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1 (32.1-45.3), 12.6 (6.3-25.2) and 11.8 (9.2-15.0) per 1000-person-years, respectively. Compared to recipients with pretransplant diabetes, recipients with NODAT experienced a lower risk of MACE (adjusted hazard ratio [HR]0.59, 95%CI 0.47-0.74]), but not cardiac death [0.97(0.61-1.55)]. The rate of MACE and cardiac death was lowest in patients without diabetes.

Patients with pretransplant diabetes incur the greatest rate of MACE and cardiac deaths after transplantation. read more Having NODAT also bear high burden of vascular events compared to those without diabetes, but the magnitude of the increased rate remains lower than recipients with pretransplant diabetes.

Patients with pretransplant diabetes incur the greatest rate of MACE and cardiac deaths after transplantation. Having NODAT also bear high burden of vascular events compared to those without diabetes, but the magnitude of the increased rate remains lower than recipients with pretransplant diabetes.

Chronic lung allograft dysfunction (CLAD) and its obstructive form, the obliterative bronchiolitis (OB), are the main long-term complications related to high mortality rate postlung transplantation. CLAD treatment lacks a significant success in survival. Here, we investigated a new strategy through inhibition of the proinflammatory mitogen- and stress-activated kinase 1 (MSK1) kinase.

MSK1 expression was assessed in a mouse OB model after heterotopic tracheal allotransplantation. Pharmacological inhibition of MSK1 (H89, fasudil, PHA767491) was evaluated in the murine model and in a translational model using human lung primary fibroblasts in proinflammatory conditions. MSK1 expression was graded over time in biopsies from a cohort of CLAD patients.

MSK1 mRNA progressively increased during OB (6.4-fold at D21 posttransplantation). Inhibition of MSK1 allowed to counteract the damage to the epithelium (56% restoration for H89), and abolished the recruitment of MHCII+ (94%) and T cells (100%) at the early inflammatory phase of OB. In addition, it markedly decreased the late fibroproliferative obstruction in allografts (48%). MSK1 inhibitors decreased production of IL-6 (whose transcription is under the control of MSK1) released from human lung fibroblasts (96%). Finally, we confirmed occurrence of a 2.9-fold increased MSK1 mRNA expression in lung biopsies in patients at 6 months before CLAD diagnosis as compared to recipients with stable lung function.

These findings suggest the overall interest of the MSK1 kinase either as a marker or as a potential therapeutic target in lung dysfunction posttransplantation.

These findings suggest the overall interest of the MSK1 kinase either as a marker or as a potential therapeutic target in lung dysfunction posttransplantation.

Posttransplant Lymphoproliferative Disorders (PTLD) encompass a spectrum of heterogeneous entities. Because the vast majority of cases PTLD arise from B cells, available data on PTLD of T or NK phenotype (T/NK-cell PTLD) are scarce, which limits the quality of the management of these patients.

All adult cases of PTLD diagnosed in France were prospectively recorded in the national registry between 1998 and 2007. Crosschecking the registry data with 2 other independent national databases identified 58 cases of T/NK-cell PTLD. This cohort was then compared with i) the 395 cases of B-cell PTLD from the registry, and of ii) a cohort of 148 T/NK-cell lymphomas diagnosed in nontransplanted patients.

T/NK-cell PTLD occurred significantly later after transplantation and had a worse overall survival than B-cell PTLD. Two subtypes of T/NK-cell PTLD were distinguished i) cutaneous (28%) and ii) systemic (72%), the latter being associated with a worse prognosis. Compared with T/NK-cell lymphomas of nontransplanted patients, overall survival of systemic T/NK-cell PTLD was worse (HR 2.64[1.76-3.94]; p<0.00001).

This difference, which persisted after adjustment on tumoral mass, histological subtype, and extension of the disease at diagnosis could be explained by the fact that transplanted patients were less intensively treated and responded less to chemotherapy.

This difference, which persisted after adjustment on tumoral mass, histological subtype, and extension of the disease at diagnosis could be explained by the fact that transplanted patients were less intensively treated and responded less to chemotherapy.

Hypothermic Machine Perfusion (HMP) is a well-established method for deceased donor kidney preservation. Normothermic Machine Perfusion (NMP) might offer similar or greater advantages. We compared the two methods in an ex vivo perfusion model using 34 porcine kidneys.

Thirty kidneys were stored on ice for 24h before undergoing 4h of HMP (n=15) or NMP (n=15) followed by 2h of normothermic ex vivo reperfusion with whole blood. Four kidneys underwent 28h of cold static storage (CSS) followed by 2h of normothermic ex vivo reperfusion. During the 2 hours of normothermic ex vivo reperfusion perfusate flow rates, urinary output and oxygen consumption rates were compared between all groups.

Porcine kidneys after HMP showed significantly higher urinary output- (5.31ml/min±2.06ml/min vs. 2.44ml/min±1.19ml/min, p=0.002), oxygen consumption- (22.71±6.27ml/min vs. 11.83±1.29ml/min, p=0.0016) and perfusate flow rates (46.24±12.49ml/min vs. 26.16±4.57ml/min, p=0.0051) than kidneys after NMP. Tunnel staining of tissue sections showed significantly higher rates of apoptosis in kidneys after NMP (p=0.027).

In our study, the direct comparison of HMP and NMP kidney perfusion in a translational model demonstrated superiority of HMP, however further in vivo studies would be needed to validate those results.

In our study, the direct comparison of HMP and NMP kidney perfusion in a translational model demonstrated superiority of HMP, however further in vivo studies would be needed to validate those results.Interpretation of gastrointestinal PET/computed tomography (PET/CT) is often complicated by anatomy including bowel folds, flexures, variant redundancy, decompressed bowel segments and physiological uptake. This makes it very difficult to identify both true positives and true negatives, compromising both sensitivity and specificity. CT enterography is increasingly being integrated into the field of nuclear medicine to address these issues. This technique uses the combination of negative/neutral contrast to distend the lumen of the gut and iodinated contrast to enhance the gastrointestinal wall and pathological findings. Apart from augmentation in the diagnostic performance, the technique also improves the quality of the imaging, confidence of the reporting physician and inter-rater agreement. Therefore, this technique has found favor among nuclear medicine physicians, in the imaging of chronic inflammatory disorders and malignancies in and of the gut. It is a feasible and easily executable procedure with minimal and manageable side-effects and should be routinely recommended in cases where interference from physiologic findings is expected.