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Biomedical subjects

K Murase

Publications and source records attributed to K Murase.

At least 91 records · Page 5Linked to original sources
PubMed1999

Effects of electrical stimulation of thalamic nucleus submedius and periaqueductal gray on the visceral nociceptive responses of spinal dorsal horn neurons in the rat.

Electrical stimulation of the nucleus submedius (Sm) has been shown to suppress the viscerosomatic reflex (VSR), which is evoked by colorectal distension (CRD). We have examined the effects of focal electrical stimulation (0.3 ms, 50 Hz, 100 microA, 10 s) of the Sm and the periaqueductal gray (PAG) on the excitatory responses evoked by CRD in spinal dorsal horn neurons within the L6-S1 region in the urethane-anesthetized Wistar rats. Extracellular recordings were made from 32 spinal excitatory CRD responses. All of these neurons were convergent neurons with cutaneous receptive fields. The majority of the neurons (27/32) were wide dynamic range (WDR) neurons (responding to noxious and non-noxious cutaneous stimuli) while the remaining five neurons were nociceptive specific (NS) neurons (responding only to noxious cutaneous stimuli). The effects of electrical stimulation applied to 28 sites within the Sm were assessed for spinal neurons. Electrical stimulation in seven sites within the Sm (25%) inhibited the CRD excitatory response of dorsal horn neurons, while in two sites (7%) the same stimulation yielded facilitation. Electrical stimulation in the majority of the sites in the Sm (19/28, 68%) did not affect spinal excitatory CRD responses. On the other hand, electrical stimulation of the PAG clearly inhibited 20 of 22 (90%) CRD excitatory responses. These results suggest that the majority of Sm neurons may suppress VSR activity at a supraspinal reflex center rather than via a descending inhibition of spinal visceral nociceptive transmission, as is the case for the PAG.

Animals↗
PubMed1999

Effects of dopamine agonists and antagonists on optical responses evoked in rat frontal cortex slices after stimulation of the subcortical white matter.

Effects of dopamine agonists and antagonists on the optical response of frontal cortical slices to stimulation of the subcortical white matter were examined using a voltage-sensitive dye and a high-speed image sensor. In the slices treated with bicuculline, stimulation of the white matter evoked optical responses propagating to the overlaying cortex. Bath application of the D1 agonist, chloro-APB (1 microM), consistently decreased the intensity of the early part of the response but increased the duration of the response occurring at the superficial layers of the cortex. Application of the D1 antagonist, SCH 23390 (1 microM), resulted in a small increase in both the intensity and the duration of the response. Bath application of the D2 agonist, quinpirole (1-10 microM), reduced the response occurring after 10 ms from stimulation. The effects of chloro-APB and quinpirole were additive. Application of the D2 antagonist, eticlopride, did not cause a significant change in the response but effectively blocked the quinpirole effects. This study suggests that although both D1 and D2 agonists reduced the peak optical response evoked in the slices of the frontal cortex, the two agonists exerted different temporal and spatial effects.

2-Amino-5-phosphonovalerate↗
PubMed1999

An alternative approach to estimation of the brain perfusion index for measurement of cerebral blood flow using technetium-99m compounds.

Cerebral blood flow (CBF) has been quantified non-invasively using the brain perfusion index (BPI) determined from radionuclide angiographic data generated by technetium-99m hexamethylpropylene amine oxime( )((99m)Tc-HMPAO) or technetium-99m ethyl cysteinate dimer( )((99m)Tc-ECD). The BPI is generally calculated using graphical analysis (GA). In the present study, BPI was measured using spectral analysis (SA), and its usefulness evaluated in comparison with GA. The BPI was calculated from the sum of spectral data obtained by SA. We applied this method to radionuclide angiographic data collected from the bilateral brain hemispheres of 20 patients with various brain diseases using (99m)Tc-HMPAO and from those of 20 patients using (99m)Tc-ECD. We also measured BPI using GA. The BPI values obtained by SA (BPI(S)) (x) and by GA (BPI(G)) (y) correlated closely (y=0.708x+0.038, r=0.945 for (99m)Tc-HMPAO and y=0.559x+0.093, r=0.931 for (99m)Tc-ECD). However, the BPI(G) values were underestimated by 22.9%+/-6.6% (mean+/-SD) for (99m)Tc-HMPAO and by 27.9%+/-7.5% for (99m)Tc-ECD as compared with the BPI(S) values. The extent of underestimation tended to increase with increasing BPI(S) values. These findings were considered to be a result of the BPI(G) values being affected by the first-pass extraction fraction of the tracer. We also compared the BPI(S) and BPI(G) values with those of CBF measured using N-isopropyl-p-[(123)I]iodoamphetamine (CBF(IMP)) in 16 patients (six for (99m)Tc-HMPAO and ten for (99m)Tc-ECD). Although both BPI(S) and BPI(G) values correlated significantly with the CBF(IMP) values, the correlation coefficient in BPI(S) was always better than that in BPI(G) (r=0.869 for (99m)Tc-HMPAO and r=0.929 for (99m)Tc-ECD in BPI(S), r=0.629 for (99m)Tc-HMPAO and r=0.856 for (99m)Tc-ECD in BPI(G)). These results suggest that SA can provide a more reliable BPI for quantifying CBF using (99m)Tc-HMPAO or (99m)Tc-ECD than the conventional method using GA. Our method will be useful especially when using a tracer with a low first-pass extraction fraction and/or when performing activation studies using pharmacological intervention.

Aged↗
PubMed1999

Endothelium-dependent contraction induced by substance P in canine cerebral arteries: involvement of NK1 receptors and thromboxane A2.

We characterized the endothelial responses to substance P (SP) in the isolated canine cerebral artery. SP caused concentration-dependent contraction at 10(-10) - 10(-7) M and relaxation at 10(-10) and 10(-9) M, which were abolished by removal of the endothelium. The SP-induced endothelium-dependent relaxation (EDR) was suppressed, while the endothelium-dependent contraction (EDC) was increased by repeated application. The EDC induced by SP (10(-7) M) was attenuated by SR-140333 (10(-9) - 10(-7) M) and CP-99994 (10(-7) M), both NK1 antagonists, but not by SR-48968 (10(-7) M), an NK2 antagonist, or four antagonistic SP analogues (10(-6) M). The EDC induced by SP (10(-7) M) was attenuated by aspirin (10(-5) M), a cyclooxygenase inhibitor, OKY-046 (10(-5) M), a TXA2 synthetase inhibitor and ONO-3708 (10(-8) M), a TXA2 antagonist. Neurokinin A (10(-7) M) but not neurokinin B (10(-7) M) caused EDC similar to that induced by SP. In conclusion, SP induces EDC via endothelial NK1 receptors and TXA2 production in canine cerebral arteries.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1999

Purification and properties of beta-N-acetylglucosaminidase from Vibrio alginolyticus H-8.

Beta-N-acetylglucosaminidase [EC 3.2.1.30] from Vibrio alginolyticus H-8 was purified by column chromatography on DEAE-Sepharose FF, phenyl-Sepharose HP, Superdex 200HR, and Mono Q. The molecular weight of the enzyme was estimated by SDS-gel electrophoresis (SDS-PAGE) to be 75 kDa. The pI was 4.6. The activity was inhibited by Ag+, Hg2+, iodoacetate, p-chloromercuribenzoate, and N-ethylmaleimide.

Journal Article↗
PubMed1999

Functional circuitry for the induction of prolonged excitation in the rat spinal dorsal horn.

The neuronal circuitry through which prolonged excitation is generated in the spinal dorsal horn was investigated using optical imaging of neuronal excitation in transverse slices of rat spinal cords. It is known that tetanic stimulation (20 Hz for 1 s) of the dorsal root that activates both A and C primary afferent fibres elicits slow intrinsic optical signals (IOS) in the dorsal horn, seen most intensely in the substantia gelatinosa (SG), lamina II, and that IOS expresses in part the slow synaptic response recorded intracellularly in dorsal horn neurons. We here report that the slow IOS within the SG were completely abolished after an incision was made at the border between the SG and the deeper laminae, but not after an incision within the deeper dorsal horn of the laminae III-V. The result demonstrates directly that, in order to generate prolonged excitation in the SG, the neuronal elements in the deeper dorsal horn must be intact. Thus, the afferent information might be received first by the deeper elements and then transmitted to the SG region, and/or collaboration between the SG and deeper elements is necessary to maintain prolonged excitation in the SG.

Animals↗
PubMed1999

A close relationship between Helicobacter pylori infection and gastric xanthoma.

BACKGROUND: Although the pathogenesis of gastric xanthoma (GX) remains unclear, an association of GX with atrophic gastritis has been reported. Helicobacter pylori is closely related to atrophic gastritis. The aim of this study was to investigate the relationship among GX, H. pylori, and atrophic gastritis. METHODS: Sixty-seven patients with GX were assessed for H. pylori infection by serum anti-H. pylori IgG antibody, in addition to the rapid urease test, culture, and histologic examination using biopsy specimens of the antrum and corpus. The findings were compared with 67 age- and sex-matched control subjects without GX. The distribution of atrophic gastritis was assessed endoscopically. The severity of atrophic gastritis was determined endoscopically and histologically. Serum pepsinogen (PG) levels were also measured. Immunohistochemical staining of GX samples for H. pylori antigen was performed. H. pylori clinical isolates from patients with GX and controls were assessed for cagA by means of polymerase chain reaction. RESULTS: The prevalence of H. pylori was significantly higher in patients with GX than in controls (94% and 72%, respectively). A significantly more extensive atrophic gastritis was present in patients with GX, as determined endoscopically and histologically, than in controls. Serum PG-I levels and the PG-I/PG-II ratio were significantly lower in the GX group than in the control group. H. pylori antigens were frequently identified in the cytoplasm of xanthoma cells in H. pylori-positive specimens of GX (54 of 63 specimens, 86%), whereas no immunoreactivity for H. pylori antigens was detected in H. pylori-negative specimens of GX. There was no significant difference in the positive rate of cagA between the two groups. CONCLUSIONS: Our results identified a close relationship among H. pylori infection, GX, and atrophic gastritis. A proportion of GXs may be provoked by H. pylori infection.

Aged↗
PubMed1999

Mechanisms of hypoxic coronary vasodilatation in isolated perfused rat hearts.

We pharmacologically investigated the potential involvement of nitric oxide (NO), prostacyclin, adenosine, adenosine triphosphate (ATP)-sensitive K (K(ATP)) channel opening and Ca2+-activated K (K(Ca)) channel opening in coronary vasodilatation during 15 min of hypoxia in isolated rat hearts perfused at a constant pressure of 70 mm Hg. The coronary flow suppressed by 10(-4) M Nomega-nitro-L-arginine methyl ester (L-NAME), which corresponds to the NO-dependent flow, decreased to almost zero during hypoxia. In contrast, the NO-dependent coronary flow amounted to approximately 40% of the total coronary flow during normoxia. The suppression of coronary flow by 10(-5) M 8-phenyltheophylline (8-PT), which corresponds to the adenosine-dependent flow, was remarkable in the middle and the late phases of a 15-min hypoxia. The coronary flow suppressed by 2 x 10(-6) M glibenclamide, which corresponds to the K(ATP) channel opening-dependent flow, depended on the agents added to the perfusate. However, there was a marked increase in coronary flow in the early phase of hypoxia in the heart perfused with the combination of 8-PT, 10(-2) M tetraethylammonium (TEA) and L-NAME. During hypoxia, the coronary flow suppressed by TEA, which corresponds mainly to the K(Ca) channel opening-dependent flow, also depended on the agents added to the perfusate. However, during reoxygenation, there was a transient significant increase in any combination of the agents. Our study suggests that hypoxia almost completely inhibits NO production, and that K(ATP) channel opening immediately after hypoxia and subsequent enhanced adenosine production cause a marked hypoxic coronary vasodilatation. It also suggests that K(Ca) channel opening causes vasodilatation during reoxygenation.

Animals↗
PubMed1999

Kinetic parameter estimation from compartment models using a genetic algorithm.

Kinetic parameters were estimated from a three-compartment fluorodeoxyglucose model with three rate constants using a genetic algorithm. The performance of the genetic algorithm was investigated by simulation studies, in which brain time-activity data (TAD) were generated using cited mean values of rate constants and the plasma TAD obtained from positron emission tomographic studies. The accuracy of kinetic parameter estimation using the genetic algorithm was compared with that using the non-linear least-squares (NLSQ) method. The margin of error in the parameters estimated using the genetic algorithm tended to be smaller than that obtained by the NLSQ method. Although not statistically significant at a noise level of 5% in the brain TAD, the difference between the two methods became significant for all parameters at a noise level of 15% or higher. Our results suggest that the genetic algorithm is a promising means of estimating kinetic parameters from compartment models, because it is more robust against statistical noise than the NLSQ method and it can be rendered highly parallel for processing.

Algorithms↗
PubMed1999

Hepatic extraction fraction of hepatobiliary radiopharmaceuticals measured using spectral analysis.

Measuring the hepatic extraction fraction (HEF) of a hepatobiliary radiopharmaceutical helps to differentiate hepatocyte from biliary tract diseases, and it is generally performed using deconvolution analysis. In this study, we measured HEF using spectral analysis. With spectral analysis, HEF was calculated from (the sum of the spectral data obtained by spectral analysis--the highest frequency component of the spectrum) divided by (the sum of the spectral data) x 100 (%). We applied this method to dynamic liver scintigraphic data obtained from six healthy volunteers and from 46 patients with various liver diseases, using 99Tcm-N-pyridoxyl-5-methyltryptophan (PMT). We also measured HEF using deconvolution analysis, in which the modified Fourier transform technique was employed. The HEF values obtained by spectral analysis correlated closely with those obtained by deconvolution analysis (r = 0.925), suggesting our method is valid. The HEF values obtained by spectral analysis decreased as the severity of liver disease progressed. The values were 100.0 +/- 0.0%, 94.7 +/- 13.6%, 76.2 +/- 27.4%, 45.7 +/- 15.6%, 82.7 +/- 24.2% and 95.2 +/- 11.8% (mean +/- S.D.) for the normal controls (n = 6), mild liver cirrhosis (n = 16), moderate liver cirrhosis (n = 11), severe liver cirrhosis (n = 5), acute hepatitis (n = 8) and chronic hepatitis groups (n = 6), respectively. The HEF was obtained more simply and rapidly by spectral analysis than by deconvolution analysis. The results suggest that our method using spectral analysis can be used as an alternative to the conventional procedure using deconvolution analysis for measuring HEF.

Aged↗
PubMed1999

Low prevalence of Helicobacter pylori in individuals with HTLV-I infection.

BACKGROUND: The prevalence of Helicobacter pylori in HIV-positive individuals is significantly lower than in HIV-negative controls. However, its prevalence in individuals infected with human T-cell leukaemia virus type I (HTLV-I), another important member of the human retrovirus family, has not been previously investigated. OBJECTIVE: To establish the prevalence of H. pylori in HTLV-I-positive individuals in the Nagasaki Prefecture, which is an area endemic for HTLV-I. METHODS: We examined sera from 146 HTLV-I-positive individuals with a mean age of 56.7 years, consisting of 45 adult T-cell leukaemia (ATL) patients, 13 HTLV-I-associated myelopathy (HAM) patients and 88 healthy carriers. Serum samples of 292 age- and sex-matched HTLV-I-negative controls were also examined. Serum anti-H. pylori immunoglobulin (Ig) G antibody was examined using an enzyme-linked immunosorbent assay kit. Twenty-eight HTLV-I-positive patients were examined endoscopically, assessed for H. pylori by culture, histology and CLO test using gastric biopsy specimens, and gastritis in these patients was also graded histologically. RESULTS: The seroprevalence of H. pylori was 48% in HTLV-I-positive individuals versus 64% in HTLV-I-negative controls (P < 0.01). In the three HTLV-I-positive groups, ATL patients and carriers had significantly lower seroprevalence of H. pylori than the HTLV-I-negative controls (P < 0.05). Assessment of H. pylori using gastric biopsy specimens also showed a significantly lower prevalence of H. pylori infection in HTLV-I-positive patients than controls (46% versus 70%, P < 0.05). Histological examination showed a significantly higher degree of activity, inflammation and glandular atrophy in the antrum and corpus in H. pylori-positive patients compared to H. pylori-negative patients. H. pylori-positive patients with HTLV-I infection had a more severe degree of glandular atrophy in the corpus than H. pylori-positive controls without HTLV-I infection. CONCLUSION: We have found a reduced prevalence of H. pylori in HTLV-I-positive individuals. Whatever the explanation, infection with HTLV-I does not predispose to the risk of H. pylori infection.

Adult↗
PubMed1999

Randomized controlled trial of lymphoblastoid interferon alpha for chronic hepatitis C (comparison of 9-MU and 6-MU doses). IFN Treatment Group of Affiliated Hospitals of the Third Department of Internal Medicine at Nagoya University School of Medicine.

OBJECTIVE: We conducted a randomized controlled trial to compare the efficacy of two different dosages of lymphoblastoid interferon alpha (IFN) for the treatment of chronic hepatitis C. METHODS: Eighty-four patients with chronic hepatitis C were enrolled and randomly assigned into the two groups; group A was treated with 6 million units (MU) and group B with 9 MU daily for the first 2 wk, and then thrice weekly for an additional 14 or 22 wk. RESULTS: Eighty patients were evaluated (39 patients in group A and 41 in group B); 14 patients in group A (35.9%) and 15 in group B (36.6%) obtained sustained response. The percentages of patients who became negative for HCV RNA at the end of the second wk differed slightly between the groups, without statistical significance (56.4% and 68.3%). When assessed in detail, patients with genotype 1 and < 1 Meq/ml of viral load became negative for HCV RNA significantly more frequently in group B (eight of eight) than in group A (three of seven) (p < 0.05) at the end of the second week, whereas the sustained response rate was similar between the groups (five of eight and four of seven). Predictors of sustained response by multivariate analysis were low viral load (< 1.0 Meq/ml) and negativity of HCV RNA at the end of the second wk of IFN. CONCLUSIONS: The results indicated that there was no difference in sustained response rate between the 6-MU and 9-MU doses. The earlier disappearance of HCV RNA, at the end of the second wk or at least by the end of the fourth week, is an essential condition for sustained response.

Antiviral Agents↗
PubMed1999

Robust suppression of afferent-induced excitation in the rat spinal dorsal horn after conditioning low-frequency stimulation.

The neuronal plasticity in the spinal dorsal horn induced after conditioning low-frequency stimulation of afferent A fibers, and its relationship with spinal inhibitory networks, was investigated with an optical-imaging method that detects neuronal excitation. High-intensity single-pulse stimulation of the dorsal root activating both A and C fibers evoked an optical response in the dorsal horn in transverse slices of 12- to 25-day-old rat spinal cords stained with a voltage-sensitive dye, RH-482. The optical response, reflecting the net excitation of neuronal elements along the thickness of each slice, was suppressed after a conditioning low-frequency stimulation (0.2-1 Hz for 10 min) to A fibers in the dorsal root. The degree of suppression was largest in the lamina II of the dorsal horn (48% reduction), where the majority of C fibers terminate, and much less in the deeper dorsal horn (5% reduction in laminae III-IV). The onset of suppression was somewhat slow; after the low-frequency stimulation, the magnitude of excitation gradually decreased, reached the maximum effect 30 min after the conditioning, and remained at the suppressed level for >1 h. Suppression was not observed when the low-frequency stimulation was given during a 20-min perfusion with a solution containing an NMDA-receptor antagonist, DL-2-amino-5-phosphonovaleric acid (30 microM). A brief application of an opioid-receptor antagonist, naloxone (0.5 microM), inhibited the induction, but not the maintenance, of low-frequency stimulus-induced suppression. However, treatments with the GABA(A) receptor antagonist bicuculline (1 microM) and the glycine receptor antagonist strychnine (0.3 microM) did not affect suppression induction and maintenance. In conclusion, conditioning low-frequency stimulation to A fibers interferes with the afferent-induced excitation in the dorsal horn. The low-frequency stimulation-induced suppression is maintained by a reduction of glutamatergic excitatory transmissions in the dorsal horn, not by an enhanced inhibition. Activation of the spinal opioid-mediated system by low-frequency stimulation, but not the inhibitory amino acid-mediated system, is necessary to initiate robust suppression. The long-term depression of afferent synaptic efficacy onto excitatory interneurons likely takes the primary role in the robust suppression of neuronal excitation in the dorsal horn.

2-Amino-5-phosphonovalerate↗
PubMed1999

Prostacyclin synthase gene transfer accelerates reendothelialization and inhibits neointimal formation in rat carotid arteries after balloon injury.

Prostacyclin (PGI2), a metabolite of arachidonic acid, has the vasoprotective effects of vasodilation, anti-platelet aggregation, and inhibition of smooth muscle cell proliferation. We hypothesized that an overexpression of endogenous PGI2 may accelerate the recovery from endothelial damage and inhibit neointimal formation in the injured artery. To test this hypothesis, we investigated in vivo transfer of the PGI2 synthase (PCS) gene into balloon-injured rat carotid arteries by a nonviral lipotransfection method. Seven days after transfection, a significant regeneration of endothelium was observed in the arteries transfected with a plasmid carrying the rat PCS gene (pCMV-PCS), but little regeneration was seen in those with the control plasmid carrying the lacZ gene (pCMV-lacZ) (percent luminal circumference lined by newly regenerated endothelium: 87. 1+/-6.9% in pCMV-PCS-transfected vessels and 6.9+/-0.2% in pCMV-lacZ vessels, P<0.001). BrdU staining of arterial segments demonstrated a significantly lower incorporation in pCMV-PCS-transfected vessels (7. 5+/-0.3% positive nuclei in vessel cells) than in pCMV-lacZ (50. 7+/-9.6%, P<0.01). Moreover, 2 weeks after transfection, the PCS gene transfer resulted in a significant inhibition of neointimal formation (88% reduction in ratio of intima/media areas), whereas medial area was similar among the groups. Arterial segments transfected with pCMV-PCS produced significantly higher levels of 6-keto-PGF1alpha, the main metabolite of PGI2, compared with the segments transfected with pCMV-lacZ (10.2+/-0.55 and 2.1+/-0.32 ng/mg tissue for pCMV-PCS and pCMV-placZ, P<0.001). In conclusion, this study demonstrated that an in vivo PCS gene transfer increased the production of PGI2 and markedly inhibited neointimal formation with accelerated reendothelialization in rat carotid arteries after balloon injury.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

[Emergency CABG for patients with LMT lesion treated by mechanical cardiac support].

We retrospectively analysed the perioperative course of 22 patients who underwent emergency CABG for severe left main trunk lesion. The causes of LMT lesion were spontaneous acute myocardial infarction in 14 patients and failed coronary intervention and coronary angiography in 8 patients. IABP was used preoperatively in all patients and additional coronary perfusion catheter were induced for two patients and PCPS was for one patient. Overall incidence in-hospital operative mortality was 22.7% (5/22), four of them were due to cardiac related causes and one of them was due to acute renal failure. Postoperative level of max CPK enzyme was significantly higher in death cases compared to survivors, 6,330 +/- 3,649 versus 1,299 +/- 1,417 IU/dl. We considered that the most important factors in surgical strategy for acute coronary syndrome with LMT lesion were as follows: improvement of hemodynamics with mechanical cardiac support by IABP or/and PCPS, protection of broad myocardial ischemia using coronary perfusion catheter and urgent surgical revascularization by emergency CABG.

Adult↗