Charge Exchange X-ray Emission Detected in Multiple Shells of Supernova Remnant G296.1-0.5

Recent high-resolution X-ray spectroscopy revealed possible presence of charge exchange (CX) X-ray emission in supernova remnants (SNRs). Although CX is expected to take place at outermost edges of SNR shells, no significant measurement has been reported so far due to the lack of nearby SNR samples. Here we present an X-ray study of SNR G296.1$-$0.5, which has a complicated multiple-shell structure, with the Reflection Grating Spectrometer (RGS) onboard XMM-Newton. We select two shells in different regions and find that in both regions O VII line shows a high forbidden-to-resonance ($f/r$) ratio that cannot be reproduced by a simple thermal model. Our spectral analysis suggests a presence of CX and the result is also supported by our new radio observation, where we discover evidence of molecular clouds associated with these shells. Assuming G296.1$-$0.5 has a spherical shock, we estimate that CX is dominant in a thin layer with a thickness of 0.2--0.3\% of the shock radius. The result is consistent with a previous theoretical expectation and we therefore conclude that CX occurs in G296.1$-$0.5.Comment: 11 pages, 8 figure

ゾウキ イショクゴ ノ メンエキ カンヨウ ニ オケル メンエキ ヨクセイ ノ イギ

京都大学0048新制・課程博士博士(医学)甲第10094号医博第2604号新制||医||828(附属図書館)UT51-2003-H515京都大学大学院医学研究科外科系専攻(主査)教授 〓 長博, 教授 米田 正始, 教授 田中 絋一学位規則第4条第1項該当Doctor of Medical ScienceKyoto UniversityDA

Homologue-based Estimations of Short-Chain Chlorinated Paraffin Emissions and Concentrations in Japan

Short-chain chlorinated paraffins (SCCPs) are persistent organic pollutants. In Japan, SCCPs are widely detected in the environment although the production and use of SCCPs have been banned. It is essential to estimate the amount and sources of SCCPs to implement countermeasures for SCCP emission. In this study, we estimated the emission and environmental concentrations of SCCP homologues in Japan from 1950 to 2050. Initially, the material flow of total SCCPs was estimated considering the material recycling process. The emission from each process during the entire life cycle of products containing SCCPs was estimated for each homologue. Volatilization factors of long-term-use products were specifically estimated from release factors and surface area, weight, and SCCP concentration of products containing SCCPs. The environmental concentrations were then estimated using the environmental fate model. In the material flow and emission estimation, parameter uncertainties, such as emission factors and SCCP application distribution, were considered, assuming each parameter follows a uniform distribution. The results of emission estimation suggested a decreasing trend of SCCP emission in recent years and continuation of this trend in the future. However, some emissions from long-term-use products may persist. In the future, products that have a long lifetime with closed-loop recycling, such as polyvinyl chloride wire-coating materials, are expected to significantly contribute to atmospheric emission. Moreover, recycled products may contain SCCPs. Based on the estimated concentration, the estimated water and sediment concentrations were within the range of the observed concentrations. Conversely, we could reduce the gap between the estimated and observed atmospheric SCCP concentrations compared with those in previous studies that did not consider the volatilization factor for each SCCP-containing product and material recycling process. However, a difference between the estimated and observed concentrations suggests that some unconsidered emission sources may exist that emit SCCPs into the atmosphere, such as SCCPs as impurities in medium-chain chlorinated paraffins, imported products containing SCCPs, and atmospheric advection from other countries. Hence, it is essential to calculate emissions from sources other than products that intentionally contain SCCPs produced in the past

Type of donor aortic preservation solution and not cold ischemia time is a major determinant of biliary strictures after liver transplantation

The development of biliary strictures (BSs) after liver transplantation (LT) continues to affect 10% to 30% of patients, causing substantial morbidity. The cause of BSs is multifactorial, including technical, immune, and, in particular, ischemic factors. The importance of adequate flushing of the peribiliary arterial tree has been stressed. We hypothesized that high-viscosity (HV) preservation solutions in the donor do not completely flush the small donor peribiliary plexus, leading to inadequate preservation of the bile ducts and posttransplant BSs. To test this hypothesis, we retrospectively compared the incidence of BSs in 2 groups of adults undergoing LT using different types of aortic preservation solution in the donor: group 1 (n = 24), low-viscosity (LV) Marshall solution; and group 2 (n = 27), HV University of Wisconsin (UW) solution. All donors in both groups received additional portal flushes with UW. All LTs were performed between November 1995 and August 1998 at 2 centers by the same surgeon, eliminating a technical bias. Terminal duct-to-duct anastomosis was performed in all recipients except 1 patient in group 1, who underwent a bile duct-to-jejunum anastomosis. BSs were first suspected on clinical and biochemical grounds and then confirmed by endoscopic retrograde cholangiopancreatography. Identical medical protocols were used in all patients. One-year patient survival rates in groups 1 and 2 were 92% and 100%, respectively (P =.9). One-year graft survival was identical to patient survival. The incidence of BSs in group 1 was 4.1% (1 of 24 patients), compared to 29.7% in group 2 (8 of 27 patients; P =.02). The BS in group 1 occurred 4 months post-LT and was anastomotic. BSs in group 2 occurred between 1 and 12 months post-LT and were anastomotic, extrahepatic, intrahepatic, or combined intrahepatic and extrahepatic. There were no significant differences in the following factors between groups 1 and 2: donor age, local versus imported liver, split-liver or full-liver transplantation, incidence of multiple vessels in the donor liver, indications for LT, recipient age, T-tube versus no T-tube, post-LT peak aspartate aminotransferase level, and treatment for rejection. There was no hepatic artery thrombosis or primary nonfunction in either group. Interestingly, cold ischemia time (CIT) was longer in group 1, which had the least incidence of BSs (692 +/- 190 v 535 +/- 129 minutes in group 2; P =.001). Follow-up was longer in group 1 (28.9 +/- 8.3 v 15.6 +/- 8 months in group 2; P =.0001). Preservation costs per procurement were 1.9 times greater in the UW group than in the Marshall group. Donor aortic flushing with an HV preservation solution leads to more frequent BSs compared with an LV preservation solution. The impact of preservation solution outweighs the previously described deleterious impact of prolonged CIT. Mixed preservation solution (Marshall solution in the aorta, UW solution in the portal vein) might protect against BS formation while providing optimal liver graft preservation, function, and survival despite a mean CIT longer than 10 hours.status: publishe

Aplastic anemia after transplantation for non-A, non-B, non-C fulminant hepatic failure: case report and review of the literature

Aplastic anemia is a rare complication of liver transplantation (<1%). However, an increasing number of cases of aplastic anemia have been recently reported when liver transplantation is performed for non-A, non-B, non-C fulminant hepatic failure. The aim of this study is to reevaluate the importance and the incidence of aplastic anemia after liver transplantation for non-A, non-B, non-C fulminant hepatic failure, and to propose preventive measures, diagnostic and management guidelines to try to reduce the incidence, morbidity and mortality associated with this complication. In this report a case of aplastic anemia after liver transplantation for non-A, non-B, non-C fulminant hepatic failure is described. In addition, the pertinent literature on aplastic anemia after liver transplantation, since the first description of that complication in 1987, is reviewed. A 20-year-old woman developed aplastic anemia 14 weeks after liver transplantation for fulminant non-A, non-B, non-C hepatitis. After failure of G-CSF treatment, she was treated with intensive immunosuppression (FK 506, ATG, high-dose steroids). She is well 1 year post-transplantation, with normal liver tests and with bone marrow recovery. Through a Medline literature search (1988-1999), we identified 30 additional cases of aplastic anemia following liver transplantation for non-A, non-B, non-C fulminant hepatic failure. Of all liver transplantations performed for that indication at five participating centers, the mean incidence of aplastic anemia was 23.2%. Mean age was 10 years (1.2-29) and the male/female ratio was 4.6. For treating aplastic anemia, different modalities were used: ATG ( n=12), ALG ( n=1), OKT 3 ( n=1), G-CSF ( n=6), a 6-HLA-compatible bone marrow transplantation ( n=3), and none ( n=12). The mortality rate remains high (39%), with infections and bleeding as the two most frequent causes of death. Based on this literature review, we conclude that aplastic anemia is a relatively common complication of liver transplantation for non-A, non-B, non-C fulminant hepatic failure in children and young adults. An unknown viral agent operating through immune-mediated mechanisms is probably responsible. The myelotoxic environment inherent to transplantation (e.g. azathioprine, trimethoprim) probably has a cumulative effect. Preventive measures (e.g. not using myelotoxic drugs) should be adopted in high-risk children and young adults transplanted for non-A, non-B, non-C fulminant hepatic failure. Early detection of bone marrow depression, a low threshold for performing a bone marrow biopsy, and prompt treatment are pivotal. Intensive standard supportive care with broad-spectrum antibiotics and anti-fungal agents is essential during phases of pancytopenia. Although spontaneous recovery has been described under maintenance immunosuppression, increased immunosuppression, in particular with ATG, may reverse the aplastic anemia and promote bone marrow recovery. In unresponsive patients, six-HLA-identical bone marrow transplantation has been successful.status: publishe

Liver transplantation for polycystic liver disease

Polycystic liver disease (PLD) may provoke massive hepatomegaly and severe physical and social handicaps. Data on orthotopic liver transplantation (OLT) for PLD are rare and conflicting. Conservative surgery (resection or fenestration) is indicated for large single cysts, but its value for small diffuse cysts is questionable. In addition, conservative surgery is not devoid of morbidity and mortality. OLT offers the prospect of a fully curative treatment, but controversy remains because those patients usually have preserved liver function. Thus, we reviewed our experience with OLT for PLD. Sixteen adult women underwent OLT for small diffuse PLD between 1990 and 1999. Mean age was 45 years (range, 34 to 56 years). Fourteen patients had combined liver and kidney cystic disease, but only 1 patient required combined liver and kidney transplantation, whereas 13 patients underwent OLT alone. Two patients had isolated PLD. Indications for transplantation were massive hepatomegaly causing physical handicaps (n = 16), social handicaps (n = 16), malnutrition (n = 4), and cholestasis and/or portal hypertension (n = 5). OLT caused no technical difficulty in 15 of 16 patients (surgery duration, 6.8 hours; range, 5 to 8 hours), with blood transfusions of 7.9 units (range, 0 to 22 units). One patient who underwent attempted liver-mass reduction pre-OLT died of bleeding and pulmonary emboli. Native liver weight was 10 to 20 kg. Posttransplantation immunosuppression consisted of cyclosporine or FK506, azathioprine, and steroids (discontinued at 3 months). Morbidity included biliary stricture (2 patients), revision for bleeding and hepatitis (1 patient), pneumothorax and subphrenic collection (1 patient), and tracheostomy (1 patient). One patient died of lung cancer 6 years posttransplantation. Both patient and graft survival rates are 87.5% (follow-up, 3 months to 9 years). Of 15 patients who underwent OLT alone, only 1 patient needed a kidney transplant 4 years after OLT. Kidney function has remained satisfactory in the other patients despite the use of cyclosporine or FK506 (last follow-up creatinine level, 1.55 mg/dL; range, 0.80 to 2.85 mg/dL). OLT had a dramatic impact on daily quality of life, enabling these patients to go back to a fully active life style. OLT offers the chance of a definitive treatment in patients with extensive, small, diffuse PLD that has evolved into severely handicapping hepatomegaly. In contrast to previous studies, combined liver and kidney transplantation is rarely needed. Patient symptoms and chances of definitive palliation offered by OLT must be balanced against the risks of transplantation and lifelong commitment to immunosuppression.status: publishe

Surgical strategy in liver transplantation for polycystic liver disease

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