Finding the Sweet Spot of Photocatalysis─A Case Study Using Bipyridine-Based CTFs.

Covalent triazine frameworks (CTFs) are a class of porous organic polymers that continuously attract growing interest because of their outstanding chemical and physical properties. However, the control of extended porous organic framework structures at the molecular scale for a precise adjustment of their properties has hardly been achieved so far. Here, we present a series of bipyridine-based CTFs synthesized through polycondensation, in which the sequence of specific building blocks is well controlled.

The lung function score and its components as predictors of overall survival and chronic graft-vs-host disease after allogeneic stem cell transplantation.

Aim: To retrospectively assess if the modified lung function score (LFS) and/or its components, forced expiratory volume within the first second (FEV1) and diffusion capacity for carbon monoxide corrected for hemoglobin level (cDLCO), predict overall survival (OS) and chronic graft-vs-host-disease (cGvHD).

Methods: We evaluated 241 patients receiving allogeneic hematopoietic stem cell transplantation (allo-HSCT) at the University of Regensburg Transplant Center between June 1998 and July 2005 in relation to their LFS, FEV1 and cDLCO, before and after HSCT.

Results: Decreased OS after allo-HSCT was related to decreased pre-transplantation values of FEV1<60% (P=0.

Salvage therapy with everolimus reduces the severity of treatment-refractory chronic GVHD without impairing disease control: a dual center retrospective analysis.

Chronic GVHD (cGVHD) remains the most important cause of late non-relapse mortality post allogeneic hematopoietic SCT (HSCT). Although first-line treatment of cGVHD with steroids is well established, evidence for second-line treatment remains limited. Here, we report a dual center retrospective analysis of the off-label salvage treatment of steroid-refractory cGVHD with everolimus.

Role of calcineurin and protein phosphatase-2A in the regulation of phosphatase inhibitor-1 in cardiac myocytes.

Inhibitor 1 (I-1) is a protein inhibitor of protein phosphatase 1 (PP1), the predominating Ser/Thr phosphatase in the heart. Non-phosphorylated I-1 is inactive, whereas I-1 phosphorylated by protein kinase A (PKA) at Thr35 is a potent PP1 inhibitor. The phosphatases that dephosphorylate I-1Thr35 and thus deactivate I-1 in the heart are not established.

Decreased protein and phosphorylation level of the protein phosphatase inhibitor-1 in failing human hearts.

Objective: The protein phosphatase inhibitor-1 (I-1) is a highly specific and potent inhibitor of type 1 phosphatases (PP1) that is active only in its protein kinase A (PKA)-phosphorylated form. I-1 ablation decreases, I-1 overexpression sensitizes beta-adrenergic signaling in the heart. It is controversial whether I-1 expression is altered in human heart failure (HF), likely because its detection in heart is difficult due to its low abundance.

Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes.

The protein phosphatase inhibitor-1 (PPI-1) inhibits phosphatase type-1 (PP1) only when phosphorylated by protein kinase A and could play a pivotal role in the phosphorylation/dephosphorylation balance. Rat cardiac PPI-1 was cloned by reverse transcriptase-polymerase chain reaction, expressed in Eschericia coli, evaluated in phosphatase assays, and used to generate an antiserum. An adenovirus was constructed encoding PPI-1 and green fluorescent protein (GFP) under separate cytomegalovirus promotors (AdPPI-1/GFP).