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Biomedical subjects

M Yoneda

Publications and source records attributed to M Yoneda.

At least 37 records · Page 2Linked to original sources
PubMed2003

Spontaneous dissecting aneurysm of middle cerebral artery: a case report with review of the literature.

We report a case of a dissecting aneurysm of the middle cerebral artery (MCA) and its treatment strategies. A 50-year-old male patient presented with occipital and neck pain for 2 days. CT scan revealed subarachnoid hemorrhage (SAH) in the region of the right sylvian fissure. A left carotid angiogram showed a dissecting aneurysm of the left MCA (M1). He was treated surgically by a pterional trans-sylvian approach. Clipping was done along with additional reinforcement by wrapping to completely obliterate the neck of the aneurysm. On reviewing the literature, we think that dissecting aneurysms seem to be one of the important causes of SAH and cerebral infarction of unverified origin. If an MCA dissecting aneurysm is identified, especially located in the proximal portion, surgical treatment must be considered. These patients merit a close follow-up.

Adult↗
PubMed2003

Metabolic fate of pitavastatin, a new inhibitor of HMG-CoA reductase: human UDP-glucuronosyltransferase enzymes involved in lactonization.

1. Pitavastatin is a potent competitive inhibitor of HMG-CoA reductase little metabolized in hepatic microsomes. Pitavastatin lactone, which can be converted back to the unchanged form, is the major metabolite of pitavastatin in humans. To clarify the mechanism of the lactonization of pitavastatin and the metabolic properties of the lactone, we performed experiments in vitro. 2. On addition of UDP-glucuronic acid, human hepatic microsomes produced pitavastatin lactone and an unknown metabolite (UM-2). UM-2 was converted to its unchanged form by enzymatic hydrolysis and to a lactone form non-enzymatically. Using several human UGT-expressing microsomes, UGT1A3 and UGT2B7 were principally responsible for glucuronidation of pitavastatin leading to lactonization. 3. No marked difference in intrinsic clearance between pitavastatin and its lactone form was detected in human hepatic microsomes. 4. Pitavastatin lactone showed no inhibitory effects on CYP2C9- and CYP3A4-mediated metabolism of model substrates in contrast to other HMG-CoA reductase inhibitors. 5. The mechanism of pitavastatin lactone formation has been clarified, in that glucuronidation by UGT occurs first followed by lactonization via an elimination reaction. It was also found that pitavastatin lactone demonstrates no drug-drug interactions.

Biotransformation↗
PubMed2002

Late infantile Hirschsprung disease-mental retardation syndrome with a 3-bp deletion in ZFHX1B.

A 48-year-old woman with late infantile onset mental retardation developed megacolon. Although the patient had no typical clinical features of Hirschsprung disease-mental retardation syndrome, a new 3-base pair deletion, eliminating an Asn, was identified in the responsible gene ZFHX1B. This suggests that screening for ZFHX1B mutations is warranted even in the absence of typical clinical features of the syndrome.

Cloning, Molecular↗
PubMed2002

Human autologous culture expanded bone marrow mesenchymal cell transplantation for repair of cartilage defects in osteoarthritic knees.

OBJECTIVE: There is no widely accepted method to repair articular cartilage defects. Bone marrow mesenchymal cells have the potential to differentiate into bone, cartilage, fat and muscle. Bone marrow mesenchymal cell transplantation is easy to use clinically because cells can be easily obtained and can be multiplied without losing their capacity of differentiation. The objective of this study was to apply these cell transplantations to repair human articular cartilage defects in osteoarthritic knee joints. DESIGN: Twenty-four knees of 24 patients with knee osteoarthritis (OA) who underwent a high tibial osteotomy comprised the study group. Adherent cells in bone marrow aspirates were culture expanded, embedded in collagen gel, transplanted into the articular cartilage defect in the medial femoral condyle and covered with autologous periosteum at the time of 12 high tibial osteotomies. The other 12 subjects served as cell-free controls. RESULTS: In the cell-transplanted group, as early as 6.3 weeks after transplantation the defects were covered with white to pink soft tissue, in which metachromasia was partially observed. Forty-two weeks after transplantation, the defects were covered with white soft tissue, in which metachromasia was observed in almost all areas of the sampled tissue and hyaline cartilage-like tissue was partially observed. Although the clinical improvement was not significantly different, the arthroscopic and histological grading score was better in the cell-transplanted group than in the cell-free control group. CONCLUSIONS: This procedure highlights the availability of autologous culture expanded bone marrow mesenchymal cell transplantation for the repair of articular cartilage defects in humans.

Aged↗
PubMed2002

Rinderpest virus H protein: role in determining host range in rabbits.

A major molecular determinant of virus host-range is thought to be the viral protein required for cell attachment. We used a recombinant strain of Rinderpest virus (RPV) to examine the role of this protein in determining the ability of RPV to replicate in rabbits. The recombinant was based on the RBOK vaccine strain, which is avirulent in rabbits, carrying the haemagglutinin (H) protein gene from the lapinized RPV (RPV-L) strain, which is pathogenic in rabbits. The recombinant virus (rRPV-lapH) was rescued from a cDNA of the RBOK strain in which the H gene was replaced with that from the RPV-L strain. The recombinant grew at a rate equivalent to the RPV-RBOK parental virus in B95a cells but at a lower rate than RPV-L. The H gene swap did not affect the ability of the RBOK virus to act as a vaccine to protect cattle against virulent RPV challenge. Rabbits inoculated with RPV-L became feverish, showed a decrease in body weight gain and leukopenia. High virus titres and histopathological lesions in the lymphoid tissues were also observed. Clinical signs of infection were never observed in rabbits inoculated with either RPV-RBOK or with rRPV-lapH; however, unlike RPV-RBOK, both RPV-L and rRPV-lapH induced a marked antibody response in rabbits. Therefore, the H protein plays an important role in allowing infection to occur in rabbits but other viral proteins are clearly required for full RPV pathogenicity to be manifest in this species.

Animals↗
PubMed2001

The role of cellular migration in the repair process of gastric epithelial cells.

The epithelial cells of stomach are continuously exposed to various toxic agents that may cause mucosal injury. The epithelial lining is rapidly replaced by cells that migrate from the proliferative zone of the gastric gland, to maintain the integrity of the gastric mucosa. Thus, cell migration is an essential part of the early process of gastric mucosal repair. After various forms of gastric injury, mucosal integrity is reestablished by the rapid migration of epithelial cells. However, the cellular mechanisms of the restitution remain unclear to date. In this report, we will review the role of cellular migration in the repair process of gastric epithelial cells in culture. It has been reported that hepatocyte growth factor (HGF) has the potency of acceleration of cellular repair process. In this review, we also report that HGF plays a leading role in the mucosal repair after damage by using a novel cell culture model.

Animals↗
PubMed2001

Effect of central urocortin on carbon tetrachloride-induced acute liver injury in rats.

The effect of intracisternal injection of urocortin, an endogenous ligand for corticotropin-releasing factor (CRF) 2 receptor, on carbon tetrachloride (CCl4)-induced acute liver injury was investigated in rats. Intracisternal injection of urocortin dose-dependently enhanced elevation of serum alanine aminotransferase and aspartate aminotransferase levels induced by CCl4. Intracisternal urocortin also aggravated CCl4-induced histological changes of the liver. The aggravating effect of central urocortin on CCl4-induced acute liver injury was abolished by chemical sympathectomy, but not by vagotomy. These data demonstrate that urocortin acts in the brain to exacerbate acute liver injury through the sympathetic nervous system and suggest a possible involvement of the CRF2 receptor in the central CRF-induced exacerbation of acute liver injury in rats.

Acute Disease↗
PubMed2001

The presence of chemokine receptor (CCR5, CXCR3, CCR3)-positive cells and chemokine (MCP1, MIP-1alpha, MIP-1beta, IP-10)-positive cells in human periapical granulomas.

The infiltration of leukocytes into inflammation sites such as observed in human periapical granulomas is considered to be mediated by chemotactic factors. In this study, we examined the presence of chemokine- and chemokine receptor-positive cells in samples obtained from human subjects by means of immunohistochemical methods. Macrophage chemotactic protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1alpha, MIP-1beta and IFN-inducible protein 10 (IP-10)-producing cells were present in periapical granulomas. In addition, chemokine receptor CCR3-, CCR5-, and CXCR3-positive cells were also present. In contrast, no factor expression was observed in clinically healthy periodontal ligament, serving as a negative control. Our findings suggest that these chemokines are responsible for modulating the process of disease, such as human apical periodontitis.

Adolescent↗
PubMed2001

Identification of volatile selenium compounds produced in the hydride generation system from organoselenium compounds.

We report a novel aqueous derivatization of selenomethionine (Semet), selenoethionine (Seet) and trimethylselenonium ion (TmSe) by NaBH4 and HCI to volatile selenium species, namely, diethyldiselenide (DeDSe), dimethyldiselenide (DMDSe), dimethylselenide (DmSe) and ethylhydrogenselenide (ESeH), in the hydride generation (HG) system. The volatile selenium compounds produced in the HG system were on-line trapped and concentrated in a U-tube that was immersed in the liquid nitrogen trap. The trapped volatile Se compounds were volatilized at 80 degrees C in a water bath, and 50-500 microL of volatile gas was injected into the GC/AED and GC/MS, respectively. It has been established that DmSe, DmDSe, and DeDSe are the predominant Se compounds that are produced in the HG system from TmSe, Semet, and Seet, respectively, followed by ESeH from Seet. Analytical methods previously employed have stated that these compounds are inactive in the HG system. Prior decomposition of Semet, Seet, and TmSe to selenous acid is essential before HG. To the best of our knowledge, current findings for the production and identification of volatile selenium compounds in the HG system are new and different from existing reports; hence, direct estimation of Semet, Seet, and TmSe is possible when coupling with a HG system using a suitable Se-specific detector.

Journal Article↗
PubMed2001

Simultaneous determination of taxol and its metabolites in microsomal samples by a simple thin-layer chromatography radioactivity assay--inhibitory effect of NK-104, a new inhibitor of HMG-CoA reductase.

The inhibitory effect of NK-104, a potent inhibitor of HMG-CoA reductase, on taxol metabolism was examined using radio-TLC. This method is described for in vitro measurement of taxol metabolites as an alternative to the commonly used HPLC assay. After incubation of 14C-taxol with human liver microsomes, the supernatants were developed using a solvent system consisting of toluene-acetone-formic acid (60:39:1, v/v) and quantified with a bioimaging analyzer. The described method provides a valuable tool for the simultaneous determination of unchanged taxol and its major metabolites. There was no inhibitory effect of NK-104 on CYP-mediated metabolism of taxol in human liver microsomes.

Antineoplastic Agents, Phytogenic↗
PubMed2001

A significant participation of leukemia inhibitory factor in regulating the reproductive function in rats: a novel action of the pleiotropic cytokine.

Leukemia inhibitory factor (LIF) is a pleiotropic cytokine exhibiting diverse biological activities in various tissues and cell types. Accumulating evidence suggests a crucial role for LIF in regulating the hypothalamo-pituitary-adrenal axis, but information is limited regarding whether the cytokine also exerts a significant influence on other endocrine systems. In this study, we examined a possible involvement of LIF in the generation of ovarian steroid-induced luteinizing hormone (LH) and prolactin (PRL) surges in the rat. Experiments were performed on both normally fed and 3-day-fasted rats, which were ovariectomized and primed with estradiol and progesterone. From 11:00 to 18:00 h, blood was collected every 30 min to measure LH and PRL. All the following substances were given intracerebroventricularly at 11:00 h. Compared to control serum, undiluted and 5-times diluted preparations of anti-rat LIF serum caused a partial but significant suppression of LH surge to a similar extent. The two different concentrations of antibody also delayed the onset of PRL surge to a comparable degree. Fasted rats were devoid of significant surges of the hormones, while 1.0 and 3.0 nmol, but not 0.3 nmol, of recombinant murine LIF given to these animals led to a partial but significant recovery of both LH and PRL surges. This stimulatory potency of LIF on both hormones was already maximal at its 1.0-nmol dose. These results demonstrate for the first time a significant participation of LIF in the generation of LH and PRL surges in the rat. A novel action of the pleiotropic cytokine is reported herein.

Animals↗
PubMed2001

Further evidence for a significant participation of the melanocortin 4 receptor in the preovulatory prolactin surge in the rat.

We previously reported that the melanocortin 4 receptor may play a significant role in mediating the preovulatory surges of luteinizing hormone and prolactin in the rat. In order to confirm this previous finding, in the present study we examined and compared the effects of intracerebroventricular administrations of 1.0 nmol of MT II (a non-selective melanocortin 3 and 4 receptor agonist) and 10 nmol of gamma(1)-melanocyte-stimulating hormone (a selective melanocortin 3 receptor agonist) on luteinizing hormone and prolactin surges in starved, gonadal steroid-primed ovariectomized female rats, which is a model deprived of inherent surges of the two hormones. MT II significantly recovered the surge of prolactin, but not of luteinizing hormone (although a tendency to increase was seen), and gamma(1)-melanocyte-stimulating hormone was without effect on both hormones. This study corroborated our previous report through a different and direct approach that the melanocortin 4 receptor, but not the melanocortin 3 receptor, plays a significant role in mediating the preovulatory prolactin surge in the rat.

Animals↗
PubMed2001

Establishment and characterization of a human B cell line from the lung tissue of a patient with scleroderma; extraordinary high level of IL-6 secretion by stimulated fibroblasts.

Progressive systemic sclerosis is a connective tissue disease of unknown aetiology. This is the first study to demonstrate induction by a human B cell line of IL-6 secretion from fibroblasts. The cell line was established from lesional lung tissue of a patient with progressive systemic sclerosis. These cells, referred to as kon-1 cells, showed characteristics of pro-B cell by flow cytometry. Although kon-1 cells alone secreted a small amount of IL-6, a co-culture of kon-1 cells with normal lung fibroblasts significantly increased IL-6 levels. Whereas IL-6 mRNA was weakly expressed in kon-1 cells alone, it was clearly expressed in cells from the co-culture. Immunocytochemical identification of IL-6 showed localization in the cytoplasm of fibroblasts. IL-6 is a pleiotropic cytokine, essential for B cell differentiation, which has been shown to stimulate the production of collagen and glycosaminoglycan. Thus, abnormally augmented B cell proliferation and the inflammatory response stimulated by these cells may cause the fibrotic changes in patients with progressive systemic sclerosis.

B-Lymphocytes↗
PubMed2001

Defect in SHAP-hyaluronan complex causes severe female infertility. A study by inactivation of the bikunin gene in mice.

Hyaluronan (HA) associates with proteins and proteoglycans to form the extracellular HA-rich matrices that significantly affect cellular behaviors. So far, only the heavy chains of the plasma inter-alpha-trypsin inhibitor (ITI) family, designated as SHAPs (serum-derived hyaluronan-associated proteins), have been shown to bind covalently to HA. The physiological significance of such a unique covalent complex has been unknown but is of great interest, because HA and the ITI family are abundant in tissues and in plasma, respectively, and the SHAP-HA complex is formed wherever HA meets plasma. We abolished the formation of the SHAP-HA complex in mice by targeting the gene of bikunin, the light chain of the ITI family members, which is essential for their biosynthesis. As a consequence, the cumulus oophorus, an investing structure unique to the oocyte of higher mammals, had a defect in forming the extracellular HA-rich matrix during expansion. The ovulated oocytes were completely devoid of matrix and were unfertilized, leading to severe female infertility. Intraperitoneal administration of ITI, accompanied by the formation of the SHAP-HA complex, fully rescued the defects. We conclude that the SHAP-HA complex is a major component of the HA-rich matrix of the cumulus oophorus and is essential for fertilization in vivo.

Alpha-Globulins↗
PubMed2001

Adaptive cytoprotection against acetic acid induced colonic injury in rats.

BACKGROUND AND AIMS: The phenomenon of prostaglandin dependent adaptive cytoprotection has been well established in the stomach and duodenum but not in the colon. This study investigated whether it also occurs in the colon. METHODS: Fisher rats received intracolonic administration (0.5 ml) of saline or acetic acid at low concentrations (0.01-5%) followed by high concentration (25%) at various intervals (10-720 min). The distal colon was removed 2 h after acetic acid (25%), and colonic injury was assessed macroscopically and histologically and scored. Indomethacin (5 mg/kg) or N(G)-nitro-L-arginine methyl ester (10 mg/kg) was injected intraperitoneally 1 h or 30 min before pretreatment with 1% acetic acid. RESULTS: Acetic acid (25%) administered into the colon induced 11.6+/-0.2 macroscopic scores and 10.0+/-0.4 histological scores in saline-pretreated rats, which were reduced to 0.3+/-0.2 and 1.8+/-0.5 by acetic acid (1%) pretreatment, respectively. The protective effect assessed macroscopically and histologically was dose related (0.01-1% acetic acid) and long lasting (maximal at 30 min and lasting up to 6 h). Indomethacin abolished the colonic adaptive cytoprotection while nitric oxide synthase inhibitor had no effect. CONCLUSIONS: These data show that prostaglandin dependent adaptive protection is induced by exposure of the colon to low concentrations of acetic acid, suggesting that endogenous defense mechanisms are increased in the colon by mild irritants.

Acetic Acid↗
PubMed2001

Central regulation of hepatic function by neuropeptides.

In addition to classical neurotransmitters, such as acetylcholine and noradrenaline, neuropeptides have been recognized as new neurotransmitters and neuromodulators. Neuropeptides are widely distributed in the central nervous system as well as in peripheral nerves, and act as neurotransmitters to regulate various physiological functions. The digestive organs are no exception, and several neuropeptides in the central nervous system are shown to act in specific brain sites and control gastrointestinal functions, such as gastric acid secretion, and gastrointestinal motility, through the autonomic nervous system. Recently, a relationship between central neuropeptides and hepatic function through the autonomic nervous system has been revealed in animal models. Thyrotropin-releasing hormone acts in the medulla, in particular in the left dorsal vagal complex, to induce stimulation of hepatic blood flow and hepatic proliferation, and protect against experimental liver injury through vagal and cholinergic pathways. Corticotropin-releasing factor injected intracisternally elicits inhibition of the hepatic blood flow and exacerbates experimental liver injury through sympathetic and noradrenergic pathways. Neuropeptide Y acts in the left dorsal vagal complex, in particular in regard to the Y1 receptor subtype, to stimulate bile secretion. Other neuropeptides such as beta-endorphin and bombesin in the brain modulate hepatic proliferation and bile secretion. Through the use of neuropeptides, new knowledge of the central and peripheral mechanisms underlying brain regulation of hepatic function will be revealed. Further studies in regard to the physiological relevance of the central action of neuropeptides on specific brain sites should be performed to unravel the underlying pathways that mediate brain-liver interaction.

Central Nervous System↗
PubMed2001

Japanese generalised osteoarthritis was associated with HLA class I--a study of HLA-A, B, Cw, DQ, DR in 72 patients.

To investigate the association between generalised osteoarthritis (GOA) and HLA-A, B, Cw, DQ and DR, we typed for HLA in 72 Japanese patients with GOA and compared with those of 1480 normal controls. The antigen frequency of HLA-Cw4 was significantly higher in the GOA group than in the control group. That of B62 was higher, but only uncorrected P values were significant. Those of HLA-Cw1 and Cw10 were significantly lower in the GOA group than in the control group. The antigen frequencies of HLA-DRB1*0101, *0401, *0405, *1001, and *1402, which were reported to be associated with rheumatoid arthritis, in the GOA group were not significantly different from those in the control group. The present study provides evidence of a significant association between Japanese GOA and HLA, which is different from that of Japanese RA. This may suggest that an immunological reaction that is different from RA plays a role in the pathogenesis of GOA.

Aged↗