Block Copolymer Self-assembly: Exploitation of Hydrogen Bonding for Nanoparticle Morphology Control via Incorporation of Triazine Based Comonomers by RAFT Polymerization.

Synthesis of polymeric nanoparticles of controlled non-spherical morphology is of profound interest for a wide variety of potential applications. Self-assembly of amphiphilic diblock copolymers is an attractive bottom-up approach to prepare such nanoparticles. In the present work, RAFT polymerization is employed to synthesize a variety of poly(N,N-dimethylacrylamide)-b-poly[butyl acrylate-stat-GCB] copolymers, where GCB represents vinyl monomer containing triazine based Janus guanine-cytosine nucleobase motifs featuring multiple hydrogen bonding arrays.

Cytoskeleton crosstalk: Casting stable actin bundles with dynamic microtubule molds.

Actin-microtubule crosstalk diversifies cytoskeletal networks. A new study provides insight into how the microtubule polymerase CKAP5 mediates actin-microtubule crosstalk. CKAP5 directs the assembly of stable actin bundles on dynamic microtubules; in turn, the actin bundles align growing microtubules along their length.

Cytoskeletal regulation of a transcription factor by DNA mimicry via coiled-coil interactions.

A long-established strategy for transcription regulation is the tethering of transcription factors to cellular membranes. By contrast, the principal effectors of Hedgehog signalling, the GLI transcription factors, are regulated by microtubules in the primary cilium and the cytoplasm. How GLI is tethered to microtubules remains unclear.

Molecular mechanisms and structural features of cardiomyopathy-causing troponin T mutants in the tropomyosin overlap region.

Point mutations in genes encoding sarcomeric proteins are the leading cause of inherited primary cardiomyopathies. Among them are mutations in the gene that encodes cardiac troponin T (TnT). These mutations are clustered in the tropomyosin (Tm) binding region of TnT, TNT1 (residues 80-180).

Mechanistic heterogeneity in contractile properties of α-tropomyosin (TPM1) mutants associated with inherited cardiomyopathies.

The most frequent known causes of primary cardiomyopathies are mutations in the genes encoding sarcomeric proteins. Among those are 30 single-residue mutations in TPM1, the gene encoding α-tropomyosin. We examined seven mutant tropomyosins, E62Q, D84N, I172T, L185R, S215L, D230N, and M281T, that were chosen based on their clinical severity and locations along the molecule.

Metastatic proximal epithelioid sarcoma in pleural effusion: cytopathologic findings and differential diagnosis.

We present a rare occurrence of metastatic proximal epithelioid sarcoma (PES) in the pleural effusion of a 23-year-old man, developed within one year of diagnosis in his gluteal soft tissue. The cytologic and immunoperoxidase findings are described. PES, due to its epithelioid morphology, can be confused with more common cancers in effusions such as adenocarcinoma and mesothelioma.

Vascular endothelial growth factor is increased by human pulmonary cells stimulated with Dermatophagoides sp. extract.

Airway remodeling may lead to increased secretion of TGF-beta. TGF-beta is known to activate fibroblasts and to stimulate the secretion of vascular endothelial growth factor (VEGF). Soluble and cell-associated VEGF have been identified in subjects with chronic severe asthma.

Effects of pentoxyfylline on mesenteric lymph node T-cells in a rat model of thermal injury.

Cutaneous burn injury-induced T lymphocyte suppression is a well-known phenomenon. In this study, we evaluated the effect of treatment of burn rats with pentoxifylline (PTX) on the burn-induced suppression of T lymphocytes. Anesthetized rats were subjected to 30% total body surface area burn by exposing skin to 95 degrees C water for 10 s.

Enteral nutritional supplementation prevents mesenteric lymph node T-cell suppression in burn injury.

Objective: To determine the effects of an immune-enhancing diet supplemented with glutamine, arginine, fish oil, and dietary nucleotides on mesenteric lymph node T-cell functional disturbances encountered after burn injury in rats.

Design: A prospective animal study.

Setting: University medical center research laboratory.

Enterococcus faecalis exacerbates burn injury-induced host responses in rats.

Pathophysiology of burn injury with complications of gram-positive infections is not well characterized. We have developed an in vivo rat model to study the effects of burn injury along with intra-abdominal inoculation of Enterococcus faecalis. We hypothesized that although burn injury or E.

Role of NFAT and AP-1 in PGE2-mediated T cell suppression in burn injury.

PGE2 is known to suppress T cell proliferation and IL-2 production in many inflammatory conditions. Previous studies from our laboratory have shown that such suppression of T cell proliferation in burn and sepsis could result from alteration in T cell activation signaling molecule p59fyn. In this study, we examined the role of downstream signaling molecules NFAT and AP-1 in PGE2-mediated suppression of T cell in burn injury.