Biomedical subjects

S Nagao

Publications and source records attributed to S Nagao.

At least 37 records · Page 2Linked to original sources

PubMed2003

The use of mild hypothermia for patients with severe vasospasm: a preliminary report.

The purpose of this study was to determine the effect of mild hypothermia on cerebral ischaemia due to severe vasospasm, which was refractory to medical and intravascular treatments and to assess the brain protection of this treatment in patients who underwent delayed aneurysm clipping after presenting with ischaemic neurological deficits. Mild hypothermia (32-34 degrees C of brain temperature) was employed in two groups: (1) Patients (Hunt and Kosnik grades I to II) who showed progressive neurological deficits due to vasospasm and did not respond to conventional therapy (Group 1) and (2) Patients who received delayed aneurysm clipping after presenting with ischaemic neurological deficits due to vasospasm (Group 2). Seven of 8 patients in both Groups showed a favorable outcome with mild hypothermia (good recovery in 5 and moderate disability in two patients). Mild hypothermia is considered to be effective on critical cerebral ischaemia due to vasospasm even after failure to response the conventional therapies and to provide brain protection in delayed aneurysm clipping.

Body Temperature↗

PubMed2002

Effects of brain hypothermia on brain edema formation after intracerebral hemorrhage in rats.

Patients with intracerebral hemorrhage (ICH) may deteriorate progressively after the initial ictus because of the brain edema around the hematoma. Recently, thrombin has become known to play an important role in the brain edema formation after ICH. In this study, we examined the effect of brain hypothermia on brain edema formation after hematoma and thrombin injection into the brain in rats and clarified the mechanism of hypothermia on brain damage. Anesthetized Sprague-Dawley rats received an injection of 100 microL of autologous blood or 10 units of bovine thrombin into the basal ganglia. Animals were divided into the normothermic and hypothermic groups, which were housed in a room at 25 degrees C and in a cold room at 5 degrees C respectively, for 24 hours. Brain water content was significantly reduced with hypothermia in the cortex (80.8 vs. 79.7% p < 0.05) after hematoma induction. After thrombin injection, brain water content was also significantly reduced with hypothermia in the basal ganglia (84.5 vs. 82.2%; p < 0.01), accompanied by a significant reduction in blood-brain barrier (BBB) permeability to Evan's blue (29.4 vs. 11.6 ng/g tissue; p < 0.05) and in accumulation of polymorphonuclear leukocytes (3.03 vs. 0.27 U of myeloperoxidase/g tissue; p < 0.01). This study indicates that brain hypothermia significantly reduces brain edema formation after hematoma and thrombin injection into the brain in rats. Inhibition of thrombin-induced BBB breakdown and inflammatory response with hypothermia appear to contribute to brain protection in this model.

Animals↗

PubMed2002

Cerebral oxygen metabolism monitoring under hypothermia for severe subarachnoid hemorrhage: report of eight cases.

OBJECTIVES: The significance of cerebral oxygen metabolism monitoring under hypothermia for severe subarachnoid hemorrhage (SAH) was studied. MATERIAL AND METHODS: Cerebral oxygen metabolism monitoring (jugular venous oxygen saturation: SjO2, arterio-jugular venous difference of oxygen: AJDO2, and oxygen extraction fraction:OEF) during hypothermia (32-34 degrees C) was evaluated in eight patients with SAH (severe vasoapasm group: five patients, and severe brain damage group: three patients). RESULTS: In favorable cases in both groups, each parameter tended to normalize during hypothermia therapy. When changes in SjO2 were normal, however, the value of AJDO2 was low in unfavorable cases in the severe vasospasm group. In unfavorable cases in the severe brain damage group, high level of SjO2 and low level of OEF and AJDO2 were shown even if hypothermia therapy was performed. CONCLUSIONS: The measurement of SjO2 and AJDO2 is useful for estimation of cerebral oxygen metabolism in patients with severe conscious disturbance after SAH under hypothermia therapy.

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PubMed2002

Increased expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and lymphocyte recruitment in murine gastritis induced by Helicobacter pylori.

Although T cell involvement in Helicobactor pylori-induced gastritis is known, mechanism about T cell recruitment is not understood. In this study we examined how mucosal addressin cell adhesion -molecule-1 (MAdCAM-1) is involved in lymphocyte recruitment in murine chronic gastritis induced by H. pylori. C57 BL/6 mice were infected with Sydney strain (SS1). Six months after infection, the stomach was removed. The expression of adhesion molecules, MAdCAM-1, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and the cell surface antigens CD4, CD8, CD45R/B220 or beta7-integrin were determined by immunohistochemistry. A significant increase in CD4 lymphocytes was observed in the body portion of stomach in SS1-infected mice and most of these CD4 cells express beta7-integrin, a known counter ligand for MAdCAM-1 molecule. Strong MAdCAM-1 expression was observed adjacent to these cells in the lamina propria as well as in the submucosa of SS1-infected stomach. Quantitative analysis showed that the area of MAdCAM-1 expression well correlated with the infiltration of beta7-integrin positive lymphocytes. On the other hand, expression of ICAM-1 or VCAM-1 in the lamina propria was few even in the SS1-infected stomach. Increased expression of MAdCAM-1 was well correlated to the location of lymphocytes, which express CD4 and beta7-integrin. These results suggest the possibility that MAdCAM-1 may be largely involved in the lymphocyte recruitment in the gastritis mucosa with H. pylori.

Animals↗

PubMed2002

Balloon-assisted guglielmi detachable coil placement in wide-necked internal carotid-ophthalmic aneurysms: a report of four cases.

We present an endovascular technique for treating wide-necked ophthalmic aneurysms using Guglielmi detachable coils with simultaneous temporary balloon protection. Four illustrative cases of wide-necked ophthalmic aneurysms treated with Guglielmi detachable coils and a temporary balloon are presented. By blocking the parent artery with a non-detachable balloon, the coils could be safely placed in these aneurysms without herniation when the balloon was deflated. All patients exhibited embolic manifestations after the procedure, and the use of simultaneous temporary balloon protection allowed more dense intra-aneurysmal coil packing. Although this technique requires manipulation of a second microcatheter and balloon, which increases its technical difficulties and is a higher-risk procedure than the standard coil placement, it can be used for patients who are not candidates for surgery. Long-term follow-up is needed to determine the final outcome of aneurysms treated by this technique.

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PubMed2001

Degradation characteristics of humic acid during photo-Fenton processes.

Changes in the molecular and structural characteristics of humic acid (HA) during photo-Fenton processes were studied. When aqueous solutions at pH 5.0, which contained HA, Fe(III), and H2O2, were irradiated (lambda > 370 nm), the concentrations of total organic carbon (TOC) decreased with increasing irradiation time, indicating that a portion of the HA was mineralized to CO2 during this process. To investigate the changes in molecular and structural characteristics, the HA was reisolated from the reaction mixtures after each period of irradiation. The increased elution volumes required for isolation by gel permeation chromatography indicated that the molecular size of HA decreased as a result of the irradiation. In the FTIR spectra, ether and epoxide functional groups were identified, after irradiation. These products could be formed via radical coupling and/or via peroxy radical addition reactions to the unsaturated groups in the HA, such as vinyl and aromatic groups. Moreover, an analysis of structural fragments in HA by pyrolysis-GC/MS showed that the cinnamic acid moieties (CA) disappeared, as a result of irradiation. In the molecular weight fractionated HA, the majority of the iron species were complexed with the high molecular weight HA fraction, and the CA levels of the high molecular weight fraction were larger than those in the low molecular weight fraction. These results are consistent with residues, as the reactive sites in the photo-Fenton systems. Therefore, the degradation of these sites in the high molecular weight fraction may serve as a factor in decreasing the molecular size of HA.

Carbon Dioxide↗

PubMed2001

Reduced sensitivity of inducible nitric oxide synthase-deficient mice to chronic colitis.

BACKGROUND: Overproduction of nitric oxide by the inducible form of nitric oxide synthase (iNOS) has been implicated in colitis. Different authors have postulated both toxic and protective effects of nitric oxide (NO) in the pathophysiology of active inflammation. The objective of this study was to examine the role of iNOS in experimental chronic colitis using iNOS-deficient mice. METHODS: For induction of colitis, mice received three cycles of 2% of dextran sodium sulfate (DSS) (M.W. 40,000) treatment in drinking water. The degree of colonic inflammation, leukocyte infiltration, and the expression of cell adhesion molecules were determined. INOS expression and nitrotyrosine were also determined by immunohistochemistry. RESULTS: After DSS treatment, a moderate colitis with marked cell infiltration was observed. Intense expression of iNOS was observed on infiltrating cells as well as on the colonic mucosal epithelium in these animals. In the iNOS-deficient mice, tissue damage was significantly diminished. No iNOS or nitrotyrosine staining was found in iNOS-deficient mice. The number of infiltrating cells and the expression of mucosal adressin cell adhesion molecule-1 were significantly attenuated in the DSS-treated colon of iNOS-deficient mice. CONCLUSION: Induction of iNOS seems to act as a critical toxic effector molecule in the pathogenesis of chronic colonic inflammation.

Animals↗

PubMed2001

Contribution of central amiloride-sensitive transport systems to the development of hypertension in spontaneously hypertensive rats.

This study was conducted to examine if central amiloride-sensitive transport systems are involved in the development and/or maintenance of hypertension in spontaneously hypertensive rats (SHR). Either amiloride (75 microg/60 microl/day) or artificial cerebrospinal fluid (aCSF, 60 microl/day) was infused centrally (i.c.v.) for 4 weeks to development (4-5-weeks-old) and maintenance (10-12-weeks-old) phases of hypertension in SHR. In development phase, amiloride i.c.v. (n=14) blunted the elevation of blood pressure (BP) compared to aCSF i.c.v. (n=9) (amiloride vs. aCSF; after 3 weeks of i.c.v., 146+/-3 vs. 166+/-5 mmHg, P<0.001). The difference of BP at 3 weeks of i.c.v. was canceled after ganglionic block with hexamethonium (115+/-4 vs. 117+/-5 mmHg). Further, pressor responsiveness to norepinephrine was augmented in amiloride i.c.v. rats (amiloride, n=11 vs. aCSF, n=6; %Delta BP at 800 ng/kg/min.: 16.9+/-1.3 vs. 10.8+/-1.4 mmHg, P<0.05) and this augmentation disappeared after ganglionic block. Pressor responsiveness to angiotensin II and cumulative sodium balance did not differ in the two groups. Intravenous administration of amiloride at the same dose did not attenuate the development of hypertension. On the other hand, in maintenance phase, amiloride i.c.v. by the same protocol as in development phase had no effect on BP in SHR. Also, amiloride i.c.v. did not affect BP in normotensive Wistar-Kyoto rats. These results suggest that central amiloride-sensitive transport systems are involved in the development, but not in the maintenance, of hypertension in SHR through the modulation of autonomic neural mechanisms.

Amiloride↗

PubMed2001

Preparation of mononuclear tungsten tris(sulfido) and molybdenum sulfido-tetrasulfido complexes with hydridotris(pyrazolyl)borate coligand and conversion of the former into sulfido-bridged bimetallic complex having Pt(mu-S)2WS core.

Treatment of [Et4N][(Me2Tp)W(CO)3] (Me2Tp = HB(3,5-dimethylpyrazol-1-yl)3) with S8 in DMF at room temperature afforded a tris(sulfido) complex [Et4N][(Me2Tp)WS3] (1a), while that of [Et4N][TpW(CO)3] (Tp = HB(pyrazol-1-yl)3) in MeCN resulted in the formation of [Et4N][TpWS3] (1b) along with [Et4N]2[[WO(S2)2]2(mu-S)] (6) as a byproduct. Under similar conditions, [Et4N][(Me2Tp)Mo(CO)3] gave a mixture of a sulfido-tetrasulfido complex [Et4N][(Me2Tp)MoS(S4)] (2a) and its monooxo analogue [Et4N][(Me2Tp)MoO(S4)], although a sulfido-tetrasulfido complex [Et4N][TpMoS(S4)] (2b) was exclusively obtained from [Et4N][TpMo(CO)3]. The reaction of 1a with [PtCl2(cod)] (cod = 1,5-cyclooctadiene) in MeCN at room temperature led to the formation of a sulfido-bridged mixed-metal complex [Et4N][(Me2Tp)WS(mu-S)2PtCl2] (10). The structures of new complexes have been determined in detail by the X-ray analyses for 1a.MeCN, 1b, 2a, 2b, 6, and 10.

Journal Article↗

PubMed2001

Effects of hypothermia on thrombin-induced brain edema formation.

Recent studies have shown that thrombin plays an important role in brain edema formation after intracerebral hemorrhage (ICH). The possible mechanisms of thrombin-induced brain edema formation include blood-brain barrier (BBB) disruption and inflammatory response involving polymorphonuclear (PMN) leukocyte. Animal experiments have revealed that moderate therapeutic hypothermia improves pathological and functional outcome in various models of brain injury. In this study, we examined the effect of hypothermia on thrombin-induced brain edema formation. Effects of hypothermia on BBB permeability and the accumulation of PMN leukocytes were also determined to clarify the protective mechanism of hypothermia in this model. Anesthetized adult rats received an injection of 10 Units of thrombin into the basal ganglia. Animals were separated into the normothermic and hypothermic groups, which were housed in a room maintained at 25 degrees C and in a cold room maintained at 5 degrees C, respectively, for 24 h after the thrombin injection. The brain temperature in rats housed in a cold room reduced temporarily to approximately 30 degrees C and then gradually recovered to 35 degrees C by the end of the observation. Brain water content in the basal ganglia was significantly reduced in rats treated with hypothermia compared to the normothermic rats (84.3+/-0.2 vs. 82.4+/-0.1%; P<0.01). The decrease of brain water content was accompanied with a significant reduction in BBB permeability to Evan's blue dye and in accumulation of PMN leukocytes. This study indicates that hypothermic treatment significantly reduces thrombin-induced brain edema formation in the rat. Inhibition of thrombin-induced BBB breakdown and inflammatory response by hypothermia appear to contribute to brain protection in this model. Hypothermic treatment may provide an approach to potentially reduce ongoing edema after ICH.

Animals↗

PubMed2001

Cytoarchitectonic subdivisions of the parabrachial nucleus in the Japanese monkey (Macacus fuscatus) with special reference to spinoparabrachial fiber terminals.

The cytoarchitectonic subnuclear organization of the parabrachial nucleus (PB) surrounding the brachium conjunctivum (BC) in the monkey was examined using the Nissl method and the anterograde axonal flow method. PB of the monkey could be divided into the following subnuclei: the dorsal area (DPBM) along the medial surface of the medial three-fourths of BC in the caudal half of medial PB (PBM), the ventral area (VPBM) along the medial surface of the lateral one-fourth of BC in the rostral two-thirds of PB, the ventrolateral part of lateral PB (PBL) lateral to BC throughout PB (EL), the ventral part of the rostral half of PBL ventral to EL (EXL), the medial part of middle PBL along the dorsal surface of BC (VL), the dorsal and lateral marginal part of PBL in the rostral two-thirds of PB (DL), the cell cluster in the dorsomedial part of the rostral half of PBL between VL and DL (CL), the dorsocentral part appearing at the level of root exit of the trochlear nerve between DL and CL and extending to the rostral end of PBL (IL), the area between DL and IL in the rostral one-seventh of PBL (SL), and Kölliker-Fuse nucleus (KF) ventral to EL and BC in the middle one-third of PB and lateral to the lateral pontine tegmentum. After the injection of biotinylated dextran amine into the upper cervical segments, labeled fibers terminated in each subdivision of PB with different densities; most heavily in IL, more heavily in DL and KF, moderately in EL and VPBM, and scarcely in the rest of PB. The present study demonstrated for the first time the subdivisions of PB in the monkey, which were essentially common to those of the rat based on the cytoarchictecture of PB and spinal fiber terminals in it.

Animals↗

PubMed2001

Expression of an embryonic intermediate filament protein in amygdaloid kindled rats.

Amygdaloid kindling is well known as an experimental model of temporal lobe epilepsy. However, the mechanism of kindling epileptogenesis remains unclear. To examine the remodelling process in kindling, we performed immunohistochemistry of nestin, an embryonic intermediate neurofilament protein, in amygdaloid kindled rats. In rats expressing focal seizures (kindling stage C3), nestin immunoreactive cells (NIC) were detected at ipsilateral piriform cortex (PC) and ipsilateral perirhinal cortex (PRh), and at PC bilaterally in fully kindled rats expressing secondary generalized seizures (kindling stage C5). Double staining with glial fibrillary acidic protein revealed that almost all reactive astrocytes at PC express nestin immunoreactivity. These results suggest that glial NIC may participate in the remodelling process at the PC and PRh areas. This is the first report of nestin expression in kindling and suggests that glial nestin at PC and PRh may play a significant role in permanent epileptogenesis in kindling.

Amygdala↗

PubMed2001

A new dysferlin gene mutation in two Japanese families with limb-girdle muscular dystrophy 2B and Miyoshi myopathy.

We found a new dysferlin gene mutation in two Japanese families, one with limb-girdle muscular dystrophy 2B and the other with Miyoshi myopathy. All patients in the limb-girdle muscular dystrophy 2B family showed apparent proximal dominant muscle atrophy and weakness, whereas a patient with Miyoshi myopathy in the second family showed distal muscle involvement at an early stage. The common clinical feature of all patients in both families was preferential involvement of calf muscles rather than the tibialis anterior muscle, which was confirmed by muscle computed tomography scan. All patients in both families shared the same homozygous alleles for chromosome 2p13 markers, and dysferlin gene analysis revealed a novel missense mutation, a G to A transition at nt 5882, which changed aspartic acid to asparagine at codon 1837. Allele-specific polymerase chain reaction analysis was used for confirmation of the mutation and for genotype analysis of the family members.

Aged↗

PubMed2001

Repeated thalamic haemorrhage: case report and review of the literature.

Recurrence of thalamic haemorrhage has rarely been reported. A 70-year-old woman had recurrent thalamic haemorrhage five-times during a period of 6 years. The first, second and fifth haemorrhages were located in the right thalamic region, and the third and fourth haemorrhages in the left thalamic region. Cranial computed tomography and magnetic resonance imaging revealed no abnormal lesion. After the first, second, and third haemorrhage with medical treatments, the patient recovered her functional ability or was at least capable of self-care at home. However, after the fourth and fifth haemorrhage, with medical therapy the patient's prognosis was severe disability. In this case, systemic blood pressure was normalized without antihypertensive agents after the first attack. However, there was an episode of sudden hypertension at each attack. Although the mechanism of rebleeding has not been clarified, rebleeding might be associated with changes of cerebral circulation following the previous haemorrhage.

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PubMed2001

Involvement of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in the pathogenesis of granulomatous colitis in rats.

Although increased expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) has been demonstrated in inflammatory sites of various diseases, its role in colitis remains unknown. In this study, we examined whether MAdCAM-1 is involved in the pathogenesis of granulomatous colitis induced by peptidoglycan-polysaccharide (PG-PS). Experimental colitis was induced by intramural injection of PG-PS to rat colon. After 3 weeks the colon was removed and the mucosal inflammation was assessed. The area of MAdCAM-1-positive venules and the subsets of infiltrating cells were determined in colonic mucosa by immunohistochemistry. In another experiment, monoclonal antibody against MAdCAM-1 was administered intraperitoneally to examine its attenuating effect on colitis. The intramural injection of PG-PS induced significant colonic inflammation with granuloma formation. The submucosa was drastically thickened with the infiltration of CD4 positive lymphocytes and ED-1 positive macrophages. Intense MAdCAM-1 expression was observed on endothelium of the submucosal venules in inflamed mucosa. Administration of anti-MAdCAM-1 antibody significantly attenuated the PG-PS-induced colonic damage and cell infiltration. Enhanced expression of MAdCAM-1 was demonstrated in venular endothelium of the inflamed colon in PG-PS-induced colitis. The attenuating effect of anti-MAdCAM-1 suggests the importance of the MAdCAM-1-dependent process in the formation of chronic granulomatous colitis.

Animals↗

PubMed2001

Expression of bone morphogenetic proteins in colon carcinoma with heterotopic ossification.

Here we report the case of a 50-year-old woman with adenocarcinoma of the colon, showing heterotopic ossification. The patient was referred to our hospital for investigation of anemia secondary to occult gastrointestinal blood loss. By colonoscopy, an irregular polypoid mass was found in the ascending colon. A biopsy of the lesion revealed moderately to poorly differentiated adenocarcinoma with heterotopic ossification. A right hemicolectomy was done and revealed areas of heterotopic bone within the tumor, but no ossification was evident in the metastatic lesions within the mesenteric lymph nodes. The formation of heterotopic bone in gastrointestinal tumors is rare and its exact mechanism is unknown. Immunohistochemical localization of bone morphogenetic proteins (BMP), known to be primary inducers of new bone formation, was determined. BMP-5 and -6 were prominent in the cytoplasm of tumor cells, and they stained weakly in osteoblast-like cells adjacent to newly formed bone. Cytoplasmic staining for BMP-2 and -4 was weak in tumor cells, osteoblast-like cells, and stromal fibroblast cells. BMP may play an important role in heterotopic ossification in colon adenocarcinoma.

Adenocarcinoma↗

PubMed2001

Increased renal expression of monocyte chemoattractant protein-1 and osteopontin in ADPKD in rats.

BACKGROUND: Human autosomal-dominant polycystic kidney disease (ADPKD) is variable in the rate of deterioration of renal function, with end-stage renal disease (ESRD) occurring in only approximately 50% of affected individuals. Evidence suggests that interstitial inflammation may be important in the development of ESRD in ADPKD. Han:SPRD rats manifest ADPKD that resembles the human disease. Homozygous cystic (Cy/Cy) rats develop rapidly progressive PKD and die near age 3 weeks. Heterozygous (Cy/+) females develop slowly progressive PKD without evidence of renal dysfunction until the second year of life, whereas heterozygous (Cy/+) males develop more aggressive PKD with renal failure beginning by 8 to 12 weeks of age. METHODS: To examine the relationship between proinflammatory chemoattractants and the development of interstitial inflammation and ultimately renal failure in ADPKD, we evaluated monocyte chemoattractant protein-1 (MCP-1) and osteopontin mRNAs and proteins in kidneys from Han:SRPD rats. RESULTS: MCP-1 and osteopontin mRNAs, expressed at low levels in kidneys from normal (+/+) animals at all ages, were markedly elevated in kidneys from 3-week-old Cy/Cy animals. In kidneys from heterozygous (Cy/+) adults of either gender, MCP-1 and osteopontin mRNAs were more abundant than normal; MCP-1 mRNA was more abundant in Cy/+ males than in females. Thus, chemoattractant mRNA expression correlated with the development of renal failure in Cy/Cy and Cy/+ rats. Osteopontin mRNA, localized by in situ hybridization, was moderately expressed in the renal medulla of normal animals; however, this mRNA was expressed at very high levels in the cystic epithelia of Cy/+ and Cy/Cy animals. MCP-1 and osteopontin proteins, localized by immunohistochemistry, were weakly detected in +/+ kidneys but were densely expressed in Cy/Cy and in adult Cy/+ kidneys, primarily over cystic epithelium. Increased expression of chemoattractants was associated with the accumulation of ED-1 positive cells (macrophages) in the interstitium of cystic kidneys. CONCLUSIONS: We suggest that proinflammatory chemoattractants have a role in the development of interstitial inflammation and renal failure in ADPKD.

Animals↗

PubMed2001

The efficacy and safety of transvenous embolisation in the treatment of intracranial dural arteriovenous fistulas.

To evaluate the role of transvenous embolisation including its efficacy and safety in the treatment of intracranial dural arteriovenous fistulas (DAVFs), we retrospectively analysed seven cases of intracranial DAVFs treated with transvenous embolisation in combination with arterial embolisation. Four DAVFs were in the cavernous sinus, two in the transverse-sigmoid sinus, and one in the inferior petrosal sinus. The transarterial and transvenous embolic agents included fibred platinum coils (FPC) and interlocking detachable coils (IDC). In all patients, the transarterial embolisation alone had failed to cure the DAVFs. After the combined transvenous embolisation, the anatomical cure was proven in five patients, and all patients were clinically cured. There were no complications in any patient. In conclusion, the transvenous embolisation is a useful and safe approach in the management of intracranial DAVFs.

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