Notes

Analyzing evidence Around Pontine Cholinergic Engagement throughout REM Sleep Generation.
Several studies have examined the role of physical activity as a predictor of heart failure (HF) mortality and morbidity. Here, we aimed to evaluate the role of self-reported physical activity as an independent risk factor of post-discharge mortality and re-hospitalization in patients hospitalized for HF, as well as study the association between physical activity and 92 plasma proteins associated with cardiovascular disease (CVD).

Four-hundred-and-thirty-four patients hospitalized for HF (mean age 75 years; 32% women) were screened for physical activity derived from questionnaires in the Swedish national public health survey. The median follow-up time to death and re-hospitalization was 835 (interquartile range, 390-1,432) and 157 (43-583) days, respectively. Associations between baseline reported physical activity, mortality and re-hospitalization risk were analyzed using multivariable Cox regression analysis. Plasma samples from 295 study participants were analyzed with a proximity extension assay consis of 4 proteins linked to cardiovascular disease.
Self-reported low weekly physical activity is associated with increased risk of mortality and re-hospitalization in patients hospitalized for HF independent of traditional risk factors. Furthermore, physical inactivity was associated with elevated levels of 4 proteins linked to cardiovascular disease.
Near-infrared spectroscopy (NIRS) provides the localization of lipid-rich components in coronary plaques. However, morphological features in NIRS-detected lipid-rich plaques (LRP) are unclear.

A total of 140
culprit lesions in 140 patients with the acute coronary syndrome (ACS) who underwent NIRS and optical coherence tomography (OCT) examinations for the culprit lesions at the time of percutaneous coronary interventions were investigated. We defined a NIRS-LRP as a lesion with a maximum lipid core burden index of 4 mm [LCBI
] > 500 in the culprit plaque. Clinical demographics, angiographic, and OCT findings were compared between the patients with NIRS-LRP (
= 54) vs. those without NIRS-LRP (
= 86). Uni- and multivariable logistic regression analyses were performed to examine the independent OCT morphological predictors for NIRS-LRP.

Clinical demographics showed no significant differences between the two groups. The angiographic minimum lumen diameter was smaller in the NIRS-LRP group than in the non- NIRS-LRP group. In OCT analysis, the minimum flow area was smaller; lipid angle, lipid length, the prevalence of thin-cap fibroatheroma, and cholesterol crystals were greater in the NIRS-LRP group than in the non-NIRS-LRP group. Plaque rupture and thrombi were more frequent in the NIRS-LRP group, albeit not significant. In a multivariable logistic regression analysis, presence of thin-cap fibroatheroma [odds ratio (OR) 2.56; 95% CI 1.12 to 5.84;
= 0.03] and cholesterol crystals (OR 2.90; 95% CI 1.20 to 6.99;
= 0.02) were independently predictive of NIRS-LRP.

In ACS culprit lesions, OCT-detected thin-cap fibroatheroma and cholesterol crystals rather than plaque rupture and thrombi were closely associated with a great lipid-core burden.
In ACS culprit lesions, OCT-detected thin-cap fibroatheroma and cholesterol crystals rather than plaque rupture and thrombi were closely associated with a great lipid-core burden.
Cardiac dysfunction including arrhythmias appear frequently in patients with cancers, which are expected to be caused mainly by cardiotoxic effects of chemotherapy. https://www.selleckchem.com/products/c1632.html Experimental studies investigating the effects of cancer cell secretion without chemotherapy on ion channel function in human cardiomyocytes are still lacking.

The human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) generated from three healthy donors were treated with gastrointestinal (GI) cancer (AGS and SW480 cells) medium for 48 h. The qPCR, patch-clamp, western blotting, immunostaining, dot blotting, bisulfite sequence, and overexpression of the ten-eleven translocation (TET) enzyme were performed for the study.

After treated with cancer cell secretion, the maximum depolarization velocity and the action potential amplitude were reduced, the action potential duration prolonged, peak Na
current, and the transient outward current were decreased, late Na
and the slowly activating delayed rectifier K
current were incgenesis of arrhythmia in cancer patients.
Myocardial fibrosis is an important pathophysiologic mechanism of cardiac involvement that leads to increased mortality in patients with autoimmune diseases (AIDs). The aim of this study was to evaluate the association between myocardial strain from speckle-tracking echocardiography (STE) and fibrosis on cardiovascular magnetic resonance (CMR) and to further explore their prognostic implications in patients with AIDs.

We prospectively included 102 AIDs patients with clinically suspected cardiac involvement and 102 age- and sex-matched healthy individuals. Patients underwent CMR for evaluation of myocardial fibrosis by late gadolinium enhancement (LGE) and T1 mapping. A semiquantitative evaluation based on the extent of LGE was used to calculate the total (tLGEs) and segmental (sLGEs) LGE score. Global longitudinal strain (GLS) was evaluated by STE in all subjects. All patients were regularly followed up every 6 months. The primary endpoint was the composite incidence of all-cause death and cardiovascular ddition to LGE in the prediction of adverse outcomes.
In AIDs patients, impaired myocardial strain on STE could reflect the presence and extent of myocardial fibrosis and provide incremental prognostic value in addition to LGE in the prediction of adverse outcomes.Severe tricuspid valve regurgitation has been for a long time a neglected valve disease, which has only recently attracted an increasing interest due to the notable negative impact on the prognosis of patients with cardiovascular disease. It is estimated that around 90% of tricuspid regurgitation is diagnosed as "functional" and mostly secondary to a primary left-sided heart disease and, therefore, has been usually interpreted as a benign condition that did not require a surgical management. Nevertheless, the persistence of severe tricuspid regurgitation after left-sided surgical correction of a valve disease, particularly mitral valve surgery, has been associated to adverse outcomes, worsening of the quality of life, and a significant increase in mortality rate. Similar results have been found when the impact of isolated severe tricuspid regurgitation has been studied. Current knowledge is shifting the "functional" categorization toward a more complex and detailed pathophysiological classification, identifying various phenotypes with completely different etiology, natural history and, potentially, an invasive management. The aim of this review is to offer a comprehensive guide for clinicians and surgeons with a systematic description of "functional" tricuspid regurgitation subtypes, an analysis centered on the effectiveness of existing surgical techniques and a focus on the emergent percutaneous procedures. This latter may be an attractive alternative to a standard surgical approach in patients with high-operative risk or isolated tricuspid regurgitation.
This study aims to describe the outcome of intravascular lithotripsy (IVL) when used with different indications and to assess the short- and long-term outcomes of IVL-facilitated percutaneous coronary intervention (PCI).

Intravascular lithotripsy can improve the results of PCI of calcified coronary lesions with a low rate of periprocedural complications.

A total of 105 consecutive patients with 110 calcified lesions underwent IVL. A total of 87
lesions were treated by IVL with the following indications 25 before attempting other balloon-based devices (primary IVL), 51 after the failure of non-compliant balloon dilatation (secondary IVL), and 11 after stent implantation because of stent under expansion (bailout IVL). In 23 lesions, IVL was used for the treatment of in-stent restenosis (ISR). Effectiveness (angiographic success) and safety [major adverse cardiovascular events (MACEs) and IVL-related procedural complications] endpoints were assessed.

Angiographic success was achieved in 84.6% of lesioexpansion.In genetic diseases like hypertrophic cardiomyopathy, reliable quantification of the expression level of mutant protein can play an important role in disease research, diagnosis, treatment and prognosis. For heterozygous β-myosin heavy chain (β-MyHC) mutations it has been shown that disease severity is related to the fraction of mutant protein in the myocardium. Yet, heart tissue from patients with genetically characterized diseases is scarce. Here we asked, if even in the case of small endomyocardial biopsies, single quantifications produce reliable results. Myocardial samples were taken from four different regions of an explanted heart of a patient with hypertrophic cardiomyopathy carrying point mutation p.Gly716Arg in β-MyHC. From both, large samples (15 mg) and small, endomyocardial biopsy-sized samples (≤ 1 mg) myosin was extracted and enzymatically digested to yield a specific peptide of interest that allowed to distinguish mutant and wild-type β-MyHC. Absolute quantification by mass spectrometry (AQUA) of the peptide of interest was performed repeatedly for both sample sizes to determine the fraction of mutant β-MyHC. Fractions of mutant β-MyHC (32% on average) showed only small differences between the four cardiac regions and for large and small samples. The standard deviations were smaller than five percentage points for all cardiac regions. The two quantification methods (large and small sample size) produce results with comparable accuracy and precision. Consequently, with our method even small endomyocardial biopsies allow reliable protein quantification for potential diagnostic purposes.Combination therapy with increased efficacy and reduced toxicity plays a crucial role in treating complex diseases, such as stroke, but it remains an insurmountable barrier to elucidate the mechanisms of synergistic effects. Here, we present a Driver-induced Modular Screening (DiMS) strategy integrated synergistic module and driver gene identification to elucidate the additive mechanisms of Baicalin (BA) and Jasminoidin (JA) on cerebral ischemia (CI) therapy. Based on anti-ischemia genomic networks BA, JA, and their combination (BJ), we obtained 4, 3, and 9 On-modules of BA, JA, and BJ by modular similarity analysis. Compared with the monotherapy groups, four additive modules (Add-module, BJ_Mod-4, 7, 9, and 13), 15 driver genes of BJ were identified by modular similarity and network control methods, and seven driver proteins (PAQR8, RhoA, EMC10, GGA2, VIPR1, FAM120A, and SEMA3F) were validated by animal experiments. The functional analysis found neuroprotective roles of the Add-modules and driver genes, such as the Neurotrophin signaling pathway and FoxO signaling pathway, which may reflect the additive mechanisms of BJ. Moreover, such a DiMS paradigm provides a new angle to explore the synergistic mechanisms of combination therapy and screen multi-targeted drugs for complex diseases.The protective effect of astragaloside IV (AS-IV) on myocardial injury after myocardial infarction has been reported. However, the underlying mechanism is still largely unknown. We established a myocardial infarction model in C57BL/6 mice and injected intraperitoneally with 10 mg/kg/d AS-IV for 4 weeks. The cardiac function, myocardial fibrosis, and angiogenesis were investigated by echocardiography, Masson's trichrome staining, and CD31 and smooth muscle actin staining, respectively. Cardiac mitochondrial morphology was visualized by transmission electron microscopy. Cardiac function, infarct size, vascular distribution, and mitochondrial morphology were significantly better in AS-IV-treated mice than in the myocardial infarction model mice. In vitro, a hypoxia-induced H9c2 cell model was established to observe cellular apoptosis and mitochondrial function. H9c2 cells transfected with silent information regulator 3 (Sirt3) targeting siRNA were assayed for Sirt3 expression and activity. Sirt3 silencing eliminated the beneficial effects of AS-IV and abrogated the inhibitory effect of AS-IV on mitochondrial division.
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