A Case of Idiopathic Thrombocytopenic Purpura Involving Diffuse Alveolar Hemorrhage

Idiopathic Thrombocytopenic Purpura（ITP） is an autoimmune disease which cause thrombocytopenia by the autoantibody against plateletmembrane glycoproteins. It usually develops petechiae, purpra of the skin and mucosal bleeding for thrombocytopenia. It is uncommon for diffuse alveolar hemorrhage to be developed by ITP. We experienced　a case of ITP in which ａ respiratory infection involved diffuse alveolar hemorrhage. Here we propose the possibility that alveolar inflammation participates in development of a diffuse alveolar hemorrhage, so it is necessary to pay enough attention to ａ respiratory infection in ITP

The Hydrogen Burning Turn-off of RS Ophiuchi 2006

We report a coordinated multi-band photometry of the RS Oph 2006 outburst and highlight the emission line free y-band photometry that shows a mid-plateau phase at y ~ 10.2 mag from day 40 to day 75 after the discovery followed by a sharp drop of the final decline. Such mid-plateau phases are observed in other two recurrent novae, U Sco and CI Aql, and are interpreted as a bright disk irradiated by the white dwarf. We have calculated theoretical light curves based on the optically thick wind theory and have reproduced the observed light curves including the mid-plateau phase and the final sharp decline. This final decline is identified with the end of steady hydrogen shell-burning, which turned out the day ~80. This turnoff date is consistent with the end of a supersoft X-ray phase observed with Swift. Our model suggests a white dwarf mass of 1.35 \pm 0.01 M_\sun, which indicates that RS Oph is a progenitor of Type Ia supernovae. We strongly recommend the y-filter observation of novae to detect both the presence of a disk and the hydrogen burning turn-off.Comment: to appear in ApJL, 4 pages including 4 figure

Phase II trial of erlotinib in patients with advanced non-small-cell lung cancer harboring epidermal growth factor receptor mutations: additive analysis of pharmacokinetics

Background: We conducted a phase II trial of erlotinib in patients with advanced non-small-cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations and evaluated the relationship between plasma concentration and efficacy of erlotinib. Methods: Patients who were previously treated but naive to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs), with advanced NSCLC harboring EGFR mutations, were enrolled. Erlotinib was given at 150 mg once daily until disease progression. The primary end point was objective response rate (ORR). Plasma trough levels of erlotinib were measured on Days 2 (D2) and 8 (D8) by high-performance liquid chromatography. Results: In total, 29 patients were enrolled from September 2008 to January 2011. ORR was 61.5 % (95 % confidence interval [CI] 40.57-79.8) of 26 assessable patients. The median progression-free survival (PFS) and overall survival (OS) were 6.3 months and 16.9 months, respectively. Skin rash was observed in 24 patients, mostly at grade 1 or 2. Grade 2 pneumonitis was observed in one patient. We collected blood samples from 16 patients. The median PFS of the high and low D8/D2 ratio group was 11.2 months and 5.7 months, respectively (p = 0.044, hazard ratio = 0.301, 95 % CI 0.094-0.968). Conclusion: Erlotinib showed an ORR comparable to that seen in previous studies for patients with NSCLC harboring EGFR mutations, although response, the primary end point, did not reach the predetermined threshold level. The D8/D2 ratio of erlotinib plasma trough levels might be a predictive factor for PFS

Polymorphisms of PTPN11 coding SHP-2 as biomarkers for ulcerative colitis susceptibility in the Japanese population.

OBJECTIVE: To identify genetic determinants of inflammatory bowel disease (IBD), we examined an association between polymorphisms of both the programmed cell death 1 gene (PDCD1) and the src homology 2 domain-containing tyrosine phosphatase 2 gene (PTPN11) and susceptibility to IBD. METHODS: Study subjects comprised 114 patients with ulcerative colitis (UC), 83 patients with Crohn\u27s disease, and 200 healthy control subjects. Five single nucleotide polymorphisms (SNPs) in PDCD1 and PTPN11 were detected by polymerase chain reaction restriction fragment length polymorphism. Subsequently, haplotypes composed of the two SNPs in PTPN11 were constructed. RESULTS: The frequencies of the Hap 1 haplotype and its homozygous Hap 1/Hap 1 diplotype of PTPN11 were significantly increased in UC patients compared to control subjects (P = 0.011 and P = 0.030, respectively). While no association was found for PDCD1 for UC or CD and none for PTPN11 for CD. CONCLUSION: PTPN11 is a genetic determinant for the pathogenesis of UC, and haplotyping of PTPN11 may be useful as a genetic biomarker to identify high-risk individuals susceptible to UC

A Case of a Patient Who Successfully Achieved Early Wound Closure by Local Negative Pressure Wound Therapy (NPWT) against Compromised Wound Healing after Arterio-Venous Graft Infection

The primary treatment strategy for arterio-venous graft (AVG) infection includes appropriate antibiotic use and removal of the infected graft. It is well known that patients with hemodialysis are likely to experience compromised wound healing, which often leads to various postoperative complications. Negative pressure wound therapy (NPWT) is a non-invasive procedure that promotes wound healing by sealing the wound under negative pressure. Although NPWT is practically accepted in general surgery, there are only a few reports of this strategy to the vascular access operation for patients with hemodialysis due to the possibility of severe bleeding. In the present report, we report a case of a patient who successfully achieved safe and early wound closure by NPWT against compromised wound healing after AVG infection