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N Sakai

Publications and source records attributed to N Sakai.

At least 163 records · Page 9Linked to original sources
PubMed2000

Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients.

Adiponectin is a novel, adipose-specific protein abundantly present in the circulation, and it has antiatherogenic properties. We analyzed the plasma adiponectin concentrations in age- and body mass index (BMI)-matched nondiabetic and type 2 diabetic subjects with and without coronary artery disease (CAD). Plasma levels of adiponectin in the diabetic subjects without CAD were lower than those in nondiabetic subjects (6.6+/-0.4 versus 7.9+/-0.5 microg/mL in men, 7.6+/-0.7 versus 11.7+/-1.0 microg/mL in women; P<0.001). The plasma adiponectin concentrations of diabetic patients with CAD were lower than those of diabetic patients without CAD (4.0+/-0.4 versus 6.6+/-0.4 microg/mL, P<0.001 in men; 6.3+/-0.8 versus 7.6+/-0. 7 microg/mL in women). In contrast, plasma levels of leptin did not differ between diabetic patients with and without CAD. The presence of microangiopathy did not affect the plasma adiponectin levels in diabetic patients. Significant, univariate, inverse correlations were observed between adiponectin levels and fasting plasma insulin (r=-0.18, P<0.01) and glucose (r=-0.26, P<0.001) levels. In multivariate analysis, plasma insulin did not independently affect the plasma adiponectin levels. BMI, serum triglyceride concentration, and the presence of diabetes or CAD remained significantly related to plasma adiponectin concentrations. Weight reduction significantly elevated plasma adiponectin levels in the diabetic subjects as well as the nondiabetic subjects. These results suggest that the decreased plasma adiponectin concentrations in diabetes may be an indicator of macroangiopathy.

Adiponectin↗
PubMed2000

Oxidized LDL-induced NF-kappa B activation and subsequent expression of proinflammatory genes are defective in monocyte-derived macrophages from CD36-deficient patients.

-CD36 is 1 of the class B scavenger receptor expressed on monocytes, monocyte-derived macrophages (Mphi), platelets, and adipocytes. In our previous studies, we reported that the uptake of oxidized low density lipoproteins (OxLDLs) is reduced by approximately 50% in Mphi from CD36-deficient patients compared with that in control subjects. Recently, we have shown that CD36 is highly expressed in human atherosclerotic aorta. Possibilities have been raised that besides the wide distribution and multifunctional characteristics of CD36, this molecule may also be involved in the mediation of intracellular signaling. The aim of the present study was to elucidate the role of CD36 in cytokine secretion and to investigate the CD36-mediated intracellular signaling stimulated by OxLDL. On addition of OxLDL or thrombospondin-1, the Mphi from CD36-deficient patients secreted significantly less amounts of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) compared with those from controls. RNase protection assay with multiprobe template sets demonstrated that after incubation with OxLDL, the mRNAs of a variety of cytokines, including genes encoding IL-1Ra, IL-1beta, IL-6, TNF-alpha and -beta, and interferon (IFN)-gamma and -beta, were significantly lower in the Mphi of patients. The addition of antibody against CD36 attenuated this OxLDL-induced response in controls. We also observed a reduced response in nuclear factor-kappa B (NF-kappa B) activity in OxLDL-stimulated Mphi from CD36-deficient patients. Unlike OxLDL, stimulation by lipopolysaccharide induced an increase in NF-kappa B activity in Mphi from CD36-deficient patients, suggesting that lipopolysaccharide-mediated signaling was conserved. These results demonstrate that in addition to the reduced OxLDL uptake that we reported previously, CD36-deficient patients may also have an impaired response of OxLDL-induced NF-kappa B activation and subsequent cytokine expression.

Arteriosclerosis↗
PubMed2000

p38 MAP kinase is required for vasopressin-stimulated HSP27 induction in aortic smooth muscle cells.

We previously showed that arginine vasopressin (AVP) stimulates heat shock protein 27 (HSP27) induction through protein kinase C activation in aortic smooth muscle A10 cells. In the present study, we examined whether the mitogen-activated protein (MAP) kinase superfamily is involved in the AVP-stimulated HSP27 induction in A10 cells. AVP stimulated the phosphorylation of p42/p44 MAP kinase and p38 MAP kinase. On the contrary, AVP had little effect on SAPK (stress-activated protein kinase)/JNK (c-Jun N-terminal kinase) phosphorylation. The HSP27 accumulation by AVP was not affected by PD98059, an inhibitor of the upstream kinase that activates p42/p44 MAP kinase. SB203580 and PD169316, specific inhibitors of p38 MAP kinase, suppressed the AVP-induced accumulation of HSP27. 12-O-tetradecanoylphorbol 13-acetate, an activator of protein kinase C, induced accumulation of HSP27 and was not inhibited by PD98059 but was inhibited by SB203580. Calphostin C and ET-18-OCH(3), inhibitors of protein kinase C, reduced the phosphorylation of p38 MAP kinase by AVP. SB203580 and PD169316 suppressed the AVP-increased levels in mRNA for HSP27. Dissociation of the aggregated HSP27 to the dissociated HSP27 was induced by AVP. These results strongly suggest that p38 MAP kinase takes part in the pathway of the AVP-stimulated induction of HSP27 in vascular smooth muscle cells.

Animals↗
PubMed2000

Phospholipase A(2) and its products are involved in the purinergic receptor-mediated translocation of protein kinase C in CHO-K1 cells.

The signal transduction involved in the purinergic stimuli-induced activation of protein kinase C (PKC) in CHO-K1 cells was investigated. Purinergic stimuli such as adenosine triphosphate and uridine triphosphate induced a transient translocation of PKC epsilon, gamma, and delta from the cytoplasm to the plasma membrane. These translocations were blocked by an inhibitor of phosphatidylinositol-specific phospholipase C (PLC), but not by an inhibitor of phosphatidylcholine-specific PLC. A diacylglycerol (DAG) analogue also induced reversible translocations of PKC gamma, epsilon, and delta from the cytoplasm to the plasma membrane, while the calcium ionophore A23187 caused a similar translocation of only the gamma subtype. These results confirm that the hydrolysis of phosphatidylinositol-2-phosphate by PLC and the subsequent generation of DAG and increase in Ca(2+ )are involved in the purinergic stimuli-induced translocation of PKC. A DAG antagonist, 1-o-hexadecyl-2-o-acetyl-glycerol, blocked the DAG analogue-induced translocations of all PKC subtypes tested but failed to inhibit the purinergic stimuli-induced translocations of PKC epsilon and gamma. The DAG antagonist could not block the ATP- and UTP-induced translocation of PKC epsilon even in the absence of extracellular Ca(2+). Co-application of the DAG antagonist and a phospholipase A(2) (PLA(2)) inhibitor such as aristolochic acid, arachidonyltrifluoromethyl ketone, or bromoenol lactone inhibited the purinergic receptor-mediated translocation of PKC epsilon although each PLA(2) inhibitor alone did not block the translocation. In contrast to the epsilon subtype, ATP-induced translocation of PKC gamma was observed in the presence of both the PLA(2) inhibitor and the DAG antagonist. However, it is noteworthy that re-translocation of PKC gamma was hastened by the PLA(2) inhibitor. Furthermore products of PLA(2), such as lysophospholipids and fatty acids, induced the translocation of PKC gamma and epsilon in a dose dependent manner, but not delta. These results indicate that, in addition to PLC and DAG, PLA(2) and its products are involved in the purinergic stimuli-induced translocation of PKC epsilon and gamma in CHO-K1 cells. Each subtype of PKC in CHO-K1 cell is individually activated in response to a purinergic stimulation.

Animals↗
PubMed2000

[Apoptotic cell death induced by actinomycin D arisen at different levels and cell cycle stages according to human cultured cell species].

Nine kinds of human cultured cells, including fetus cells (smooth chorion trophoblast cells, amnion epithelial cells and HE-21), adult non-carcinoma cells (HCF), and carcinoma cells (KATO-III, COLO 201, Lu-134-AH, SK-OV-3 and SKG-3a) were stimulated with Actinomycin (Act.) D for 24 h. Apoptosis induction was investigated by agarose gel electrophoresis for DNA fragmentation analysis and by flow cytometric analysis of stained cells using in situ terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP nick-end labeling TUNEL) staining techniques for the quantification of apoptosis, and simultaneously using propidium iodide for the gain of some information about cell cycle. By agarose gel electrophoresis, DNA fragmentation of these cells except amnion epithelial and SKG-3a cells was detected, depending on concentration of Act. D. Using flow cytometric analysis, these cells were separated into four groups according to the information about cell cycle. Group 1 included amnion epithelial and SKG-3a cells, which were TUNEL negative. In group 2, all cell populations at G0/G1 and G2/M phases of HCC, KATO-III and SK-OV-3 were TUNEL staining positive. A portion of each G0/G1 or G2/M phase cell of Lu-134-AH and COLO 201 in group 3 was TUNEL stain positive. In group 4, G2/M phase cells of smooth chorion trophoblast cells and HE-21 were mostly stained and a small population of G0/G1 phase cells were also TUNEL stain positive. These results show that the stages of the cell cycle at which apoptosis was arisen by Act. D stimulation were significantly different depending on the cells types.

Amnion↗
PubMed2000

Genomic organization of the human chondromodulin-1 gene containing a promoter region that confers the expression of reporter gene in chondrogenic ATDC5 cells.

Chondromodulin-1 (ChM-1) is a cartilage-specific glycoprotein that stimulates the growth of chondrocytes and inhibits the tube formation of endothelial cells. To clarify the tissue-specific expression and the role of ChM-1 in pathophysiological conditions, we analyzed the structure of the human ChM-1 gene and its promoter. On the screening of a human genomic cosmid library using the human ChM-1 complimentary DNA (cDNA) as a probe, two clones were obtained that contained ChM-1 cDNA. The restriction enzyme map and nucleotide sequence revealed the human ChM-1 gene consisting of seven exons and exon-intron boundaries. The human ChM-1 gene was assigned to chromosome 13q14-21 by fluorescence in situ hybridization (FISH) using the clone as a probe. A primer extension analysis using total RNA extracted from human cartilage revealed a major transcription start site with the sequence CGCT+1GG. The region approximately 3-kilobase (kb) nucleotides upstream of the translation start site was then sequenced and analyzed in terms of promoter activity. We found that a region 446 base pairs (bp) upstream of the start site had promoter activity in COS7, HeLa, and ATDC5 cells. In structure the promoter is a TATA-less type without a GC-rich region. The transcription factors Sox9, Og12, and Cart-1 did not affect the promoter activity. The transcription factor Ying-Yang1 suppressed the promoter activity but GABP protein did not change the promoter activity. The construct containing -446/+87 fused to the SV40 enhancer and green fluorescent protein (GFP) exhibited expression of GFP corresponding to the differentiation of ATDC5 cells to mature chondrocytes. These results suggest that the element -446/+87 confers the cartilage-specific expression of this gene by some factor(s) other than Sox9, Og12, and Cart-1.

Animals↗
PubMed2000

Induction of a 55-kDa PKN cleavage product by ischemia/reperfusion model in the rat retina.

PURPOSE: To investigate the physiological role of a protein kinase, PKN, and its relation to apoptosis in vivo. METHODS: An ischemia/reperfusion model of the rat retina was created by elevating the intraocular pressure. Retinal samples were obtained after ischemic insult (15-45 minutes) followed by reperfusion (1-7 days). The effect of ischemia on the fragmentation of PKN was examined by immunoblotting and immunocytochemical procedures using the antibody against PKN. N-methyl-D-aspartate (NMDA) or a caspase-3 inhibitor (DEVD-CHO) was administered intravitreally to investigate its effect on the induction of PKN fragmentation. The retinal cell loss in each sample was evaluated by toluidine blue staining. RESULTS: Ischemia induced a 55-kDa PKN cleavage fragment corresponding to the molecular size of the constitutively active fragment of PKN. The appearance of the cleavage fragment depended on the duration of reperfusion and correlated with the occurrence of retinal cell loss. Immunocytochemical analysis revealed that ischemia increased PKN immunoreactivity in the inner layers of the retina. DEVD-CHO significantly inhibited the appearance of the 55-kDa fragment and protected against retinal cell loss. The administration of NMDA also induced cleavage of PKN. CONCLUSIONS: PKN is specifically cleaved by caspase-3 or a related protease during apoptosis in vivo, and PKN cleavage is at least partially initiated by activation of the NMDA receptor.

Animals↗
PubMed2000

[A survey on drug-related service by homehelper in the Japanese home care system].

The purposes of this study are a) to determine whether homehelpers attend to drug-related service of elder care-recipients at home and b) to determine what cooperating human resources were utilized. A structured questionnaire survey was conducted in 1997 with 403 homehelpers who provided in home care to dependent elderly person. Of the total, 19% subjects did deal with care recipients' medication. Regarding the type of service, the highest proportion of subjects had assisted by picking up medicine from pharmacy and talking it to the care recipients' home. Results showed that physicians and home visiting nurses were the most depended upon human resources in the home health care system among health, medical and welfare facilities. Results also suggested that many homehelpers are not aware that pharmacists are readily available resources for providing home health care. Hence we conclude that the respondents tend to rely on physicians or home visiting nurses to respond to care recipients care, and pharmacists should be made aware of the necessity of providing the appropriate drug-related information to physicians or home visiting nurses.

Adult↗
PubMed2000

A case of subarachnoid hemorrhage presenting with temporary blindness disclosed by Xe CT-CBF study.

A 69-year-old male with right oculomotor palsy caused by non-ruptured right internal carotid-posterior communicating artery aneurysm suddenly became blind after cerebral angiography. He lost consensual response of left eye, in spite of no preretinal hemorrhage. Xenon computed tomography(Xe-CT) showed moderate cerebral blood flow(CBF) decrease of bilateral posterior cerebral artery territories at the values of 26.9 ml/100 g/min(left) and 28.3 ml/100 g/min(right), which were about 30% under our control value. However, MR T2-weighted imaging demonstrated no cerebral infarction. Two weeks later, regional CBF values were improved and 6 months later his visual acuity were almost cured. We conclude that Xe-CT CBF study supports the hypothesis of the temporary blindness due to the optic chiasm and nerves injuries by subarachnoid hemorrhage.

Aged↗
PubMed2000

[Coil embolization for incidental aneurysms in patients with chronic renal failure: midterm clinical results of two cases].

In spite of recent advances in perioperative management, the risk of neurosurgical intervention for patients with chronic renal failure is still considered too high. In this study, coil embolization for incidental aneurysms in such patients is demonstrated in reference to midterm results. A 42-year-old woman with a history of hemodialisis for 7 years presented with subcortical hemorrhage in her right frontal lobe. The magnetic resonance angiography (MRA) demonstrated a distal anterior cerebral artery aneurysm, but it was considered to be unrelated to the hemorrhage. Two and a half months after the hemorrhage the aneurysm was embolized with interlocking detachable coils. Thirty months after embolization, the angiogram revealed the coil compaction and the recanalization of the aneurysm neck. However, 54 months after embolization, the figure of the embolized aneurysm and neck remnant was the same as the previous findings. A 69-year-old woman with a history of hemodialisis for 5 years suddenly experienced left hemiparesis. Computed tomography revealed cerebral infarction in the right frontoparietal white matter. In addition, a left middle cerebral artery aneurysm was unexpectedly found on the MRA. Five months after the onset of the attack, the aneurysm was embolized with a Guglielmi detachable coli. An angiogram obtained 24 months after the embolization showed the aneurysm to be almost completely obliterated. In considering the therapeutic risks and benefits for incidental aneurysms of patients with chronic renal failure, intra-vascular surgery could be recommended as a less invasive treatment.

Adult↗
PubMed2000

Immunohistochemical analysis of beta-catenin in N-ethyl-N-nitrosourea-induced rat gliomas: implications in regulation of angiogenesis.

Angiogenesis plays an important role in the development of malignant brain tumors. We postulated the involvement of beta-catenin, which is associated with not only cell adhesion but also tumorigenesis in some neoplasms, in angiogenesis in brain tumors. We performed an immunohistochemical analysis of beta-catenin for vascular cells (VC) in 45 N-ethyl-N-nitrosourea (ENU)-induced rat gliomas and rat normal brain tissues. As a result, beta-catenin was found concentrated in the vascular cell-cell junction and internal surface of the vascular lumen in all normal brains. In contrast, proliferating VC in tumors were stained homogeneously in the cytoplasms of 35 cases (77.8%), among which nuclear staining was also recognized in 12 cases (26.7%). The proliferative potential of VC, which was evaluated by nucleolar organizer region-associated argyrophilic protein (AgNOR), was higher in all types of tumors than in normal brains, and was basically in parallel with the degree of malignancy of the tumors. Thus, it was suggested that the tumor vessels proliferate under a relationship with the proliferative potential of the tumors, and the intracellular localization of beta-catenin is changed under the influence of proliferative potentials of VC. beta-catenin in normal VC is considered to maintain the polarity of the vascular structure, and thus aberrant localization of beta-catenin may result in the loss of structural polarity of the tumor vessels.

Animals↗
PubMed2000

Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects.

Apolipoprotein L is a newly recognized component of human plasma lipoproteins. Mainly associated with apoA-I-containing lipoproteins, it is a marker of distinct HDL subpopulations. In an effort to gain inference as to its as yet unknown function, we studied biological determinants of apoL levels in human plasma. The distribution of apoL in normal subjects is asymmetric, with marked skewing toward higher values. No difference was found in apoL concentrations between males and females, but we observed an elevation of apoL in primary hypercholesterolemia (10.1 vs. 8.5 microgram/mL in control), in endogenous hypertriglyceridemia (13.8 microgram/mL, P < 0.001), combined hyperlipidemia phenotype (18.7 g/mL, P < 0.0001), and in patients with type II diabetes (16.2 microgram/mL, P < 0.02) who were hyperlipidemic. Significant positive correlations were observed between apoL and the log of plasma triglycerides in normolipidemia (0.446, P < 0.0001), endogenous hypertriglyceridemia (0.435, P < 0.01), primary hypercholesterolemia (0.66, P < 0.02), combined hyperlipidemia (0.396, P < 0.04), hypo-alphalipoproteinemia (0.701, P < 0.005), and type II diabetes with hyperlipidemia (0.602, P < 0. 01). Apolipoprotein L levels were also correlated with total cholesterol in normolipidemia (0.257, P < 0.004), endogenous hypertriglyceridemia (0.446, P = 0.001), and non-insulin-dependent diabetes mellitus (NIDDM) (0.548, P < 0.02). No significant correlation was found between apoL and body mass index, age, sex, HDL-cholesterol or fasting glucose and glycohemoglobin levels. ApoL levels in plasma of patients with primary cholesteryl ester transfer protein deficiency significantly increased (7.1 +/- 0.5 vs. 5.47 +/- 0.27, P < 0.006).

Adult↗
PubMed2000

Sensible human projects: haptic modeling and surgical simulation based on measurements of practical patients with MR elastography--measurement of elastic modulus.

To provide realistic surgical simulation, 3D visualization and haptic feedback are important. In the existing surgical simulators, the fidelity of the deformation and haptic feedback is limited because they are based on the subjective evaluation of the expert-user and not on an objective model-based evaluation. To obtain accurate elastic modulus of whole human tissues, we have started a new project called the Sensible Human Project (SHP). This paper deals with establishing the measurement of elastic modulus by the magnetic resonance elastography (MRE) technique, as a first step of the SHP Project.

Computer Simulation↗
PubMed2000

[A case of Klebsiella pneumoniae infection causing a buccal abscess complicated with multiple lung abscesses].

A 51 year-old man fitted with a dental prosthesis was hospitalized with buccal swelling, fever and chest pain. Laboratory data showed marked inflammatory changes, and chest radiography and CT scanning revealed small nodular shadows within the lung. A diagnosis of multiple lung abscesses secondary to a buccal abscess possibly caused by the prosthesis was made from needle aspiration biopsies of the lung nodules and of a buccal lesion. Klebsiella pneumoniae was isolated from these lesions and from a blood culture. The patient was successfully treated with antibiotics and by surgical drainage of the buccal abscess. It is important to note that the patient was immunodeficient at the time as a result of diabetes and alcohol intoxication.

Abscess↗
PubMed2000

[Combined endovascular stent implantation and coil embolization for the treatment of a vertebro-basilar fusiform aneurysm: technical case report].

We describe a case of the combined application of endovascular stent implantation and Guglielmi detachable coil packing for the treatment of a vertebro-basilar fusiform aneurysm and review the literature on stent placement to treat cerebral aneurysms. A 70-year-old female presented with an acute headache from subarachnoid hemorrhage. A fusiform aneurysm with a broad-based neck and dome, measuring 15 mm, involving the union of the vertebral arteries and the proximal basilar artery was demonstrated on cerebral angiography. The aneurysm was judged to be inoperable and treated conservatively. Twelve days later the patient was transferred to our hospital for endovascular therapy. An intravascular stent (MultiLink) was placed across the base of the aneurysm through the right vertebral artery. After this, coil placement in the aneurysm around the stent was performed via a microcatheter guided from the left vertebral artery. After that a microcatheter was guided from the right vertebral artery through the interstices of the stent into the aneurysm, and additional coils were placed. Final angiography showed subtotal occlusion of the aneurysm and excellent blood flow of the parent artery through the stent. There were no new neurological deficits. Neither rerupture nor ischemic event has occurred. The use of stents provides another treatment for managing the difficult entity of intracranial aneurysms.

Acute Disease↗
PubMed2000

[Stress fracture].

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Arthritis, Rheumatoid↗
PubMed2000

[A case of high-age minimal change nephrotic syndrome relapse after 18-year remission and effective treatment with steroid and cyclosporin combined therapy].

We describe the clinical course of a 69-year-old woman, who suffered from minimal change nephrotic syndrome(MCNS) after long-term remission. In 1979, she was admitted to Kanazawa University Hospital due to MCNS verified by renal biopsy and was treated with oral prednisolone(initially 40 mg/day) for two years. She suffered from edema again in 1999 with massive proteinuria. Renal biopsy revealed minor glomerular abnormality without any deposition of immunoglobulins or complements. Electron microscopic findings showed extensive foot process effacement. Therefore, we diagnosed this case as a recurrence of MCNS. She was treated with the combination of methylprednisolone pulse therapy(500 mg, 3 days), oral prednisolone(20 mg/day) and cyclosporin(CyA, 3 mg/kg/day), which could induce earlier complete remission. These results suggest that recurrence after long-term remission could occur in adult-onset MCNS and that the combination therapy of prednisolone and CyA may be effective for the induction of early remission in MCNS.

Administration, Oral↗