An epidemic of arsenic neuropathy from a spiked curry.
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Arsenic Poisoning↗
Biomedical subjects
K Ogawa
Publications and source records attributed to K Ogawa.
A novel serum protein that is selectively produced by cytotoxic lymphocytes.
Cytotoxic lymphocytes such as CTL and NK cells play principal roles in the host defense mechanisms. Monitoring these effector cells in vivo is helpful to understand the immune responses in disorders such as cancer and infectious diseases. In this study, we identified a novel secretory protein, killer-specific secretory protein of 37 kDa (Ksp37), as a Th1-specific protein by a subtractive cloning method between human Th1 and Th2 cells. In peripheral blood leukocytes, Ksp37 expression was limited to Th1-type CD4(+) T cells, effector CD8(+) T cells, gammadelta T cells, and CD16(+) NK cells. Most of these Ksp37-expressing cells coexpressed perforin, indicating that Ksp37 is selectively and commonly expressed in the lymphocytes that have cytotoxic potential. Ksp37 was released at constant rate from both unstimulated and stimulated PBMCs in vitro and also detected in normal human sera. In healthy individuals, serum Ksp37 levels were significantly higher in children (mean +/- SD; 984 +/- 365 ng/ml for age 0-9) than in adults (441 +/- 135 ng/ml for age 20-99), consistent with reported differences in the absolute counts of blood T and NK cells between children and adults. In patients with infectious mononucleosis, transient elevation of serum Ksp37 levels was observed during the early acute phase of primary EBV infection. These results suggest that Ksp37 may be involved in an essential process of cytotoxic lymphocyte-mediated immunity and that Ksp37 may also have clinical value as a new type of serum indicator for monitoring cytotoxic lymphocytes in vivo.
Adolescent↗
Clinicopathological and prognostic significance of thymidine phosphorylase and proliferating cell nuclear antigen in gastric carcinoma.
We have reported that thymidine phosphorylase (dThdPase) is identical to platelet derived-endothelial cell growth factor and that it has an angiogenic activity in vitro and in human carcinoma tissues as well as gastric carcinoma. Recently, we revealed that dThdPase may have an another function(s) besides angiogenesis in vitro and in human solid tumors. Using immunohistochemistry, we examined retrospectively whether the expression of dThdPase was correlated with tumor growth, comparing it with the proliferating cell nuclear antigen labeling index (PCNA LI) and examining their prognostic significance in 116 patients with gastric carcinoma. A direct correlation of these two factors was observed (R=0.659, P<0.001). A multivariate Cox regression analysis showed that both dThdPase positivity and PCNA LI were independent prognostic factors, as were depth of invasion and lymph node metastasis. Furthermore, the patients with dThdPase-positive/high PCNA LI tumors had the worst prognoses. The combination of dThdPase and PCNA expression is a better tool for predicting the prognosis of patients with gastric carcinoma than the expression of either of them alone. These results raise the possibility that dThdPase may have a function(s) involved in tumor growth besides angiogenesis.
Adult↗
Cloning and functional characterization of chicken p160 coactivator family members.
The factors SRC-1, TIF2 and ACTR were identified as interacting with nuclear receptors in a highly ligand-dependent manner. Because the molecular mass of each of these factors is approximately 160 kDa, they are collectively termed p160 coactivators. So far, p160 coactivators have been cloned from human, mouse and Xenopus. We report here the cloning of the chicken homologues of p160 coactivator members. As in human and mouse, chicken has three p160 coactivators. Each gene encodes an approximately 160 kDa protein which exhibits 70-80% amino acid sequence identity to human and mouse p160 coactivators. Chicken p160 coactivators also have the property of interacting with several liganded nuclear receptors. Moreover, we describe an imperfect LXXLL sequence, termed NR box 4, which is located downstream of NR box 3 and conserved between evolutionarily diverse species. The loss of NR box 4 results in a decrease of interaction with the nuclear receptor, which indicates that NR box 4 is required for efficient interaction.
Acetyltransferases↗
Establishment of rat hepatocellular carcinoma cell lines with differing metastatic potential in nude mice.
For better understanding of cancer metastasis, we have established an in vivo model for induction of highly metastatic hepatocellular carcinomas (HCC) in male F344 rats. From 1 tumor, 4 cell lines with differing metastatic potential (C1, C2, C6, C5F) were established by subcloning using the limited-dilution cloning technique. Two other lines, N1 and L2, arose from another primary HCC and a lung metastatic lesion, respectively. Although cell adhesion of each cell line in culture medium was different, tumors developing in the subcutis of nude mice after transplantation were all moderately differentiated HCC with a trabecular pattern. On subcutaneous injection into nude mice, all 6 cell lines proved to be tumorigenic in the injection site and C5F was highly metastatic to the lung. With injection into the tail vein, N1 and L2 formed frequent metastases in the lung as well as in lymph nodes. Using intraperitoneal injection, C1, C6, N1 and L2 showed marked disseminated growth in the abdominal cavity with bloody ascitis. Northern blot analysis revealed expression of known metastasis-related genes, KAI1 and heparanase, to be decreased in C5F, but no differences in expression of nm23-H1 were evident. A point mutation in the GSK-3beta phosphorylation site of the beta-catenin gene was found in L2. These transplantable HCC cell lines that have different metastatic ability should be useful for elucidation of mechanisms of metastasis.
Animals↗
Beta-D-glycosylamidines: potent, selective, and easily accessible 1-glycosidase inhibitors.
Beta-D-glycosylamidines, in which a glycon is connected via an N-glycoside linkage with a substituted amidine (aglycon), were synthesized in two steps from the corresponding sugars and served as stable and potent beta-glycosidase inhibitors with high selectivity according to the glycon- and alpha, beta-specificities of the enzymes.
Amidines↗
Chrysotile asbestos fibers mediate transformation of Escherichia coli by exogenous plasmid DNA.
The ability of chrysotile asbestos fibers to introduce the exogenous plasmid pUC18 into Escherichia coli JM109 cells was tested. Cells were transformed with pUC18 DNA although the frequency of transformation was quite low: 759+/-301 transformants were obtained per microgram of pUC18. Plasmids were purified from E. coli which had been transformed by mediation with chrysotile asbestos. Following this, the plasmids were confirmed to be pUC18 by Southern hybridization. This asbestos-mediated transformation was optimal within 5 min when 10 mg ml(-1) of asbestos was used. Plasmids up to 7.69 kb were introduced by this method.
Asbestos, Serpentine↗
First report of the invasive eel pest Pseudodactylogyrus bini in North America and in wild American eels.
We detected 2 species of monogenean gill worms, Pseudodactylogyrus bini (Kikuchi, 1929) Gusev, 1965 and P. anguillae (Yin & Sproston, 1948) Gusev, 1965 (Monopisthocotylea: Pseudodactylogyridae), on American eel Anguilla rostrata in 2 rivers in South Carolina, USA. One of these, P. anguillae, was reported 5 yr ago from Nova Scotia; as well as in South Carolina, we also discovered it in 2 localities in Chesapeake Bay. Differences in the morphologies of specimens of either species of worm from North America and northeastern Asia were negligible. Similarly, the level of variation in sequences in the ITS2 (internal transcribed spacers) region of ribosomal RNA was minor, and not consistent with geographical origin. These data indicate that these monogeneans invaded North America only recently, possibly in parallel with the nematode Anguillicola crassus (which is known to have been introduced with commercial imports of foreign eels). We map the current global occurrence of these monogeneans, and conclude that their dispersal from northeastern Asia was largely as a result of the eel trade, and has probably been secondarily augmented by longshore migration of infected eels, and possibly also by transport in ballast waters. With present technology, all eel stocks must still be collected from the wild; unless shipments are disinfected at quarantine, these and other eel pathogens (such as A. crassus) are likely to continue to colonise other regions of the world.
Animals↗
Prostaglandin D2 selectively induces chemotaxis in T helper type 2 cells, eosinophils, and basophils via seven-transmembrane receptor CRTH2.
Prostaglandin (PG)D2, which has long been implicated in allergic diseases, is currently considered to elicit its biological actions through the DP receptor (DP). Involvement of DP in the formation of allergic asthma was recently demonstrated with DP-deficient mice. However, proinflammatory functions of PGD2 cannot be explained by DP alone. We show here that a seven-transmembrane receptor, CRTH2, which is preferentially expressed in T helper type 2 (Th2) cells, eosinophils, and basophils in humans, serves as the novel receptor for PGD2. In response to PGD2, CRTH2 induces intracellular Ca2+mobilization and chemotaxis in Th2 cells in a Galphai-dependent manner. In addition, CRTH2, but not DP, mediates PGD2-dependent cell migration of blood eosinophils and basophils. Thus, PGD2 is likely involved in multiple aspects of allergic inflammation through its dual receptor systems, DP and CRTH2.
Base Sequence↗
Dynamics of antigen-specific helper T cells at the initiation of airway eosinophilic inflammation.
Bronchial asthma is characterized by chronic eosinophilic inflammation of the bronchial mucosa in which Th2 cells play crucial roles. Ovalbumin-reactive Th2 clones were labeled with a fluorescent-probe then infused into unprimed mice to elucidate the dynamics of antigen-specific T cells involved in allergic inflammation. Infiltration of not only labeled antigen-specific T cells, but also unlabeled nonspecific CD4(+) T cells into the bronchial mucosa following inhaled antigen challenge was detectable under confocal microscopy and flow cytometry. Accordingly, labeled T cells in the spleen were decreased, whereas those in hilar lymph nodes were increased upon antigen challenge. Approximately 45% of antigen-specific T cells that migrated into the lungs bore CD25, while another early activation marker, CD69, was expressed on 80% of the migrated T cells. Accordingly, antigen challenge to the mice induced in situ proliferation of antigen-specific T cells as well as bronchial epithelial cells in the lungs. Expression of vascular cell adhesion molecule (VCAM)-1, but not intercellular adhesion molecule (ICAM)-1, on the vascular endothelium in the lungs was enhanced following antigen challenge. Nevertheless, treatment with anti-VCAM-1 antibody, and also anti-ICAM-1 antibody strongly suppressed the accumulation of T cells, suggesting that both VCAM-1 and ICAM-1 are essential for antigen-stimulated T cell mobilization into peripheral tissues. Our current study visualized the kinetics and the mechanism of antigen-specific T cell migration in response to local challenge with a protein antigen.
Adoptive Transfer↗
Resistance of primary cultured mouse hepatic tumor cells to cellular senescence despite expression of p16(Ink4a), p19(Arf), p53, and p21(Waf1/Cip1).
Primary cultured mouse hepatic cells become senescent within a short period, although rare cells form colonies from which continuously proliferating cell lines can be established. In contrast, hepatic tumor (HT) cells show little senescence and higher colony-forming capacity. To assess this difference, we investigated p16(Ink4a)/p19(Arf)/p53/p21(Waf1/Cip1) expression in primary normal and HT cells, together with cell lines established from both. In primary normal cells, p16(Ink4a)/p19(Arf) were expressed only in association with senescence and disappeared at later stages of colony formation. In contrast, primary HT cells showed sustained p16(Ink4a)/p19(Arf) expression from the beginning. No p16(Ink4a)/p19(Arf) alterations, such as deletion, mutations, or hypermethylation, were detected in the primary HT cells, although most cell lines derived from either normal or HT cell colonies lost p16(Ink4a) or p19(Arf) expression owing to hypermethylation or homozygous deletion of p16(Ink4a)/p19(Arf). On the other hand, primary normal and HT cells and most cell lines showed constitutively elevated expression of p53/p21(Waf1/Cip1), with a further increment after ultraviolet ir-radiation, indicating a functionally normal p53 pathway. These results indicate that primary HT cells are resistant to senescence despite retaining p16(Ink4a)/p19(Arf)/p53/p21(Waf1/Cip1) expression and that loss of p16(Ink4a)/p19(Arf) function is associated only with establishment of the cell lines.
Alkylating Agents↗
Anaplastic meningioma with papillary, rhabdoid, and epithelial features: a case report.
A 74-year-old man manifested disturbed consciousness and right hemiparesis. Computed tomography revealed a left frontal parasagittal meningeal tumor with extensive peritumoral brain edema and skull invasion. Subtotal removal was performed. Five years later, he underwent two more operations of massive recurrences. Pathological studies revealed anaplastic meningioma with two different histological areas. One was an epithelial and meningothelial area, and the other was a papillary and rhabdoid area. In the papillary and rhabdoid area, small tumor cells with a high nucleus/cytoplasm ratio proliferated densely around the dilated central capillaries with a pseudopapillary pattern. Many rhabdoid cells (vimentin ++, cytokeratin AE1/AE3 +, epithelial membrane antigen [EMA] + +) tended to be distributed far from the central capillaries. There were many mitotic figures near the central vessels. Dense MIB1-positive nuclei were also observed near the central vessels. The trabecular pattern of the tumor cells in the epithelial area was quite different from the histological features of chordoid meningioma.
Aged↗
Mitral valve replacement through right thoracotomy after coronary arterial bypass grafting with functioning conduits.
A 67-year-old man who had undergone coronary artery bypass grafting 3 years previously suffered from severe mitral regurgitation associated with Streptococcal infective endocarditis. He was placed in New York Heart Association functional class III. Preoperative angiography demonstrated good opacification of all 3 conduits implanted in the previous operation. We replaced the mitral valve through an anterolateral right thoracotomy, approaching the mitral valve as an alternative to redoing sternotomy to minimize potential injury to patent grafts. His postoperative course was uneventful. After a 1-month course of antibiotics, the patient was discharged as New York Heart Association class II and at present, 3 months after discharge, is doing well. This approach is an effective alternative to redoing sternotomy for mitral valve operation, especially in patients undergoing a previous coronary arterial bypass grafting via median sternotomy.
Aged↗
Toxicity and mutagenesis of chrysotile asbestos to Agrobacterium radiobacter.
The mutation of Agrobacterium radiobacter cells exposed to chrysotile asbestos was examined by the random amplified polymorphic DNA (RAPD) method. Approximately 1.4 kbp of DNA in A. radiobacter, which was not amplified strongly in the cells that were not exposed to asbestos, was amplified in the cells that were exposed to asbestos. Mutation in genomic DNA of A. radiobacter was found to be induced by asbestos. Specific DNA that was amplified by asbestos present in PCR products and that which exists latently in genomic DNA were cloned, and these sequences were then determined and compared. It was shown that one of the mutations by the asbestos in the A. radiobacter occurred only in the primer annealed region and was a point mutation or deletion.
Asbestos, Serpentine↗
Indocyanine green and fluorescein hyperfluorescence at the site of occlusion in branch retinal vein occlusion.
BACKGROUND: In patients with branch retinal vein occlusion (BRVO), we investigated the presence of indocyanine green (ICG) and fluorescein hyperfluorescence at the site of occlusion. We also assessed the association of this feature with the clinical outcome of these patients. METHODS: Both indocyanine green (ICG) videoangiography and fluorescein angiography (FAG) were performed in 21 eyes with BRVO of less than 1 month duration. Deterioration of the disease was defined clinically as an increase in retinal hemorrhages or retinal edema. Capillary nonperfusion was quantified with computer image analysis from the FAG pictures. RESULTS: ICG videoangiography showed focal hyperfluorescence along the venous wall at the site of the affected A-V crossing in 9 of the 21 eyes, and FAG showed this feature in 10 eyes. The ICG hyperfluorescence was more prominently and focally detected than the hyperfluorescence on FAG, which was sometimes diffusely seen throughout the whole occluded area. Eight of the nine eyes showing ICG hyperfluorescence had clinical deterioration with an increase in retinal hemorrhage or edema. This deterioration occurred more frequently in eyes with hyperfluorescence and/or late leakage than in ones without these features. The mean nonperfused area was significantly larger in eyes with hyperfluorescence than in eyes without these features. CONCLUSION: The ICG hyperfluorescence at the site of A-V crossing is associated with disease deterioration in patients with fresh BRVO. The ICG hyperfluorescence was more easily detectable than the hyperfluorescence on FAG, although the difference in sensitivity between the two methods is not great.
Adult↗
Cause of death in renal transplant patients: a comparison between azathioprine and ciclosporin.
The results of renal transplantation have improved due to advances in immunosuppression techniques of preservation, and pre- and postoperative treatments; however, both morbidity and mortality remain serious problems. To decrease the morbidity and mortality rates we analyzed the causes of death after renal transplantation in our hospital. Between 1972 and 1999, we performed 364 renal transplantations, 257 of which were living-related and 107, cadaveric. There were 178 patients given azathioprine and 186 given ciclosporin. The survival rate of the patients on ciclosporin therapy was much better than that of those on azathioprine therapy. Of the total 364 renal transplant patients, 59 (16.2%) died, and 28 (47.5%) of these 59 deaths occurred within 1 year after renal transplantation. The causes of death were infection in 19 (32.2%) patients, gastrointestinal diseases in 16 (27.1%), cardiovascular diseases in 11 (18.6%), cerebrovascular diseases in 6 (10.2%), suicide in 3 (5.1%), and other causes in 4 (6.8%). These findings reinforce that early diagnosis and treatment are essential to decrease the morbidity and mortality rates assoiated with renal transplantation.
Azathioprine↗
Glutamate is not involved in the MPP+-induced dopamine overflow in the striatum of freely moving C57BL/6 mice.
The role of glutamate in the N-methyl-4-phenyldihydropyridinium (MPP+) toxicity has been argued in the past decade. However, the effects of glutamate efflux and NMDA antagonist on MPP+-induced dopamine overflow have not been documented. To clarify this, we perfused MPP+ through a microdialysis probe in the striatum of freely moving mature C57BL/6 mice. The 60-min perfusion of 10 and 100 microM MPP+ strikingly increased dopamine levels to 28- and 93-fold of the basal values, respectively. In contrast, an administration of MPP+ did not induce marked glutamate release: the MPP+-perfusion slightly increased the glutamate level at 100 microM, but not at 10 microM. The addition of 100 microM (+)-MK-801 or 200 microM (+/-)-AP-7 to the perfusate did not attenuate MPP+-induced dopamine overflow. The extent of dopamine release only depended on the amount of MPP+ accumulation into the cells. These results indicated that, at least in the striatum, neither glutamate release nor the NMDA antagonist, including (+)-MK-801, could regulate MPP+-evoked dopamine overflow.
1-Methyl-4-phenylpyridinium↗
Norharman, an indoleamine-derived beta-carboline, but not Trp-P-2, a gamma-carboline, induces apoptotic cell death in human neuroblastoma SH-SY5Y cells.
Carbolines, azaheterocyclic amines derived from indoleamines, have various biological activities, such as neurotoxicity of beta-carbolines and potent mutagenicity of gamma-carbolines. In this study, structural significance among these carbolines was investigated in relation to the types of cell death, apoptosis and necrosis, using human neuroblastoma SH-SY5Y cells. DNA damage was quantitatively analyzed by a single-cell gel electrophoresis assay. DNA damage was induced by both beta-carbolines, harman and norharman, and gamma-carbolines, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 3-amino-4-methyl-5H-pyrido[4,3-b]indole (Trp-P-2), in a dose dependent manner. Gamma-carbolines were more potent to damage DNA than beta-carbolines. Alkaline lysis of the cells prevented DNA damage induced by beta-carboline, and pre-treatment of the cells with cycloheximide, an inhibitor of protein synthesis, reduced DNA damage caused by norharman. Morphological observation showed condensed and fragmented nuclei typical for apoptosis, in the cells treated with norharman. Thus, DNA damage induced by norharman was proved to be apoptotic. However, harman, which had a methyl substitution at the position 1, might induce necrosis in the cells. On the other hand, gamma-carbolines, Trp-P-1 and Trp-P-2, directly damaged DNA. Thus, the nitrogen atom at the gamma-position and/or an amino group in carboline structure would be required to induce the direct DNA cleavage.
Apoptosis↗