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On page 1 showing 1 ~ 11 papers out of 11 papers

Increased expression of sialyl Lewis A and sialyl Lewis X in liver metastases of human colorectal carcinoma.

  • N Yamada‎ et al.
  • Invasion & metastasis‎
  • 1995‎

Sialyl Lewis A (SLA) and sialyl Lewis X (SLX) have been shown to be specific ligands for endothelial leukocyte adhesion molecule-1 (ELAM-1), and may be involved in the process of adhesion between cancer cells and endothelium. We used immunohistochemical methods to study the expression of SLA, SLX and CEA in both primary tumors and matched metastatic liver lesions of colorectal carcinomas. Specimens from primary tumors and matched liver metastases from 24 patients with colorectal carcinomas were studied immunohistochemically. The degree of expression of CEA in liver metastases was similar to that in primary tumors, but SLA and SLX were expressed on a larger proportion of tumor cells in liver metastases than in primary tumors. Our findings suggest that colorectal carcinoma cells expressing SLA and/or SLX form metastatic liver tumors. They also suggest that expression of SLA and SLX in primary of colorectal carcinoma can be used as a prognostic indicator of metastasis.


Mass spectrometry proves under-O-glycosylation of glomerular IgA1 in IgA nephropathy.

  • Y Hiki‎ et al.
  • Kidney international‎
  • 2001‎

The IgA1 molecule, which is predominantly deposited in glomeruli in IgA nephropathy (IgAN), is a unique serum glycoprotein because it has O-glycan side chains in its hinge region. Our study was conducted to investigate the O-glycan structure in the glomerular IgA1 in IgAN.


Environmental enrichment brings a beneficial effect on beam walking and enhances the migration of doublecortin-positive cells following striatal lesions in rats.

  • S Urakawa‎ et al.
  • Neuroscience‎
  • 2007‎

Rats raised in an enriched environment (enriched rats) have been reported to show less motor dysfunction following brain lesions, but the neuronal correlates of this improvement have not been well clarified. The present study aimed to elucidate the effect of chemical brain lesions and environmental enrichment on motor function and lesion-induced neurogenesis. Three week-old, recently weaned rats were divided into two groups: one group was raised in an enriched environment and the other group was raised in a standard cage for 5 weeks. Striatal damage was induced at an age of 8 weeks by injection of the neuro-toxins 6-hydroxydopamine (6-OHDA) or quinolinic acid (QA) into the striatum, or by injection of 6-OHDA into the substantia nigra (SN), which depleted nigrostriatal dopaminergic innervation. Enriched rats showed better performance on beam walking compared with those raised in standard conditions, but both groups showed similar forelimb use asymmetry in a cylinder test. The number of bromodeoxyuridine-labeled proliferating cells in the subventricular zone was increased by a severe striatal lesion induced by QA injection 1 week after the lesion, but decreased by injection of 6-OHDA into the SN. Following induction of lesions by striatal injection of 6-OHDA or QA, the number of cells positive for doublecortin (DCX) was strongly increased in the striatum; however, there was no change in the number of DCX-positive cells following 6-OHDA injection into the SN. Environmental enrichment enhanced the increase of DCX-positive cells with migrating morphology in the dorsal striatum. In enriched rats, DCX-positive cells traversed the striatal parenchyma far from the corpus callosum and lateral ventricle. DCX-positive cells co-expressed an immature neuronal marker, polysialylated neural cell adhesion molecule, but were negative for a glial marker. These data suggest that environmental enrichment improves motor performance on beam walking and enhances neuronal migration toward a lesion area in the striatum.


Astrocytes are more vulnerable than neurons to cellular Ca2+ overload induced by a mitochondrial toxin, 3-nitropropionic acid.

  • A Fukuda‎ et al.
  • Neuroscience‎
  • 1998‎

The differential effects of 3-nitropropionic acid on cultured neurons and astrocytes (of cortical and striatal origin) were examined by studying intracellular Ca2+ changes using imaging techniques with fura-2. The neurons and astrocytes whose intracellular Ca2+ concentration was recorded were identified later by immunocytochemical staining for microtubule-associated protein 2 and glial fibrillary acidic protein, respectively. 3-Nitropropionic acid (1.7 mM) irreversibly increased intracellular Ca2+ in astrocytes (27%) and, to a significantly smaller extent, in neurons (10%). The latency to onset of the intracellular Ca2+ increase was longer in neurons (45 min) than in astrocytes (29 min). Thus, a differential susceptibility of astrocytes and neurons was observed. The 3-nitropropionic acid-induced astrocytic and neuronal Ca2+ accumulations were both due to influx of Ca2+, as the increases were absent in Ca2+-free medium. An inhibitor of the Na+-Ca2+ exchanger (2',4'-dichlorobenzamil), greatly reduced the intracellular Ca2+ increase in astrocytes, but not in neurons. This indicates that the intracellular Ca2+ increase in astrocytes is primarily mediated by a reverse operation of the Na+-Ca2+ exchange system, whereas in neurons it is mediated by a different mechanism. In addition, we noted that astrocytic cell death occurred in 9% of cells at 60 min or more after the start of a 40 min perfusion with 3-nitropropionic acid, while only 4% of neurons died. In astrocytes, cell death was preceded by blebbing of the cell membrane, and by a sustained increase in intracellular Ca2+ followed by an abrupt further elevation occurring just before cellular collapse. The present results indicate that astrocytes are more vulnerable than neurons to 3-nitropropionic acid-induced cellular Ca2+ overload and toxicity, and hence support the hypothesis that, in part, 3-nitropropionic acid-induced neurotoxicity could be secondary to astrocytic cell death caused by Ca2+ overload.


Estrogen protects against while testosterone exacerbates vulnerability of the lateral striatal artery to chemical hypoxia by 3-nitropropionic acid.

  • H Nishino‎ et al.
  • Neuroscience research‎
  • 1998‎

Gender differences in the vulnerability of the lateral striatal artery (1STR artery) to systemic intoxication with 3-nitropropionic acid (3-NPA, succinate dehydrogenase inhibitor) were studied. Subcutaneous injection of 3-NPA (20 mg/kg once a day for 2 days) induced striatal selective lesions in half of male rats associated with motor symptoms (rolling, paddling, recumbency, etc) while female rats were resistant. Lesions were located in the lateral striata and characterized by astroglial necrotic cell death, enhanced immunoreaction to factor VIII-related antigen, edema, extravasation of IgG and sometimes bleeding. The motor and histological disturbances were highly sex-dependent and modulated by changes in hormonal levels. Males were more susceptible than females. Castration had little effect but ovariectomy enhanced the vulnerability. Replacement therapy with testosterone increased while estradiol or tamoxifen suppressed the vulnerability in ovariectomized females. Investigation of the arterial architecture of the brain often revealed rectangular and acute angled branchings in the centrolateral striatum where the ISTR artery feeds. A parallel in vitro toxicity study demonstrated that an extreme Ca++ overload and a strong cellular swelling resulted in astrocytic cell death. Data suggest that 1STR artery and astrocytes are highly vulnerable to 3-NPA intoxication in males. The greater vulnerability of the ISTR artery may contribute to the pathogenesis of neurodegenerative diseases, striatal bleeding, etc. Protective effects of estrogen and tamoxifen may mediate gender differences often observed in these disorders and suggest their potential use as therapeutic agents for these disorders.


[Immunological aspects of asthmatic children in remission].

  • T Noma‎ et al.
  • Arerugi = [Allergy]‎
  • 1993‎

Allergen-activated T cells secrete several kinds of bioactive lymphokines such as IL2, IL3, IL4, IL5 and IFN-gamma. They function as helpers in IgE production involved in immediate type hypersensitivity and/or effector cells in delayed type hypersensitivity in allergic patients. The acquisition of interleukin 2 (IL2) responsiveness by specific antigen-stimulated cells is generally an essential event for the induction of specific immunological phenomena. To investigate the immunological changes in asthmatic children in remission, the induction of IL2-responsiveness and production by Df (Dermatophagoides farinae)-stimulated patient lymphocytes, and Df-induced IFN-gamma production by patient lymphocytes were evaluated. The patients were divided into 3 groups. The remission group (I) consisted of those patients who had had no or only a few asthmatic attacks for more than 2 years without medication. The group of active asthma were divided into 2 groups according to attack frequency and severity (II, partial remission; III, active asthma). IL2 responsiveness and production by Df-stimulated lymphocytes from group II and III were increased. As symptoms improved, the extent of the response subsided to a level comparable to that of normal individuals (group III). IFN-gamma production by Df-stimulated lymphocytes from patients with active asthma was lower than that of normal lymphocytes. In contrast, lymphocytes from patients in complete remission group (I) induced far greater IFN-gamma generation than those from normal and group II and III patients in a Df antigen-dependent manner, which might downregulate Df-induced hyperreactivity for Df-mediated allergic response.(ABSTRACT TRUNCATED AT 250 WORDS)


Kinetic Interpretation of the Importance of OATP1B3 and MRP2 in Docetaxel-Induced Hematopoietic Toxicity.

  • A Yamada‎ et al.
  • CPT: pharmacometrics & systems pharmacology‎
  • 2014‎

Neutropenia is a lethal dose-limiting toxicity of docetaxel. Our previous report indicated that the prevalence of severe docetaxel-induced neutropenia is significantly associated with genetic polymorphisms in solute carrier organic anion transporter 1B3 (SLCO1B3) (encoding organic anion-transporting polypeptide 1B3 (OATP1B3)) and ATP-binding cassette subfamily C2 (ABCC2) (encoding multidrug-resistant-associated protein 2 (MRP2)). Therefore, we investigated their significance in docetaxel-induced neutropenia. In vitro experiments suggested their possible involvement in the hepatic uptake of docetaxel and its efflux from bone marrow cells. To further characterize a quantitative impact of OATP1B3 and MRP2 on neutropenia, we used an in silico simulation of the neutrophil count in docetaxel-treated subjects with functional changes in OATP1B3 and MRP2 in a pharmacokinetic/pharmacodynamic model. The clinically reported odds ratios for docetaxel-induced neutropenia risk were explained by the decreased function of OATP1B3 and MRP2 to 41 and 32%, respectively. These results suggest that reduced activities of OATP1B3 and MRP2 associated with systemic exposure and local accumulation in bone marrow cells, respectively, account for the docetaxel-induced neutropenia observed clinically.


Identification of pentosidine as a native structure for advanced glycation end products in beta-2-microglobulin-containing amyloid fibrils in patients with dialysis-related amyloidosis.

  • T Miyata‎ et al.
  • Proceedings of the National Academy of Sciences of the United States of America‎
  • 1996‎

beta-2-Microglobulin (beta-2m) is a major constituent of amyloid fibrils in patients with dialysis-related amyloidosis (DRA). Recently, we found that the pigmented and fluorescent adducts formed nonenzymatically between sugar and protein, known as advanced glycation end products (AGEs), were present in beta-2m-containing amyloid fibrils, suggesting the possible involvement of AGE-modified beta-2m in bone and joint destruction in DRA. As an extension of our search for the native structure of AGEs in beta-2m of patients with DRA, the present study focused on pentosidine, a fluorescent cross-linked glycoxidation product. Determination by both HPLC assay and competitive ELISA demonstrated a significant amount of pentosidine in amyloid-fibril beta-2m from long-term hemodialysis patients with DRA, and the acidic isoform of beta-2m in the serum and urine of hemodialysis patients. A further immunohistochemical study revealed the positive immunostaining for pentosidine and immunoreactive AGEs and beta-2m in macrophage-infiltrated amyloid deposits of long-term hemodialysis patients with DRA. These findings implicate a potential link of glycoxidation products in long-lived beta-2m-containing amyloid fibrils to the pathogenesis of DRA.


Neurochemical and metabolic consequences of elevated cerebrospinal fluid quinolinic acid concentrations in rat brain.

  • K Maeda‎ et al.
  • Neuroscience research‎
  • 1997‎

Quinolinic acid (QUIN) is an endogenous excitatory amino acid, which is elevated in brain tissues or cerebrospinal fluid (CSF) in several acute and chronic inflammatory central nervous system (CNS) diseases. The functional significance of this elevation is unknown but speculations of excitotoxicity have been raised. We have begun to address the pathologic consequences of elevated CSF QUIN by studying the effects of intracerebroventricular (i.cv) administration of QUIN on regional choline acetyltransferase (ChAT) activity, somatostatin content and glucose metabolism in the rat brain. QUIN (12 and 60 nmol) i.cv administration once a day for 7 days (total dose; 84 and 420 nmol, respectively) had minimal effect on somatostatin content and no effect on ChAT activity. In contrast, following continuous i.cv infusion of QUIN for 14 days using an osmotic minipump (480 nmol), ChAT activity dropped in the hippocampus and the striatum and somatostatin content was reduced in the frontal cortex, hippocampus, striatum and amygdala. Moreover, following the QUIN infusion, glucose utilization decreased in the basal nucleus of Meynert, frontal cortex, and portions of the basal ganglia and the limbic system. These results indicate that subchronic i.cv infusion of QUIN to rats results in selective regional neurochemical and metabolic changes distributed throughout the CNS. These results suggest target brain areas and transmitter systems which may be associated with neurologic syndromes characterized by elevated CSF QUIN levels.


Localization of glucokinase-like immunoreactivity in the rat lower brain stem: for possible location of brain glucose-sensing mechanisms.

  • F Maekawa‎ et al.
  • Endocrinology‎
  • 2000‎

Pancreatic glucokinase (GK) is considered an important element of the glucose-sensing unit in pancreatic beta-cells. It is possible that the brain uses similar glucose-sensing units, and we employed GK immunohistochemistry and confocal microscopy to examine the anatomical distribution of GK-like immunoreactivities in the rat brain. We found strong GK-like immunoreactivities in the ependymocytes, endothelial cells, and many serotonergic neurons. In the ependymocytes, the GK-like immunoreactivity was located in the cytoplasmic area, but not in the nucleus. The GK-positive ependymocytes were found to have glucose transporter-2 (GLUT2)-like immunoreactivities on the cilia. In addition, the ependymocytes had GLUT1-like immunoreactivity on the cilia and GLUT4-like immunoreactivity densely in the cytoplasmic area and slightly in the plasma membrane. In serotonergic neurons, GK-like immunoreactivity was found in the cytoplasm and their processes. The present results raise the possibility that these GK-like immunopositive cells comprise a part of a vast glucose-sensing mechanism in the brain.


Acute 3-nitropropionic acid intoxication induces striatal astrocytic cell death and dysfunction of the blood-brain barrier: involvement of dopamine toxicity.

  • H Nishino‎ et al.
  • Neuroscience research‎
  • 1997‎

Mechanisms underlying the selective vulnerability of the lateral striatal area to the toxic effects of 3-nitropropionic acid (3-NPA) were investigated in rats. A single exposure to 3-NPA (20 mg/kg, s.c.) induced no deficits in behavior and histology, but subsequent injection produced motor symptoms, catalepsy, lip smacking, abnormal gait, paddling, rolling, opisthotonos, tremor, recombence, somnolence and so on, in 30% of the animals within a few hours. Diffusion-weighted magnetic resonance imaging of the brains revealed an area of high signal intensity in the bilateral striata. By this stage (within a few hours), striatal astrocytes had become swollen and disintegrated. Extravasation of immunoglobulin G was detected, indicating blood-brain barrier (BBB) dysfunction. Electron microscopy revealed edema and disorganization of structures inside the astrocytic end-feet around the branches of the lateral striatal artery. Neurons were less vulnerable than astrocytes to the 3-NPA injury. Treatment of the rats with D2 receptor agonist prior to exposure to 3-NPA attenuated the behavioral abnormalities and histological damage whereas pretreatment with D2 antagonist exacerbated these changes. The concentrations of extracellular dopamine (DA) and dihydroxyphenyl acetic acid (DOPAC) were both increased in rats exposed to 3-NPA. In vitro imaging of astrocytes revealed a progressive increase in [Ca2+]i after superfusion with 3-NPA, and the 'ceiling' level was maintained even after extensive washing. DA superfusion also increased the astrocytic [Ca2+]i and this increase was reversible. Data indicate that 3-NPA-induced striatal damage was associated with astrocytic cell death and dysfunction of the BBB. Intracellular edema and extreme Ca2+ overload induced by the toxin were further aggravated by an increase in the level of DA activity. These factors acting either singly or in combination may trigger astrocyte destruction.


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