphine group received oral clonidine 5 microg/kg 90 min before arriving in the operating room and epidural morphine 2 mg before induction of general anesthesia, the clonidine-placebo group received oral clonidine 5 microg/kg and no epidural morphine, and the placebo-morphine group received no clonidine and epidural morphine 2 mg. An epidural catheter was placed at the L1-2 or L2-3 interspace, and 1.5% lidocaine was used for surgical anesthesia in all patients. General anesthesia was then induced with propofol, and maintained with a continuous infusion of propofol and 67% nitrous oxide in oxygen during surgery. Four patients were subsequently withdrawn from the study. After surgery, patient-controlled analgesia using IV morphine was used to assess analgesic requirement. Morphine consumptions determined every 6 h after surgery in the clonidine-morphine and placebo-morphine groups were significantly less than the clonidine-placebo group until 12 h after surgery, whereas those of the clonidine-morphine group were significantly less than the placebo-morphine group from 13 to 42 h after surgery. Visual analog (pain) scale (VAS) scores in the clonidine-morphine group were significantly lower than the placebo-morphine group at 48 h at rest, and at 1, 24, 36, and 48 h with movement. Similarly, VAS scores in the clonidine-morphine group were significantly lower than the clonidine-placebo group at 1 and 6 h both at rest and with movement, whereas VAS scores in the clonidine-placebo group were significantly lower than the placebo-morphine group at 24, 36, and 48 h at rest and with movement. The incidence of nausea and pruritus was similar between groups. We conclude that the combination of oral clonidine and epidural morphine produces more potent and longer lasting postoperative analgesia than either drug alone without increasing the incidence of adverse effects after major gynecologic surgeries. IMPLICATIONS: A small dose of epidural morphine is often used for postoperative analgesia. We found that oral clonidine premedication 5 microg/kg improves the analgesic efficacy of epidural morphine without increasing the incidence of adverse side effects.

Administration, Oral↗
PubMed1999

Antipsychotic-induced life-threatening 'esophageal dyskinesia'.

We report two patients with lingual dyskinesia and complaints of food regurgitation following long-term antipsychotic therapy. Esophageal contrast radiography revealed dyskinetic movements extending from the pharynx to the upper portion of the esophagus. The elevation of intraesophageal pressure was confirmed by esophageal manometry. The dyskinetic movements almost disappeared along with improvement of lingual dyskinesia following the administration of sulpiride in one patient. Another patient suddenly died due to asphyxiation of foods before the beginning of treatment. We termed this life-threatening movement, 'esophageal dyskinesia'. It should be emphasized that 'esophageal dyskinesia' associated with lingual dyskinesia is a potentially fatal adverse reaction to antipsychotic therapy.

Aged↗
PubMed1999

Retrograde temporal order amnesia resulting from damage to the fornix.

Some amnesic patients show an impairment of temporal order memory that cannot be accounted for by content memory deficits. The performance of an amnesic patient on memory tasks assessing the patient's content and temporal memories for remotely acquired material is described, after a lesion including the bilateral anterior fornix and adjacent anterior thalamus. The patient displayed a deficit in the temporal order tasks for remotely acquired information. Neither frontal cognitive deficits nor recognition deficits can account for this patient's poor temporal memory. This retrograde temporal order memory impairment without content memory deficits were not seen in previously reported thalamic amnesic patients. Accordingly, the present patient's poor retrograde temporal memory could hardly be explained by only a thalamic lesion. It is concluded that the patient's impairment of temporal order memory for the retrograde material is probably due to the direct disconnection between the frontal lobe and the hippocampus by disruption of the fornix.

Amnesia↗
PubMed1999

Role of somatosensory feedback from tools in realizing movements by patients with ideomotor apraxia.

In order to investigate the underlying mechanism of ideomotor apraxia, we studied 9 patients who could not mime using tools despite the ability to manipulate actual tools normally. In all the mime tasks, visually presented tools or model gestures by examiners were fundamentally ineffectual in improving the patients' performances. Even the remarkable improvement demonstrated when using actual tools disappeared immediately after the subjects took their hands off them. In a further experiment, 4 of the 9 patients were required to pretend to use tools while holding a stick, resulting in significant improvements or normal miming. These findings suggest that the somatosensory feedback continuously supplied from a handheld tool is a crucial component in enabling patients with ideomotor apraxia to actually use tools.

Acoustic Stimulation↗
PubMed1999

Three cases of Darier's disease in a family showing marked heterogeneous clinical severity.

We report a Japanese family in which two sisters and their mother with Darier's disease showed apparent heterogeneous clinical severity. The elder sister had extensive skin lesions typical of Darier's disease on the scalp, face, neck, axillae and chest. The skin lesions of the younger sister were less severe. The mother had had skin lesions due to Darier's disease with moderate severity since her teenage years. The lesions had gradually involuted as she grew older, leaving only postinflammatory pigmentation around the neck. Thus, spontaneous remission of skin lesions, rare in Darier's disease, and heterogeneous clinical severity between and within generations were noted in this family.

Adult↗