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For a two-period closed-loop supply chain (CLSC) consisting of a manufacturer and a retailer, Stackelberg game analyses are conducted to examine pricing and warranty decisions under two warranty models depending on who offers warranty for new and remanufactured products and the corresponding benchmark models with a warranty for new products only. Next, we identify the conditions under which warranty for remanufactured products is offered and investigate how this warranty affects the CLSC operations. Subsequently, comparative studies are carried out to examine equilibrium decisions, profitability and consumer surplus of the CLSC between the two warranty models. Analytical results show that offering warranty for remanufactured products does not affect new product pricing in period 2, but influences the pricing of new products in period 1 and remanufactured products in period 2, thereby enhancing remanufacturing, individual and channel profitability, and consumer surplus. Compared to the retailer warranty for remanufactured products, the manufacturer warranty can attain a more equitable profit distribution. If the warranty cost advantage of the manufacturer (retailer) is significant relative to that of the retailer (the manufacturer), the manufacturer (retailer) arises as a natural choice to offer warranty for remanufactured products as this decision enhances both profitability and consumer surplus. [ABSTRACT FROM AUTHOR]

The epicardium is the important outermost mesothelial/epithelial layer of the heart that serves as a signaling center for cardiac development and repair. During heart development, epicardial cells undergo a process known as epithelial-to-mesenchymal transition to form diverse mesenchymal cell lineages, such as fibroblasts, coronary vascular smooth muscle cells, and pericytes. However, it is not clear whether the reverse process, mesenchymal-to-epithelial transition (MET), takes place in the mammalian heart. In this study, we performed apical resection on neonatal hearts and used Fap-CreER;Ai9 labeling to track activated fibroblasts in the injured cardiac regions. We found that these fibroblasts underwent MET to generate epicardial cells during heart regeneration. To our knowledge, this is the first report of MET occurring in vivo during heart development and regeneration. Our findings suggest that it is feasible to directly convert fibroblasts into epicardial cells, providing a novel approach to generate epicardial cells. [ABSTRACT FROM AUTHOR]

Triglyceride droplets can be stored within cardiac adipocytes (CAs) and cardiomyocytes in the heart. Cardiac adipocytes reside in three distinct regions: pericardial, epicardial, and intramyocardial adipose tissues. In healthy individuals, cardiac adipose tissues modulate cardiovascular functions and energy partitioning, which are, thus, protective. However, ectopic deposition of cardiac adipose tissues turns them into adverse lipotoxic, prothrombotic, and pro‐inflammatory tissues with local and systemic contribution to the development of cardiovascular disorders. Accumulation of triglyceride droplets in cardiomyocytes may lead to lipotoxic injury of cardiomyocytes and contribute to the development of cardiac hypertrophy and dysfunction. Here, we summarize the roles of CAs and myocardial triglyceride droplets under physiological and pathological conditions and review the cellular sources of CAs in heart development and diseases. Understanding the functions and cellular origins of cardiac fat will provide clues for future studies on pathophysiological processes and treatment of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Disseminated candidiasis has become one of the leading causes of hospital-acquired blood stream infections with high mobility and mortality. However, the molecular basis of host defense against disseminated candidiasis remains elusive, and treatment options are limited. Here we report that the E3 ubiquitin ligase CBLB directs polyubiquitination of dectin-1 and dectin-2, two key pattern-recognition receptors for sensing Candida albicans, and their downstream kinase SYK, thus inhibiting dectin-1- and dectin-2-mediated innate immune responses. CBLB deficiency or inactivation protects mice from systemic infection with a lethal dose of C. albicans, and deficiency of dectin-1, dectin-2, or both in [Cblb.sup.-/-] mice abrogates this protection. Notably, silencing the Cblb gene in vivo protects mice from lethal systemic C. albicans infection. Our data reveal that CBLB is crucial for homeostatic control of innate immune responses mediated by dectin-1 and dectin-2. Our data also indicate that CBLB represents a potential therapeutic target for protection from disseminated candidiasis., C. albicans is the most common cause of fungal infections in humans and has become one of the leading causes of hospital-acquired blood stream infections. Despite the availability of several [...]

Cancers from lung and esophagus are the leading causes of cancer-related deaths in China and share many similarities in terms of histological type, risk factors and genetic variants. Recent genome-wide association studies (GWAS) in Chinese esophageal cancer patients have demonstrated six high-risk candidate single nucleotide polymorphisms (SNPs). Thus, the present study aimed to determine the risk of these SNPs predisposing to lung cancer in Chinese population.A total of 1170 lung cancer patients and 1530 normal subjects were enrolled in this study from high-incidence areas for esophageal cancer in Henan, northern China. Five milliliters of blood were collected from all subjects for genotyping. Genotyping of 20 high-risk SNP loci identified from genome-wide association studies (GWAS) on esophageal, lung and gastric cancers was performed using TaqMan allelic discrimination assays. Polymorphisms were examined for deviation from Hardy-Weinberg equilibrium (HWE) using Х2 test. Bonferroni correction was performed to correct the statistical significance of 20 SNPs with the risk of lung cancer. The Pearson's Х2 test was used to compare the distributions of gender, TNM stage, histopathological type, smoking and family history by lung susceptibility genotypes. Kaplan-Meier and Cox regression analyses were carried out to evaluate the associations between genetic variants and overall survival.Four of the 20 SNPs identified as high-risk SNPs in Chinese esophageal cancer showed increased risk for Chinese lung cancer, which included rs3769823 (OR = 1.26; 95% CI = 1.107-1.509; P = 0.02), rs10931936 (OR = 1.283; 95% CI = 1.100-1.495; P = 0.04), rs2244438 (OR = 1.294; 95% CI = 1.098-1.525; P = 0.04) and rs13016963 (OR = 1.268; 95% CI = 1.089-1.447; P = 0.04). All these SNPs were located at 2q33 region harboringgenes of CASP8, ALS2CR12 and TRAK2. However, none of these susceptibility SNPs was observed to be significantly associated with gender, TNM stage, histopathological type, smoking, family history and overall survival.The present study identified four high-risk SNPs at 2q33 locus for Chinese lung cancer and demonstrated the shared susceptibility loci at 2q33 region for Chinese lung and esophageal cancers.