Unexpected selective gas adsorption on a 'non-porous' metal organic framework

A metal organic framework Cu(tpt)BF 4· 3 4 H 2O was synthesized as a potential carbon capture material, with the aim being to exploit the Lewis base interaction of the incorporated ligand functionalities with acidic gas. The material displays high thermal stability but an exceptionally low surface area; however, this contrasts starkly with its ability to capture carbon dioxide, demonstrating significant activated diffusion within the framework. The full characterization of the material shows a robust structure, where the CO 2 sorption is 120% greater than current industrial methods using liquid amine solutions; the thermal energy required for sorbent regeneration is reduced by 65%, indicating the true industrial potential of the synthesized material

Regulation of Cardiac Stress Signaling by Protein Kinase D1

In response to pathological stresses such as hypertension or myocardial infarction, the heart undergoes a remodeling process that is associated with myocyte hypertrophy, myocyte death, and fibrosis. Histone deacetylase 5 (HDAC5) is a transcriptional repressor of cardiac remodeling that is subject to phosphorylation-dependent neutralization in response to stress signaling. Recent studies have suggested a role for protein kinase C (PKC) and its downstream effector, protein kinase D1 (PKD1), in the control of HDAC5 phosphorylation. While PKCs are well-documented regulators of cardiac signaling, the function of PKD1 in heart muscle remains unclear. Here, we demonstrate that PKD1 catalytic activity is stimulated in cardiac myocytes by diverse hypertrophic agonists that signal through G protein-coupled receptors (GPCRs) and Rho GTPases. PKD1 activation in cardiomyocytes occurs through PKC-dependent and -independent mechanisms. In vivo, cardiac PKD1 is activated in multiple rodent models of pathological cardiac remodeling. PKD1 activation correlates with phosphorylation-dependent nuclear export of HDAC5, and reduction of endogenous PKD1 expression with small interfering RNA suppresses HDAC5 shuttling and associated cardiomyocyte growth. Conversely, ectopic overexpression of constitutively active PKD1 in mouse heart leads to dilated cardiomyopathy. These findings support a role for PKD1 in the control of pathological remodeling of the heart via its ability to phosphorylate and neutralize HDAC5

MOXI Is a Mitochondrial Micropeptide That Enhances Fatty Acid β-Oxidation

Summary: Micropeptide regulator of β-oxidation (MOXI) is a conserved muscle-enriched protein encoded by an RNA transcript misannotated as non-coding. MOXI localizes to the inner mitochondrial membrane where it associates with the mitochondrial trifunctional protein, an enzyme complex that plays a critical role in fatty acid β-oxidation. Isolated heart and skeletal muscle mitochondria from MOXI knockout mice exhibit a diminished ability to metabolize fatty acids, while transgenic MOXI overexpression leads to enhanced β-oxidation. Additionally, hearts from MOXI knockout mice preferentially oxidize carbohydrates over fatty acids in an isolated perfused heart system compared to wild-type (WT) animals. MOXI knockout mice also exhibit a profound reduction in exercise capacity, highlighting the role of MOXI in metabolic control. The functional characterization of MOXI provides insight into the regulation of mitochondrial metabolism and energy homeostasis and underscores the regulatory potential of additional micropeptides that have yet to be identified. : Micropeptide regulator of β-oxidation (MOXI) is encoded by a muscle-enriched RNA transcript misannotated as non-coding. MOXI localizes to the inner mitochondrial membrane where it interacts with the trifunctional protein to modulate fatty acid β-oxidation and exercise capacity. Keywords: micropeptide, fatty acid oxidation, metabolism, mitochondria, trifunctional protein, noncoding RN

Perioperative Aspirin Use is Associated with Bleeding Complications During Robotic Partial Nephrectomy

INTRODUCTION AND OBJECTIVE: Daily aspirin use following cardiovascular intervention is commonplace and creates concern regarding bleeding risk in patients undergoing surgery. Despite its cardio-protective role, aspirin is often discontinued 5-7 days prior to major surgery due to bleeding concerns. Single institution studies have investigated perioperative outcomes of aspirin use in robotic partial nephrectomy (RPN). We sought to evaluate the outcomes of perioperative aspirin (pASA) use during RPN in a multicenter setting. METHODS: We performed a retrospective evaluation of patients undergoing RPN at 5 high volume RPN institutions. We compared perioperative outcomes of patients taking pASA (81 mg) to those not on aspirin. We analyzed the association between pASA use and perioperative transfusion. RESULTS: Of 1565 patients undergoing RPN, 228 (14.5%) patients continued pASA and were older (62.8 vs. 56.8 years, p \u3c0.001) with higher Charlson scores (mean 3 vs. 2, p \u3c0.001). pASA was associated with increased perioperative blood transfusions (11% vs. 4%, p \u3c0.001) and major complications (10% vs. 3%, p \u3c0.001). On multivariable analysis, pASA was associated with increased transfusion risk (OR 1.94, 1.10-3.45, 95% CI). CONCLUSIONS: In experienced hands, perioperative aspirin 81 mg use during RPN is reasonable and safe, however, there is a higher risk of blood transfusions and major complications. Future studies are needed to clarify the role of antiplatelet therapy in RPN patients requiring pASA for primary or secondary prevention of cardiovascular events

Confocal SERS mapping of glycan expression for the identification of cancerous cells

Lectin-functionalized silver nanoparticles have been successfully designed for use as molecular imaging agents to investigate carbohydrate-lectin interactions at the surface of mammalian cells, using surface-enhanced Raman scattering (SERS). Carbohydrate-lectin interactions are key to many cellular processes and are responsible for controlling an array of cellular interactions. In this study, lectin-functionalized silver nanoparticles were used to detect the expression of carbohydrate species at the cellular interface. The carbohydrate-lectin interactions were demonstrated using three different lectin species for three distinct cell types. Due to the known difference between the expressions of glycans in cancerous versus noncancerous cells of the same origin, this approach has been expanded to study both cancerous and noncancerous prostate cells. This has been achieved via confocal SERS mapping of the expression of the key glycan, sialic acid, on the surface of each of these cell types. In achieving such discrimination, a novel method has been created by which glycan expression can be reproducibly monitored. Comparative studies were performed using both fluorescence and SERS. SERS provided an increased discrimination over fluorescence when analyzing cell subsets to discriminate between cancerous and noncancerous cells. The success of this method means that it could be used to complement the current gold standard histopathological techniques