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Biomedical subjects

Y Masaki

Publications and source records attributed to Y Masaki.

At least 37 records · Page 2Linked to original sources
PubMed2000

Quantitative evaluation of a directly depolarized area induced by high-output pacing on the cardiac muscle.

Quantitative information is needed on the directly depolarized area (DDA) induced by high-output energy during a precise mapping procedure to detect the origin of a tachycardia. In the present study, a DDA caused by high-output energy was quantitatively evaluated in the exposed canine heart. In 8 dogs, the right atrial and ventricular surfaces were exposed through a right thoracotomy and pacing with various outputs was delivered from the epicardial surface. A comb-shaped 16 polar electrode array and/or a 224 polar mat electrode array were used for recording the epicardial electrograms. The local activation time was measured at each electrode site, and the relationship of the distance between the electrode location from the pacing site and the local activation time was plotted and fitted to a primary regression line. The intercept of the regression line on the horizontal axis was defined as the radius of the 'DDA' and this was evaluated at each pacing output. The radius of the DDA was 0.6+/-0.1 mm with a 2 V and 3.8+/-0.2 mm with a 10 V output when it was evaluated in a direction perpendicular to the fiber orientation of the pectinate muscle, 0.8+/-0.1 mm with a 2 V and 4.1+/-0.3 mm with a 10 V output in a direction parallel to the pectinate muscle fiber orientation, and 0.9+/-0.3 mm with a 2 V and 3.6+/-0.5 mm with a 10 V output in the right ventricle. The DDA extended according to the increase in stimulation outputs at all sites, and there was no significant difference in the pacing site or the direction of the stimulation propagation. The DDA caused by high-output energy is a purely physical phenomenon that depends only on stimulation output and tissue resistance. The diameter of the DDA exceeded 4 mm (ie, the size of a standard tip electrode for catheter ablation) when pacing was delivered with an output greater than 6 V.

Animals↗
PubMed2000

[Histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto's disease) accompanied by hemophagocytosis and salivary gland swelling in a patient with systemic lupus erythematosus].

After 2 years of steroid therapy that had effectively controlled her systemic lupus erythematosus, a 37-year-old woman presented with fever, erythema (face, upper chest), and low CH50. Increased oral steroid (prednisolone from 15 mg to 40 mg) and intravenous methylprednisolone (mPSL) (80 mg for 3 days) alleviated these symptoms except for the fever. Subsequently, the patient's fever worsened and leukocytopenia, abnormal liver function, lymphadenopathy (neck, axilla), and salivary gland swelling developed. Lymph node histology revealed features characteristic of Kikuchi-Fujimoto's disease (KFD). Laboratory examinations showed WBC 600/microliter, Hb 9.5 g/dl, platelets 90,000/microliter, GOT 766 IU/l, GPT 646 IU/l, LDH 4,228 IU/l, TG 1,622 mg/dl, and ferritin 6,330 ng/ml. Serum interferon gamma was also elevated (673 U/ml). Because a bone marrow smear revealed hemophagocytosis, mPSL pulse therapy (1 g for 3 days) was started for treatment of hemophagocytic syndrome. The fever promptly disappeared, and the patient's clinical symptoms resolved within 2 weeks. The abnormal laboratory data related to KFD and hemophagocytosis returned to normal within 4 weeks after the initiation of mPSL pulse therapy. We speculated that the hemophagocytosis and salivary gland involvement in this patient were also symptoms of KFD. This case indicated that corticosteroid pulse therapy is effective for KFD with serious clinical symptoms.

Adult↗
PubMed2000

Frequency of a 30-base pair deletion in the latent membrane protein-1 gene in Epstein-Barr virus-associated lymphomas in Japan.

The association of Epstein-Barr virus (EBV) with various lymphoid malignancies has been reported. The precise pathogenesis of EBV in malignancies has not yet been elucidated. Latent membrane protein-1 (LMP-1) and Epstein-Barr nuclear antigen-2 (EBNA-2) genes are suspected to be tumorigenic genes. Previous studies suggest that a deletion within the LMP-1 gene may increase the oncogenic potential of EBV. In this study, we analyzed the sequence within the carboxy terminal end of the LMP-1 gene in paraffin-embedded specimens from T-cell lymphomas, Hodgkin's disease (HD), and the buffy coat of peripheral blood from healthy individuals in Japan. Polymerase chain reaction (PCR) was performed using primers spanning the carboxy terminal region of the LMP-1 gene, and sequence analysis was performed to show the exact location of the deletion. The PCR product of the Raji cell line was 161 base pairs (bp), and the LMP-1 gene with deletion was 30 bp shorter in a direct sequence of PCR products. The 30-bp deletion was located in position 168285-168256 of the Raji cell. A deletion within the LMP-1 gene was found in 4 of 25 cases (16%) of EBV-positive T-cell lymphomas, 4 of 10 cases (40%) of EBV-positive HD cases, and 2 of 13 specimens (15%) with amplified PCR products from 49 healthy individuals. The incidence of the 30-bp deletion within the LMP-1 gene in HD was comparable to that of subjects in the United States and Brazil, but the deletion was not found in a high proportion of EBV-positive T-cell lymphoid malignancies. No statistical significance was found regarding the clinical outcome between patients with a deletion within the LMP-1 gene and patients with wild-type LMP. This deletion cannot be considered as simply causing the pathogenesis of EBV-associated lymphoid malignancies in Japan.

Adult↗
PubMed1999

Flumazenil antagonizes midazolam-induced airway narrowing during nasal breathing in humans.

We measured nasal resistance (Rn) while awake, during midazolam-induced sedation and after antagonism with flumazenil (n = 9). Nasal and oral airflow were measured. Rn was calculated by dividing the difference between maximal nasal mask and oropharyngeal pressures by inspiratory airflow at minimum pharyngeal pressure. During sedation, two subjects developed obstructive apnoeic events and four subjects had snoring events. Each apnoea was ended by mechanisms other than a change in breathing route. After antagonism with flumazenil, apnoeic and snoring events were abolished. Rn during midazolam sedation (median 1.46 (25th percentile 1.00, 75th 2.61) kPa litre-1 s) was significantly greater than before midazolam (0.29 (0.25, 0.48) kPa litre-1 s) and after flumazenil (0.41 (0.25, 0.58) kPa litre-1 s) (P < 0.01 in each subject). We conclude that midazolam increased Rn, sometimes leading to obstruction, and flumazenil abolished this increase in Rn.

Adult↗
PubMed1999

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

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

Anesthetics, Local↗
PubMed1999

Underglycosylation of IgA1 hinge plays a certain role for its glomerular deposition in IgA nephropathy.

This study was performed to isolate and investigate the IgA1 that could accumulate in glomeruli (glomerulophilic IgA1). IgA1 was fractionated by the electric charge and the reactivity to Jacalin. Serum IgA1 of IgA nephropathy patients was separated and fractionated using a Jacalin column and subsequent ion-exchange chromatography. The fractions were divided into three groups of relatively cationic (C), neutral (N), and anionic (A). IgA1 was also divided into Jacalin low (L), intermediate (I), and high (H) affinity fractions by serial elution using 25, 100, and 800 mM galactose. The left kidneys of Wistar rats were perfused with 2, 5, or 10 mg of each group of IgA1. The rats were sacrificed 15 min, 30 min, 3 h, or 24 h after the perfusion. The accumulation of each IgA1 in the glomeruli was then observed by immunofluorescence. The IgA1 of the fractions N and H separated by the two methods was definitely accumulated in the rat glomeruli with a similar pattern. The electrophoresis revealed that the macromolecular IgA1 was increased in fraction H compared with other fractions. Therefore, Jacalin high-affinity IgA1(fraction H) was applied on a diethylaminoethyl column and divided into electrically cationic (HC), neutral (HN), and anionic (HA). Only the asialo-Galbeta1,3GalNAc chain was identified in the fraction HN IgA1 by gas-phase hydrazinolysis. Furthermore, the IgA1 fraction was strongly recognized by peanut agglutinin, Vicia Villosa lectins, and antisynthetic hinge peptide antibody. These results indicated that the IgA1 molecules having the underglycosylated hinge glycopeptide played a certain role in the glomerular accumulation of IgA1 in IgA nephropathy.

Animals↗
PubMed1999

[Evaluation of the histologic criteria for the diagnosis of Sjögren's syndrome].

OBJECTIVE: The most important diagnostic criterion in Sjögren's syndrome (SS) is considered to be the histologic focus score of the labial salivary glands. The focus score is defined as the number of lymphocytic foci per 4 mm2 of the salivary gland according to the criterion of Chisholm & Mason. On the other hand, in the criteria of the Sjögren's Disease Research Committee of the Ministry of Health and Welfare in Japan it is defined as the number of lymphocytic foci per a lobule of the salivary gland. By setting the limited criteria for SS on the basis of objective signs of both dry eyes and dry mouth, we compared the usefulness of these two diagnostic criteria for the diagnosis of SS in terms of the sensitivity, the specificity and laboratory data. METHODS: The biopsy of labial salivary glands was performed in 245 patients (230 females and 15 males, with a mean age of 54.9 years) who were suspected of SS in our hospital during the time between 1975 and 1996. Labial salivary glands were histologically assessed and the focus score was calculated according to the criterion of Chisholm & Mason and to that of the Sjögren's Disease Research Committee, respectively. RESULTS: The average area per a lobule of the salivary gland was 0.70 mm2. According to the limited criteria for SS, the Japanese histologic diagnostic criteria showed a higher specificity (93.3%) and a lower sensitivity (23.5%). The sensitivity of the criterion of Chisholm & Mason was 72.1%, and the specificity was 80.0%. The margin of the lobule was sometimes difficult to be identified because of the fatty change and fibrosis in some salivary glands. CONCLUSIONS: By comparing the two different histologic criteria using our limited criteria, it was better to use the histologic criterion of Chisholm & Mason as a criterion for the diagnosis of SS than that of the Sjogren's Disease Research Committee of the Ministry of Health and Welfare in Japan in terms of the sensitivity, the specificity and laboratory data.

Adult↗
PubMed1999

[Effect of adrenaline on vagus nerve reflexes].

INTRODUCTION: Dizziness or syncope may occur during treatment of nasal disease. These symptoms are considered imputable to the vagovagal reflex, which is partly involved in neurogenic syncope. In response to trigeminal nerve stimulation, the vagus nerve causes a sudden fall in heart rate and blood pressure. Elevation in blood adrenaline level during pain or tension was noted, and its effects on vagovagal reflexes were studied. MATERIALS AND METHODS: Ten cats were used in the experiment. The vagus nerve was exposed on the right side of the neck by making an incision in the trachea, and a platinum electrode was attached to the vagus nerve on nerve's distal side. The head was tilted a 30 degree angle. The cats were divided into control and adrenaline-treated groups, and changes in cerebral blood flow, heart rate, and arterial pressure were compared between the two groups after electric stimulation of the vagus nerve. Cerebral blood flow was measured by the hydrogen clearance method. 1) Control group The vagus nerve was electrically stimulated for 1 minute. 2) Adrenaline-treated group The vagus nerve was electrically stimulated for 1 minute following 30 seconds of intravenous administration of adrenaline. RESULTS: Cerebral blood flow was significantly decreased in both the control and adrenaline-treated groups after electric stimulation, but the decrease was significantly greater in the latter group at all sites of measurement. Whereas heart rate and arterial pressure were significantly decreased in the control group, these variables in the adrenaline-treated group showed no significant change despite the greater decrease in cerebral blood flow. DISCUSSION: Heart rate, blood pressure, and cerebral blood flow were all significantly decreased after electric stimulation of the vagus nerve. These changes were considered owing to a fall in blood pressure due to vasodilation resulting from bradycardia and a relative decrease in sympathetic nervous tension resulting from electric stimulation. On the other hand, in the adrenaline-treated group, neither heart rate nor blood pressure showed any significant change, but cerebral blood flow was significantly decreased at all sites of measurement despite an adrenaline load. This contradictory results may be accounted for by the powerful beta 2-activity of adrenaline. The greater decrease in cerebral blood flow in the adrenaline-treated than in the control group can be attributed to decreased peripheral vascular resistance by its beta 2-activity. In the field of otorhinolaryngology the trigeminal region is often involved in the treatment of nasal disorders so that vagovagal reflexes are often encountered. The results of this study counsels caution in the treatment involving the trigeminal region.

Adrenergic beta-2 Receptor Agonists↗
PubMed1999

Epstein-Barr virus study in malignant lymphoma in Sjögren's syndrome.

The association of Epstein-Barr virus (EBV) with Sjögren's syndrome (SS) is controversial. Reports suggest there is an increased risk of developing lymphoid malignancy in SS. Among our 425 cases of SS, 17 cases of malignant lymphoma (4%), 16 cases of non-Hodgkin's lymphoma (NHL), and 1 case of Hodgkin's disease were found. We looked for an association between EBV and 14 cases of NHL, 13 cases of B-cell lymphoma, and 1 case of T-cell lymphoma in which tissue specimens were available. Epstein-Barr virus-encoded RNA in situ hybridization study and polymerase chain reaction (PCR) study using primers to detect the Bam HI W fragment of EBV with DNA extracts were positive in 2 NHLs: 1 diffuse, large B-cell-type lymphoma, 1 out of 13 cases (8%) of B-cell lymphoma, and 1 angioimmunoblastic T-cell lymphoma with dysproteinemia. In the Bam HI W PCR study of DNA obtained from the labial small salivary glands of 55 cases with SS, 3 cases (5%) were positive. These 3 cases were not associated with malignant lymphoma. Our study revealed that EBV association in SS did not lead to an increased occurrence.

Aged↗
PubMed1998

Dissemination of Epstein-Barr virus associated B-cell lymphoma of the brain after development of immunological incompetence with Evans syndrome.

A 54-year-old female with Epstein-Barr virus (EBV)-associated B-cell lymphoma of the brain and Evans syndrome is presented. After treatment of the lymphoma with irradiation to the brain and chemotherapy she developed Evans syndrome with autoimmune hemolytic anemia and thrombocytopenia. Further immunosuppressive treatment for Evans syndrome caused the dissemination of EBV-associated B-cell lymphoma. The dissemination of EBV-associated B-cell lymphoma was confirmed by in situ hybridization with EBV encoded small RNAs (EBER), polymerase chain reaction with Bam HI-W fragment of EBV and lymphocyte determined membrane antigen (LYDMA) and immunohistochemistry with latent membrane protein (LMP). Since only a few cases of lymphomas associated with EBV occurring during autoimmune diseases have been reported, this is an illustrative case.

Autoimmune Diseases↗