MCPIP as wound therapy

Disclosed herein are methods and compositions of treating a subject suffering from a wound. In exemplary examples, the method involves elevating MCPIP levels in a subject in need. Elevating MCPIP levels may involve direct administration (e.g. delivery of protein) or indirect administration (e.g. delivery vehicle capable of increasing expression of MCPIP)

MCPIP as wound therapy

Disclosed herein are methods and compositions of treating a subject suffering from a wound. In exemplary examples, the method involves elevating MCPIP levels in a subject in need. Elevating MCPIP levels may involve direct administration (e.g. delivery of protein) or indirect administration (e.g. delivery vehicle capable of increasing expression of MCPIP)

Quantitative Determination of the Critical Points of Mott Metal-Insulator Transition in Strongly Correlated Systems

The Mottness is at the heart of the essential physics in a strongly correlated system as many novel quantum phenomena occur at the metallic phase near the Mott metal-insulator transition. We investigate the Mott metal-insulator transition in a strongly-correlated electron system based on the Hubbard model. The on-site moment evaluated by the dynamical mean-field theory is employed to depict the Mott metal-insulator transition. Conveniently, the on-site moment is a more proper order parameter to quantitatively determine the Mott critical point, in comparison with the corresponding quasiparticle coherent weight. Moreover, this order parameter also gives a consistent description of two distinct forms of the critical points of the Mott metal-insulator transition.Comment: 6 pages, 4 figure

Relação entre a Razão Nitrogênio Ureico/Creatinina e Prognóstico de Insuficiência Cardíaca em Todo o Espectro da Fração de Ejeção

Resumo Fundamento Em pacientes com insuficiência cardíaca (IC), devido à relativa deficiência do volume sanguíneo, a ativação do sistema neuro-hormonal leva à vasoconstrição renal, que afeta o teor de nitrogênio ureico (NU) e creatinina (C) no organismo, sendo que NU e C são facilmente afetados por outros fatores. Portanto, a razão NU/C pode ser utilizada como mais um marcador para o prognóstico da IC. Objetivo Explorar o prognóstico do desfecho adverso da IC no grupo NU/C alta em comparação com o grupo NU/C baixa em todo o espectro da fração de ejeção. Métodos De 2014 a 2016, pacientes sintomáticos hospitalizados com IC foram recrutados e acompanhados para observar desfechos cardiovasculares adversos. Foram realizadas análise logística e a análise COX para determinar a significância. Valores de p<0,05 foram considerados estatisticamente significativos. Resultados Na análise de regressão logística univariada, o grupo NU/C alta apresentou maior risco de desfecho adverso na insuficiência cardíaca com fração de ejeção reduzida (ICFEr) e insuficiência cardíaca com fração de ejeção preservada (ICFEp). A análise de regressão logística multivariada mostrou que o risco de morte cardíaca no grupo ICFEr foi maior do que no grupo NU/C baixa, enquanto o risco de morte por todas as causas foi significativo apenas em 3 meses (p<0,05) (Ilustração Central). O risco de morte por todas as causas no grupo NU/C alta no grupo ICFEP foi significativamente maior do que no grupo NU/C baixa em dois anos. Conclusão O grupo NU/C alta está relacionado ao risco de mau prognóstico da ICFEP, não sendo inferior ao valor preditivo da fração de ejeção do ventrículo esquerdo (FEVE)

CT-guided microcoil localization for scapula-blocked pulmonary nodules using penetrating lung puncture before video-assisted thoracic surgery

PURPOSETo retrospectively analyze the effectiveness and safety of computed tomography (CT)-guided microcoil localization for scapula-blocked pulmonary nodules using penetrating lung puncture prior to video-assisted thoracic surgery (VATS).METHODSOne hundred thirty-eight patients with 138 pulmonary nodules were included in this single-center retrospective study. Among them, 110 patients who underwent CT-guided microcoil localization using the routine puncture technique formed the routine group; the other 28 patients who underwent the CT-guided microcoil localization using the penetrating lung puncture technique formed the penetrating lung group. The main outcomes were the success rate and complication rate of the two groups.RESULTSThe localization success rate was 95.5% (105/110) in the routine group and 89.3% (25/28) in the penetrating lung group (P = 0.205). There was no statistical difference in any of the complications (pneumothorax, intrapulmonary hemorrhage, or moderate and severe chest pain) in both groups (P = 0.178, P = 0.204, P = 0.709, respectively). Localization procedure time was significantly increased in the penetrating lung group compared with the routine group (31.0 ± 3.0 min vs. 21.2 ± 2.8 min, P < 0.001).CONCLUSIONCT-guided microcoil localization for scapula-blocked pulmonary nodules using penetrating lung puncture prior to VATS resection is effective and safe. However, the deployment of the microcoil using penetrating lung puncture required more time than the routine puncture method

Role Of Mcp-1 In Cardiovascular Disease: Molecular Mechanisms And Clinical Implications

Many of the major diseases, including cardiovascular disease, are widely recognized as inflammatory diseases. MCP-1 (monocyte chemotactic protein-1) plays a critical role in the development of cardiovascular diseases. MCP-1, by its chemotactic activity, causes diapedesis of monocytes from the lumen to the subendothelial space where they become foam cells, initiating fatty streak formation that leads to atherosclerotic plaque formation. Inflammatory macrophages probably play a role in plaque rupture and the resulting ischaemic episode as well as restenosis after angioplasty. There is strong evidence that MCP-1 plays a major role in myocarditis, ischaemia/reperfusion injury in the heart and in transplant rejection. MCP-1 also plays a role in cardiac repair and manifests protective effects under certain conditions. Such protective effects may be due to the induction of protective ER (endoplasmic reticulum) stress chaperones by MCP-1. Under sustained ER stress caused by chronic exposure to MCP-1, the protection would break down resulting in the development of heart failure. MCP-1 is also involved in ischaemic angiogenesis. The recent advances in our understanding of the molecular mechanisms that might be involved in the roles that MCP-1 plays in cardiovascular disease are reviewed. The gene expression changes induced by the signalling events triggered by MCP-1 binding to its receptor include the induction of a novel zinc-finger protein called MCPIP (MCP-1-induced protein), which plays critical roles in the development of the pathophysiology caused by MCP-1 production. The role of the MCP-1/CCR2 (CC chemokine receptor 2) system in diabetes, which is a major risk factor for cardiovascular diseases, is also reviewed briefly. MCP-1/CCR2- and/or MCPIP-targeted therapeutic approaches to intervene in inflammatory diseases, including cardiovascular diseases, may be feasible. © The Authors Journal compilation © 2009 Biochemical Society

Inflammation, Endoplasmic Reticulum Stress, Autophagy, And The Monocyte Chemoattractant Protein-1/Ccr2 Pathway

Electroless copper(Cu) deposition on multi-walled carbon nanotube(MWCNT) activated with silver nitrate was developed and the mechanism was proposed. The CuMWCNT hybrid nanowires with MWCNT coated with about 30 nm uniform and continuous crystalline Cu layer which have preferred crystal orientation along the (111) planes were fabricated. Conduction behaviors of the Cu/MWCNT hybrid nanowires demonstrated by electrical measurements and possible reasons were provided. The deposition presents an electroless, simple, and inexpensive process to fabricate Cu/MWCNT hybrid nanowire that may be targeted to connect at specific locations on larger-scale circuits in the near future. © 2011 The Electrochemical Society

Protection Against Lipopolysacharide-Induced Myocardial Dysfunction in Mice by Cardiac-Specific Expression of Soluble Fas

The mechanisms responsible for myocardial dysfunction in the setting of sepsis remain undefined. Fas ligation with its cognate ligand (FasL) induces apoptosis and activates cellular inflammatory responses associated with tissue injury. We determined whether interruption of Fas/FasL interaction by cardiac-specific expression of soluble Fas (sFas), a competitive inhibitor of FasL, would improve myocardial dysfunction and inflammation in a lipopolysacharide (LPS)-induced mouse model of sepsis. Wild-type (WT) and sFas transgenic mice were injected intraperitoneally with 10 mg/kg LPS or with an equivalent volume of saline. At 18 h after LPS administration, echocardiographic evaluation revealed a significant decrease in left ventricular fractional shortening in the WT mice, whereas the fractional shortening was preserved in the sFas mice. Activation of nuclear factor-kappa B (NF-κB) and the increase in the transcript levels of proinflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 resulting from LPS treatment were attenuated in the myocardium of sFas mice. sFas expression also inhibited LPS-induced upregulation of Toll-like receptor 4 (TLR-4) and inducible nitric oxide synthase (iNOS), and formation of peroxynitrite in the myocardium. LPS-induced increase in caspase-3/7 activity and apoptotic cell death were suppressed in sFas mice compared with WT mice. LPS-induced lung injury and increase in lung water content were also significantly reduced in sFas mice. These data indicate that neutralization of FasL by expression of sFas significantly preserves cardiac function and reduces inflammatory responses in the heart, suggesting that Fas/FasL signaling pathway is important in mediating the deleterious effects of LPS on myocardial function

Cerium Oxide Nanoparticles Inhibits Oxidative Stress And Nuclear Factor-Κb Activation In H9C2 Cardiomyocytes Exposed To Cigarette Smoke Extract

Cigarette smoke contains and generates a large amount of reactive oxygen species (ROS) that affect normal cellular function and have pathogenic consequences in the cardiovascular system. Increased oxidative stress and inflammation are considered to be an important mechanism of cardiovascular injury induced by cigarette smoke. Antioxidants may serve as effective therapeutic agents against smoke-related cardiovascular disease. Because of the presence of oxygen vacancies on its surface and self-regenerative cycle of its dual oxidation states, Ce3+ and Ce4+, cerium oxide (CeO2) nanoparticles offer a potential to quench ROS in biological systems. In this study, we determined the ability of CeO2 nanoparticles to protect against cigarette smoke extract (CSE)-induced oxidative stress and inflammation in cultured rat H9c2 cardiomyocytes. CeO2 nanoparticles pretreatment of H9c2 cells resulted in significant inhibition of CSE-induced ROS production and cell death. Pretreatment of H9c2 cells with CeO2 nanoparticles suppressed CSE-induced phosphorylation of IκBα, nuclear translocation of p65 subunit of nuclear factor-κB (NF-κB), and NF-κB reporter activity in H9c2 cells. CeO2 nanoparticles pretreatment also resulted in a significant down-regulation of NF-κB-regulated inflammatory genes tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and inducible nitric-oxide synthase and further inhibited CSE-induced depletion of antioxidant enzymes, such as copper zinc superoxide dismutase, manganese superoxide dismutase, and intracellular glutathione content. These results indicate that CeO2 nanoparticles can inhibit CSE-induced cell damage via inhibition of ROS generation, NF-κB activation, inflammatory gene expression, and antioxidant depletion and may have a great potential for treatment of smoking-related diseases. Copyright © 2011 by The American Society for Pharmacology and Experimental Therapeutics