Svenstrupthorhauge6641

For estimated prevalence of 5480 control subjects, echocardiographic screens in those with normal left ventricular ejection fraction were performed. Of 533 systolic HF cases, 143 (26.8%) had systolic PR during indexed hospitalization. Among 143 cases, 86% systolic PR disappeared during late follow-up. In control subjects, 0.3% (18/5480) had systolic PR. Systolic PR correlated to RV dysfunction, estimated PVR, E/e', sign of low cardiac output, and pulmonary oedema. Systolic PR was associated independently with further cardiovascular events (hazard ratio 2.266, 95% confidence interval 1.682-3.089, P<0.0001) including cardiovascular death and HF rehospitalization.

Systolic PR is not uncommon in systolic HF and is associated with high PVR and RV dysfunction. Systolic PR significantly impacts cardiovascular outcome.

Systolic PR is not uncommon in systolic HF and is associated with high PVR and RV dysfunction. Systolic PR significantly impacts cardiovascular outcome.

Patients hospitalized for heart failure (HF) had worse in-hospital outcomes during the first wave of the COVID-19 pandemic. However, their long-term outcomes are unknown. We describe long-term outcomes among patients who survived to hospital discharge compared with patients hospitalized in 2019 from two referral centers in London during the COVID-19 pandemic.

In total, 512 patients who survived their hospitalization for acute HF in two South London referral centers between 7 January and 14 June 2020 were included in the study and compared with 725 patients from the corresponding period in 2019. The primary outcome was all-cause mortality. The demographic characteristics of patients admitted in 2020 were similar to the 2019 cohort. Median (IQR) follow-up was 622 (348-691) days. All-cause mortality after discharge remained significantly higher for patients admitted in 2020 compared with the equivalent period in 2019 (P<0.01), which may relate to observed differences in place of care with fewer patients being managed on specialist cardiology wards during the COVID-19 pandemic.

Hospitalization for HF during the first wave of the COVID-19 pandemic was associated with higher all-cause mortality among patients who survived to discharge. Further studies are necessary to identify predictors of these adverse outcomes to improve outpatient management during a critical period in the management of acute HF.

Hospitalization for HF during the first wave of the COVID-19 pandemic was associated with higher all-cause mortality among patients who survived to discharge. Further studies are necessary to identify predictors of these adverse outcomes to improve outpatient management during a critical period in the management of acute HF.Severe COVID-19 is reflected by significant changes in urine peptides. Based on this observation, a clinical test predicting COVID-19 severity, CoV50, was developed and registered as in vitro diagnostic in Germany. We have hypothesized that molecular changes displayed by CoV50, likely reflective of endothelial damage, may be reversed by specific drugs. Such an impact by a drug could indicate potential benefits in the context of COVID-19. To test this hypothesis, urinary peptide data from patients without COVID-19 prior to and after drug treatment were collected from the human urinary proteome database. The drugs chosen were selected based on availability of sufficient number of participants in the dataset (n > 20) and potential value of drug therapies in the treatment of COVID-19 based on reports in the literature. In these participants without COVID-19, spironolactone did not demonstrate a significant impact on CoV50 scoring. Empagliflozin treatment resulted in a significant change in CoV50 scoring, indicative of a potential therapeutic benefit. The study serves as a proof-of-principle for a drug repurposing approach based on human urinary peptide signatures. The results support the initiation of a randomized control trial testing a potential positive effect of empagliflozin for severe COVID-19, possibly via endothelial protective mechanisms.Flexible and soft bioelectronics display conflicting demands on miniaturization, compliance, and reliability. Here, the authors investigate the design and performance of thin encapsulation multilayers against hermeticity and mechanical integrity. Partially cracked organic/inorganic multilayer coatings are demonstrated to display surprisingly year-long hermetic lifetime under demanding mechanical and environmental loading. The thin hermetic encapsulation is grown in a single process chamber as a continuous multilayer with dyads of atomic layer deposited (ALD) Al2 O3 -TiO2 and chemical vapor deposited Parylene C films with strong interlayer adhesion. Upon tensile loading, tortuous diffusion pathways defined along channel cracks in the ALD oxide films and through tough Parylene films efficiently postpone the hermeticity failure of the partially cracked coating. The authors assessed the coating performance against prolonged exposure to biomimetic physiological conditions using coated magnesium films, platinum interdigitated electrodes, and optoelectronic devices prepared on stretchable substrates. Designed extension of the lifetime preventing direct failures reduces from over 5 years yet tolerates the lifetime of 3 years even with the presence of critical damage, while others will directly fail less than two months at 37 °C. This strategy should accelerate progress on thin hermetic packaging for miniaturized and compliant implantable electronics.In this study, we describe a new rat model of vertebral inflammation-induced caudal intervertebral disc degeneration (VI-IVDD), in which IVD structure was not damaged and controllable segment and speed degeneration was achieved. VI-IVDD model was obtained by placing lipopolysaccharide (LPS) in the caudal vertebral bodies of rats. Rat experimental groups were set as follows normal control group, group with a hole drilled in the middle of vertebral body and not filled with LPS (Blank group), group with a hole drilled in the middle of vertebral body and filled with LPS (Mid group), and group with hole drilled in the vertebral body in proximity of IVD and filled with LPS (NIVD group). Radiological results of VI-IVDD rats showed a significant reduction in the intervertebral space height and decrease in MRI T2 signal intensity. Histological stainings also revealed that the more the nucleus pulposus and endplate degenerated, the more the annulus fibrosus structure appeared disorganized. Immunohistochemistry analysis demonstrated that the expression of Aggrecan and collagen-II decreased, whereas that of MMP-3 increased in Mid and NIVD groups. Abundant local production of pro-inflammatory cytokines was detected together with increased infiltration of M1 macrophages in Mid and NIVD groups. Apoptosis ratio remarkably enhanced in Mid and NIVD groups. Interestingly, we found a strong activation of the cyclic GMP-AMP synthase /stimulator of interferon gene signalling pathway, which is strictly related to inflammatory and degenerative diseases. In this study, we generated a new, reliable and reproducible IVDD rat model, in which controllable segment and speed degeneration was achieved.

For early-stage non-small cell lung cancer (NSCLC), surgical resection is considered the most effective treatment strategy and curative treatment. Unfortunately, even after complete resection, almost half of all patients with stage I-IIIA NSCLC relapse and die. Although the possibility of a cure for postoperative recurrence of NSCLC is significantly low, the course of subsequent treatment can possibly affect overall survival (OS). Here, we examined the association of relapse-free survival (RFS) and post-progression survival (PPS) with OS in patients with postoperative recurrence of NSCLC.

We evaluated 128 patients with NSCLC who underwent complete resection between January 2007 and December 2018. The association between RFS and PPS on OS was examined at the patient level.

Spearman's rank correlation and linear regression analyses revealed that PPS was strongly correlated with OS (r=0.83, p < 0.05, R

=0.72), whereas RFS was weakly associated with OS (r=0.56, p < 0.05, R

=0.37). Additionally, the performance status at relapse and administration of tyrosine kinase inhibitors were significantly correlated with PPS.

PPS was significantly more strongly correlated with OS than was RFS in patients with postoperative recurrence of NSCLC. These results suggest that therapy following postoperative recurrence affects OS. Therefore, it is necessary to validate these promising results in a large prospective study.

PPS was significantly more strongly correlated with OS than was RFS in patients with postoperative recurrence of NSCLC. These results suggest that therapy following postoperative recurrence affects OS. Therefore, it is necessary to validate these promising results in a large prospective study.Pressure injury (PI) is still a significant public health problem to be solved. Accurate prediction can lead to timely prophylaxis and therapy. However, the currently used Braden score shows insufficient predictive validity. We aimed to develop a nomogram to predict PI development in critically ill patients. We extracted data from Medical Information Mart for Intensive Care-IV v1.0. Variable selection was based on univariate logistic regression and all-subset regression. The area under the receiver operating characteristic curve (AUC) was used to assess the performance of the nomogram and Braden score. Decision curve analysis (DCA) was performed to identify and compare the clinical usefulness between the nomogram model and Braden score. We have developed a novel and practical nomogram that accurately predicts pressure ulcers. The AUC of the new model was better than that of the Braden score (P  less then  .001). DCA showed that the nomogram model had a better net benefit than the Braden score at any given threshold. This finding needs to be confirmed by external validation as well as multicentre prospective studies.Primary lymphedema, a rare disease, has a genetic cause in ~40% of patients. PARP inhibitor Recently, loss-of-function mutations in PIEZO1, which encodes the mechanotransducer protein PIEZO1, were described as causing primary lymphedema, when gain-of-function PIEZO1 mutations were attributed to dehydrated hereditary stomatocytosis type-1 (DHS), a dominant red cell hemolytic disorder, with ~20% of patients having perinatal edema. Lymphedema was diagnosed in a 36-year-old man from a three-generation DHS family, with a PIEZO1-allele harboring 3 missense mutations in cis. Four affected family members had severe fetal and neonatal edema, most severe in the proband, whose generalized edema with prevailing ascites resolved after 8 months. Our patient's intermittent lower limb-lymphedema episodes during hot periods appeared at puberty; they became persistent and bilateral at age 32. Clinical Stemmer's sign confirmed lymphedema. Lower leg lymphoscintigraphy showed substantial dermal backflow in both calves, predominantly on the right. Noncontrast magnetic resonance lymphography showed bilateral lower limb lymphedema, dilated dysplastic lymphatic iliac, and inguinal trunks. Exome-sequencing analysis identified no additional pathogenic variation in primary lymphedema-associated genes. This is the first description of well-documented lymphedema in an adult with PIEZO1-DHS. The pathophysiology of PIEZO1-associated primary lymphedema is poorly understood. Whether it infers overlapping phenotypes or different mechanisms of gain- and loss-of-function PIEZO1 mutations deserves further investigation.