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Single-cell RNA sequencing evaluation associated with mouse follicular somatic cellular material.
Heart disease is the leading cause of death in the United States among both adults and infants. In adults, 5-year survival after a heart attack is less then 60%, and congenital heart defects are the top killer of liveborn infants. Problematically, the regenerative capacity of the heart is extremely limited, even in newborns. Furthermore, suitable donor hearts for transplant cannot meet the demand and require recipients to use immunosuppressants for life. Tissue engineered myocardium has the potential to replace dead or fibrotic heart tissue in adults and could also be used to permanently repair congenital heart defects in infants. In addition, engineering functional myocardium could facilitate the development of a whole bioartificial heart. Here, we review and compare in vitro and in situ myocardial tissue engineering strategies. In the context of this comparison, we consider three challenges that must be addressed in the engineering of myocardial tissue recapitulation of myocardial architecture, vascularization of the tissue, and modulation of the immune system. In addition to reviewing and analyzing current progress, we recommend specific strategies for the generation of tissue engineered myocardial patches for heart regeneration and repair.Background Italy has one of the world's oldest populations, and suffered one the highest death tolls from Coronavirus disease 2019 (COVID-19) worldwide. Older people with cardiovascular diseases (CVDs), and in particular hypertension, are at higher risk of hospitalization and death for COVID-19. Whether hypertension medications may increase the risk for death in older COVID 19 inpatients at the highest risk for the disease is currently unknown. Methods Data from 5,625 COVID-19 inpatients were manually extracted from medical charts from 61 hospitals across Italy. From the initial 5,625 patients, 3,179 were included in the study as they were either discharged or deceased at the time of the data analysis. Primary outcome was inpatient death or recovery. Mixed effects logistic regression models were adjusted for sex, age, and number of comorbidities, with a random effect for site. Results A large proportion of participating inpatients were ≥65 years old (58%), male (68%), non-smokers (93%) with comorbidities (66%). Isoproterenol sulfate purchase Each additional comorbidity increased the risk of death by 35% [adjOR = 1.35 (1.2, 1.5) p less then 0.001]. Use of ACE inhibitors, ARBs, beta-blockers or Ca-antagonists was not associated with significantly increased risk of death. There was a marginal negative association between ARB use and death, and a marginal positive association between diuretic use and death. Conclusions This Italian nationwide observational study of COVID-19 inpatients, the majority of which ≥65 years old, indicates that there is a linear direct relationship between the number of comorbidities and the risk of death. Among CVDs, hypertension and pre-existing cardiomyopathy were significantly associated with risk of death. The use of hypertension medications reported to be safe in younger cohorts, do not contribute significantly to increased COVID-19 related deaths in an older population that suffered one of the highest death tolls worldwide.Heart failure is a serious comorbidity and the most common cause of mortality in diabetes patients. Diabetic cardiomyopathy (DCM) features impaired cellular structure and function, culminating in heart failure; however, there is a dearth of specific clinical therapy for treating DCM. Protein homeostasis is pivotal for the maintenance of cellular viability under physiological and pathological conditions, particularly in the irreplaceable cardiomyocytes; therefore, it is tightly regulated by a protein quality control (PQC) system. Three evolutionarily conserved molecular processes, the unfolded protein response (UPR), the ubiquitin-proteasome system (UPS), and autophagy, enhance protein turnover and preserve protein homeostasis by suppressing protein translation, degrading misfolded or unfolded proteins in cytosol or organelles, disposing of damaged and toxic proteins, recycling essential amino acids, and eliminating insoluble protein aggregates. In response to increased cellular protein demand under pathological insults, including the diabetic condition, a coordinated PQC system retains cardiac protein homeostasis and heart performance, on the contrary, inappropriate PQC function exaggerates cardiac proteotoxicity with subsequent heart dysfunction. Further investigation of the PQC mechanisms in diabetes propels a more comprehensive understanding of the molecular pathogenesis of DCM and opens new prospective treatment strategies for heart disease and heart failure in diabetes patients. In this review, the function and regulation of cardiac PQC machinery in diabetes mellitus, and the therapeutic potential for the diabetic heart are discussed.Background Rs13216675 T>C polymorphism, an SNP (single-nucleotide polymorphism) close to the gap junction protein alpha 1 (GJA1) gene, has been reported to be associated with risk of atrial fibrillation (AF); however, the results remained inconclusive. We aimed to perform a systematic review to clarify the relationship between rs13216675 and risk of AF. Materials and methods We systematically searched the databases of PubMed, EMBASE, Web of Science, and the Chinese National Knowledge Infrastructure up to July 15, 2020. Data were synthesized using the random-effects model. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the relationship between rs13216675 and risk of AF. Results Seven studies involving 39,827 cases and 458,466 controls were analyzed in the meta-analysis. The overall pooled OR of rs13216675 polymorphism for AF was significant (OR = 1.10, 95% CI = 1.07-1.12, P less then 0.001) under the additive genetic model. Subgroup analyses revealed that rs13216675 polymorphism was significantly associated with AF in both Asians (OR = 1.12, 95% CI = 1.07-1.17, P less then 0.001) and Europeans (OR = 1.09, 95% CI = 1.06-1.12, P less then 0.001). When data were stratified by control sources, rs13216675 polymorphism was significantly related to AF in studies with both population-based controls (OR = 1.09, 95% CI = 1.07-1.12) and hospital-based controls (OR = 1.12, 95% CI = 1.07-1.17). No evidence of publication bias was detected. Conclusion Our meta-analysis suggested that rs13216675 was significantly related to risk of AF and, therefore, might serve as a potential biological marker of AF.Background Non-invasive Doppler waveform (DW) analysis is a widely adopted method for detecting and evaluating lower extremity peripheral artery disease (PAD). Previous investigations have reported that broad heterogeneity in the description of Doppler waveforms is reduced by using a classification method. The reliability of arterial Doppler classification, however, is unknown. Purpose The purpose of this study is to assess the reliability of a 4-category arterial DW classification method among Chinese sonographers. Methods During a national ultrasound conference in China attendees were invited to classify thirty arterial Doppler waveforms. After viewing a 4-category (triphasic, biphasic, monophasic, and other) arterial Doppler waveform descriptor presentation, attendees were asked to classify 15 continuous wave (CW) and 15 pulsed wave (PW) Doppler waveforms. Their responses were recorded via mobile phone and the reliability of this 4-category classification was estimated by Fleiss' Kappa inter-rater statistical analysis. Results One hundred and seventy-eight attendees participated in the analysis. The Kappa coefficient of Fleiss (κ) for all attendees was 0.522 (p less then 0.005) with 95% confidence interval (CI) 0.520-0.523. The reliability of the waveform descriptor triphasic was the highest (κ = 0.621, p less then 0.005), and other was the lowest (κ = 0.341, p less then 0.005). Conclusion The inter-rater reliability of a 4-category arterial Doppler waveform classification by Chinese sonographers is considered weak (κ = 0.522, CI95% 0.520-0.523, p less then 0.005). This study reinforces the importance of assessing DW classification reliability and the development of DW descriptors that are more accurately predictive of clinical hemodynamic events.Background The elevated gamma-glutamyltransferase (GGT) activity is regarded as an indicator of cardiovascular disease, with males having higher values than females. The greater incidence of idiopathic pulmonary arterial hypertension (IPAH) is observed in women, whereas prognosis is poor in men. The present study aims to investigate the potential association of GGT on male patients. Methods Serum GGT levels were measured in 338 consecutive adult IPAH patients, who underwent bone morphogenetic protein receptor type 2 (BMPR2) genetic counseling, and matched with healthy subjects by sex and age. The followed interval was 48 ± 34 months. Results Increased serum GGT levels were more common in patients with IPAH than controls (p less then 0.001). GGT values were significantly higher in male patients than those of females (p less then 0.001). Compared with female patients with BMPR2 mutation, GGT level in male patients with BMPR2 mutation was further increased (p = 0.002). Higher GGT levels were associated with worse hemodynamics and Nterminal pro B-type natriuretic peptide in all patients. However, males with a GGT concentration ≥ 53 U/L had a worse survival than those of females. Contrarily, if GGT concentration less then 53 U/L, there was no survival difference between male and female patients. After adjustment for relevant variables of clinical features and hemodynamics, baseline higher GGT levels remained increased risks of all-cause mortality in males rather than females. During rehospitalization follow-up, male patients still had significantly higher values of GGT than females. Conclusions Increased GGT levels were correlated with BMPR2 mutation, hemodynamic dysfunction, and poor outcomes in male patients with IPAH. Further studies are needed to explain the origin of abnormal GGT and its potential pathogenesis in men.Coronary heart disease (CHD) is common in patients with diabetes mellitus (DM), however, the relevant mechanism remains elusive. The whole blood gene expression profiles of healthy control, patients with DM, patients with DM and CHD (DMCHD) were used to performed weight gene correlation network analysis (WGCNA) to identify the gene modules associated with DM-related atherogenesis. The candidate module was significantly involved in immune- and T cell activity-related biological process. GSEA results suggested that lysosome and apoptosis were enriched in DM and DMCHD samples. The protein-protein-KEGG pathway network may reveal the potential transcriptional regulatory network involving in DM-related atherosclerosis. Nineteen genes (RTKN, DCP1B, PDZD4, CACNA2D2, TSEN54, PVRIG, PLEKHF1, NKG7, ZAP70, NUDCD3, SLAMF6, CCDC107, NAG6, ZDHHC14, EOMES, VIL2, WDR54, DMAP1, and PMPCA) were considered as DM-related atherogenesis genes (DRAGs). The Gene Set Variation Analysis (GSVA) score of the DRAG set gradually increased in the control, DM and DMCHD. ROC curve analysis showed that ZAP70, TSEN54, and PLEKHF1 may be potential blood circulation biomarkers for DMCHD in patients with DM. In conclusion, we identified nineteen hallmark genes involving in DM-related atherogenesis and constructed a potential transcriptional regulatory network involving in DM-related atherosclerosis.
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