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The gap formation induced by a giant planet is important in the evolution of the planet and the protoplanetary disc. We examine the gap formation by a planet with a new formulation of one-dimensional viscous discs which takes into account the deviation from Keplerian disc rotation due to the steep gradient of the surface density. This formulation enables us to naturally include the Rayleigh stable condition for the disc rotation. It is found that the derivation from Keplerian disc rotation promotes the radial angular momentum transfer and makes the gap shallower than in the Keplerian case. For deep gaps, this shallowing effect becomes significant due to the Rayleigh condition. In our model, we also take into account the propagation of the density waves excited by the planet, which widens the range of the angular momentum deposition to the disc. The effect of the wave propagation makes the gap wider and shallower than the case with instantaneous wave damping. With these shallowing effects, our one-dimensional gap model is consistent with the recent hydrodynamic simulations. [ABSTRACT FROM PUBLISHER]

We present results of a 1.1-mm deep survey of the AKARI Deep Field South (ADF-S) with AzTEC mounted on the Atacama Submillimetre Telescope Experiment (ASTE). We obtained a map of 0.25-deg area with an rms noise level of 0.32-0.71 mJy. This is one of the deepest and widest maps thus far at millimetre and submillimetre wavelengths. We uncovered 198 sources with a significance of 3.5σ-15.6σ, providing the largest catalogue of 1.1-mm sources in a contiguous region. Most of the sources are not detected in the far-infrared bands of the AKARI satellite, suggesting that they are mostly at given the detection limits. We constructed differential and cumulative number counts in the ADF-S, the Subaru/ XMM-Newton Deep Field and the SSA 22 field surveyed by AzTEC/ASTE, which provide currently the tightest constraints on the faint end. The integration of the best-fitting number counts in the ADF-S finds that the contribution of 1.1-mm sources with fluxes of 1 mJy to the cosmic infrared background (CIB) at 1.1 mm is 12-16 per cent, suggesting that the large fraction of the CIB originates from faint sources of which the number counts are not yet constrained. We estimate the cosmic star formation rate density contributed by 1.1-mm sources with 1 mJy using the best-fitting number counts in the ADF-S and find that it is lower by about a factor of 5-10 compared to those derived from UV/optically selected galaxies at . The fraction of stellar mass of the present-day universe produced by 1.1-mm sources with 1 mJy at is ∼20 per cent, calculated by the time integration of the star formation rate density. If we consider the recycled fraction of >0.4, which is the fraction of materials forming stars returned to the interstellar medium, the fraction of stellar mass produced by 1.1-mm sources decreases to ≲10 per cent. [ABSTRACT FROM AUTHOR]

We investigated the relationship between supermassive black hole (SMBH) mass and host starburst luminosity in Seyfert galaxies and Palomar–Green quasi-stellar objects, focusing on the host galaxy morphology. Host starburst luminosity was derived from the 11.3 μm polycyclic aromatic hydrocarbon luminosity. We found that the SMBH masses of elliptical-dominated host galaxies are more massive than those of disc-dominated host galaxies statistically. We also found that the SMBH masses of disc-dominated host galaxies seem to be suppressed even under increasing starburst luminosity. These findings imply that final SMBH mass is strongly regulated by host galaxy morphology. This can be understood by considering the radiation drag model as the SMBH growth mechanism, taking into account the radiation efficiency of the host galaxy. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) galaxies have been selected from the Galaxy Evolution Explorer deep imaging survey. The presence of a far-UV (FUV) drop-out in their spectral energy distributions (SEDs) proved to be a very complete (83.3 per cent) but not very efficient (21.4 per cent) tool for identifying Lyman break galaxies (LBGs) at z∼ 1. In this paper, we explore the physical properties of these galaxies and how they contribute to the total star formation rate (SFR). We divide the LBG sample into two subclasses: red LBGs (RLBGs) detected at which are mainly luminous infrared (IR) galaxies (LIRGs) and blue LBGs (BLBGs) undetected at down to the MIPS/GTO limiting flux density of 83 μJy. Two of the RLBGs are also detected at 70 μm. The median SED of the RLBGs is similar (above ) to that of a luminous dusty starburst at , HR10. However, unlike local luminous and ultraluminous IR galaxies, RLBGs are UV bright objects. We suggest that these objects contain a large amount of dust but that some bare stellar populations are also directly visible. The median SED of the BLBGs is consistent with their containing the same stellar population as the RLBGs (i.e. a 250–500 Myr old, exponentially decaying star formation history) but with a lower dust content. The luminosity function (LF) of our LBG sample at is similar to the LF of near-UV (NUV) selected galaxies at the same redshift. The integrated luminosity densities of LBGs and NUV-selected galaxies are very consistent. Making use of the RLBG sample, we show that SFRs estimated from UV measurements and corrected using the IRX−β method provide average total SFRTOT in agreement with the sum of the UV and IR contributions: SFR UV+ SFR dust. However, IRX−β-based SFRTOT shows a large dispersion. Summing up the detected UV (1150-Å rest-frame) and IR-based SFRs of the detected objects, we find that only one-third of the total (i.e. UV + dust) LBG SFR resides in BLBGs and two-thirds in RLBGs, even though most LBGs at z∼ 1 are BLBGs. On the other hand, the total SFR of LBGs accounts for only 11 per cent of the total SFR at . Finally, we observe a regular decrease in the luminosity ratio Ldust/ LFUV from to for UV-selected samples. [ABSTRACT FROM AUTHOR]

Receptors for platelet-derived growth factor (PDGF) are abundantly expressed on synovial fibroblast-like (SFL) cells from patients with rheumatoid arthritis (RA), and stimulation with PDGF enhances both the anchorage-dependent and -independent growth of RA–SFL cells. To elucidate the molecular mechanisms responsible for the excessive growth of RA–SFL cells and to seek a novel molecular-targeting therapy for RA, we examined the expression of adapter proteins and the effect of the specific inhibition of PDGF receptor activation by imatinib mesylate. Cultured SFL cells were used in the present study after 2–5 passages. The anchorage-dependent and -independent growth patterns of the SFL cells were evaluated using a tetrazolium-based assay and colony formation in 0·3% agar, respectively. Adapter proteins Gab1 and Gab2 were expressed in RA–SFL cells, and both proteins were rapidly (< 1 min) tyrosine-phosphorylated after the stimulation of RA–SFL cells with 10 ng/ml of PDGF and, to a lesser extent, after stimulation with 100 ng/ml of epidermal growth factor (EGF). The inhibition of PDGF receptor tyrosine kinase activation by 1 µM or less of imatinib mesylate specifically suppressed the PDGF-dependent, but not EGF-dependent, tyrosine phosphorylation of various proteins. Moreover, imatinib mesylate abolished both the anchorage-dependent and -independent proliferation of RA–SFL cells induced by PDGF stimulation. These results suggest that Gab adapter proteins are expressed and likely to be involved in the growth signalling of rheumatoid synovial cells and that imatinib mesylate, a key drug in the treatment of chronic myeloid leukaemia, may also be effective for the treatment of RA. [ABSTRACT FROM AUTHOR]

Summary Background The most characteristic change in psoriasis vulgaris is markedly increased, persistent keratinocyte proliferation. The underlying mechanism of excessive epidermal growth is controversial. We previously found and reported that T-cadherin was expressed in keratinocytes and confined to the basal layer of mouse and human skin. Invasive cutaneous squamous cell carcinoma showed a loss of T-cadherin expression. Another study showed that T-cadherin was a negative growth regulator of epidermal growth factor in T-cadherin transfectant neuroblastoma cells. Objectives To obtain insight into the role of T-cadherin in keratinocyte proliferation and to investigate further the pathogenesis of psoriasis vulgaris, we examined the expression of T-cadherin, as well as E- and P-cadherin, in psoriasis vulgaris. Methods Four untreated active psoriatic skin samples from psoriasis vulgaris patients and four normal human skin samples from plastic surgery were collected, cryosectioned and immunohistochemically stained by antihuman T-, P- and E-cadherin antibodies. Further, the immunofluorescence intensities of T- and P-cadherin on the basal layer of the epidermis were quantitatively measured by the histogram function of LSM 510 software installed in a Zeiss laser scanning confocal microscope. The data were statistically analysed by Student's t -test. Results It was observed that T-cadherin was weakly and discontinuously expressed on the basal layer of psoriatic skin, while it was intensively expressed on all basal keratinocytes in normal human skin. In contrast, P-cadherin was strongly expressed throughout the entire epidermal layer in psoriatic skin samples, although its expression is restricted to the basal cell layer in normal human skin. There were no obvious differences in E-cadherin expression between normal human skin and psoriatic skin. Statistical analyses showed that the immunofluorescence intensity of T-cadherin in the basal cell layer of psoriatic skin (35 ± 9·08) was significantly decreased compared with that in normal human skin (131·75 ± 3·49, P = 2·46 × 10[sup -6] ). There was a significant increase (P = 0·00139) in the immunofluorescence intensity of P-cadherin in the basal layer of psoriatic skin (68·25 ± 12·13) compared with normal human skin (26 ± 4·90). Conclusions The present study demonstrates that there is downregulation of T-cadherin expression and upregulation of P-cadherin expression in psoriatic skin, which are considered to be involved in the hyperproliferation of keratinocytes in psoriasis vulgaris. [ABSTRACT FROM AUTHOR]

SUMMARY We have reported that tyrosine phosphorylation and expression of the T cell receptor zeta chain (TCR ζ) was decreased in two systemic lupus erythematosus (SLE) patients with an abnormal TCR ζ lacking exon-7. To examine further the TCR ζ defect and any possible relationship with specific clinical features, we studied the expression of TCR ζ in peripheral blood T cells from 44 patients with SLE, 53 with other rheumatic diseases (30 rheumatoid arthritis (RA), 11 systemic sclerosis (SSc) and 12 primary Sjögren's syndrome(SjS)) and 39 healthy individuals. Flow cytometric analysis demonstrated a significant decrease in the expression of TCR ζ in SLE (P < 0·001), but not in the other rheumatic diseases. Immunoprecipitation experiments confirmed that the expression of TCR ζ in SLE T cells was decreased dramatically (normal: 111·4 ± 22·6%, SLE: 51·6 ± 37·4%, P < 0·0001). The decrease in TCR ζ did not correlate with disease activity, or with the dose of prednisolone (PSL). There were, however, three SLE patients in whom the level of TCR ζ expression normalized after treatment, suggesting that mechanisms responsible for the TCR ζ defect appear to be heterogeneous. These results confirm the defective expression and altered tyrosine phosphorylation of TCR ζ in a large proportion of SLE patients, suggesting that it may play an important role in T cell dysfunction in SLE. [ABSTRACT FROM AUTHOR]

SUMMARY The objective of our study was to investigate the possibility of Fas ligand protein abnormalities in certain types of Sjögren's syndrome patients with enlarged exocrine glands. Fas ligand expression by lymphocytes infiltrating the lachrymal glands and by peripheral blood monocytes in Sjögren's syndrome patients with enlarged exocrine glands was assessed immunohistologically and by immunoblotting. Cytotoxicity of peripheral blood monocytes and sensitivity to steroids in Sjögren's syndrome patients with enlarged exocrine glands were studied by functional assay. Minimal Fas ligand expression was detected in the lymphocytes of the lachrymal glands and a decreased level of Fas ligand was found in peripheral blood monocytes as assessed by immunoblotting. Functional assay confirmed the decreased cytotoxicity of lymphocytes in Sjögren's syndrome patients with enlarged exocrine glands, and that it is not affected by anti-Fas ligand antibody. By contrast, the sensitivity of lymphocytes in Sjögren's syndrome patients with enlarged exocrine glands to steroids was increased. These observations suggest that abnormal expression and function of Fas ligand occurs in Sjögren's syndrome patients with enlarged exocrine glands. [ABSTRACT FROM AUTHOR]

To investigate the mechanism of the downregulation of T-cell receptor ζ chain (TCRζ) expression in the peripheral blood T cells (PBTs) of systemic lupus erythematosus (SLE) patients, we analyzed the 3′ untranslated region (3′UTR) of TCRζ mRNA, because the 3′UTR in mRNA is responsible for posttranscriptional regulation. Use of the reverse transcriptase polymerase chain reaction (RT-PCR) to amplify the 917 bp TCRζ 3′UTR cDNA demonstrated that the short variant cDNA (355 bp), expressed as an alternatively spliced 3′UTR with 562-bp deletion, was predominated in the PBTs of 11 of 14 SLE patients, whereas mainly the wild-form cDNA (917 bp) was detected in the PBTs of seven negative controls (two systemic sclerosis patients, five normal controls) and in two T-cell line hybridomas. Semiquantitative PCR also revealed the predominant expression of the TCRζ mRNA with alternatively spliced 3′UTR (TCRζ mRNA/as-3′UTR), and a decreased expression of TCRζ mRNA with the wild form 3′UTR (TCRζ mRNA/w-3′UTR) in SLE T cells. However, there was no difference in the expression of the open reading frame (ORF) TCRζ mRNA between the negative controls and SLE patients. The TCRζ protein expression level according to Western blot analysis correlated well with that of TCRζ mRNA/w-3′UTR ( r= 0.931) and reversibly with TCRζ mRNA/as-3′UTR ( r=−0.614), but not with ORF TCRζ mRNA ( r=−0.296). It can be concluded that the reduced expression of TCRζ mRNA/w-3′UTR and the predominant expression of TCRζ mRNA/as-3′UTR lead to downregulation of the TCRζ protein in SLE T cells. [ABSTRACT FROM AUTHOR]

Transplanting a germinal vesicle (GV) from an aged woman's oocyte into a younger ooplasm has been proposed as a possible way to reduce the incidence of oocyte aneuploidy which is considered to be responsible for age-related infertility. In this study, we have assessed the efficiency of each step involved in nuclear transplantation—specifically cell survival, nuclear-cytoplasmic reconstitution, and the capacity of the reconstituted oocytes for in-vitro maturation. In addition, we have evaluated the fertilizability and karyotypic status of the manipulated oocytes by intracytoplasmic sperm injection (ICSI) and fluorescent in-situ hybridization technique respectively. Nuclear transplantation was accomplished with an overall efficiency of 73%. Due to the limited availability of materials, most nuclear transplantation procedures were performed between sibling oocytes. The maturation rate of 62% following reconstitution was comparable with that of control oocytes, as was the incidence of aneuploidy among the reconstituted oocytes. The ICSI results of the reconstituted oocytes yielded a survival rate of 77%, a fertilization rate of 52%, and a satisfactory early embryonic cleavage. Furthermore, in a limited number of observations where the nucleus of an aged oocyte was transferred into a younger ooplasm, there was an appropriate chromosomal segregation. These findings demonstrate that human oocytes reconstituted with GV nuclei are able to undergo maturation, fertilization, and early embryo cleavage, and maintain a normal ploidy. Although in-vitro maturation seems to be a limiting step, this technique would allow us to investigate further the nuclear-ooplasmic relationship during meiotic maturation. [ABSTRACT FROM PUBLISHER]

Although great progress has been made in both the investigation and treatment of infertility, a considerable number of patients still fail to conceive. Spermatogenic failure and/or oocyte ageing appear to be responsible for a large proportion of cases. The use of donor gametes may bring legal, ethical and even social problems of acceptance that can discourage infertile couples from the donor route. Fortunately, emerging reproductive technologies and preliminary results from animal experiments provide some hope for alternative sources of gametes through which these infertile patients can finally conceive their own genetic child. In conjunction with intracytoplasmic sperm injection (ICSI), fertilization of human oocytes with immature sperm precursors, e.g. spermatids and even secondary spermatocytes, has resulted in healthy babies. Pregnancies have also resulted from the use of spermatids derived from in-vitro spermatogenesis. In the mouse, even primary spermatocytes appear able to participate in normal embryogenesis. In view of the possibility for transplantation and even xenotransplantation of spermatogonia to a host testis in animals, a similar use of human male stem cells might provide an attractive source for the treatment of males with arrested spermatogenesis, as well as male cancer patients. Transplantation of somatic cell nuclei and their haploidization within oocytes may prove to be a practical way of eradicating age-related aneuploidy and so constitute an innovative source of healthy oocytes. Most importantly, however, the safety of the procedures described here needs to be proven before their application to the human arena. Finally, we discuss the implications of cytoplasmic quality and of genetic imprinting in the context of these manipulations. [ABSTRACT FROM AUTHOR]

Trypanosoma cruzi was transformed with the Plasmodium yoelii gene encoding the circumsporozoite (CS) protein, which contains the well-characterized CD9+ T cell epitope, SYVPSAEQI. In vivo and in vitro assays indicated that cells infected with the transformed T. cruzi could process and present this malaria parasite-derived class I MHC-restricted epitope. Immunization of mice with recombinant influenza and vaccinia viruses expressing the SYVPSAEQI epitope induced a large number of specific CD8+ T cells that strongly suppressed parasitemia and conferred complete protection against the acute T. cruzi lethal infection. CD8+ T cells mediated this immunity as indicated by the unrelenting parasitemia and high mortality observed in immunized mice treated with anti-CD8 antibody. This study demonstrated, for the first time, that vaccination of mice with vectors designed to induce CD8+ T cells is effective against T. cruzi infection. [ABSTRACT FROM PUBLISHER]

Transplanting a germinal vesicle (GV) to another enucleated oocyte provides a possible way to avoid age-related aneuploidy in metaphase II (MII) oocytes from older women. This study was conducted to examine the efficiency of each step of nuclear transplantation as reflected in the survival and maturation capacity of immature mouse oocytes subjected to this procedure. GV stage oocytes were retrieved from unstimulated ovaries. A GV removed with a small amount of cytoplasm (karyoplast) was transferred subzonally into a previously enucleated oocyte, which was then exposed to direct current to promote fusion. Such reconstituted oocytes were placed in culture to allow maturation, and some that had extruded a first polar body were fixed and processed for chromosome analysis. Each step of nuclear transplantation - survival, enucleation, grafting, and reconstitution - was successful in >90%, with the overall efficiency of reconstitution being 80%. The observation of normal karyotypes confirmed that the procedure did not increase chromosomal aneuploidy. An electrolytic medium, revealed to be superior for the reconstitution procedure, also allowed haploidization of the transplanted nucleus. These findings suggest that this technique can be applied to study the effects of a 'younger' woman's ooplasm on the disjunction of an 'older' woman's chromosomes during meiosis I. [ABSTRACT FROM AUTHOR]

To disclose the mechanism of aberrant function of peripheral blood lymphocytes (PBL) in SLE, we focused on the catalytic function of CD45, and determined the CD45 PTPase activity in SLE patients. The sample population consisted of 32 SLE patients with different disease activity. PTPase activity of cell lysates immunoprecipitated by anti-CD45 MoAb was assayed against phosphotyrosine analogue PNPP, followed by measuring the release of para-nitro phenol at 410nm. CD45 PTPase activity of PBL was significantly decreased in SLE patients, compared with that of normal controls and patients with systemic sclerosis (964 ± 265. 1202 ± 172. 1210 ± 125. respectively: SLE versus normal, P < 0.05). It was correlated with SLE Disease Activity Index (SLEDAI) score (r = 0.597, P = 0.0006), but not with the dose of prednisolone (r = 0.214, P = 0.2657), indicating that CD45 PTPase activity became reduced when the disease was active, but it was not affected by prednisolone. Moreover, it was not corrected by in vitro culture with or without stimulation. The expression of CD45 on PBL was comparable between normal and SLE, raising a possibility that it may be due to aberrant regulation of catalytic function of CD45 in SLE. Given the evidence that tyrosine phosphorylation of cellular proteins by tyrosine kinases and phosphatases is one of the key biochemical events in the signal transduction pathway, the decreased CD45 PTPase activity in SLE may account for the defective signal transduction via TCR/CD3. leading to dysregulated effect or function of the lymphocytes. [ABSTRACT FROM AUTHOR]

To elucidate the mechanism of ocular surface allergic disease, we focused on IL-4, which is one of the key factors in regulating IgE production, and thus determined the concentration of IL-4 in tears. IL-4 concentration was determined in the tears of 15 patients with seasonal allergic conjunctivitis, 15 vernal keratoconjunctivitis (VKC), 10 giant papillary conjunctivitis (GPC), 10 patients with non-allergic conjunctivitis and post-cataract surgical conjunctivitis as intermediate conjunctivitis, and 10 normal subjects using a highly sensitive sandwich ELISA. The mean level of IL-4 in normal controls was low, and seasonal allergic conjunctivitis, VKC and GPC showed a significant elevation (P < 0.05), respectively. IL-4 of VKC and GPC were also significantly higher than allergic conjunctivitis, and non-allergic conjunctivitis and post-cataract surgical conjunctivitis were not higher than normal. These results raise the possibility that the increased level of IL-4 in tears could play a role in allergic disease and its severity in patients. [ABSTRACT FROM AUTHOR]

To address the molecular mechanism underlying the functional defects of peripheral T cells in systemic lupus erythematosus (SLE), we focused on early signaling events. We demonstrated that protein expression of the TCR ξ chain was significantly decreased in peripheral T cells from patients with SLE compared to normal controls and patients with systemic sclerosis (SSc). Among those patients showing decreased TCR ξ chain expression, we found two patients with pronounced TCR ξ chain abnormalities, including an aberrant 14 kDa form in one and only trace expression in the other. RT-PCR, SSCP and subsequent cloning of the transcripts revealed that bases 468-503, corresponding to exon 7, were deleted in both patients. Since exon 7 spans the GTP/GDP binding site and N-terminal tyrosine in the third ITAM domain of TCR ξ chain, the transcript lacking exon 7 may be responsible for altered signal transduction via TCR in these SLE patients. [ABSTRACT FROM PUBLISHER]

We have investigated the mutagenicity of oxidative DNA damage induced in V79 Chinese hamster lung fibroblast, and measured 8-hydroxydeoxyguanosine (8OHdG) levels as an indicator of this damage. A hydroxyl radical generator, N,N'-bis(2-hydroxyperoxy-2-methoxyethyl)-1,4,5,8-naphthalene-tetra -carboxylic-diimide (NP-III), induced 8OHdG in V79 upon irradiation with 366 nm ultraviolet light (UV) for 15 min. 8OHdG was determined by HPLC with electrochemical detection after anaerobic sample processing. The 8OHdG level in the cells treated without NP-III was 0.49 per 10(5) dG, whereas levels in the cells treated with 5, 10 or 20 microM NP-III and UV irradiation were 1.84, 4.06 or 6.95 per 10(5) dG, respectively. The 8OHdG induced by 20 microM NP-III with UV irradiation decreased rapidly, and the half-life of the induced 8OHdG was approximately 6 h. NP-III with UV irradiation also induced DNA strand breaks in all cells uniformly, as determined by single cell gel assay. Mutant frequencies at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus in V79 were determined as the number of 6-thioguanine-resistant cells per 10(6) cells. Mutant frequency of the cells without NP-III was 8.0, and frequencies of the cells treated with 5, 10 or 20 microM NP-III and UV irradiation were 14.9, 20.6 or 24.7 respectively. Treatment with 20 microM NP-III and UV irradiation decreased the cell number, determined 3 days after the treatment, to 20.8%. These findings indicate that acutely induced oxidative DNA damage including mutagenic 8OHdG is only weakly mutagenic in V79. [ABSTRACT FROM PUBLISHER]

The in-vivo antifungal activity of benanomicin A administered intravenously or subcutaneously was compared with that of amphotericin B and fluconazole using animal models of systemic infections with Candida albicans, Aspergillus fumigatus and Cryptococcus neoformans. The efficacy of benanomicin A in C. albicans infection was more pronounced when administered in multiple doses than in a single dose. This was also true of fluconazole, but not of amphotericin B, which showed no difference between single and multiple dosings. Benanomcin A eradicated C. albicans cells from the kidneys of infected mice in a manner comparable to that of amphotericin B, but more effectively than fluconazole. The histopathological findings obtained from the kidneys of the C. albicans-infected mice confirmed the therapeutic efficacy of benanomicin A. The subcutaneous ED50 values of benanomicin A were 1.30 mg/kg/day (C. albicans) and 19.0 mg/kg/day (A. fumigatus) which were intermediate between those of amphotericin B and fluconazole in the two models. The subcutaneous ED50 value of benanomicin A for C. neoformans was 21.5 mg/kg/day, which was higher than that of amphotericin B. [ABSTRACT FROM AUTHOR]

Benanomicin A showed a broad antifungal spectrum, inhibiting the growth of all test strains of 41 yeasts, 23 dimorphic fungi, 23 dematiaceous fungi, 16 aspergilli, and 19 dermatophytes, with the exception of 12 zygomycetic strains. The MIC values of benanomicin A were comparable to those of amphotericin B against Cryptococcus. Rhodotorula, Trichosporon, Geotrichum, Sporothrix, and some dermatophytes, but were two to eightfold higher than those of amphotericin B against other fungal pathogens tested. The action of benanomicin A was fungicidal. [ABSTRACT FROM AUTHOR]

Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis. We present a case of a 56-year-old male with ECD. As time progressed, involvement of the orbital fossa, cranial convexity, spinal cord, brain stem, thyroid, lung, retroperitoneum, lower extremity bones and skin were found. Previously reported cases reveal the frequency of ECD with spinal cord involvement is rare. Although this was a presumed diagnosis based on other lesions, our case is the first in which both intramedullary and epidural masses are present. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which discusses a case of a 68-year-old Japanese man diagnosed with paraneoplastic pemphigus (PNP) and has triple malignancies in the mucous membrane pemphigoid.

Rheumatoid arthritis (RA) is a chronic inflammatory disease mediated by the production of various cytokines such as tumor necrosis factor (TNF), interleukin-1 and interleukin-6 (IL-6). Tocilizumab (TCZ) is a humanized anti-human IL-6 receptor monoclonal antibody that was created in Japan. TCZ inhibits both of soluble form and membrane bounded IL-6 receptor-mediated signaling transduction through gp130 pathway. TCZ is using widely in the treatment of RA refractory to DMARDs and TNF blockers. However, until now no data have been available for the efficacy and safety in daily practice in the real world. Therefore, we conducted to investigate the efficacy and safety of TCZ through a multicenter retrospective study in Japan.In total, 229 patients received 8mg/kg of TCZ every 4 weeks treatment from the approval in May 2008 to March 2009. Disease activity and disability were assessed by DAS28-ESR and health assessment questionnaire disability index (HAQ-DI). Safety was analyzed based on events for which a causal relationship to TCZ could not be ruled out. Last observation carrying forward (LOCF) method was used in each analysis.In the 24 weeks treatment period, TCZ showed excellent efficacy for reducing signs and symptoms (DAS remission rate was 40.7% at week 24) and were well tolerated in active RA patients including the anti-TNF therapy-refractory population. For the future investigation, we will evaluate the efficacy of TCZ for the joint damage for 52 weeks treatment of TCZ, and the result will be presented in this session. [ABSTRACT FROM PUBLISHER]