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Follicular helper T (Tfh) cells contribute to various immune responses as well as to the pathogenesis of several immune diseases. However, the precise mechanism underlying the onset or development of autoimmunity via Tfh cells remains unclear. Herein, the detailed relationship between autoimmune disease and Tfh cells was analyzed using a murine model for Sjögren syndrome (SS) wherein the mice underwent neonatal thymectomy. Germinal center (GC) development was promoted in this SS model along with an increase of Tfh cells and GC B cells. The severity of the autoimmune lesions was correlated with the number of Tfh cells detected in the spleen of the SS model mice. In addition, treatment with an anti-CD20 monoclonal antibody effectively suppressed the autoimmune lesions with a reduction of Tfh cells and GC B cells. Comprehensive gene analysis revealed that several genes associated with Tfh cell differentiation, including achaete-scute homologue 2 (Ascl2), were up-regulated in peripheral CD25−CD4+T cells in SS model mice compared with those in control mice. Moreover, an experiment using CD4CreBcl6fl/flmice that received neonatal thymectomy treatment demonstrated that Ascl2 contributes to the Tfh cell differentiation associated with autoimmunity during the early stages, independent of Bcl6. In conclusion, our results indicate that abnormal Tfh cell differentiation via Ascl2 regulation might contribute to the pathogenesis of autoimmunity.

Epithelial cell rests of Malassez (ERM) are quiescent epithelial remnants of the Hertwig’s epithelial root sheath (HERS) that are involved in the formation of tooth roots. ERM cells are unique epithelial cells that remain in periodontal tissues throughout adult life. They have a functional role in the repair/regeneration of cement or enamel. Here, we isolated odontogenic epithelial cells from ERM in the periodontal ligament, and the cells were spontaneously immortalized. Immortalized odontogenic epithelial (iOdE) cells had the ability to form spheroids and expressed stem cell-related genes. Interestingly, iOdE cells underwent osteogenic differentiation, as demonstrated by the mineralization activity in vitro in mineralization-inducing media and formation of calcification foci in iOdE cells transplanted into immunocompromised mice. These findings suggest that a cell population with features similar to stem cells exists in ERM and that this cell population has a differentiation capacity for producing calcifications in a particular microenvironment. In summary, iOdE cells will provide a convenient cell source for tissue engineering and experimental models to investigate tooth growth, differentiation, and tumorigenesis.

Epithelial cell rests of Malassez (ERM) are quiescent epithelial remnants of the Hertwig's epithelial root sheath (HERS) that are involved in the formation of tooth roots. ERM cells are unique epithelial cells that remain in periodontal tissues throughout adult life. They have a functional role in the repair/regeneration of cement or enamel. Here, we isolated odontogenic epithelial cells from ERM in the periodontal ligament, and the cells were spontaneously immortalized. Immortalized odontogenic epithelial (iOdE) cells had the ability to form spheroids and expressed stem cell-related genes. Interestingly, iOdE cells underwent osteogenic differentiation, as demonstrated by the mineralization activity in vitroin mineralization-inducing media and formation of calcification foci in iOdE cells transplanted into immunocompromised mice. These findings suggest that a cell population with features similar to stem cells exists in ERM and that this cell population has a differentiation capacity for producing calcifications in a particular microenvironment. In summary, iOdE cells will provide a convenient cell source for tissue engineering and experimental models to investigate tooth growth, differentiation, and tumorigenesis.

Both autoimmunity and tumor immunity are immune responses against self-tissues or cells. However, the precise similarity or difference between them remains unclear. In this study, to understand a novel mechanism of tumor immunity, we performed transplantation experiments with a murine autoimmune model, C57BL/6J (B6)/lpr mice. A melanoma cell line, B16F10 cells, or granulocyte macrophage colony-stimulating factor- overexpressing B16F10 (B16F10/mGM) cells were transplanted into B6 or B6/lpr mice. Tumor growth by transplanted B16F10/mGM cells was significantly accelerated in B6/lpr mice compared with that in B6 mice. The accumulation of M1 macrophages in the tumor tissues of B6/lpr recipient mice was significantly lower compared with that in the control mice. In vitro co-culture experiment showed that impaired differentiation into M1 macrophages was observed in B6/lpr mice. The number of tumor vessels and vascular endothelial growth factor (VEGF) expression were also significantly enhanced in the tumor tissues of B6/lpr mice compared with those in the B6 mice. Moreover, VEGF expression was correlated with the increased expression of hypoxia-inducible factor-1α in the tumor tissues of B6/lpr mice. These results suggest that dysfunctional tumor immunity and enhanced angiogenesis in autoimmunity influence tumor growth.

Both autoimmunity and tumor immunity are immune responses against self-tissues or cells. However, the precise similarity or difference between them remains unclear. In this study, to understand a novel mechanism of tumor immunity, we performed transplantation experiments with a murine autoimmune model, C57BL/6J (B6)/lprmice. A melanoma cell line, B16F10 cells, or granulocyte macrophage colony-stimulating factor- overexpressing B16F10 (B16F10/mGM) cells were transplanted into B6 or B6/lprmice. Tumor growth by transplanted B16F10/mGM cells was significantly accelerated in B6/lprmice compared with that in B6 mice. The accumulation of M1 macrophages in the tumor tissues of B6/lprrecipient mice was significantly lower compared with that in the control mice. In vitroco-culture experiment showed that impaired differentiation into M1 macrophages was observed in B6/lprmice. The number of tumor vessels and vascular endothelial growth factor (VEGF) expression were also significantly enhanced in the tumor tissues of B6/lprmice compared with those in the B6 mice. Moreover, VEGF expression was correlated with the increased expression of hypoxia-inducible factor-1αin the tumor tissues of B6/lprmice. These results suggest that dysfunctional tumor immunity and enhanced angiogenesis in autoimmunity influence tumor growth.

To examine cross‐sectionally whether intraabdominal fat area (IAFA), i.e., visceral fat, and liver fat assessed by computed tomography (CT) are independently associated with hyperuricemia. Subjects were 801 Japanese men not taking antidiabetic, antihypertensive, or urate‐lowering medications, without any history of renal disease, cardiovascular disease, or cancer, and with serum creatinine <1.5 mg/dl. Abdominal, thoracic, and thigh fat areas were measured by CT. Total fat area (TFA) was the sum of these fat areas. Total subcutaneous fat area (TSFA) was TFA minus IAFA. Liver fat was assessed by liver‐to‐spleen (L/S) ratio measured by CT. Hyperuricemia was defined as serum uric acid level >7.0 mg/dl. Its association with adiposity was tested using logistic regression. The prevalence of hyperuricemia was 19.6% (157 men). Both greater IAFA and lower L/S ratio were independently associated with hyperuricemia in models that simultaneously included IAFA and L/S ratio: multiple‐adjusted odds ratios of hyperuricemia for quintiles 3, 4, and 5 of IAFA were 2.16 (95% confidence interval [95% CI] 1.02–4.59), 2.41 (95% CI 1.13–5.16), and 4.00 (95% CI 1.81–8.85), respectively, compared to quintile 1, and the L/S ratios for quintiles 3, 2, and 1 were 2.34 (95% CI 1.16–4.75), 2.15 (95% CI 1.06–4.34), and 2.79 (95% CI 1.35–5.76), respectively, compared to quintile 5. Both IAFA and L/S ratio remained significant even after adjusting for abdominal subcutaneous fat area, TFA, TSFA, body mass index, or waist circumference. Of all fat measurements, IAFA had the strongest association with hyperuricemia by Akaike's information criteria. Greater amounts of both visceral fat and liver fat were independently associated with hyperuricemia.

Neonatal thymectomy in certain mouse strains is known to induce organ-specific autoimmunity due to impaired functions of T cells, including Foxp3+regulatory T (Treg) cells in the thymus. The precise mechanism underlying the induction of autoimmunity by neonatal thymectomy remains unclear. One possibility is that depletion of Tregcells breaks down peripheral tolerance. We examined the functions of Tregcells by using a murine Sjögren syndrome model of NFS/sldmice that underwent neonatal thymectomy. The ratio of Tregcells to effector memory phenotype T cells in thymectomy mice was significantly lower than that of nonthymectomy mice. In addition, in vitroinduction of peripherally induced Tregcells by transforming growth factor-β (TGF-β) using naive T cells from Sjögren syndrome model mice was severely impaired. The mRNA expression of TGF-β receptor I and II and Smad3 and -4 in the TGF-β–induced signal transduction pathway of Tregcells in this Sjögren syndrome model were lower than those of control mice. In addition, Tregcells in this Sjögren syndrome model exhibited an interferon-γ–producing Th1-like phenotype that resembled effector T cells. In conclusion, these results suggest that abnormal expansion and differentiation of Tregcells and inflammatory cytokines produced by Tregcells contribute to the development of autoimmunity.

Using a simulation, we investigate the effects of the light source size and derive an effective method for suppression of the subfringes that appear in ArF Talbot lithography, which has been proposed for submicron pattern transfer applications. The appearance of the subfringes, which were caused by interference, was related to the size of the light source. If an appropriate light source size is chosen, then, a large process window can be obtained. Guidelines for source size selection are given.

Several autoimmune diseases are known to develop in postmenopausal women. However, the mechanism by which estrogen deficiency influences autoimmunity is unknown. Aromatase is an enzyme that converts androgens to estrogens. Herein, we used female aromatase gene knockout (ArKO) mice as a model of estrogen deficiency to investigate the molecular mechanism that underlies the onset and development of autoimmunity. Histological analyses showed that inflammatory lesions in the lacrimal and salivary glands of ArKO mice increased with age. Adoptive transfer of spleen cells or bone marrow cells from ArKO mice into recombination activating gene 2 knockout mice failed to induce the autoimmune lesions. Expression of mRNA encoding proinflammatory cytokines and monocyte chemotactic protein-1 increased in white adipose tissue of ArKO mice and was significantly higher than that in wild-type mice. Moreover, an increased number of inflammatory M1 macrophages was observed in white adipose tissue of ArKO mice. A significantly increased monocyte chemotactic protein-1 mRNA expression of the salivary gland tissue in ArKO was found together with adiposity. Furthermore, the autoimmune lesions in a murine model of Sjögren syndrome were exacerbated by administration of an aromatase inhibitor. These results suggest that aromatase may play a key role in the pathogenesis of Sjögren syndrome–like lesions by controlling the target organ and adipose tissue–associated macrophage.

Introduction:IL-1 plays key roles in the biological functions of various cells. In particular, many roles of IL-1 in the immune system have been discovered by numerous studies. This review focuses on the association of IL-1 with the pathogenesis of autoimmunity.Areas covered:An overview of the biological functions of the IL-1 family and the IL-1 receptors (IL-1Rs), including the maintenance of systemic or local homeostasis, and the signaling pathway through IL-1/IL-1R in various immune systems are described. Several functions of IL-1 in the pathogenesis of Sjögren's syndrome (SS) have been demonstrated with a focus on the immune responses and target tissues in SS. In addition to the role of IL-1 in the immune responses in SS, the function of IL-1 in ocular mucosa lesions in SS has been described. Lastly, there is an overview of possible therapeutic strategies for IL-1 inhibition in SS.Expert opinion:IL-1 plays critical roles in the onset and development of SS by controlling systemic or local immune responses and maintaining the survival and mucosal defense of target epithelial cells. The inhibition of the pathogenic functions of IL-1 may be beneficial for treating SS.

Forkhead box p3-positive (Foxp3+) regulatory T cells (Tregcells) participate in maintaining peripheral immune tolerance and suppressing autoimmunity. We recently reported that in situpatrolling by C-C-chemokine receptor 7 (CCR7)+Tregcells in target organs is essential for controlling autoimmune lesions in Sjögren's syndrome. In the present study, the molecular mechanism underlying CCR7-mediated Tregcell migration was investigated in a mouse model. The impaired migratory response of Ccr7−/−Tregcells to sphingosine 1-phosphate (S1P) occurred because of defective association of S1P receptor 1 (S1P1) with a G coupled–protein. In addition, T-cell receptor (TCR)- and S1P1-mediated Ras-related C3 botulinum toxin substrate 1 (Rac-1), extracellular signal-related kinase (ERK), and c-Jun phosphorylation required for activator protein 1 (AP-1) transcriptional activity were significantly impaired in Ccr7−/−Tregcells. Surprisingly, the abnormal nuclear localization of Foxp3 was detected after abrogation of the c-Jun and Foxp3 interaction in the nucleus of Ccr7−/−Tregcells. These results indicate that CCR7 essentially controls the migratory function of Tregcells through S1P1-mediated AP-1 signaling, which is regulated through its interaction with Foxp3 in the nucleus.

Faint Object Camera and Spectrograph (FOCAS) is a versatile common-use optical instrument for the 8.2 m Subaru Telescope, offering imaging and spectroscopic observations. FOCAS employs grisms with resolving powers ranging from 280 to 8200 as dispersive optical elements. A grism is a direct-vision grating composed of a transmission grating and prism(s). FOCAS has five grisms with replica surface-relief gratings including an echelle-type grism, and eight grisms with volume-phase holographic (VPH) gratings. The size of these grisms is 110 mm $\times$106 mm in aperture with a maximum thickness of 110 mm. We employ not only the dichromated gelatin, but also the hologram resin as a recording material for VPH gratings. We discuss the performance of these FOCAS grisms measured in the laboratory, and verify it by test observations, and show examples of astronomical spectroscopic observations.

It is well established that cytochrome c is released from mitochondria when the permeability transition (PT) of this organelle is induced by Ca2+. Our previous study showed that valinomycin also caused the release of cytochrome c from mitochondria but without inducing this PT (Shinohara, Y., Almofti, M. R., Yamamoto, T., Ishida, T., Kita, F., Kanzaki, H., Ohnishi, M., Yamashita, K., Shimizu, S., and Terada, H. (2002) Permeability transition-independent release of mitochondrial cytochrome c induced by valinomycin. Eur. J. Biochem. 269, 5224–5230). These results indicate that cytochrome c may be released from mitochondria with or without the induction of PT. In the present study, we examined the protein species released from valinomycin- and Ca2+-treated mitochondria by LC-MS/MS analysis. As a result, the proteins located in the intermembrane space were found to be specifically released from valinomycin-treated mitochondria, whereas those in the intermembrane space and in the matrix were released from Ca2+-treated mitochondria. These results were confirmed by Western analysis. Furthermore to examine how the protein release occurred, we examined the correlation between the species of released proteins and those of the abundant proteins in mitochondria. Consequently most of the proteins released from mitochondria treated with either agent were highly expressed proteins in mitochondria, indicating that the release occurred not selectively but in a manner dependent on the concentration of the proteins. Based on these results, the permeabilization effects of Ca2+and valinomycin on the inner and outer mitochondrial membranes are discussed.

It is well established that cytochrome cis released from mitochondria when the permeability transition (PT) of this organelle is induced by Ca2+. Our previous study showed that valinomycin also caused the release of cytochrome cfrom mitochondria but without inducing this PT (Shinohara, Y., Almofti, M. R., Yamamoto, T., Ishida, T., Kita, F., Kanzaki, H., Ohnishi, M., Yamashita, K., Shimizu, S., and Terada, H. (2002) Permeability transition-independent release of mitochondrial cytochrome c induced by valinomycin. Eur. J. Biochem.269, 5224–5230). These results indicate that cytochrome cmay be released from mitochondria with or without the induction of PT. In the present study, we examined the protein species released from valinomycin- and Ca2+-treated mitochondria by LC-MS/MS analysis. As a result, the proteins located in the intermembrane space were found to be specifically released from valinomycin-treated mitochondria, whereas those in the intermembrane space and in the matrix were released from Ca2+-treated mitochondria. These results were confirmed by Western analysis. Furthermore to examine how the protein release occurred, we examined the correlation between the species of released proteins and those of the abundant proteins in mitochondria. Consequently most of the proteins released from mitochondria treated with either agent were highly expressed proteins in mitochondria, indicating that the release occurred not selectively but in a manner dependent on the concentration of the proteins. Based on these results, the permeabilization effects of Ca2+and valinomycin on the inner and outer mitochondrial membranes are discussed.

Although it has been well documented that aberrant major histocompatibility complex class II molecules may contribute to the development of autoimmune disorders, the precise mechanisms responsible for their tissue-specific expression remain unknown. Here we show that estrogen deficiency induces aberrant class II major histocompatibility complex expression in exocrine glands via interactions between epithelial cells and plasmacytoid dendritic cells. Relatively modest but functionally significant expression levels of major histocompatibility complex class II and class II transactivator molecules were observed in the exocrine glands of ovariectomized (Ovx) C57BL/6 (B6) mice, but were not seen in the exocrine glands of control B6 mice. We observed that the salivary dendritic cells adjacent to the apoptotic epithelial cells positive for terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, were activated in Ovx mice, but were not activated in control mice. We obtained evidence that the salivary gland cells express both interferon regulatory factor-1 and class II transactivator type IV molecules in Ovx mice. Salivary gland cells from Ovx mice were also capable of inducing the activation of antigen-specific T cells from OT-II transgenic mice. These findings indicate that estrogen deficiency initiates class II transactivator type IV mRNA expression in exocrine glands via interactions between epithelial cells and plasmacytoid dendritic cells, suggesting that plasmacytoid dendritic cells play a pivotal role in gender-based autoimmune disorders in postmenopausal women.

Bisphenol A (BPA) is a representative endocrine disruptor that may have adverse effects on human health. Since the development of oral tolerance during infancy may play an important role in the prevention of food allergies, we examined whether transmaternal exposure to BPA influences the development of oral tolerance. To measure antigen-specific responses, female wild-type mice mated with male ovalbumin (OVA)-specific T-cell receptor transgenic (TCR-tg) mice were fed with BPA during pregnancy and while nursing. OVA was administered to OVA-TCR-tg offspring during their weaning period. Oral administration of both high and low doses of OVA suppressed OVA-specific cell proliferation and cytokine production in both BPA-exposed and nonexposed control mice, but the OVA-mediated suppression was significantly more diminished by the BPA exposure. The accumulation of CD4CD25Foxp3T cells was diminished in the BPA-exposed offspring. Moreover, after low dose OVA administration, serum OVA-specific IgG1 and IgG2a levels were higher in the BPA-exposed offspring than in nonexposed ones. Taken together, our results indicate that transmaternal exposure to BPA seems to modulate the mechanisms underlying tolerance induction; therefore, BPA may partially interrupt the development of oral tolerance.

Bisphenol A (BPA) is a representative endocrine disruptor that may have adverse effects on human health. Since the development of oral tolerance during infancy may play an important role in the prevention of food allergies, we examined whether transmaternal exposure to BPA influences the development of oral tolerance. To measure antigen-specific responses, female wild-type mice mated with male ovalbumin (OVA)-specific T-cell receptor transgenic (TCR-tg) mice were fed with BPA during pregnancy and while nursing. OVA was administered to OVA-TCR-tg offspring during their weaning period. Oral administration of both high and low doses of OVA suppressed OVA-specific cell proliferation and cytokine production in both BPA-exposed and nonexposed control mice, but the OVA-mediated suppression was significantly more diminished by the BPA exposure. The accumulation of CD4+CD25+Foxp3+T cells was diminished in the BPA-exposed offspring. Moreover, after low dose OVA administration, serum OVA-specific IgG1 and IgG2a levels were higher in the BPA-exposed offspring than in nonexposed ones. Taken together, our results indicate that transmaternal exposure to BPA seems to modulate the mechanisms underlying tolerance induction; therefore, BPA may partially interrupt the development of oral tolerance.

The voltage-dependent anion channel (VDAC) is a pore-forming protein expressed in the outer membrane of eukaryotic mitochondria. Three isoforms of it, i.e., VDAC1, VDAC2, and VDAC3, are known to be expressed in mammals; however, the question as to which is the main isoform in mitochondria is still unanswered. To address this question, we first prepared standard VDACs by using a bacterial expression system and raised various antibodies against them by using synthetic peptides as immunogens. Of the three bacterially expressed VDAC isoforms, VDAC3 showed faster migration in SDS-polyacrylamide gels than VDAC1 and VDAC2, although VDAC2 is longer than VDAC1 and VDAC3, due to a 12-amino acid extension of its N-terminal region. Even with careful structural characterization of the expressed VDACs by LC-MS/MS analysis, serious structural modifications of VDACs causing changes in their migration in SDS-polyacrylamide gels were not detected. Next, immunoreactivities of the raised antibodies toward these bacterially expressed VDAC isoforms were evaluated. Trials to prepare specific antibodies against the three individual VDAC isoforms were not successful except in the case of VDAC1. However, using a synthetic peptide corresponding to the highly conserved region among the three VDACs, we were successful in preparing an antibody showing essentially equal imunoreactivities toward all three VDACs. When mitochondrial outer membrane proteins of various rat tissues were subjected to 2-dimensional electrophoresis followed by immunoblotting with this antibody, six immnoreactive protein spots were detected. These spots were characterized by LC-MS/MS analysis, and the signal intensities among the spots were compared. As a result, the signal intensity of the spot representing VDAC1 was the highest, and thus, VDAC1 was concluded to be the most abundantly expressed of the three VDAC isoforms in mammalian mitochondria.

Bronchial asthma (BA) often develops in children with atopic dermatitis (AD). Identification of factors that could predict the development of asthma in children with AD is useful for early intervention.

Early intervention strategies in allergic diseases will be dependent on identification of newborns at high risk for later development of atopic disease. In this cohort study of 106 neonates, we investigated whether cytokine production property and responsiveness to IL-12 of neonatal CD4+T cells were associated with the subsequent development of atopic disease and whether a skewed cytokine production property was intrinsic to helper T cells. To exclude the effects of contaminating cells, highly purified cord blood CD4+T cells were stimulated with anti-CD3 MAb and recombinant B7-2 molecule in the presence or absence of IL-12. Production of IL-13 and interferon-? was determined by ELISA. The infants were assessed at 12 mo for the development of atopic diseases. CD4+T cells of neonates who manifested allergic symptoms (atopic group) produced higher levels of IL-13 compared with those of the nonatopic group in both the presence and absence of IL-12. No significant difference was noted between the two groups with respect to interferon-? production. Moreover, higher IL-13 production was also observed in neonates with chronic eczema than those with short-term eczema. Our data suggest that increased production of IL-13 by neonatal CD4+T cells is a useful marker of newborns at high risk for subsequent development of atopic diseases and that an intrinsic abnormality of CD4+T cell is associated with the pathogeneses of atopic disease, especially atopic dermatitis in infants.

Early intervention strategies in allergic diseases will be dependent on identification of newborns at high risk for later development of atopic disease. In this cohort study of 106 neonates, we investigated whether cytokine production property and responsiveness to IL-12 of neonatal CD4T cells were associated with the subsequent development of atopic disease and whether a skewed cytokine production property was intrinsic to helper T cells. To exclude the effects of contaminating cells, highly purified cord blood CD4T cells were stimulated with anti-CD3 MAb and recombinant B7-2 molecule in the presence or absence of IL-12. Production of IL-13 and interferon- was determined by ELISA. The infants were assessed at 12 mo for the development of atopic diseases. CD4T cells of neonates who manifested allergic symptoms (atopic group) produced higher levels of IL-13 compared with those of the nonatopic group in both the presence and absence of IL-12. No significant difference was noted between the two groups with respect to interferon- production. Moreover, higher IL-13 production was also observed in neonates with chronic eczema than those with short-term eczema. Our data suggest that increased production of IL-13 by neonatal CD4T cells is a useful marker of newborns at high risk for subsequent development of atopic diseases and that an intrinsic abnormality of CD4T cell is associated with the pathogeneses of atopic disease, especially atopic dermatitis in infants.

Although the Kozu Island Volcano, one of the Izu Islands Volcanoes in the south part Central Japan, is an active volcano, there is no record of the eruption for about 1100 years since the last eruption in 833 A.D. Since 1988, frequent earthquake swarms are observed around the Kozu Island, and the uplift of 2–4 cm/yr is observed on the island by tidal observations. Station velocities detected by GPS measurements since 1989 show velocities that differ from the convergent velocity of the Philippine Sea plate calculated from plate motion models. A local GPS network with 12 stations is occupied around the volcano, and the GPS measurements are repeated every about six month since July 1996. Inflated deformation of 2–4 cm/yr are detected from the GPS measurements and the pressure source is estimated to be located in the northeastern part of the island at a depth of 2.1 km using Mogi solution. Negative gravity changes of more than 30 microgal are also measured above the pressure source in the period November 1998 to July 1999, consistent with uplift.

• GeneralL. Castle and C. Findlay. Pacific Trade in Services. Sydney, Wellington, London, and Boston: Allen & Unwin, in association with the Pacific Trade and Development Conference Secretariat and the Australian National University, 1988. Pp. 294.Denys Lombard and Jean Aubin, editors. Marchands et Hommes d'Affaires Asiatiques. Paris: Editions de l'Ecole des Hautes Etudes en Sciences Sociales, 1988. Pp. 375. Plates, maps, tables. 260F, paper.R.J. May and William J. O'Malley, editors. Observing Change in Asia. Essays in Honour of J.A.C. Mackie. Bathurst: Crawford House Press, 1989. Pp. x, 265. Tables, acknowledgments, notes, bibliographies, index.Amin Saikal, editor. Refugees in the Modern World. Canberra Studies in World Affairs Number 25. Canberra: Department of International Relations, Research School of Pacific Studies, Australian National University, 1989. Pp. 125.• China and inner AsiaArif Dirlik and Maurice Meisner, editors. Marxism and the Chinese Experience. Armonk, New York and London: M.E. Sharpe, 1989. Pp. 384. Index, contents, acknowledgements, introduction, notes.Michael S. Duke, editor. Modern Chinese Women Writers: Critical Appraisals. New York: M.E. Sharpe, Inc., 1989. Pp. 272.Thomas Heberer. China and its National Minorities, Autonomy or Assimilation? Armonk and London: M.E. Sharpe, 1989. Pp. 165. Contents, preface, notes, glossary, illustrations, tables, maps, bibliography, index. $39.95, cloth.Ray Huang. China: A Macro History. Armonk, New York: M.E. Sharpe, 1987. Pp. xix, 277. Maps, line drawings, chronological charts, index.Huang Tsung-hsi. The Records of Ming Scholars. Edited by Julia Ching with the collaboration of Chaoying Fang. Honolulu: University of Hawaii Press, 1987. Pp. xxi, 336. Acknowledgements, note, abbreviations, glossary, introduction, bibliographies, index. US$27.00, cloth.Ono Kazuko. Chinese Women in a Century of Revolution 1850-1950. Edited by Joshua A. Fogel. Stanford: Stanford University Press, 1989. Pp. v, 255. Prefaces, introduction by Joshua A. Fogel and Susan Mann, chronology, notes, supplementary references, index. Hardcover.Colin Mackerras, Kevin Bucknall, Russell Trood. The Beijing Tragedy: Implications for China and Australia. Australia-Asia Papers No. 51. Brisbane: Centre for the Study of Australia-Asia Relations, Griffith University, 1989. Pp. ii, 93. $6.00, paper.Zhang Xinxin and Sang Ye. Chinese Lives: An Oral History of Contemporary China. Edited by W.J.F Jenner and Delia Davin. London: Penguin Books, 1989. Pp. v, 367. Contents, preface, editor's introduction, author's note, chronology, map, Chinese titles and sources. $14.99, paper.Chinese Lives: An Oral History of Contemporary China is an abridged English language version of Beijingren: Yibaige putongrende zishu (Shanghai: Wenyi Chubanshe, 1986, repr. 1987; 616 pp.).• Japan and Northeast AsiaTheodore C. Bestor. Neighborhood Tokyo. Stanford: Stanford University, 1989. Pp. x, 268. Acknowledgements, appendixes, notes, bibliography, index. Cloth.Scott S. Burnett, editor. Korean-American Relations: Documents Pertaining to the Far Eastern Diplomacy of the United States. Volume 3. The Period of Diminishing Influence, 1896-1905. Honolulu: University of Hawaii Press, 1989. Pp. xiii, 304. Introduction. US$24.Yur-Bok Lee. West Goes East: Paul Georg Von Mollendorff and Great Power Imperialism in Late Yi Korea. Honolulu: University of Hawaii Press, 1988. Pp. x, 295. Preface, notes, bibliography, index, illustrations. US$29.00.Stephen E. Marsland. The Birth of the Japanese Labor Movement: Takano Fusataro and the Rodo Kumiai Kiseikai. Honolulu: University of Hawaii Press, 1989. Pp. ix, 271. Preface, appendixes, notes, bibliography, index. US$27.00, cloth.Robert A. Scalapino and Hongkoo Lee, editors. Korea-US Relations: The Politics of Trade and Security Berkeley: Institute of East Asian Studies, University of California, 1988. Research Papers and Policy Studies Number 25. Pp. vi, 242. Introduction, contributors. US$17.00, paper.Tanizaki Jun'ichirô. A Cat, Shôzô and Two Women. Translated by Matsui Sakuko. The University of Sydney East Asian Series, Wild Peony, Sydney, 1988.Karel van Wolferen. The Enigma of Japanese Power: People and Politics in a Stateless Nation. London: Macmillan, 1989. Pp. 496. Acknowledgements, notes, index. Hardcover.Paul Varley and Kumakura ISAO, editors. Tea in Japan: Essays on the History of Chanoyu. Honolulu: University of Hawaii Press, 1989. Pp. vii, 285. Contents, preface, glossary, index, black-and-white and colour photographs. $25.00, cloth.• Southeast AsiaSharom Ahmat and Sharon Siddique, editors. Islamic Society, Higher Education and Development in Southeast Asia. Singapore: Institute of Southeast Asian Studies, 1986. Pp. xii, 219. Contents, foreword, acknowledgements, contributors, introduction. S$18.40, paper.William J. Duiker. Historical Dictionary of Vietnam. Asian Historical Dictionaries No. 1. Metuchen NJ & London: The Scarecrow Press Inc., 1989. Pp. xiv, 269. Preface, maps, appendices, bibliography. $32.50, cloth.Charles Higham. The Archaeology of Mainland Southeast Asia. Cambridge: Cambridge University Press, 1989. Pp. xvi, 387. Maps, illustrations. $99.00.Ruurdje Laarhoven. Triumph of Moro Diplomacy: The Maguindanao Sultanate in the 17th Century. Quezon City: New Day Publishers, 1989. Pp. xx, 268. Foreword, acknowledgements, abbreviations, introduction, maps, appendices, reference notes, glossary, bibliography. $14.25, paper. Distributed outside the Philippines by the Cellar Book Shop, Detroit.Donald H. Mcmillen, editor. Conflict Resolution in Kampuchea: Proceedings of the Third International Conference on Indochina. Brisbane: Centre for the Study of Australian-Asian Relations, 1989. Pp. 151. $10.00, paper.Vincente L. Rafael. Contracting Colonialism: Translation and Christian Conversion in Tagalog Society under Early Spanish Rule. Ithaca and London: Cornell University Press, 1988. Pp. 230. Plates, bibliography.Garry Rodan. The Political Economy of Singapore's Industrialization: National State and International Capital. London: Macmillan, 1989. Pp. xvii, 266. Preface, acknowledgements, list of tables, index, abbreviations, notes and bibliography. £35, cloth.Friedrich Seltmann. Die Kalang: Eine Volksgruppe auf Java und ihre Stamm-Mythe, ein Beitrag zur Kulturgeschichte Javas. Stuttgart: Franz Steiner Verlag Wiesbaden GmbH, 1987. Pp. 430. Tabular overview, indices, glossary, seventeen sketches, forty-five black-and-white photos, eight colour photographs, maps. DM244, cloth.Yoshikazu Takaya. Agricultural Development of a Tropical Delta: A Study of the Chao Phraya Delta. Translated by Peter Hawkes. English-Language Series no. 17, monographs of the Center for Southeast Asian Studies, Kyoto University. Honoloul: University of Hawaii Press, 1987. Pp. xviii, 269.

Oxidation of 4-alkylphenols 1by 1-( tert-butylperoxy)-1,2-benziodoxol-3(1 H)-one ( 2) in the presence of tert-butyl hydroperoxide affords selectively 4-( tert-butylperoxy)-2,5-cyclohexadien-1-ones 3in good yields. Evidence for the involvement of free-radicals is reported.

The rates (RS) of the oxygen exchange reaction of alkylarsonates (methyl-, butyl-, hexyl-, and benzyl-) and dialkylarsinates (dimethyl- and dibutyl-) with solvent water were measured in the pH range greater than 6, and at temperatures between 30 and 0 °C. For arsonates, the rate (R) is expressed by the following rate law: R= k1[A2-] + k2[HA-] + k3[H2A] + k4[HA-]2+ k5[HA-][H2A] + k6[H2A]2, where A2-, HA-, and H2A designate R'AsO32-, R'AsO3H-, and R'AsO3H2(R' = alkyl), respectively. For arsinates, R= k1[R'2AsO2-] + k2[R'AsO2H] (pH > 9). The exchange rates of arsonates at 0 and 30 °C were analyzed in terms of the rate law to obtain the values of the rate constants (k1–k6). The activation parameters were obtained for the k1paths of both arsonates and arsinates, which are the reaction between R'AsO32-or R'2AsO2-and water. It is noticeable that the values of the activation entropies of the arsonates were found to be negative, while those of the arsinate were found to be positive. It was suggested that the oxygen exchange of arsonate ions proceeds via an SN2 mechanism, while that of arsinates preceeds via SN1.

The first total synthesis of (8R) and (8S) methyl β-d-glucopyranosyl helianthenate B was accomplished using the Cadiot-Chodkiewicz coupling reaction as a key step. Significant differences were observed in the resonances between the 1H-NMR and 13C-NMR spectra of the diastereomers. Based on these results, the absolute configurations of glucopyranosyloxymethine in methyl β-d-glucopyranosyl helianthenate A to E (1-5) were reconfirmed to be the (R) configuration.

Background:Galectin-9 (Gal-9), a member of the galectin family, plays a crucial role in inflammation and tumorigenesis involving angiogenesis, cell adhesion, immune escape, and cancer cell survival. In acute myeloid leukemia (AML), Gal-9 is highly expressed in some AML cell lines and binds with T-cell immunoglobulin- and mucin-domain-containing molecule-3 (Tim-3) on T cells and leukemic stem cells. The Tim-3/Gal-9 pathway may be associated with disease progression by inducing T-cell dysregulation and mediating autocrine proliferation of leukemic cells. However, the role of the pathway in myelodysplastic syndromes (MDS) remains unclear. In the current study, we investigated the prognostic impact of plasma Gal-9 levels and the pathophysiological roles of Gal-9 and Tim-3 in MDS.

No relevant conflicts of interest to declare.

No relevant conflicts of interest to declare.

Introduction: The immunophenotypic analysis of plasma cells using flow cytometry (FCM) is useful for the diagnosis for multiple myeloma (MM) and the detection of MM cells after treatment. CD138 is a well-known surface marker identifying plasma cells, although decreased CD138 expression on plasma cells is frequently observed in MM patients with relapsed or progressive disease. Thus, more stable MM antigens are needed. The SLAM family molecule CD229 has recently been reported to be specifically overexpressed on MM cells including their clonogenic precursors, suggesting that it may be a good marker to identify MM cells. Furthermore, some surface antigens, i.e., costimulatory molecule CD86 (B7-2), its receptor CD28, IL-6 receptor (CD126), insulin-like growth factor-1 (CD221), and coinhibitory molecule B7-H1 (PD-L1, CD274), were reported to be associated with poor prognosis. This study aimed to validate the potential of CD229 as a new MM cell marker and the efficacy of immunophenotypes on MM cells as prognostic markers in a multicenter study.