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A Shimada

Publications and source records attributed to A Shimada.

At least 19 recordsLinked to original sources
PubMed2006

Sensory system-predominant distribution of leukotriene A4 hydrolase and its colocalization with calretinin in the mouse nervous system.

Leukotriene B4 is a potent lipid mediator, which has been identified as a potent proinflammatory and immunomodulatory compound. Although there has been robust evidence indicating that leukotriene B4 is synthesized in the normal brain, detailed distribution and its functions in the nervous system have been unclear. To obtain insight into the possible neural function of leukotriene B4, we examined the immunohistochemical distribution of leukotriene A4 hydrolase, an enzyme catalyzing the final and committed step in leukotriene B4 biosynthesis, in the mouse nervous system. Immunoreactivity for leukotriene A4 hydrolase showed widespread distribution with preference to the sensory-associated structures; i.e. neurons in the olfactory epithelium and vomeronasal organ, olfactory glomeruli, possibly amacrine cells, neurons in the ganglion cell layer and three bands in the inner plexiform layer of the retina, axons in the optic nerve and tract up to the superior colliculus, inner and outer hair cells and the spiral ganglion cells in the cochlea, vestibulocochlear nerve bundle, spinal trigeminal tract, and lamina II of the spinal cord. Double immunofluorescence staining demonstrated that most of the leukotriene A4-hydrolase-immunopositive neurons coexpressed calretinin, a calcium-binding protein in neurons. The ubiquitous distribution of leukotriene A4 hydrolase was in sharp contrast with the distribution of leukotriene C4 synthase [Shimada A, Satoh M, Chiba Y, Saitoh Y, Kawamura N, Keino H, Hosokawa M, Shimizu T (2005) Highly selective localization of leukotriene C4 synthase in hypothalamic and extrahypothalamic vasopressin systems of mouse brain. Neuroscience 131:683-689] which was confined to the hypothalamic and extrahypothalamic vasopressinergic neurons. These results suggest that leukotriene B4 may exert some neuromodulatory function mainly in the sensory nervous system, in concert with calretinin.

Animals↗
PubMed2006

Stress-relaxation and microscopic dynamics of rabbit periodontal ligament.

The aim of the present study was to examine the structural basis for the stress-relaxation behaviour of the periodontal ligament (PDL). Seventeen 4-month-old rabbits were used. A tooth-PDL-bone segment was cut in a rectangular prism from the incisor of a dissected mandible. The specimen was mounted in a testing machine built on a video stereomicroscope. Following preconditioning, each specimen was stretched to a deformation of 35 microm and then the deformation was kept constant for 300 s to obtain a stress-relaxation curve. Thereafter, stress-relaxation tests were repeated sequentially at deformations of 55, 75, and 95 microm. Polarised-light video-stereomicroscopic images of the specimens were simultaneously recorded and analysed with the stress-relaxation curves. The image analysis revealed that during stress-relaxation, the brightness of the birefringent fibres tended to initially increase rapidly and then do so gradually. There were negative correlations between the brightness and relaxation modulus at the four deformations. The decreases of normalised relaxation modulus for 300 s were less at greater deformation levels. The stress-relaxation process was well described by a function with three exponential decay terms and a constant. These findings suggest that during stress-relaxation of the PDL, the alignment of the collagen molecules and fibrils within the stretched fibres may occur, which could be driven by the strain energy imparted to the specimen on initial stretching.

Animals↗
PubMed2006

The expressions of insulin-like growth factors, their receptors, and binding proteins are related to the mechanism regulating masseter muscle mass in the rat.

OBJECTIVE: The mechanism regulating skeletal muscle mass is unclear. The purpose of the present study was to investigate the extent to which insulin-like growth factors (IGFs), their receptors (IGFRs), and binding proteins (IGFBPs) are involved in the regulation of skeletal muscle mass. DESIGN: We measured the mRNA expression levels for IGFs, IGFRs, and IGFBPs in the rat masseter muscle hypertrophied by oral administration of clenbuterol for 3 weeks and determined the correlations between the weight of masseter muscle and the mRNA expression levels. RESULTS: The mRNA expression levels for IGF-I and II, IGFR1 and 2, and IGFBP4 and 6 showed clenbuterol-induced elevations and positive correlations with the weight of masseter muscle. That for IGFBP3 only exhibited a clenbuterol-induced decrease and a strong negative correlation with the weight of masseter muscle. The mRNA expression levels for IGFBP2 and 5 showed no significant changes between the control and clenbuterol groups, and no significant correlations. IGFBP1 mRNA was not detectable. CONCLUSION: These results suggest that IGF-I, II, IGFR1 and 2, and IGFBP3, 4 and 6 are related to the mechanism regulating masseter muscle mass in the rat.

Adrenergic beta-Agonists↗
PubMed2006

Apical vulnerability to dendritic retraction in prefrontal neurones of ageing SAMP10 mouse: a model of cerebral degeneration.

The SAMP10 mouse is a model of accelerated ageing in which senescence is characterized by age-related atrophy of the cerebral cortex and limbic structures, poor learning and memory task performance with depressive behaviour and cholinergic and dopaminergic alterations. Here we studied age-related changes in the dendritic arbors and spine density of pyramidal cells in the medial prefrontal cortex of SAMP10 mice using a quantitative Golgi method. Dendrites of prefrontal neurones gradually retracted with ageing towards the soma with the relative preservation of overall complexity. Apical dendrites were much more severely affected than basal dendrites. The combined length of the apical dendrites and spine density were decreased by 45% and 55%, respectively, in mice at 12 months, compared with mice at 3 months of age. Immunohistochemical and immunoblot analyses indicated that expression of microtubule-associated protein (MAP) 2, a marker of dendrites, decreased in an age-related manner not only in the anterior cortex but also in the posterior cortex and olfactory structures in SAMP10 mice. Decreased expression of MAP2 mRNA caused the decrease in MAP2 protein expression. These results suggest that retraction of apical, but not of basal dendrites, with a loss of spines in prefrontal neurones, appears to be responsible for poor learning and memory performance in aged SAMP10 mice. It is also suggested that age-related dendritic retraction occurs in a wide area including the entire cerebral cortex and olfactory structures.

Aging↗
PubMed2005

Clinical and immunogenetic characteristics of fulminant type 1 diabetes associated with pregnancy.

OBJECTIVE: The objective of this study was to characterize the clinical and immunogenetic features of Japanese pregnancy-associated fulminant type 1 diabetes (PF). A group of patients with PF was compared with a group of patients of child-bearing age with fulminant type 1 diabetes that was not associated with pregnancy (NPF) in a nationwide survey conducted from 2000-2004. PATIENTS: The clinical characteristics of the 22 patients in the PF group were compared with those of the 48 patients in the NPF group. Human leukocyte antigen (HLA) class II DR and DQ genotyping of 17 PF and 20 NPF patients was performed. RESULTS: Arterial pH was significantly lower (P = 0.0366), and amylase values tended to increase in PF patients compared with NPF patients (P = 0.0515). In 22 PF patients, 18 developed disease during pregnancy (26.3 wk; range, 7-38), whereas four cases occurred immediately after delivery (10.5 d; range, 7-14 d). Twelve cases that developed during pregnancy resulted in stillbirth (67%), and five of the six fetal cases that survived were delivered by cesarean section. The haplotype frequency of HLA DRB1*0901-DQB1*0303 in PF was significantly higher than those in NPF (P = 0.0244) and controls (P = 0.0001), whereas that of DRB1*0405-DQB1*0401 in NPF was significantly higher than those in PF (P = 0.0162) and controls (P < 0.0001). CONCLUSIONS: The clinical symptoms of PF patients were more severe than those of NPF patients, and the prognosis of their fetuses was extremely poor. The type 1 diabetes-susceptible HLA class II haplotype is distinct in PF and NPF patients, suggesting that different HLA haplotypes underlie the presentation of PF or NPF.

Adolescent↗
PubMed2005

Localization and role of metallothioneins in the olfactory pathway after exposure to mercury vapor.

We have investigated the localization and physiological roles of metallothioneins (MTs) in the olfactory pathway after exposure to mercury (Hg0) vapor. Male MT-null and wild-type mice were examined for the distribution of mercury, MT immunoreactivity and MT-III mRNA expression. There were no signs of histological changes in MT-null or wild-type mice. Light and electron microscopy of the samples stained with autometallography demonstrated chronological transfer of exposed mercury granules to the olfactory bulb by way of the olfactory tract. Basal expression of MT-I and -II immunoreactivity was observed in supporting cells, basal cells and acinar cells of the Bowman's gland of the olfactory mucosa in wild-type mice even without mercury exposure. In situ hybridization showed that signals for MT-III mRNA dominated in the olfactory cells of the olfactory mucosa, neurons in the olfactory bulb and those of brain in MT-null and wild-type mice. No difference in these findings was observed between samples taken at any interval after mercury exposure.

Animals↗
PubMed2005

Protective role for cytosolic phospholipase A2alpha in autoimmune diabetes of mice.

Cytosolic phospholipase A(2)alpha (cPLA(2)alpha) plays an important role in arachidonate pathway. To investigate the contribution of cPLA(2)alpha to autoimmune diabetes, we established non-obese diabetic (NOD) mouse, an excellent model for human type 1 diabetes, deficient in cPLA(2)alpha. These mice showed severe insulitis and a higher incidence of diabetes. In their macrophages, decreased prostaglandin E(2) (PGE(2)) induced by cPLA(2)alpha deficiency, and the increase in production of tumor necrosis factor (TNF)-alpha were observed. These results suggested that cPLA(2)alpha plays a protective role in progression of insulitis and development of autoimmune diabetes by suppression of TNF-alpha production from macrophages.

Animals↗
PubMed2005

Different contribution of class II HLA in fulminant and typical autoimmune type 1 diabetes mellitus.

AIMS/HYPOTHESIS: Fulminant type 1 diabetes, which is characterised by a markedly acute onset of diabetes and an absence of islet-related autoantibodies, accounts for 20% of type 1 diabetes in Japan. We aimed to clarify the contribution of the HLA subtype to fulminant type 1 diabetes in Japanese. METHODS: We determined the serological subtypes of HLA-A, -DR and -DQ in 115 patients with fulminant type 1 diabetes, 98 patients with typical type 1A diabetes and 190 normal control subjects. RESULTS: The frequency of HLA-DR4, but not DR9, was significantly higher in fulminant type 1 diabetes, while those of HLA-DR1, DR2, DR5 and DR8 were significantly lower than those in controls. In contrast, DR9 but not DR4 was more frequent and DR2 was extremely rare in typical type 1A diabetes. Haplotype analysis revealed that DR4-DQ4 was significantly more frequent, and both DR2-DQ1 and DR8-DQ1 were less frequent in fulminant diabetes. In type 1A diabetes, DR2-DQ1 was extremely rare while DR9-DQ3 was significantly more frequent. In the combination analysis, the homozygotes of DR4-DQ4 in fulminant type 1 diabetes and DR9-DQ3 in typical type 1A diabetes indicated high odds ratios (13.3 and 13.3, respectively). CONCLUSIONS/INTERPRETATION: Our results suggest that class II HLA contributes to the development of fulminant type 1 diabetes. Susceptibility and resistance of the HLA subtype to type 1 diabetes are distinct between fulminant and typical autoimmune type 1 diabetes.

Adolescent↗
PubMed2005

Association between hydration volume and symptoms in terminally ill cancer patients with abdominal malignancies.

BACKGROUND: To explore the association between hydration volume and symptoms during the last 3 weeks of life in terminally ill cancer patients. PATIENTS AND METHODS: This was a multicenter, prospective, observational study of 226 consecutive terminally ill patients with abdominal malignancies. Primary responsible physicians and nurses evaluated the severity of membranous dehydration (dehydration score calculated from three physical findings), peripheral edema (edema score calculated from seven physical findings), ascites and pleural effusion (rated as physically undetectable to symptomatic), bronchial secretion, hyperactive delirium (Memorial Delirium Assessment Scale), communication capacity (Communication Capacity Scale), agitation (Agitation Distress Scale), myoclonus and bedsores. RESULTS: Patients were classified into two groups: the hydration group (n=59) who received 1 l or more of artificial hydration per day, 1 and 3 weeks before death, and the non-hydration group (n=167). The percentage of patients with deterioration in dehydration score in the final 3 weeks was significantly higher in the non-hydration group than the hydration group (35% versus 14%; P=0.002), while the percentages of patients whose symptom scores for edema, ascites and pleural effusion increased were significantly higher in the hydration group than the non-hydration group (44% versus 29%, P=0.039; 29% versus 8.4%, P <0.001; 15% versus 5.4%, P=0.016; respectively). After controlling for multiple covariates and treatment settings, the association between hydration group and dehydration/ascites score was statistically significant. Subgroup analysis of patients with peritoneal metastases identified statistically significant interaction between hydration group and dehydration/pleural effusion score. There were no significant differences in the degree of bronchial secretion, hyperactive delirium, communication capacity, agitation, myoclonus or bedsores. CONCLUSIONS: Artificial hydration therapy could alleviate membranous dehydration signs, but could worsen peripheral edema, ascites and pleural effusions. It is suggested that the potential benefits of artificial hydration therapy should be balanced with the risk of worsening fluid retention symptoms. Further clinical studies are strongly needed to identify the effects of artificial hydration therapy on overall patient well-being, and an individualized treatment and close monitoring of dehydration and fluid retention symptoms is strongly recommended.

Abdominal Neoplasms↗
PubMed2005

Immunohistochemical and ultrastructural findings related to the blood--brain barrier in the blood vessels of the cerebral white matter in aged dogs.

Immunohistochemical and ultrastructural analysis of canine brain tissue was performed to determine whether cerebral capillaries, which form the blood--brain barrier (BBB), display age-related morphological changes in the white matter (WM). A slight decrease in laminin immunolabelling was detected in the basement membranes (BMs) of capillaries in the WM of old dogs, as compared with that in the brains of young dogs. The Prussian blue DAB post-DAB enhancement method detected iron present in macrophages and astrocytes in the WM. Copper/zinc superoxide dismutase, MT-I and -II and MT-III immunoreactivity was detected mainly in reactive astrocytes in the WM of aged dogs. Ultrastructurally, collagen-like fibrils were detected to a variable degree in the spaces between the BMs of capillary endothelial cells and astrocytes in the WM of some aged dogs. These results suggest that age-related morphological changes in capillaries of the WM are associated with BBB dysfunction, leading to the exudation of serum constituents, including harmful substances (e.g., iron), thereby causing tissue damage by oxidative injury. These factors may play a role in the pathogenesis of severe degenerative changes in the WM of aged dogs.

Aging↗
PubMed2005

Renal dysplasia with unilateral renal agenesis in a dog.

This report describes a renal dysplastic lesion associated with renal agenesis in a 3-year-old dog with chronic renal failure. Haematological examination revealed non-regenerative anaemia, azotaemia, increased creatinine and hyperphosphataemia. At necropsy, the right kidney and right ureter could not be identified. The left kidney was slightly enlarged, with a reduced cortico-medullary ratio. Histologically, the medulla of the left kidney had persistent mesenchyme and primitive tubules (tall pseudostratified columnar epithelium), dilated collecting ducts lined by flattened epithelium, and adenomatoid proliferation of cuboidal epithelium; fetal or immature glomeruli could not be identified. To our knowledge, this is the first report of a renal dysplastic lesion with unilateral agenesis in animals.

Animals↗
PubMed2005

Highly selective localization of leukotriene C4 synthase in hypothalamic and extrahypothalamic vasopressin systems of mouse brain.

While leukotriene C4 (LTC4) was originally identified as a potent bronchoconstrictor, the compound has versatile biological activities besides inflammatory reactions. Although the high content of LTC4 has been reported in the hypothalamus and median eminence, the precise localization of the compound remained obscure. To elucidate its possible functions in the neuroendocrine systems, we determined immunohistochemical localization of LTC4 synthase, a key enzyme to produce LTC4 using mouse brains. Light microscopy and confocal laser scanning microscopy showed that LTC4 synthase was selectively localized in the vasopressinergic magnocellular neurons of the hypothalamic paraventricular, supraoptic and suprachiasmatic nuclei and in the retrochiasmatic area, as well as in axons that emanated from these neurons to the pars nervosa of the pituitary gland. At subcellular level, however, LTC4 synthase and arginine vasopressin appeared to localize differently within individual neurons. LTC4 synthase immunoreactivity was also observed in the axons of the extrahypothalamic system including the bed nucleus of the stria terminalis, lateral habenular nucleus, midbrain central gray, medial amygdaloid nucleus and ventral septal area, although this immunoreactivity was relatively minor. The other brain regions did not contain LTC4 synthase immunoreactivity. The distribution of LTC4 synthase did not overlap with that of either oxytocin or luteinizing hormone releasing hormone. Therefore, LTC4 is considered to be involved in neural functions of the brain magnocellular vasopressinergic system such as water retention. LTC4 may also be involved in extrahypothalamic vasopressinergic neural functions including the regulation of learning and memory, social recognition memory, sexual and aggressive behavior, etc.

Animals↗
PubMed2005

The cytoplasmic expression of E-cadherin and beta-catenin in bovine trophoblasts during binucleate cell differentiation.

Binucleate cells are endocrine cells generated by the acytokinesis and endoreduplication of the trophectoderm in the ruminant placenta. These cells are migratory and secrete hormones into the maternal circulation after fusing with uterine epithelial cells. In this study, we performed immunohistochemistry for E-cadherin and beta-catenin in bovine placenta and a bovine trophoblast cell line (BT-1). We found that E-cadherin and beta-catenin were distributed not only at the cell to cell boundary but throughout the cytoplasm in binucleate cells, although they were concentrated at the cell to cell boundary in epithelial cells in bovine placenta. Moreover, beta-catenin was detected in the nuclei of binucleate cells. Binucleate cells after fusion with uterine epithelial cells (feto-maternal hybrid cells) in the maternal side showed no intracellular expression of E-cadherin and beta-catenin. The transformation into binucleate cells in the BT-1 cell line was also accompanied by the cytoplasmic accumulation of E-cadherin and beta-catenin. We further demonstrated that levels of cytoplasmic beta-catenin were well correlated with the DNA content of binucleate cells in BT-1. The dynamic changes in the distribution of E-cadherin and beta-catenin suggest an important role in binucleate cells, including the rearrangement of cadherin-mediated cell adhesions during cell migration and the onset of endoreduplication probably via the nuclear transfer of beta-catenin.

Actins↗
PubMed2005

Toxicological screening for the effects of short-term exposure of sidestream cigarette smoke on angiogenesis.

Angiogenesis is a fundamental process that ensures adequate metabolic supply to tissues in numerous biological and pathological states, including tumorigenesis. Cigarette smoking causes numerous adverse effects, some of which are associated with disruption of the normal process of angiogenesis. It is believed that sidestream cigarette smoke severely affects different components that help in the normal process of angiogenesis. Sidestream cigarette smoke is composed primarily of smoke that emanates from the burning end of a cigarette, and contaminants that diffuse through the cigarette paper. The aim of the current study was to ascertain the toxicological effects of different sidestream cigarette smoke solutions (SSCSS) on angiogenesis by using chicken chorioallantoic membrane (CAM) assay. Decrease in total vascular area, diameter of secondary and tertiary blood vessels, cell proliferation, migration of blood vessels toward ectoderm, and number of capillary plexuses formation was observed by application of SSCSS. Scanning microscopy also revealed deviation in pattern formed by the major capillary plexuses and the fibrillar elements of the mesoderm SSCSS in treated CAMs. It is concluded that SSCSS may hinder the normal process of angiogenesis resulting in abnormal blood supply to tissues and decreased repair and remodeling, which are common problems among smoke-exposed individuals. Further study is required to delineate the effects of different chemicals in SSCSS on angiogenesis.

Animals↗
PubMed2004

N-acetyl-cysteine accelerates transfer of diabetes into non-obese diabetic scid mice.

AIMS/HYPOTHESIS: Type 1 diabetes mellitus is caused by autoimmune pancreatic beta cell destruction, and the destructive process involves several molecular mechanisms including oxygen-reactive species. A cysteine derivative, N-acetyl-cysteine, is widely used as an antioxidant, but the role of N-acetyl-cysteine in the protection of pancreatic beta cells in type 1 diabetes remains unclear. The aim of this study was to clarify the effect of N-acetyl-cysteine on beta cells using an adoptive transfer system in a murine model of type 1 diabetes. METHODS: Splenocytes from diabetic female non-obese diabetic mice were transferred into female non-obese diabetic scid/ scid recipients to induce diabetes. Just after transfer, N-acetyl-cysteine was administered to non-obese diabetic scid recipients. Two weeks after transfer, the pancreas of the recipients was examined histologically, and cytokine mRNA expression in the pancreas was analysed. In vitro, CD4-positive splenocytes from diabetic donor mice were stimulated with anti-CD3 and anti-CD28 antibodies with or without N-acetyl-cysteine. RESULTS: Treatment with N-acetyl-cysteine significantly accelerated the transfer of diabetes into non-obese diabetic scid recipients. Treatment with N-acetyl-cysteine accelerated the infiltration of mononuclear cells accompanied by CD8-positive cells into the intra-islet region of the recipient's pancreas, and enhanced interferon-gamma mRNA expression in the pancreas. In vitro, treatment with N-acetyl-cysteine enhanced interferon-gamma and interleukin-2 production by CD4-positive splenocytes of the diabetic donor mice. CONCLUSIONS/INTERPRETATION: N-acetyl-cysteine accelerates the transfer of diabetes into non-obese diabetic scid mice and this effect is accompanied by the promotion of local infiltration and T-helper cell type 1 responses.

Acetylcysteine↗