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Resurrection species possess unusual anatomical features that could confer stress tolerance (thick cell walls) without compromising the photosynthetic capacity (high chloroplast exposure). This mechanism is particularly successful in resurrection ferns, which display higher photosynthesis than their desiccation-sensitive counterparts.

Gp91-containing NADPH oxidases (NOX2) are a significant source of myocardial superoxide production. An increase in NOX2 activity accompanies atrial fibrillation (AF) induction and electrical remodelling in animal models and predicts incident AF in humans; however, a direct causal role for NOX2 in AF has not been demonstrated. Accordingly, we investigated whether myocardial NOX2 overexpression in mice (NOX2-Tg) is sufficient to generate a favourable substrate for AF and further assessed the effects of atorvastatin, an inhibitor of NOX2, on atrial superoxide production and AF susceptibility.

NOX2-Tg mice showed a 2-2.5-fold higher atrial protein content of NOX2 compared with wild-type (WT) controls, which was associated with a significant (2-fold) increase in NADPH-stimulated superoxide production (2-hydroxyethidium by HPLC) in left and right atrial tissue homogenates (P = 0.004 and P = 0.019, respectively). AF susceptibility assessed in vivo by transoesophageal atrial burst stimulation was modestly increasial NOX2-derived superoxide is an independent predictor of postoperative AF in humans and contributes to atrial oxidative stress early after AF induction. Whilst experimental models have reported an association of NOX2 with AF-induced remodelling, a causal link between NOX2 activity and AF remains to be established. Here we show that overexpression of the human NOX2 gene in mice resulted in a 2-fold higher atrial superoxide production and a modest increase in AF susceptibility, independent of atrial electrical or structural remodelling. Short-term treatment with atorvastatin normalized atrial superoxide in NOX2-Tg mice without affecting AF susceptibility. Together these findings indicate that atrial NOX2-derived superoxide is more likely a biomarker of AF risk than a primary driver of AF development, and that NOX2 inhibition is unlikely to prevent the new-onset of AF.

Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting joints and blood vessels. Despite low levels of low-density lipoprotein cholesterol (LDL-C), RA patients exhibit endothelial dysfunction and are at increased risk of death from cardiovascular (CV) complications, but the molecular mechanism of action is unknown.We aimed in the present study to identify the molecular mechanism of endothelial dysfunction in a mouse model of RA and in patients with RA.

Endothelium-dependent relaxations to acetylcholine were reduced in aortae of two TNFα transgenic mouse lines with either mild (Tg3647) or severe (Tg197) forms of RA in a time- and severity-dependent fashion as assessed by organ chamber myograph. In Tg197, TNFα plasma levels were associated with severe endothelial dysfunction. LOX-1 receptor was markedly upregulated leading to increased vascular oxLDL uptake and NFκB-mediated enhanced Arg2 expression via direct binding to its promoter resulting in reduced NO bioavailability and vascular cGMP lMP levels. Anti-TNFα treatment improved both articular symptoms and endothelial function by reducing LOX-1, vascular oxLDL and Arg2 levels.

Machine learning (ML)-based predictive models are increasingly common in neurosurgery, but typically require large databases of discrete variables for training. Natural language processing (NLP) can extract meaningful data from unstructured text.

To present an NLP model that predicts nonhome discharge and a point-of-care implementation.

We retrospectively collected age, preoperative notes, and radiology reports from 595 adults who underwent meningioma resection in an academic center from 1995 to 2015. A total of 32 algorithms were trained with the data; the 3 best performing algorithms were combined to form an ensemble. Predictive ability, assessed by area under the receiver operating characteristic curve (AUC) and calibration, was compared to a previously published model utilizing 52 neurosurgeon-selected variables. We then built a multi-institutional model by incorporating notes from 693 patients at another center into algorithm training. Permutation importance was used to analyze the relative importance of each input to model performance. selleck inhibitor Word clouds and non-negative matrix factorization were used to analyze predictive features of text.

The single-institution NLP model predicted nonhome discharge with AUC of 0.80 (95% CI=0.74-0.86) on internal and 0.76 on holdout validation compared to AUC of 0.77 (95% CI=0.73-0.81) and 0.74 for the 52-variable ensemble. The multi-institutional model performed similarly well with AUC=0.78 (95% CI=0.74-0.81) on internal and 0.76 on holdout validation. Preoperative notes most influenced predictions. The model is available at http//nlp-home.insds.org.

ML and NLP are underutilized in neurosurgery. Here, we construct a multi-institutional NLP model that predicts nonhome discharge.

ML and NLP are underutilized in neurosurgery. Here, we construct a multi-institutional NLP model that predicts nonhome discharge.

Myocarditis is associated with formidable symptoms and increased risk of adverse outcomes. Current approaches mostly rely on symptomatic treatments, warranting novel concepts for clinical practice. The aim of this study was to investigate the microRNA (miRNA) expression profile of Balb/c mice with experimental autoimmune myocarditis (EAM), choose a representative miRNA to antagonize after review of available literature and test its effects on myocardial inflammation in vitro and in vivo.

Methods Phase 1 EAM was induced in 12 male Balb/c mice, 10 animals served as controls. After sacrifice, next-generation sequencing (NGS) of the microRNA expression profile was performed. Based on these results, H9C2 cells and human ventricular cardiac fibroblasts exposed to lipopolysaccharide (LPS) were treated with the selected candidate antagomiR-21a-5p. Phase 2 EAM was induced in 48 animals. Thereof, 24 animals were either treated with antagomiR-21a-5p or negative control oligonucleotide in a nanoparticle formulation. Transthoracic echocardiography (TTE) was performed on days 0,7,14 and 21.

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