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Biomedical subjects

R Ogawa

Publications and source records attributed to R Ogawa.

At least 37 records · Page 2Linked to original sources
PubMed2002

An anatomical and clinical study of the dorsal intercostal cutaneous perforators, and application to free microvascular augmented subdermal vascular network (ma-SVN) flaps.

We report a two-part anatomical and clinical study whose aim was to map the dominant dorsal intercostal cutaneous perforators (DICPs), which are useful for microvascular augmentation of flaps raised from the skin of the back called subdermal vascular network (SVN) flaps, and to test their reliability in the clinical setting. In the anatomical arm of the study, using preserved cadavers, we macroscopically confirmed the location of DICPs, and performed micro-angiography of the dorsal skin to find each dominant DICP. In the clinical arm of the study, we confirmed the location of the dominant DICP during microvascular augmented SVN flap transfer. Postoperatively, posteroanterior radiographs of the chest were taken to locate vessel clips used to ligate the DICPs. The combined study results showed that the dominant DICP is the sixth or seventh in most instances, but there are some anatomical variations. If no dominant DICP is found in the sixth or seventh spaces, at least one DICP that is of sufficient calibre for microvascular augmentation can usually be found in the general vicinity, such as the fifth, eighth or ninth spaces. The clinical application of microvascular augmented SVN flaps, both pedicled and free, is presented.

Adult↗
PubMed2002

Synthesis and immunological effect of thymic humoral factor-gamma-2 analogues.

Nine analogues of thymic humoral factor (THF)-gamma-2 were prepared by the solid-phase method, and their in vitro restoring effect on the impaired blastogenic response of phytohemagglutinin(PHA)-stimulated T-lymphocytes of uremic patients with infectious diseases were examined. The results were as follows: [Arg6]-THF-gamma-2 exhibited higher restoring activity than that of our synthetic THF-gamma-2. [Sar4]-, [Val1]-, [Arg3]-, [Gly5]-, and [Asn3]-THF-gamma-2 were also active but less potent than that of our synthetic THF-gamma-2. Three other peptides, [beta-Ala4]-, [Arg2]-, and [Gln2]-THF-gamma-2, did not show any restoring activity on the impaired blastogenic response of uremic patients with infectious disease.

Amino Acid Sequence↗
PubMed2002

Synthesis and immunological effect of thymic humoral factor-gamma 2 analogues.

Nine analogues of thymic humoral factor (THF)-gamma 2 were prepared by the solid-phase method and their in vitro restoring effect on the impaired blastogenic response of phytohemagglutinin(PHA)-stimulated T-lymphocytes of uremic patients with infectious diseases were examined. The results were as follows: [Arg6]-THF-gamma 2 exhibited higher restoring activity than that of our synthetic THF-gamma 2. [Sar4]-, [Val1]-, [Arg3]-, [Gly5]-, and [Asn3]-THF-gamma 2 were also active, but less potent than that of our synthetic THF-gamma 2. Three other peptides, [beta Ala4]-, [Arg2]-, and [Gln2]-THF-gamma 2, did not show any restoring activity on the impaired blastogenic response of uremic patients with infectious disease.

Humans↗
PubMed2002

The effects of intravenous lignocaine on haemodynamics and seizure duration during electroconvulsive therapy.

Electroconvulsive therapy (ECT) is commonly associated with acute hyperdynamic cardiovascular responses, and we hypothesize that intravenous lignocaine can blunt this response. We have measured the effect of lignocaine 1.5 mg/kg i.v. on heart rate and mean arterial pressure during electroconvulsive therapy. Furthermore, we also assessed seizure duration using both the cuff method and two-lead electroencephalography. We studied 25 patients using a randomized, double-blind, placebo-controlled crossover study design. Patients in the control group were given intravenous saline 0.075 ml/kg, and those in the lignocaine group were given intravenous lignocaine 2% 1.5 mg/kg, and this treatment was conducted one minute before intravenous propofol 1.5 mg/kg to induce unconsciousness. Succinylcholine 1.5 mg/kg was then administered intravenously and electrical stimulation was administered after fasciculation. Measurements were taken at the baseline, prior to succinycholine, prior to electroconvulsive therapy and at the peak response after electroconvulsive therapy. Intravenous lignocaine significantly reduced the increases in heart rate after electroconvulsive therapy, as compared with the placebo. The use of intravenous lignocaine was, however, associated with a remarkably shortened seizure duration. Due to the reduction in seizure duration, routine administration of intravenous lignocaine may not be advisable since it may interfere with the psychotherapeutic efficacy of electroconvulsive therapy. However, intravenous lignocaine medication for electroconvulsive therapy is potentially useful for reducing tachycardia in high-risk patients and reducing the severity of propofol injection pain in comparison with a placebo.

Adult↗
PubMed2001

Intra-bone marrow injection of allogeneic bone marrow cells: a powerful new strategy for treatment of intractable autoimmune diseases in MRL/lpr mice.

Intractable autoimmune diseases in chimeric resistant MRL/lpr mice were treated by a new bone marrow transplantation (BMT) method consisting of fractionated irradiation, 5.5 Gy x 2, followed by intra-bone marrow (IBM) injection of whole bone marrow cells (BMCs) from allogeneic normal C57BL/6 (B6) mice (5.5 Gy x 2 + IBM). In MRL/lpr mice treated with this method, the number of donor-derived cells in the bone marrow, spleen, and liver rapidly increased (almost 100% donor-derived cells by 14 days after the treatment), and the number of donor-derived hemopoietic progenitor cells concomitantly increased. Furthermore, donor-derived stromal cells were clearly detected in the cultured bone pieces from MRL/lpr mice treated with 5.5 Gy x 2 + IBM. All the recipients thus treated survived more than 1 year (> 60 weeks after birth) and remained free from autoimmune diseases. Autoantibodies decreased to almost normal levels, and abnormal T cells (Thy1.2(+)/B220(+)/CD4(-)/CD8(-)) disappeared. Hematolymphoid cells were reconstituted with donor-derived cells, and newly developed T cells were tolerant to both donor (B6)-type and host (MRL/lpr)-type major histocompatibility complex determinants. Successful cooperation was achieved among T cells, B cells, and antigen-presenting cells when evaluated by in vitro antisheep red blood cell responses. These findings clearly indicate that this new strategy (IBM-BMT) creates the appropriate hemopoietic environment for the early recovery of hemopoiesis and donor cell engraftment, resulting in the complete amelioration of intractable autoimmune diseases in chimeric resistant MRL/lpr mice without recourse to immunosuppressants. This strategy would therefore be suitable for human therapy.

Animals↗
PubMed2001

Comparison of control of Listeria by nitric oxide redox chemistry from murine macrophages and NO donors: insights into listeriocidal activity of oxidative and nitrosative stress.

The physiological function of nitric oxide (NO) in the defense against pathogens is multifaceted. The exact chemistry by which NO combats intracellular pathogens such as Listeria monocytogenes is yet unresolved. We examined the effects of NO exposure, either delivered by NO donors or generated in situ within ANA-1 murine macrophages, on L. monocytogenes growth. Production of NO by the two NONOate compounds PAPA/NO (NH2(C3H6)(N[N(O)NO]C3H7) and DEA/NO (Na(C2H5)2N[N(O)NO]) resulted in L. monocytogenes cytostasis with minimal cytotoxicity. Reactive oxygen species generated from xanthine oxidase/hypoxanthine were neither bactericidal nor cytostatic and did not alter the action of NO. L. monocytogenes growth was also suppressed upon internalization into ANA-1 murine macrophages primed with interferon-gamma (INF-gamma) + tumor necrosis factor-alpha (TNF-alpha or INF-gamma + lipid polysaccharide (LPS). Growth suppression correlated with nitrite formation and nitrosation of 2,3-diaminonaphthalene elicited by stimulated murine macrophages. This nitrosative chemistry was not dependent upon nor mediated by interaction with reactive oxygen species (ROS), but resulted solely from NO and intermediates related to nitrosative stress. The role of nitrosation in controlling L. monocytogenes was further examined by monitoring the effects of exposure to NO on an important virulence factor, Listeriolysin O, which was inhibited under nitrosative conditions. These results suggest that nitrosative stress mediated by macrophages is an important component of the immunological arsenal in controlling L. monocytogenes infections.

2-Naphthylamine↗
PubMed2001

Epidural anesthesia with lidocaine reduces propofol injection pain.

PURPOSE: To determine whether epidural lidocaine reduces the severity of propofol injection pain compared with iv lidocaine. METHODS: A prospective, randomized double-blind clinical study was conducted in 120 female patients scheduled for elective gynecological laparotomy. A lumbar epidural catheter and an iv catheter placed in the cephalic vein of the non-dominant hand were used in all patients. Patients of the control group (Group C) were given epidural normal saline followed by iv normal saline then iv propofol. Patients of Group E were given epidural 2% lidocaine (0.08 mL.cm(-1)) followed by iv normal saline and then propofol. Patients of Group V were given epidural normal saline followed by iv 2% lidocaine (0.05 mL.kg(-1)) then propofol. Pain was scored as no pain=0, minimal pain=1, moderate pain=2, severe pain=3. RESULTS: The pain scores, in group E; 1 (0-2) and group V; 2 (0-2), were significantly lower than in group C; 2 (1-3); median (25th-75th percentile) (P <0.001). There was no difference in pain score between groups E and V The plasma lidocaine concentration 15 min after epidural lidocaine was 2.74 +/- 0.54 microg.ml(-1), compared with 1.54 +/- 0.31 microg.mL(-1) at three minutes after iv lidocaine. CONCLUSION: Epidural and iv lidocaine equally reduced the severity of propofol injection pain despite higher lidocaine plasma concentrations in epidurally administered lidocaine.

Adult↗
PubMed2001

Syntheses of two deacetyl-thymosin beta4 analogs and their anti-inflammatory effect on carrageenin-induced edema in the mouse paw.

Two [Met(0)6]deacetyl-thymosin beta4 analogs containing Phe(4F) or Tyr(Me) at position 12 were synthesized by the manual solid-phase method, and their anti-inflammatory effect on carrageenin-induced edema in the mouse paw was studied. Fluorination of the para-position of Phe12 resulted in a marked antiinflammatory effect on carrageenin-induced edema in the mouse paw compared with that of our synthetic [Met(0)6]deacetyl-thymosin beta4, but the other analog, [Met(0)6, Tyr(Me)12]deacetyl-thymosin beta4, showed a marked reduction of the anti-inflammatory effect.

Animals↗
PubMed2001

Enhancement of hyperthermia-induced apoptosis by a free radical initiator, 2,2'-azobis (2-amidinopropane) dihydrochloride, in human histiocytic lymphoma U937 cells.

To elucidate the mechanism how a free radical initiator, 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH), induces cell death at hyperthermic temperatures, apoptosis in a human histiocytic lymphoma cell line, U937, was investigated. Free radical formation deriving from the thermal decomposition of AAPH was examined by spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). An assay for DNA fragmentation, observation of nuclear morphological changes, and flow cytometry for phosphatidylserine (PS) externalization were used to detect apoptosis and revealed enhancement of 44.0 degrees C hyperthermia-induced apoptosis by free radicals due to AAPH. However, free radicals alone derived from AAPH did not induce apoptosis. Hyperthermia induced the production of lipid peroxidation (LPO), an increase in intracellular Ca2+ concentration ([Ca2+]i) and enhanced expression of the type 1 inositol 1,4,5-trisphosphate receptor (IP3R1). The effects of hyperthermia on LPO and [Ca2+]i were enhanced markedly by the combination with AAPH. A significant decrease in Bcl-2 expression, increase in Bax expression, a loss of mitochondrial membrane potential (delta psi m) and a marked increase in cytochrome c expression were found only in cells treated with hyperthermia and AAPH. Although an intracellular Ca2+ ion chelator, BAPTA-AM, completely inhibited DNA fragmentation, water-soluble vitamin E, Trolox, only partially suppressed DNA fragmentation and the increase in [Ca2+]i. In contrast, LPO was inhibited completely by Trolox, but no inhibition by BAPTA-AM was found. These results suggest that apoptosis induced by hyperthermia alone is due to the increase in [Ca2+]i arising from increased expression of IP3R1 and LPO. Additional increase in [Ca2+]i due to increased LPO and the activation of mitochondria-caspase dependent pathway play a major role in the enhancement of apoptosis by the combination with hyperthermia and AAPH.

Amidines↗
PubMed2001

T lymphocyte activation and restenosis after percutaneous transluminal coronary angioplasty.

We investigated the relation between the activation of T lymphocytes and the occurrence of restenosis after percutaneous transluminal coronary angioplasty (PTCA) in 10 stable angina patients. Recent studies have suggested that PTCA causes an inflammatory response, which may affect restenosis after angioplasty. Soluble interleukin-2 receptor (sIL-2R) is a useful marker to evaluate the activation of T lymphocytes. sIL-2R was measured before and 2 h after successful PTCA, and 3-month follow-up coronary angiography was done to observe restenosis. Four of 10 patients showed restenosis. The restenosis group of 4 patients had a higher level of sIL-2R after PTCA than the no-restenosis group of 6 patients (495 vs. 274 U/ml, p < 0.01). This study suggests that sIL-2R may offer prognostic information after elective PTCA and identify a subgroup of patients at high risk for clinical restenosis in a few months.

Aged↗
PubMed2001

Orally administered clonidine significantly reduces pain during injection of propofol.

We examined the analgesic effects of orally administered clonidine on pain induced by injection of propofol (Diprivan; 2,6-diisopropyl phenol). Female patients (n=81) were randomly allocated to one of two groups: oral clonidine (5.5 microg kg(-1)) followed by i.v. propofol and a control group given placebo followed by i.v. propofol. The median pain score in the group receiving clonidine, using a four-point scale (0=no pain, 1=minimal pain, 2=moderate pain, 3=severe pain) was 1 (0-2), significantly lower than in the control group [2 (1-3), median (25-75 percentiles), P<0.001].

Administration, Oral↗
PubMed2001

The effects of diltiazem on hemodynamics and seizure duration during electroconvulsive therapy.

UNLABELLED: Electroconvulsive therapy (ECT) is often associated with acute hyperdynamic responses, and we hypothesize that diltiazem can blunt this response. We measured the effect of a 10-mg dose of diltiazem on heart rate and mean arterial pressure during ECT. Furthermore, we assessed seizure duration by using both the cuff method and two-lead electroencephalogram. We studied 18 patients with a randomized, double-blinded, placebo-controlled cross-over study design. Diltiazem significantly reduced heart rate and mean arterial pressure just after medication, and it also significantly reduced the increases in these variables after ECT, as compared with the placebo. The use of diltiazem was, however, associated with a shortened seizure duration, possibly making ECT less effective. Because of the reduction in seizure duration, the routine administration of diltiazem may not be advisable because it can possibly interfere with the psychotherapeutic efficacy of ECT. However, diltiazem medication for ECT is potentially useful for reducing tachycardia and hypertension in high-risk patients. IMPLICATIONS: Diltiazem can blunt acute hyperdynamic responses after electroconvulsive therapy, but seizure duration is also significantly reduced, possibly making this therapy less effective.

Adult↗
PubMed2001

A prostaglandin E2 receptor subtype EP1 receptor antagonist (ONO-8711) reduces hyperalgesia, allodynia, and c-fos gene expression in rats with chronic nerve constriction.

UNLABELLED: Chronic constriction injury (CCI) of the sciatic nerve in rats induces persistent mechanical hyperalgesia and allodynia. CCI is widely known as a model of neuropathic pain, and many studies using this model have been reported. Recently, c-fos has been used as a neural marker of pain, and various studies have assessed the relationship between hyperalgesia and c-fos expression in the lumbar spinal cord. In this study, we examined the role of a prostaglandin E2 receptor subtype EP1 receptor antagonist (ONO-8711) in a rat CCI model. EP1 receptor antagonist (EP1-ra) oral administration from day 8 to day 14 significantly reduced hyperalgesia and allodynia in the three pain tests on day 15. EP1-ra treatment from day 8 to 14 also reduced c-fos-positive cells in laminae I-II, III-IV, and V-X compared with saline treatment. A single dose of EP1-ra treatment on day 8 significantly reduced hyperalgesia and allodynia at 1 h and 2 h after administration, but the efficacy was not observed at 24 h. We conclude that EP1-ra treatment may be useful for hyperalgesia and allodynia and that EP1 receptor mechanisms are involved in the maintenance of c-fos gene expression induced by nerve injury. IMPLICATIONS: We examined whether a prostaglandin E2 receptor subtype EP1 receptor antagonist abrogates neuropathic pain induced by chronic constriction injury model in rats. The EP1 receptor antagonist significantly reduced hyperalgesia, allodynia, and c-fos positive cells. These findings suggested that EP1 receptor antagonists may have a role in treatment of neuropathic pain.

Animals↗
PubMed2001

Molecular mechanisms for alpha2-adrenoceptor-mediated regulation of synoviocyte populations.

The sympathetic nervous system has been indicated to influence the severity of inflammatory disease including rheumatoid arthritis. In this study, we elucidated the effects of catecholamine on the synovial cell populations. Stimulation with epinephrine or norepinephrine for 1-2 weeks dose- and time-dependently increased the number of synovial A (macrophage-like) cells but decreased that of B (fibroblast-like) cells. These responses in A and B cells were inhibited by the alpha2-antagonist yohimbine, the G-protein inactivator pertussis toxin and the phospholipase C (PLC) inhibitor U-73122. Furthermore, the protein kinase C (PKC) inhibitor calphostin C and mitogen-activated protein (MAP) kinase inhibitors PD98059 and wortmannin also abolished the norepinephrine effects on A and B cell numbers. In A cells cloned from an A and B cell mixture, norepinephrine also increased the cell number. In immunoblotting and immunocytostaining analyses, among the PKC isozymes, only PKC betaII immunoreactivity was observed in the cytoplasm of unstimulated A and B cells. After alpha2-adrenoceptor stimulation, PKC betaII immunoreactivity increased in the plasma membranes of both A and B cells with decreases in the cytoplasm. These findings indicated that alpha2-adrenoceptor stimulation of type A and B synoviocytes produced an increase and a decrease in the respective cell number, probably through Gi-coupled PLC activation and the resulting stimulation of the PKC betaII/MAP kinase.

Adrenergic alpha-Agonists↗
PubMed2001

Activation of the adenosine triphosphate sensitive mitochondrial potassium channel is involved in the cardioprotective effect of isoflurane.

The adenosine triphosphate-dependent potassium (K(ATP)) channel has been proposed to play an important role in the cardioprotective effect of isoflurane (ISO). However, the question of whether the K(ATP) channel, sarcolemmal or mitochondrial is the main contributor to the effect has not been clarified. The major aim of the present study was to determine whether or not the mitochondrial potassium channel was a site of action for ISO. Whether there was an acute "memory phase", in which drugs were not detected in the tissues, but the protective effect still remained in the ischemic preconditioning (IP) -like effect of ISO was also investigated. Dangling participle isolated rat hearts, a 20-min normothermic nonperfused phase was maintained to produce a global ischemia. Under these ischemic conditions, the effects of ISO, sodium 5-hydroxydecanoate (5HD: a selective mitochondrial K(ATP) channel antagonist), and ISO combined with 5HD on cardiac performance were examined. To all these four groups, (non-treated group, ISO group, 5HD group and ISO plus 5HD group, n=6 each) drugs were given for 30 min. After 10 min of drug-free perfusion (pre-ischemia restabilization period), 20 min of ischemia followed. Then the cardiac performance and the creatine kinase (CK) release during the reperfusion period were tested. In the non treated group and 5HD group, cardiac performance was stable during the treated period and pre-ischemia the restabilization period. In the ISO group and ISO plus 5HD group, heart rate (HR), left ventricular (LV) systolic pressure, and LV maximum rate of development of tension (dP/dtMax) during the drug-treated period became gradually and linearly worse. However, these values were the same as in the non-treated group and 5HD group at the end of the pre-ischemia restabilization period. So 5HD itself had no hemodynamic effect; nor did it have any influence on the actions of ISO. At the end of the pre-ischemia restabilization period, the significant hemodynamic differences among the groups diminished and ISO was not detected in the solution. In the post-reperfusion period, except for the ISO group, (non treated group, 5HD group and ISO plus 5HD group) cardiac performances were drastically decreased. ISO significantly ameliorated the dysfunction of cardiac output, LV systolic pressure and LV+dP/dtMax. The CK level in the coronary effluent during reperfusion was also significantly reduced by ISO. 5HD completely inhibited these cardiac effects of ISO. Activation of the adenosine triphosphate sensitive mitochondrial potassium channel is involved in the cardioprotective effect of ISO, and the action of this agent has an acute"memory phase" like ischemic preconditioning.

Adenosine Triphosphate↗
PubMed2001

Study on the treatment of tracheobronchial stenosis using expandable metallic stents.

The purpose of this study is to clarify the clinical usefulness of Gianturco-Z stent (G-Z stent) for the management of malignant and benign tracheobronchial stenosis. Seventy-three stents were used in 30 patients. In 20 cases, we used the so-called "stent-in-stent" method. Twenty-four patients were grade 5, and 6 were grade 4 according to the Hugh-Jones classification of respiratory status. The technical success rates, clinical condition, respiratory status, blood gas analysis, survival rate, and complications were reviewed on the basis of the patients'medical records and radiographs. All stents were successfully placed in the appropriate position. After the procedure, respiratory status improved in 97% (29/30) of the patients. PaO(2) increased statistically (p<0.05), and PaCO(2) decreased one week after the treatment. Mean survival of 30 patients after stent placement was 123 days. Mean survival in 9 malignant patients treated in combination with radiotherapy (182 days) was statistically longer (p<0.01) than in those treated without radiotherapy (65 days, n=20). The tracheobronchial burn patient who received a combination of stent placement and post operative radiotherapy survived 540 days. No major complications were encountered during or after the procedure. Only 3 minor complications were observed: 1 stent migration, 1 partial rupture of the stent, and 1 stent deformation. G-Z stent treatment with the "stent-in-stent" technique is useful for palliation of malignant and benign tracheobronchial stenosis, and should contribute to improving the quality of life in patients with advanced cancer.

Adult↗