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Biomedical subjects

K Taga

Publications and source records attributed to K Taga.

At least 37 records · Page 2Linked to original sources
PubMed1999

Effects of naloxone and morphine on acute hypoxic survival in mice.

OBJECTIVE: To investigate a role of the opiate system during acute hypoxic hypoxia, the effects of naloxone and morphine on hypoxic survival rate were investigated in awake adult mice. DESIGN: Prospective, randomized, animal trial. SETTING: University research laboratory. SUBJECTS: Male dd-Y mice (n = 864 in experiment I, n = 144 in experiment II, n = 30 in experiment III). INTERVENTIONS: The animals were placed in an airtight plastic chamber into which a continuous flow of 8 L/min 5% oxygen-95% nitrogen was passed. MEASUREMENTS AND MAIN RESULTS: One and 5 mg/kg naloxone had no significant effect on the survival rate of mice subjected to acute hypoxic hypoxia, whereas 10 mg/kg naloxone decreased the survival rate. On the other hand, 2 and 5 mg/kg morphine was shown to have a protective action against acute hypoxic hypoxia. The protective effects of 5 mg/kg morphine against hypoxia was even antagonized by 5 mg/kg naloxone, which did not itself show any significant effect on the survival rate. The oxygen consumption in the morphine-treated (5 mg/kg) mice was significantly (p < .05) lower (87.0% +/- 4.6%; mean +/- SE) than that in the saline-treated animals. CONCLUSIONS: The present study suggests that the endogenous opiate system does not play a significant role on the pathophysiology caused by acute hypoxic hypoxia and that the improved survival of the hypoxic animals by morphine is at least partly attributable to its depressant effect on oxygen consumption.

Analgesics, Opioid↗
PubMed1999

Target cell-induced apoptosis in IL-2-activated human natural killer cells.

We demonstrated that tumor cells induce cell death in lymphokine-activated NK (LAK) cells, but not in non-activated NK cells. Cell death in LAK cells involves nuclear condensation and DNA cleavage, all of which are characteristic features of apoptosis. The mechanism involves signaling through integrins and requires src family tyrosine kinases and protease activities. Engagement of an apoptotic signal molecule, Fas, may also trigger LAK cell death by apoptosis. It appears that LAK cells rapidly die by apoptosis after attacking tumor cells. This phenomenon may provide a means for potential tumor target cells to escape from natural immunosurveillance during therapeutic interventions such as those using IL-2 or LAK cells.

Apoptosis↗
PubMed1999

[Anesthetic management for pericardial fenestration in a hypertrophic cardiomyopathy (HCM) patient with massive pericardial effusion].

A 65 year-old male with HCM had progressively increased pericardial effusion. He also had atrial fibrillation (af), cardiac systolic dysfunction and chronic renal failure needing hemofiltration. Pericardial fenestration was carried out to improve diastolic function. Anesthetic management with fentanyl plus low-dose propofol infusion and postoperative analgesia with epidural morphine were effective for hemodynamic stability to prevent myocardial depression and to control ventricular response to atrial fibrillation. Intraoperative trans-esophageal echocardiography (TEE) monitoring was very useful for fluid therapy, inotropic support and estimation of systolic and diastolic function.

Aged↗
PubMed1998

Differential inhibitory effects of thiopental, thiamylal and phenobarbital on both voltage-gated calcium channels and NMDA receptors in rat hippocampal slices.

Although it is known that there are some pharmacological differences between the structurally similar barbiturates, the underlying mechanism of action remains unclear. We have compared the effects of thiopental, thiamylal and phenobarbital on both voltage-gated calcium channels (VGCC) and N-methyl-D-aspartate (NMDA) receptors in rat hippocampal slices by determining changes in intracellular calcium ([Ca2+]i). Experiments were performed in adult rat hippocampal slices perfused with Krebs solution (37 degrees C). Concentrations of [Ca2+]i in the pyramidal cell layer of the CA1 region were measured using a calcium indicator dye, fura-2. To activate VGCC and NMDA receptors, slices were exposed to K+ 60 mmol litre-1 (< or = 60 s) and NMDA 100 mumol litre-1 (30 s), respectively. Thiopental, thiamylal and phenobarbital were present 5 min before, during and 1 min after high K+ or NMDA application. Both thiamylal and thiopental (50-600 mumol litre-1) attenuated the increases in [Ca2+]i produced by high K+ or NMDA in a concentration-dependent manner, while phenobarbital 50-1000 mumol litre-1 only slightly attenuated the [Ca2+]i increase produced by high K+ at concentrations of more than 200 mumol litre-1 and was ineffective on the [Ca2+]i response produced by NMDA. Although the increases in [Ca2+]i caused by membrane depolarization with high K+ were reduced equally with thiamylal and thiopental, thiamylal was more effective in attenuating the increase in [Ca2+]i produced by NMDA receptor activation than thiopental. We conclude that the depressant effects of barbiturates on both VGCC and NMDA receptors varied between agents. Differential inhibition of both VGCC and NMDA receptors may determine the pharmacological properties of barbiturates and their ability to protect neurones against ischaemia.

Anesthetics, Intravenous↗
PubMed1998

Headache after attempted epidural block: the role of intrathecal air.

BACKGROUND: Postmeningeal puncture headache (PMPH) is typically attributed to the loss of cerebrospinal fluid (CSF). However, when it occurs after an attempted epidural puncture, it may be due to either CSF loss or, potentially, to the subarachnoid injection of air used as a part of "loss-of-resistance" testing. This study was performed to examine the relation between intrathecal air and PMPH. METHODS: Using a loss-of-resistance test with an air-filled (n = 1,812; air group) or saline-filled (n = 1,918; saline group) syringe, epidural block was performed in patients with acute or chronic pain. The dura was judged to be perforated not only when backflow of CSF was recognized in the needle but also when signs and symptoms solely attributable to meningeal perforation were seen, such as high spinal blockade or severe motor blockade. The incidence, onset time, and duration of PMPH in the air and saline groups were compared. In all patients with signs of meningeal perforation, brain computed tomography was examined. RESULTS: The incidence of PMPH in the air group (32 cases) was significantly higher than that in the saline group (5 cases), although the occurrences of meningeal perforation between the air (48 cases) and saline (51 cases) groups did not differ significantly. Intrathecal air bubbles were detected on brain computed tomography in both the deep supraspinal structures such as the ventricles, Silvian fissures and cisterns, and the superficial subarachnoid space in 30 of 32 patients with PMPH in the air group, whereas no intrathecal air bubbles were seen in the saline group. PMPH was significantly more rapid in onset and shorter in duration in the air group than that in the saline group. CONCLUSIONS: The use of air for loss-of-resistance testing during epidural block was associated with a higher incidence of PMPH, which might be attributable to subarachnoid air injection and CSF leakage.

Adolescent↗
PubMed1998

Thiopental inhibits increases in [Ca2+]i induced by membrane depolarization, NMDA receptor activation, and ischemia in rat hippocampal and cortical slices.

BACKGROUND: This study examined the effects of thiopental on intracellular calcium ([Ca2+]i) changes induced by membrane depolarization, N-methyl-D-aspartate (NMDA) receptor activation, and ischemia. METHODS: Experiments were performed in brain slices prepared from Wistar rats. [Ca2+]i measurements were taken on the CA1 pyramidal cell layer of the hippocampus or layers II to III of the somatosensory cortex using the fura-2 fluorescence technique. Membrane depolarization and NMDA receptor activation were induced by exposing slices to 60 mM K+ and 100 microM NMDA, respectively. In vitro ischemia was induced by superfusing slices with glucose-free Krebs solution equilibrated with 95% nitrogen and 5% carbon dioxide. Thiopental was applied 5 min before application of high K+ and NMDA, or before in vitro ischemia. RESULTS: Ischemia for 15 min produced a characteristic [Ca2+]i increase in both hippocampal and cortical slices. Thiopental prolonged the latency to the appearance of the [Ca2+]i plateau and reduced the magnitudes of increase in [Ca2+]i 8, 10, and 15 min after the onset of ischemia. Thiopental also suppressed the high K+- and NMDA-induced [Ca2+]i increases. The NMDA-induced [Ca2+]i increases were attenuated to a greater extent in cortical slices than were those in hippocampal slices. The inhibition of thiopental on the 200-microM NMDA-mediated [Ca2+]i response was confirmed in cultured cortical neurons. CONCLUSIONS: The results indicate that thiopental attenuates ischemia-induced [Ca2+]i increases in the hippocampus and cortex in vitro, probably because of its inhibition of both voltage-gated calcium channels and NMDA receptors. The regionally different inhibition of thiopental on NMDA receptors may relate to its region-specific action against ischemia.

Anesthetics, Intravenous↗
PubMed1997

Prior brain injury protects death from local anaesthetic-induced convulsion.

Minor brain injury was inflicted with a small hypodermic needle at four sites from the scalp 7 days before the production of convulsion by i.p. injection of 100 mg/kg lidocaine in mice. The latency to convulsion and survival rate were significantly longer and higher, respectively, in the brain-injured group than in the sham-operated one. Thus, the results suggest that a protective mechanism develops in the injured brain against asphyxia caused by lidocaine convulsion.

Anesthetics, Local↗
PubMed1997

NMDA induces a biphasic change in intracellular pH in rat hippocampal slices.

As alterations in intracellular pH (pH(i)) tend to exert a profound effect on the properties of cells, this study was undertaken to examine NMDA-induced changes in pH(i) in rat hippocampal slices using the BCECF fluorescent technique. The 'resting' pH(i) in the CA1 pyramidal cell layers was 6.93 +/- 0.07 (mean +/- S.D., n = 72 slices) in 25 mM HCO3-/5% CO2-buffered solution at 37 degrees C. Exposure of hippocampal slices to NMDA in the range of 10-1000 microM produced a biphasic change in pH(i): an initial transient alkaline shift was followed by a long-lasting acid shift. Dizocilpine (10 microM) but not CNQX (40 microM) blocked the NMDA-induced changes in pH(i). In 0 Ca medium (0 mM Ca2+ supplemented 1 mM EGTA, referred to as 0 Ca), pH(i) acid shift caused by NMDA (20 microM) declined by about 11%, whereas the initial alkaline shift almost completely disappeared. In an independent experiment, the NMDA-induced increase in intracellular Ca2+ ([Ca2+]i) was reduced by more than 80% in 0 Ca medium. Glucose substitution using equimolar pyruvate (as an energy-yielding substrate) suppressed this NMDA-induced pH(i) acid shift by two-thirds, while the NMDA-induced pH(i) alkaline shift was enhanced. Fluoride (10 mM), a glycolytic inhibitor, abolished NMDA-induced pH(i) acid shift. Furthermore, the lactate content of hippocampal slices was markedly increased following exposure to NMDA. In conclusion, activation of NMDA receptors in rat hippocampal slices evokes a biphasic change in pH(i). The initial alkaline shift is suggested to be associated with calcium influx, and the following acid shift may be caused by an increase in lactate production through the acceleration of glycolysis, as well as the increased [Ca2+]i. The pH(i) acid shift produced by the increased lactate may contribute to proton modulation of the NMDA receptor and NMDA-induced cell injury or death.

Animals↗
PubMed1997

Transient neuronal depolarization induces tolerance to subsequent forebrain ischemia in rats.

BACKGROUND: Minor cortical injury has previously been shown to improve survival in animals subjected to ischemic insults. Although the mechanism by which an ischemia-tolerant state is achieved is not clear, transient neuronal depolarization is thought to play a central role in the development of the tolerance. One way of producing transient neuronal depolarization is by the induction of cortical spreading depression (CSD). The present study was conducted to evaluate the effect of preischemic transient depolarization, induced by CSD, on postischemic neuronal outcome in rats. METHODS: Unilateral CSD was induced by application of KCl to the frontal cortex (CSD hemisphere) in three groups of isoflurane-anesthetized rats (CSD groups; n = 8/group). Sham animals (n = 12) did not undergo CSD. In a fifth group (n = 8), ketamine was administered during KCl application to inhibit CSD. One, three, or seven days after CSD, animals were subjected to forebrain ischemia produced by bilateral carotid artery occlusion. Injury to the striatum, hippocampus, and cortex was evaluated in hematoxylin and eosin-stained brain sections 3 days after ischemia. RESULTS: Preischemic CSD reduced postischemic injury in the ipsilateral cortex. The ratio of the number of injured neurons in the CSD hemisphere to that in the non-CSD hemisphere was significantly less in the groups subjected to CSD 1 day (0.51 +/- 0.33), 3 days (0.56 /- 0.22), and 7 days (0.40 +/- 0.17) before ischemia than in the sham operated group (1.11 +/- 0.47). In the ketamine group (CSD inhibition), there were no differences in the extent of injury in the two hemispheres (ratio = 0.84 +/- 0.47). Injury to the striatum and hippocampus was similar among the groups. Within each group, injury to these subcortical structures in the CSD hemisphere was not different from that in the non-CSD hemisphere. CONCLUSIONS: The data suggest that preischemic depolarization induced by CSD results in an adaptive response that reduces the vulnerability of cortical neurons to subsequent ischemic injury (ischemic tolerance).

Animals↗
PubMed1997

Epidemiological study on infectious diarrheal diseases in children in a coastal rural area of Kenya.

Diarrheal diseases are major causes of morbidity and mortality among children in developing countries. We have analyzed the causative agents of diarrhea in children under five years of age who resided in rural environments but attended a hospital in Malindi, a coastal town in Kenya. Bacterial diarrhea was found in 239 (27.7%) of 862 patients with diarrhea. Diarrheagenic Escherichia coli, including enteropathogenic, enterotoxigenic, and enterohaemorrhagic strains, was isolated from 119 (13.8%) patients, followed by Salmonella spp. (63 cases, 7.3%) and Shigella spp. (56 cases, 6.5%). Intestinal parasites were found in 109 (12.6%) of the patients. Entamoeba histolytica and Giardia lamblia were found in 67 (7.8%) and 42 (4.9%) of the cases, respectively. Rotavirus was found in 69 (16.1%) of 428 cases, a part of the 862 cases. Significant differences in age distribution were seen in diarrheal cases due to Campylobacter spp., G. lamblia, and rotavirus. No significant seasonal incidence of specific pathogens was found, but the number of diarrheal patients was significantly correlated to rainfall. Drinking water was contaminated with bacteria at concentrations ranging from 10(3) to 10(6) CFU/ml in 98% of the households and by coliform bacteria at concentrations of 10(2) to 10(5) CFU/ml in 72% of the households. These results suggest that the main routes of infection may be contaminated drinking water and fecal-oral transmission of enteric pathogens. Consequently, we propose that the enhancement of hygienic practice through health education is a feasible control measure of diarrhea in the study area.

Age Distribution↗
PubMed1996

Target cell-induced apoptosis of interleukin-2-activated human natural killer cells: roles of cell surface molecules and intracellular events.

We previously reported that natural killer (NK)-sensitive target cells, K562, kill interleukin-2-stimulated (lymphokine-activated killer [LAK]) but not unstimulated NK cells. We have now investigated the molecular basis of this phenomenon. Soluble monoclonal antibody (MoAb) to CD18 inhibited 75% of K562-induced DNA fragmentation and membrane disruption, whereas blocking MoAb to Fas partially inhibited only the DNA fragmentation. MoAbs to CD2, CD11a, CD11b, B7, or CD16 had limited or no effect on K562-induced death of LAK cells. Receptor ligation with either immobilized MoAb to CD18 or Fas induced membrane disruption and DNA degradation in LAK cells independently of K562, and MoAb to CD18, CD11a, or CD11b enhanced DNA fragmentation induced by anti-Fas. Fas-L-transfected Raji cells also killed LAK cells, but only if Fas-L expression was amplified. K562 cells rapidly triggered protein phosphorylation in LAK cells, and the tyrosine kinase inhibitor, Herbimycin A, inhibited DNA fragmentation and membrane disruption. Protease inhibitors strongly suppressed K562-mediated DNA fragmentation of LAK cells, but not membrane disruption. In conclusion, (1) K562-induced death of LAK cells involves primarily CD18, although other molecules, such as Fas, may also be involved; (2) K562-mediated apoptosis of LAK cells requires tyrosine phosphorylation and protease activity; (3) engagement of Fas by immobilized MoAb or Fas-L on target cells can also kill LAK cells; and (4) Fas-immobilized MoAb synergizes with coimmobilized MoAb to CD11a, CD11b, or CD18 for LAK cell killing. Activation-induced death of NK cells may represent a mechanism for NK cell regulation.

Antibodies, Monoclonal↗
PubMed1996

Target-induced death by apoptosis in human lymphokine-activated natural killer cells.

Activated human natural killer (NK) cells undergo rapid apoptotic cell death after ligand binding to the Fc receptor (CD16). We examined whether human NK cells die after engagement in cytolytic functions. Peripheral blood NK cells, with and without prior activation in vitro with interleukin-2 (IL-2), were tested for the occurrence of cell death after incubation with K562, the prototype NK-sensitive target cell. A proportion (15.2%) of NK cells that were stimulated for 3 days with IL-2 and then incubated for 4 hours with K562 cells showed rapid cell death, but NK cells not stimulated with IL-2 did not. This cell death was found to involve nuclear condensation and fragmentation and DNA cleavage, all of which are characteristic of apoptosis. These data indicate that a proportion of activated human NK cells undergo apoptosis as they engage in target cell lysis. Target-induced NK cell death may represent an important mechanism for regulation of inflammatory processes involving NK cells.

Apoptosis↗
PubMed1996

Somatosensory evoked potentials recorded from the posterior pharynx to stimulation of the median nerve and cauda equina.

Somatosensory evoked potentials (ppSEPs) in response to stimulation of the median nerve at the wrist and the cauda equina at the epidural space (the L4 level) were recorded from the posterior wall of the pharynx in 15 patients who underwent spinal surgery under general anesthesia, using disc electrodes attached to the endotracheal tube, and compared with segmental spinal cord potentials (seg-SCPs) that were recorded simultaneously from the posterior epidural space (PES). ppSEPs consisted of the initially positive spike (P9) followed by slow positive (P13) and negative (N22) waves. The P13 and N22 of ppSEPs had phase reversal relationship with the P2 and N2 recorded from the PES, respectively. The peak latencies of P9 (9.40 +/- 0.7 ms) (mean +/- SD), P13 (13.1 +/- 0.9 ms), and N22 (22.0 +/- 2.1 ms) of ppSEPs coincided with those of P1, N1 and P2 of seg-SCPs, respectively, ppSEPs were recorded more clearly with a reference electrode on the dorsal surface of the neck than with the reference electrode at the earlobe or back of the hand. The threshold and maximal stimulus intensities were also similar between the ppSEPs and seg-SCPs. Thus, the P9, P13, and N22 components of ppSEPs were thought to have the same origin as the P1, N1 and P2 of seg-SCPs, respectively. Therefore, the P9, P13 and N22 of ppSEPs may reflect incoming volleys through the root, synchronized activities of the interneurons and primary afferent depolarizations (PAD), respectively. ppSEPs in response to cauda equina stimulation showed that the latencies of the two initial components (4.6 +/- 0.4 and 6.4 +/- 0.6 ms) corresponded to those of the SCPs recorded from the PES (4.6 +/- 0.3 and 6.3 +/- 0.5 ms), suggesting that these potentials reflect impulses conducting through the spinal cord, similar to epidurally recorded SCPs.

Adult↗
PubMed1996

[Isolation of Vibrio cholerae in imported frozen seafood and their cholera-enterotoxin production].

A survey study for Vibrio cholerae in imported seafood was conducted during January 1991 to December 1994. A total of 7,439 specimens (approximately 20% of all imported food) were randomly picked up and examined for contamination of V. cholerae. Among these, V. cholerae O1 were isolated from 9 specimens, but they were all cholerae enterotoxin (CT)-negative. In terms of V. cholerae non-O1, a total of 2,803 specimens (37.4%) were contaminated with this vibrio. Shrimp, especially the ones still in their shells and imported from Asian countries such as India and Indonesia, were highly contaminated with V. cholerae. Although no strains of V. cholerae O1 isolated in this study produced CT, 2 strains of V. cholerae non-O1 were proved to be CT-producers. Taking together the high contamination of V. cholerae in imported seafood and a part of those strains producing CT, we believe that careful survey for the possible contamination of V. choleare in imported seafood is necessary.

Cholera Toxin↗
PubMed1995

Epstein-Barr virus as an agent of haematological disease.

Epstein-Barr virus (EBV) encodes genes that permit its persistence in human B lymphocytes and genes that ensure its replication in epithelial cells. Immune restraints on the virus are usually so effective that most EBV infections are limited to a minute fraction of B lymphocytes and of epithelial cells. As a result, most EBV infections are never symptomatic. Occasionally, the virus causes disease, often with the cooperation of the immune system or other less characterized cofactors. Infectious mononucleosis, a generally self-limited lymphoproliferative illness common in adolescents and young adults, is due to primary EBV infection and to the brisk cellular immune response it elicits. Lymphoproliferative disorders of EBV-infected B cells arise almost exclusively when cellular immunity is grossly compromised. EBV-positive Burkitt's lymphoma contain a translocated and deregulated c-myc oncogene and EBV-positive non-Hodgkin's lymphomas are characterized by the presence of Reed-Sternberg's and Hodgkin's cells, features that have not been directly linked to EBV. Many recent observations, however, including evidence that virus infection precedes malignant transformation and is often associated with a characteristic pattern of viral gene expression, provide continued interest in the relationship between the virus and these haematological malignancies.

Adolescent↗
PubMed1995

Relationship between tissue ischemia and venous endothelin-1 during abdominal aortic aneurysm surgery.

OBJECTIVES: Several substances may be released from ischemic tissues with the declamping shock that occurs during abdominal aortic aneurysm surgery. To clarify the relationship between tissue ischemia and venous endothelin-1 (ET-1) level in humans, plasma ET-1 and oxygen content in the iliac vein were measured before anesthesia, after the induction of anesthesia, after the release of the proximal and first distal clamps, after the release of the second distal clamp, and 1 hour after the second clamping. DESIGN: Prospective study. SETTING: A University hospital. PARTICIPANTS: Seven patients who underwent abdominal aneurysmectomy and replacement with bifurcated graft. INTERVENTIONS: A 20G catheter was inserted into the radial artery for the direct measurement of blood pressure and for collecting arterial blood. An 18G, 20-cm catheter was inserted into the femoral vein for collecting venous blood from the lower extremities. MEASUREMENTS AND MAIN RESULTS: The arterial and venous ET-1 levels did not change after the induction of anesthesia. Immediately after the initial release of the proximal and distal clamps, venous oxygen content dramatically decreased from 11.3 to 3.6 mL/dL (vol%) with significant increases in venous ET-1 concentration from 2.3 to 4.9 pg/mL. Concomitant with the decrease in venous oxygen content, venous plasma pH and base excess decreased with increase in PCO2, suggesting that ischemic changes in tissues distal to the cross-clamp may occur during aortic clamping. Venous ET-1 levels were significantly correlated with venous oxygen content, pH, PO2, oxygen saturation, base excess, blood sodium concentration, and potassium concentration. One hour after the second declamping, the venous ET-1 level remained high in comparison with the preanesthetic level, whereas the venous oxygen content returned to the preanesthetic level. There was no correlation between venous plasma ET-1 and venous plasma norepinephrine or epinephrine concentration. CONCLUSIONS: Tissue ischemia may increase venous ET-1 levels in humans. Factor(s) other than tissue ischemia may provoke the increase in venous ET-1 that occurs after the release of the second distal clamp.

Aged↗
PubMed1995

Human and viral interleukin-10 in acute Epstein-Barr virus-induced infectious mononucleosis.

Human interleukin 10 (hIL-10), a product of monocytes, T cells, and B cells, shares extensive structural and functional similarity with viral IL-10 (vIL-10), a product of Epstein-Barr virus (EBV) replication. With two ELISAs, one that recognizes both hIL-10 and vIL-10 and the other specific for vIL-10, IL-10 was measured in serum or plasma and in saliva from 50 patients with acute EBV-induced infectious mononucleosis and from 19 normal subjects. In serum or plasma, 60% of the patients had measurable hIL-10 and/or vIL-10 and 18% had measurable vIL-10. In saliva, 20% of the patients had detectable hIL-10 and/or vIL-10 and none had detectable vIL-10. In contrast, hIL-10 and/or vIL-10 was undetectable in all 19 normal serum or plasma samples (P < .001 vs. patient samples). Among normal saliva samples, 21% had detectable hIL-10 and/or vIL-10 but none had detectable vIL-10. Thus, most patients with acute EBV-induced infectious mononucleosis transiently have abnormally high levels of circulating IL-10.

Acute Disease↗