Beebeklinge2094

This study analyzed the efficacy of tailored recommendations to control cardiovascular risk factors at 1-year follow-up in a population-based randomized controlled trial in individuals aged 35-74 years with no history of cardiovascular disease at baseline. Total, low-density lipoprotein (LDL), and high-density lipoprotein cholesterol and systolic and diastolic blood pressure (BP) were measured at baseline and at 1-year follow-up. The primary outcome was the quantitative change in total cholesterol. To estimate the differences within and between groups, McNemar and Student t-tests were applied according to an intention-to-treat strategy. We enrolled 955 individuals [52.3% women; mean age, 50 years (standard deviation 10)]. Finally, 1 participant in each group presented a cardiovascular event and 768 were reexamined at 1-year follow-up. Intervention and control groups showed significant increases in total cholesterol [5.49 (standard deviation 1.02) to 5.56 (1.06) mmol/L and 5.34 (0.94) to 5.43 (0.93) mmol/L, respectively]. Men in the intervention group showed significant decreases in systolic and diastolic BP [117.2 (14.6) to 115.6 mmHg (14.1) and 77.9 (9.7) to 76.5 mmHg (9.7), respectively]; no changes were found in the rates of total cholesterol less then 5.2 mmol/L and LDL cholesterol less then 3.0 mmol/L. In the control group, both values were significantly decreased (43.5 to 36.4% and 26.4 to 20.8%, respectively) in men. In the stratified analysis, women showed no differences in any of the outcomes. In conclusion, an intervention with tailored recommendations increased mean total cholesterol values. The intervention effect was higher in men who maintained blood lipids at optimal levels and had decreased BP values.

High sodium intake can up-regulate the level of renal serum- and glucocorticoid-inducible kinase-1 (SGK1), which plays a pivotal role in controlling blood pressure via activation of the epithelial sodium channel (ENaC), which can lead to salt-sensitive hypertension. Increased potassium intake, or a vegetarian diet, counteracts salt-sensitive hypertension, but the underlying mechanisms are not fully understood.

Bioinformatics and molecular modeling were used to identify G-quadruplex (G4) and their conformations in the SGK1 promoter. CD spectra and UV melting dynamics were measured to study the stability of G4 as influenced by potassium/sodium balance and resveratrol. RT-PCR and Western blot were employed to study the effects of potassium and resveratrol on the SGK1 isoform expression.

The SGK1 gene encodes a G4 structure in the proximal upstream of promoter-2; the G4 structure is stabilized by potassium or resveratrol, but destabilized by sodium. Super-physiological levels of sodium stimulate the transcription of all SGK1 isoforms, whereas resveratrol or potassium supplementation inhibits the transcription of iso-2 and iso-3, but not iso-1.

Stabilizing the G4 by potassium or resveratrol induces alternative promoter usage and/or pre-mRNA splicing in the transcription of SGK1.

Potassium/sodium ion balance or resveratrol binding can act to regulate G4 molecular switches for controlling SGK1 gene expression, thereby presenting a new avenue for drug development.

Potassium/sodium ion balance or resveratrol binding can act to regulate G4 molecular switches for controlling SGK1 gene expression, thereby presenting a new avenue for drug development.

A cohort of children prenatally exposed to the 1945 atomic bombings in Japan revealed harmful effects of ionizing radiation in a variety of measures of cognitive function, including mental retardation. Here we examined cognitive function in the non-affected, now elderly, cohort.

From 2011-2015, using the Cognitive Abilities Screening Instrument and a maternal uterine radiation dose estimated with the 2002 dosimetry system, we evaluated 303 prenatally exposed subjects and their non-exposed controls from the Adult Health Study of the Radiation Effects Research Foundation, excluding those who had shown marked cognitive effects earlier. About 11% of the subjects were exposed to more than 250 mGy. We examined a self-reported disease history and, using regression analysis, evaluated the relationship between cognitive function and radiation exposures, adjusting for demographic factors.

None of the subjects reported a history of dementia. We also did not find a significant radiation effect on cognitive functiontudy or refusal of Cognitive Abilities Screening Instrument evaluation. read more Further investigations using various endpoints in other populations prenatally exposed to radiation are warranted.

Small studies have noted benefit with the use of catheter-directed therapy (CDT) versus standard of care in treatment of pulmonary embolism, but none have focused on the variability of clinical practice with this modality.

International Classification of Diseases (ICD) codes were used to retrospectively identify consecutive adult patients admitted to an intensive care unit (ICU) with pulmonary embolism over a 2-year period. We evaluated inpatient mortality and major bleeding and assessed treatment variation.

Of 284 patients included, 46 underwent CDT (9 massive pulmonary embolism, 37 submassive pulmonary embolism). Significantly more patients who underwent standard treatment had a history of congestive heart failure and diabetes. Obesity, higher troponin levels, and right heart strain were significantly more likely in the CDT group. No significant difference in inpatient mortality or major bleeding events was observed between the treatment groups. Tissue plasminogen activator use varied widely in the CDT group, and inferior vena cava filter utilization was significantly more common in the CDT group (18; 41%) compared with the standard group (40; 17%) (P < 0.01).

In this study, no significant difference in inpatient mortality or major bleeding was found in patients in the intensive care unit with pulmonary embolism who underwent CDT compared with standard care. It may be beneficial to standardize this procedure given the potential benefit of CDT in patients with submassive pulmonary embolism.

In this study, no significant difference in inpatient mortality or major bleeding was found in patients in the intensive care unit with pulmonary embolism who underwent CDT compared with standard care. It may be beneficial to standardize this procedure given the potential benefit of CDT in patients with submassive pulmonary embolism.

Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time.

The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality.

In total, 433 patients were distributed among the following groups confirmed COVID-19 (n=186), 22% with myocardial injury (n=41); and ruled out COVID-19 (n=247), 21.5% with myocardial injury (n=52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P <.001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group HR, 3.54; 95%CI, 1.70-7.34; P=.001; ruled out COVID-19 group HR, 5.57; 95%CI, 1.70-18.20; P=.004). The predictive model analyzed by ROC curves was similar in the 2 groups (P=.701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864).

Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.

Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.

The ankle-brachial index (ABI) is an indicator of peripheral artery disease (PAD). The aim of this study was to assess the association between PAD, measured with the ABI, and cognitive function in persons with overweight or obesity and metabolic syndrome.

Cross-sectional study conducted with baseline data from the PREDIMED-Plus study, which included 4898 participants (after exclusion of those without ABI measurements) aged between 55 and 75 years, and with overweight or obesity and metabolic syndrome. At the baseline assessment, we measured the ABI with a standardized protocol and assessed the presence of other cardiovascular risk factors (eg, diabetes, dyslipidemia, hypertension). Cognitive function was evaluated using several tests validated for the Spanish population (mini-mental state examination [MMSE], phonological and semantic verbal fluency test, WAIS-III working memory index [WMI], parts A and B of the trail making test (TMT), and clock drawing test). Generalized linear models were used to assess the association between the ABI and cognitive function.

Among the participants, 3.4% had PAD defined as ABI ≤ 0.9, and 3.3% had arterial calcification defined as ABI ≥ 1.4. PAD was associated with age, systolic blood pressure and obesity indicators, while arterial calcification was also associated with obesity and diabetes. No significant associations were observed between cognitive function and ABI or PAD.

In our sample, the presence of PAD increased with age, blood pressure, and obesity. No significant association was observed between ABI, PAD, or cognitive function.

In our sample, the presence of PAD increased with age, blood pressure, and obesity. No significant association was observed between ABI, PAD, or cognitive function.Alzheimer's disease (AD), an age-dependent neurodegenerative disorder, is the main cause of dementia. Common hallmarks of AD include the amyloid β-peptide (Aβ) aggregation, high levels of hyperphosphorylated tau protein (p-tau) and failure in redox homeostasis. To date, all proposed drugs affecting Aβ and/or p-tau have been failed in clinical trials. A decline in the expression of the transcription factor Nrf2 (nuclear factor-erythroid 2-p45 derived factor 2) and its driven genes (NQO1, HO-1, and GCLC), and alteration of the Nrf2-related pathways have been observed in AD brains. Nrf2 plays a critical role in maintaining cellular redox homeostasis and regulating inflammation response. Nrf2 activation also provides cytoprotection against increasing pathologies including neurodegenerative diseases. These lines of evidence imply that Nrf2 activation may be a novel AD treatment option. Interestingly, recent studies have also demonstrated that Nrf2 interferes with several key pathogenic processes in AD including Aβ and p-tau pathways. The current review aims to provide insights into the role of Nrf2 in AD. Also, we discuss the progress and challenges regarding the Nrf2 activators for AD treatment.In mammals, the Keap1-Nrf2-ARE pathway (henceforth, "the Nrf2 pathway") and autophagy are major intracellular defence systems that combat oxidative damage and maintain homeostasis. p62/SQSTM1, a ubiquitin-binding autophagy receptor protein, links the Nrf2 pathway and autophagy. Phosphorylation of p62 dramatically enhances its affinity for Keap1, which induces Keap1 to release Nrf2, and the p62-Keap1 heterodimer recruits LC3 and mediates the permanent degradation of Keap1 in the selective autophagy pathway. Eventually, Nrf2 accumulates in the cytoplasm and then translocates into the nucleus to activate the transcription of downstream genes that encode antioxidant enzymes, which protect cells from oxidative damage. Since Nrf2 also upregulates the expression of the p62 gene, a p62-Keap1-Nrf2 positive feedback loop is created that further enhances the protective effect on cells. Studies have shown that the p62-activated noncanonical Nrf2 pathway is an important marker of neurodegenerative diseases. The p62-Keap1-Nrf2 positive feedback loop and the Nrf2 pathway are involved in eliminating the ROS and protein aggregates induced by AD.