A Spectral Study of the Black Hole Candidate XTE J1752-223 in the High/Soft State with MAXI, Suzaku and Swift

We report on the X-ray spectral analysis of the black hole candidate XTE\ J1752--223 in the 2009--2010 outburst, utilizing data obtained with the MAXI/Gas Slit Camera (GSC), the Swift/XRT, and Suzaku, which work complementarily. As already reported by Nakahira et al. (2010) MAXI monitored the source continuously throughout the entire outburst for about eight months. All the MAXI/GSC energy spectra in the high/soft state lasting for 2 months are well represented by a multi-color disk plus power-law model. The innermost disk temperature changed from $\sim$0.7 keV to $\sim$0.4 keV and the disk flux decreased by an order of magnitude. Nevertheless, the innermost radius is constant at $\sim$41 $D_{3.5}(\cos{\it i})^{-1/2}$ km, where $D_{3.5}$ is the source distance in units of 3.5 kpc and $i$ the inclination. The multi-color disk parameters obtained with the MAXI/GSC are consistent with those with the Swift/XRT and Suzaku. The Suzaku data also suggests a possibility that the disk emission is slightly Comptonized, which could account for broad iron-K features reported previously. Assuming that the obtained innermost radius represents the innermost stable circular orbit for a non-rotating black hole, we estimate the mass of the black hole to be 5.51$\pm$0.28 $M_{\odot}$ $D_{3.5}(\cos{\it i})^{-1/2}$, where the correction for the stress-free inner boundary condition and color hardening factor of 1.7 are taken into account. If the inclination is less than 49$^{\circ}$ as suggested from the radio monitoring of transient jets and the soft-to-hard transition in 2010 April occurred at 1--4% of Eddignton luminosity, the fitting of the Suzaku spectra with a relativistic accretion-disk model derives constraints on the mass and the distance to be 3.1--55 $M_{\odot}$ and 2.3--22 {\rm kpc}, respectively. This confirms that the compact object in XTE J1752--223 is a black hole.Comment: 12 pages including 7 figures and 4 tables, accepted for publication in PAS

Japan Society of Gynecologic Oncology guidelines 2015 for the treatment of vulvar cancer and vaginal cancer

BackgroundVulvar cancer and vaginal cancer are relatively rare tumors, and there had been no established treatment principles or guidelines to treat these rare tumors in Japan. The first version of the Japan Society of Gynecologic Oncology (JSGO) guidelines for the treatment of vulvar cancer and vaginal cancer was published in 2015 in Japanese.ObjectiveThe JSGO committee decided to publish the English version of the JSGO guidelines worldwide, and hope it will be a useful guide to physicians in a similar situation as in Japan.MethodsThe guideline was created according to the basic principles in creating the guidelines of JSGO.ResultsThe guidelines consist of five chapters and five algorithms. Prior to the first chapter, basic items are described including staging classification and history, classification of histology, and definition of the methods of surgery, radiation, and chemotherapy to give the reader a better understanding of the contents of the guidelines for these rare tumors. The first chapter gives an overview of the guidelines, including the basic policy of the guidelines. The second chapter discusses vulvar cancer, the third chapter discusses vaginal cancer, and the fourth chapter discusses vulvar Paget’s disease and malignant melanoma. Each chapter includes clinical questions, recommendations, backgrounds, objectives, explanations, and references. The fifth chapter provides supplemental data for the drugs that are mentioned in the explanation of clinical questions.ConclusionOverall, the objective of these guidelines is to clearly delineate the standard of care for vulvar and vaginal cancer with the goal of ensuring a high standard of care for all women diagnosed with these rare diseases

Distribution of Virulence Markers among <em>Vibrio vulnificus</em> Isolates of Clinical and Environmental Origin and Regional Characteristics in Japan

<div><h3>Background</h3><p><em>Vibrio vulnificus</em> is an opportunistic human pathogen that is widely distributed in estuarine environments and is capable of causing necrotizing fasciitis and sepsis. In Japan, based on epidemiological research, the incidences of <em>V. vulnificus</em> were concentrated in Kyusyu, mainly in coastal areas of the Ariake Sea. To examine the virulence potential, various genotyping methods have recently been developed. This study aimed to investigate the distribution of virulence markers among <em>V. vulnificus</em> isolates of clinical and environmental origin in three coastal areas with different infection incidences and to determine whether these isolates have the siderophore encoding gene <em>viuB</em>.</p> <h3>Methodology/Principal Findings</h3><p>We examined the distribution of genotypes of the 16S ribosomal ribonucleic acid (rRNA) gene, <em>vvhA</em>, <em>vcg</em>, and capsular polysaccharide (CPS), and the presence of <em>viuB</em> in 156 isolates collected from patients and environmental samples in Japan. The environmental samples were collected from three coastal areas: the Ariake Sea, Ise & Mikawa Bay, and Karatsu Bay. The results showed disparity in the ratios of genotypes depending on the sample origins. <em>V. vulnificus</em> isolates obtained from patients were classified into the clinical type for all genotypes. In the environmental isolates, the ratios of the clinical type for genotypes of the 16S rRNA gene, <em>vvhA</em>, and <em>vcg</em> were in the order of the Ariake Sea>Ise & Mikawa Bay>Karatsu Bay. Meanwhile, CPS analysis showed no significant difference. Most isolates possessed <em>viuB</em>.</p> <h3>Conclusions</h3><p>Many <em>V. vulnificus</em> belonging to the clinical type existed in the Ariake Sea. Three coastal areas with different infection incidences showed distinct ratios of genotypes. This may indicate that the distribution of clinical isolates correlates with the incidence of <em>V. vulnificus</em> infection.</p> </div

Distribution of genotypes and <i>viuB</i> proportion of <i>V. vulnificus</i> according to clinical and Ariake Sea isolates.

a<p>NA, not amplified.</p><p>rRNA, ribosomal ribonucleic acid; CPS, capsular polysaccharide.</p

Map of sampling points.

<p>The prefectures indicated by dots are areas where <i>V. vulnificus</i> infections occurred. 1, Saga; 2, Nagasaki; 3, Fukuoka; 4, Kumamoto; and 5, Aichi prefectures.</p

Ratio of genotypic profile according to isolate origins.

<p>The ratio of profile of clinical and environmental isolates is shown. The three main genotypic profiles were combined. Profile 1 (clinical type) consisted of 16S rRNA gene type B, <i>vvhA</i> type 1, and <i>vcg</i> C-type; profile 2 (non-clinical type) consisted of type A, type 2, and E-type; and profile 4 consisted of type B, type 2 and C-type. Other combination types were set to untypeable.</p

Distribution of genotypes and <i>viuB</i> proportion of <i>V. vulnificus</i> according to environmental isolate origins.

a<p>NA, not amplified.</p><p>rRNA, ribosomal ribonucleic acid; CPS, capsular polysaccharide.</p

Decreased Amyloidogenicity Caused by Mutational Modulation of Surface Properties of the Immunoglobulin Light Chain BRE Variable Domain

Amyloid formation by immunoglobulin light chain (LC) proteins is associated with amyloid light chain (AL) amyloidosis. Destabilization of the native state of the variable domain of the LC (V_L) is known to be one of the critical factors in promoting the formation of amyloid fibrils. However, determining the key residues involved in this destabilization remains challenging, because of the existence of a number of intrinsic sequence variations within V_L. In this study, we identified the key residues for destabilization of the native state of amyloidogenic V_L in the LC of BRE by analyzing the stability of chimeric mutants of BRE and REI V_L; the latter immunoglobulin is not associated with AL amyloidosis. The results suggest that the surface-exposed residues N45 and D50 are the key residues in the destabilization of the native state of BRE V_L. Point mutations at the corresponding residues in REI V_L (K45N, E50D, and K45N/E50D) destabilized the native state and increased amyloidogenicity. However, the reverse mutations in BRE V_L (N45K, D50E, and N45K/D50E) re-established the native state and decreased amyloidogenicity. Thus, analyses using chimeras and point mutants successfully elucidated the key residues involved in BRE V_L destabilization and increased amyloidogenic propensity. These results also suggest that the modulation of surface properties of wild-type V_L may improve their stability and prevent the formation of amyloid fibrils