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Biomedical subjects

Y Nakai

Publications and source records attributed to Y Nakai.

At least 109 records · Page 6Linked to original sources
PubMed1999

Specific immunoglobulin E, interleukin-4, and soluble vascular cell adhesion molecule-1 in sera in patients with seasonal allergic rhinitis.

This study included 23 nonatopic volunteers and 84 patients with seasonal allergic rhinitis due to Japanese cedar pollen. Serum interleukin-4 (IL-4) and soluble vascular cell adhesion molecule-1 (sVCAM-1) in the patients were significantly higher than those in the nonatopic individuals, even outside of the pollen season. Both the good responders and the poor responders to antihistamine tablets showed significant increases in IL-4 and specific IgE during the pollen season, whereas such seasonal increases were not observed in the good responders to immunotherapy. Seasonal increases in IL-4 were significantly correlated with those of specific IgE. However, seasonal increases in sVCAM-1 were not significant. Seasonal increases in sVCAM-1 were not significantly different between the good responders and the poor responders to pharmacotherapy or immunotherapy. In conclusion, serum IL-4 and sVCAM-1 are increased in patients with seasonal allergic rhinitis, even outside of the pollen season; this finding might suggest underlying preponderant in vivo activation of T helper cell-2-like cells and inflammatory events in seasonal allergic rhinitis. A seasonal increase in IL-4 in sera might be at least partly involved in the seasonal increase in specific IgE in sera. Immunotherapy's inhibitory effect on IL-4 production and specific IgE response might be one of its working mechanisms.

Adult↗
PubMed1999

Decrease of serum levels of soluble CD23 during immunotherapy in patients with perennial allergic rhinitis.

There is increasing in vitro evidence that soluble CD23 (sCD23) is capable of potentiating the synthesis of human IgE and is likely involved in the expression of allergic diseases. Our study has aimed at investigating whether serum sCD23 is elevated in patients with perennial allergic rhinitis as compared to nonatopic controls, whether sCD23 in perennial allergic rhinitis fluctuates during the natural course in untreated patients, and whether sCD23 is decreased by immunotherapy. This study included 139 patients with perennial allergic rhinitis due to Dermatophagoides farinae who gave informed consent to participation. They were divided into 2 groups--an untreated group and an immunotherapy group--according to their treatment background. Thirty-one nonallergic, healthy volunteers were included to serve as controls. Symptom scores and serum concentrations of IgE specific to D. farinae and sCD23 were examined twice in each patient: at enrollment (first evaluation) and on a variant time course after enrollment (second evaluation). Serum concentrations of sCD23 were measured by a sandwich enzyme-linked immunosorbent assay. The level of sCD23 in patients with perennial allergic rhinitis was significantly higher than that in nonatopic controls (p < .0001). The level of sCD23 in perennial allergic rhinitis was correlated with the level of specific IgE against D. farinae. The sCD23 level did not fluctuate during the natural course for a span of 2.8 +/- 2.7 years in untreated patients (p = .1337), but was significantly decreased in patients who received immunotherapy for 2.7 +/- 2.2 years (p < .0001). The rate of decrease in sCD23 was significantly correlated with the rate of decrease in specific IgE (rs = .523, p < .0001) and symptom scores (rs = .450, p < .0001). In conclusion, the reduction in sCD23 during immunotherapy is probably related to the decrease in specific IgE and also plays a role in mediating its clinical effect.

Adult↗
PubMed1999

Plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptors in patients with anorexia nervosa.

Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with numerous immunological and metabolic activities. To study the role of TNF-alpha on the pathophysiology of anorexia nervosa and its complications, plasma concentrations of TNF-alpha, 2 soluble TNF receptors (sTNF-RI and sTNF-RII), and leptin were measured in 20 female patients with anorexia nervosa (AN) and 20 age-matched normal women (N). Plasma TNF-alpha concentrations in AN were significantly higher than those in N (4.1 +/- 0.6 pg/mL vs. 1.6 +/- 0.1 pg/mL; P < 0.01). Although no significant difference was observed in plasma sTNF-RI concentrations between the two groups, plasma sTNF-RII concentrations in AN were significantly higher than those in N (2094.0 +/- 138.5 pg/mL vs. 1569.5 +/- 84.0 pg/mL; P < 0.01). Plasma concentrations of TNF-alpha and sTNF-RII after treatment of 8 anorectic patients were not different from those before treatment, although body fat mass and plasma leptin concentrations significantly increased after treatment. Plasma TNF-alpha concentrations were not related to body fat mass in anorectic patients. These results suggest that the adipose tissue may not be the immediate source of TNF-alpha in anorectic patients and that TNF-alpha may contribute to the pathophysiology of immunological and metabolic abnormalities in anorexia nervosa.

Adult↗
PubMed1999

Antagonism of saikosaponin-induced prostaglandin E2 release by baicalein in C6 rat glioma cells.

There are several Kampo medicines (Chinese herbal medicines) containing both Bupleuri Radix and Scutellariae Radix, which are used for the treatment of inflammation. Saikosaponins are derived from Bupleuri Radix, and baicalein is from Scutellariae Radix. The present study was undertaken to investigate the pharmacological interaction of saikosaponin b1 and baicalein in prostaglandin E2 (PGE2) release from C6 rat glioma cells in vitro. Saikosaponin a, b1 and d potently stimulated PGE2 release, while saikosaponin b2 and c moderately stimulated PGE2 release. Saikosaponin b1 caused an irreversible elevation of intracellular Ca2+ concentration, which was eliminated by removing extracellular Ca2+. On the other hand, baicalein inhibited saikosaponin b1-induced PGE2 release in a concentration-dependent manner. These results suggest that saikosaponins are activators of PGE2 release, and baicalein is one of the functional inhibitors of PGE2 release by saikosaponins.

Animals↗
PubMed1999

Image-guided procedures in brain biopsy.

Image-guided procedures, such as computed tomography (CT)-guided stereotactic and ultrasound-guided methods, can assist neurosurgeons in localizing the relevant pathology. The characteristics of image-guided procedures are important for their appropriate use, especially in brain biopsy. This study reviewed the results of various image-guided brain biopsies to ascertain the advantages and disadvantages. Brain biopsies assisted by CT-guided stereotactic, ultrasound-guided, Neuronavigator-guided, and the combination of ultrasound and Neuronavigator-guided procedures were carried out in seven, eight, one, and three patients, respectively. Four patients underwent open biopsy without a guiding system. Twenty of 23 patients had a satisfactory diagnosis after the initial biopsy. Three patients failed to have a definitive diagnosis after the initial procedure, one due to insufficient volume sampling after CT-guided procedure, and two due to localization failure by ultrasound because the lesions were nonechogenic. All patients who underwent biopsy using the combination of ultrasound and Neuronavigator-guided methods had a satisfactory result. The CT-guided procedure provided an efficient method of approaching any intracranial target and was appropriate for the diagnosis of hypodense lesions, but tissue sampling was sometimes not sufficient to achieve a satisfactory diagnosis. The ultrasound-guided procedure was suitable for the investigation of hyperdense lesions, but was difficult to localize nonechogenic lesions. The combination of ultrasound and Neuronavigator methods improved the diagnostic accuracy even in nonechogenic lesions such as malignant lymphoma. Therefore, it is essential to choose the most appropriate guiding method for brain biopsy according to the radiological nature of the lesions.

Aged↗
PubMed1999

[Esophageal reconstruction for esophageal stricture after corrosive injury].

Swallowing a corrosive agent (alkali or acid) often causes severe pharyngeal, laryngeal or esophageal stricture (caustic stenosis), which is usually very difficult to treat. This paper reports two cases of esophageal stricture treated by esophagoplasty. Both cases had attempted suicide by swallowing a sodium hydroxide solution or acid. Case 1 was a 66-year-old man found to have severe hypopharynx and thoracic esophagus stenosis with supraglottic stricture. The supraglottic stricture was reconstructed with an ileocolon graft and laryngectomy. The intestinal anastomosis was patent, but the peristaltic motion in the ileocolon was not good. The patient continues to have difficulty achieving sufficient oral feeding and to receive supplemental feeding via a jejunostomy. Case 2 was a 81-year-old woman with severe thoracic esophagus stenosis after gastrectomy. The lesion was reconstructed with a jejenum graft. The intestinal anastomosis was patent. She achieved oral alimentation of both liquids and solids without aspiration after surgery. Esophagectomy in these cases can be difficult and hazardous due to extensive fibrosis and many adhesions to adjacent structures. In both cases, the reconstructed intestine passed through the ante-sternal route, so there was severe scar formation in the mediastinum, and an esophago-skin fistula formed in the cervical skin. Cervical vessels and intestinal vessels were anastomosed for blood supply to the reconstructed intestinal tract. This method is useful because it is safe and results in good deglution.

Aged↗
PubMed1999

[A case of multiple myeloma presenting with a subcutaneous mass: significance of "dural tail sign" in the differential diagnosis of the meningeal tumors].

A 65-year-old female was admitted to our hospital with a 6-month history of a gradually enlarging subcutaneous mass in the frontal region. Neurological examination on admission showed no significant abnormality. Skull X-P showed an osteolytic lesion of the frontal bone. External carotid angiogram demonstrated a tumor stain fed by the middle meningeal artery. Computed tomography (CT) showed a slightly high density mass with a marked homogeneous enhancement. MRI revealed an iso-intensity mass on both T1- and T2-weighted images. Gd-DTPA-enhanced T1-weighted images showed a mass with a marked homogeneous enhancement with the "dural tail sign" in the dura adjacent to the tumor. The tumor was totally removed; this mass was diagnosed as a multiple myeloma. No tumor cells were seen in the dura adjacent to the tumor and the mechanism of dural enhancement around the tumor was not clear. However, it is possible that the "dural tail" is due to increased vascular permeability of the dural vessels. Although the "dural tail" sign has been considered as a highly specific feature of meningioma, multiple myeloma can show the same findings on MRI. Therefore, it is important to consider the possibility of multiple myeloma in the differential diagnosis of meningeal tumors.

Aged↗
PubMed1999

[Transient cortical blindness and convulsion mimicking a hemorrhagic complication during embolization of the cerebellar AVM].

We report a case of transient cortical blindness and convulsions during embolization of the cerebellar AVM. A 29-year-old man was admitted to our hospital with subarachnoid hemorrhage. Cerebral angiography showed the right cerebellar AVM fed by the right superior cerebellar artery. Preoperative embolization of the AVM was performed. During embolization, the patient lost consciousness suddenly and appeared to be in a decerebrate posture. About 15 minutes later, the patient came around and complained of total blindness. Cerebral angiography revealed the disappearance of the aneurysm and AVM. There were no abnormal findings in the vertebrobasilar system. Computed tomography obtained just after the procedure, showed considerable contrast enhancement of the occipital lobes. Two hours later, a repeat computed tomography showed clearance of contrast enhancement. Magnetic resonance imaging obtained 12 hours after the procedure, showed no evidence of infarction in the occipital lobes. Two days after, the patient's sight gradually returned. Seven days after the procedure, the patient recovered completely. We speculated that these clinical features might be convulsions due to contrast material. In the reported cases, convulsions and transient cortical blindness due to non-ionic low osmolar contrast materials is a rare complication. This case suggested disruption of the blood-brain barrier demonstrated by the computed tomography appearance of contrast enhancement in the occipital lobes.

Adult↗
PubMed1999

Excimer laser-induced hydroxyl radical formation and keratocyte death in vitro.

PURPOSE: To characterize the type of reactive oxygen species (ROS) produced by excimer photoablation of aqueous solutions and to show the effects of ROS and antioxidants on corneal stromal cells in vitro. METHODS: Electron spin-resonance spectroscopy was performed using the spin-trapping agent 5,5-dimethyl-1-pyrroline N-oxide (DMPO) for the detection of the superoxide anion and the hydroxyl radical in an acellular DMPO solution irradiated with the excimer laser. Hydroxyl radicals were produced by the Fenton reaction in vitro by the mixture of hydrogen peroxide and ferrous iron (Fe2+), and the effects on cultured corneal fibroblasts were observed by fluorescent microscopy using the cell death marker, propidium iodide (PI) and TdT-mediated dUTP nick-end labeling (TUNEL). RESULTS: Excimer photoablation of a 1% DMPO solution produced a species-specific spin-trapping adduct for the hydroxyl radical ('OH), but not for the superoxide anion or other unidentified free radical. The signals were inhibited dose dependently by the hydroxyl radical scavenger dimethylsulfoxide (DMSO) and an L-ascorbic acid analogue, EPCK-1. The production of *OH in the supernatant of cultured rabbit corneal fibroblasts by the Fenton reaction caused an increase in PI (+) and TUNEL (+) cells by 90 minutes, which was significantly inhibited by the addition of DMSO. CONCLUSIONS: Hydroxyl radicals may be partly responsible for stromal fibroblast cell apoptosis after excimer photoablation.

Animals↗
PubMed1999

Genistein inhibits the regulation of active sodium-potassium transport by dopaminergic agonists in nonpigmented ciliary epithelium.

PURPOSE: To determine whether dopamine receptor stimulation regulates Na,K-ATPase-mediated ion transport in cultured nonpigmented ciliary epithelium (NPE). METHODS: Using a rabbit NPE cell line, active Na-K transport activity was determined by measuring ouabain-sensitive potassium (86Rb) uptake in cell monolayers. Western blot analysis of membrane material obtained from cell homogenates was conducted to examine tyrosine phosphorylation of membrane proteins. RESULTS: Ouabain-sensitive potassium (86Rb) uptake was inhibited in the presence of either dopamine or the D1-selective agonist SKF82958. The response was suppressed by SCH23390, a D1 antagonist, but not by sulpiride, a D2-selective antagonist. Quinpirole, a D2-selective agonist, did not cause inhibition of ouabain-sensitive potassium (86Rb) uptake. Cyclic adenosine monophosphate (cAMP) was detectably increased in SKF82958-treated cells, although the concentration of SKF required to elevate cell cAMP was higher than the concentration needed to inhibit ouabain-sensitive potassium (86Rb) uptake. The protein kinase A inhibitor H89 prevented the 86Rb uptake response to SKF82958. Genistein, an inhibitor of tyrosine kinases, also prevented the 86Rb uptake response to SKF82958. Membrane material isolated from cells exposed to SKF82958 showed an increase in the density of several phosphotyrosine bands. These changes in phosphotyrosine immunoblot density were not observed in material isolated from cells that received either genistein or SCH23390 before SKF82958 treatment. CONCLUSIONS: The results of this study suggest D1 agonists cause a reduction of Na,K-ATPase-mediated ion transport by a mechanism that could involve a tyrosine kinase step.

Animals↗
PubMed1999

[Phase I study of gemcitabine hydrochloride (LY 188011) combination therapy with cisplatin in the patients with non-small cell lung cancer].

The combination Phase I study of gemcitabine hydrochloride with cisplatin was conducted in the patients with non-small cell lung cancer (NSCLC) at 5 investigation sites. Gemcitabine was administrated on day 1, 8 and 15 and cisplatin on day 1 of each 28-day cycle. The dosage of cisplatin was fixed to 80 mg/m2 and the dosage of Gemcitabine was gradually escalated in 3 dosing level from 600, 800 to 1,000 mg/m2. The maximum tolerated dose (MTD) and the recommended dose was determined with Continual Reassessment Method. For each dose level, 6 cases, 3 cases and 6 cases were registered respectively and all 15 cases were evaluable. In the dose level 3 with 1,000 mg/m2 of gemcitabine and 80 mg/m2 of cisplatin, grade 4 neutropenia was observed as DLT in 3 out of 6 cases, thus dose level 3 was considered as MTD and the recommended dose. Major adverse events were leukopenia, neutropenia, nausea/vomiting and anorexia. The incidence of such adverse events seemed to be dose-dependent and especially the grade of neutropenia seemed to be more serious as the dose increased. Also, the grade of liver function tests abnormal seemed to be more serious as the dose increased but the incidence as well as the grade did not have tendency of dose-dependent in another events including renal function tests abnormal. On the other hand, as to the efficacy PR was observed in 4 out of 15 cases. Based upon the results, it is necessary to discuss further the efficacy in the recommended dose in the combination therapy of gemcitabine and cisplatin.

Adenocarcinoma↗
PubMed1999

The FLS mouse: a new inbred strain with spontaneous fatty liver.

BACKGROUND AND PURPOSE: A new strain of mouse, named FLS (fatty liver Shionogi), which develops spontaneous fatty liver without obesity, was established by inbreeding. Morphologic, physiologic, and genetic characterization of the strain was done. METHODS: Characteristics of male FLS mice were compared with those of the sister strain, dd Shionogi (DS), which does not develop spontaneous fatty liver. A genetic cross experiment was performed by mating FLS with C3H/He/Shi mice. RESULTS: The hepatocytes of neonatal FLS mice contained fine lipid droplets throughout the lobules, and large lipid droplets appeared as mice aged. Liver triglyceride concentrations of FLS mice were fivefold higher than those of DS mice, but serum lipid concentrations and the lipoprotein profile did not indicate abnormalities. Higher plasma aspartate transaminase and alanine transaminase activities in FLS, compared with DS mice, suggested hepatocellular lesions. The genetic cross experiment suggested that the fatty liver formation is a complex polygenic trait. CONCLUSION: The FLS mice develop a progressive hepatic steatosis without obesity and diabetes. The FLS mouse might be a good model for investigating hepatic disorders accompanied by fatty liver unrelated to alcoholism or obesity.

Adipose Tissue↗
PubMed1998

PACAP protects hippocampal neurons against apoptosis: involvement of JNK/SAPK signaling pathway.

We have demonstrated that the ischemia-induced apoptosis of neurons in the CA1 region of the rat hippocampus was prevented by either intracerebroventricular or intravenous infusion of pituitary adenylate cyclase-activating polypeptide (PACAP). However, the molecular mechanisms underlying the anti-apoptotic effect of PACAP remain to be determined. Within 3-6 h after ischemia, the activities of members of the mitogen-activated protein (MAP) kinase family, including extracellular signal-regulated kinase (ERK), Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK), and p38 were increased in the hippocampus. The ischemic stress had a potent influence on the MAP kinase family, especially on JNK/SAPK. PACAP inhibited the activation of JNK/SAPK after ischemic stress. Secretion of interleukin-6 (IL-6) into the cerebrospinal fluid was intensely stimulated after PACAP infusion. IL-6 inhibited the activation of JNK/SAPK, while it activated ERK. These observations suggest that PACAP and IL-6 act to inhibit the JNK/SAPK signaling pathway, thereby protecting neurons against apoptosis.

Animals↗