3% versus 46.7%,  = 0.01). Also, primary nonfunction rates were lower in the cDCD using NRP group (4.5% versus 6.4% cDCD-RR and 10.2% DBD). Patient survival rates were >90% in all groups. No differences were found in graft survival rates at 1 y. The use of abdominal NRP improves early function recovery of KT from cDCD, making their outcomes comparable with those of DBD.The use of abdominal NRP improves early function recovery of KT from cDCD, making their outcomes comparable with those of DBD.In the era of antibiotic resistance, in silico prediction of bacterial resistome profiles, likely to be associated with inactivation of new potential antibiotics is of utmost importance. Despite this, to the best of our knowledge, no tool exists for such prediction. Therefore, under the rationale that drugs with similar structures have similar resistome profiles, we developed two models, a deterministic model and a stochastic model, to predict the bacterial resistome likely to neutralize uncharacterized but potential chemical structures. The current version of the tool involves the prediction of a resistome for Escherichia coli and Pseudomonas aeruginosa. The deterministic model on omitting two diverse but relatively less characterized drug classes, polyketides and polypeptides showed an accuracy of 87%, a sensitivity of 85%, and a precision of 89%, whereas the stochastic model predicted antibiotic classes of the test set compounds with an accuracy of 72%, a sensitivity of 75%, and a precision of 83%. The models have been implemented in both a standalone package and an online server, uCAREChemSuiteCLI and uCARE Chem Suite, respectively. In addition to resistome prediction, the online version of the suite enables the user to visualize the chemical structure, classify compounds in 19 predefined drug classes, perform pairwise alignment, and cluster with database compounds using a graphical user interface. uCARE Chem Suite can be browsed at https//sauravsaha.shinyapps.io/ucarechemsuite2/, and uCAREChemSuiteCLI can be installed from1. CRAN (https//cran.r-project.org/package=uCAREChemSuiteCLI) and2. GitHub (https//github.com/sauravbsaha/uCAREChemSuiteCLI).uCARE Chem Suite can be browsed at https//sauravsaha.shinyapps.io/ucarechemsuite2/, and uCAREChemSuiteCLI can be installed from1. CRAN (https//cran.r-project.org/package=uCAREChemSuiteCLI) and2. GitHub (https//github.com/sauravbsaha/uCAREChemSuiteCLI).Secreted frizzled-related protein 5 (SFRP5) plays a pivotal role in regulating the development of many tissues and organs, however, as an inhibitor of Wnt signaling, the role of SFRP5 in vitiligo remains unknown. Hence, we speculated that SFRP5 might be associated with melanogenesis in melanocytes by regulating Wnt signaling in vitiligo. In this study, we found that SFRP5 was overexpressed in the skin lesions of patients with vitiligo. Compared with that in normal epidermal melanocytes (PIG1), the expression of SFRP5 was increased in vitiligo melanocytes (PIG3V). To investigate the effect of SFRP5 on melanin synthesis, PIG1 cells were infected with recombinant SFRP5 adenovirus (AdSFRP5), and PIG3V cells were infected with recombinant siSFRP5 adenovirus (AdsiSFRP5). The results showed that SFRP5 overexpression inhibited melanin synthesis in PIG1 cells through downregulation of microphthalmia-associated transcription factor (MITF) and its target proteins via suppression of the Wnt/β-catenin signaling pathway. Accordingly, SFRP5 silencing increased melanin synthesis and activated the Wnt signaling pathway in PIG3V cells. Moreover, SFRP5 overexpression also downregulated the transcriptional activity of T cell factor/lymphoid enhancer factor (TCF/LEF) in PIG1 cells. Furthermore, this inhibitory effect of SFRP5 on melanin synthesis was reversed by treatment with the β-catenin agonist, SKL2001. The inhibitory action of SFRP5 in pigmentation was further confirmed in vivo using a nude mouse model. Hence, our results indicate that SFRP5 can inhibit melanogenesis in melanocytes. Additionally, our findings showed that SFRP5 plays a vital role in the development of vitiligo, and thus may serve as a potential therapeutic target for vitiligo.Cancer is a disease of altered signaling and metabolism, causing uncontrolled division and survival of transformed cells. A host of molecules, factors, and conditions have been designated as underlying causes for the inception and progression of the disease. An enormous amount of data is available, system-wide interaction networks of the genes and proteins are generated over the years and have now reached up to a level of saturation, where we need to shift our focus to the more advanced and comprehensive methods and approaches of data analysis and visualization. Even with the availability of enormous literature on this one of the most pressing pathological conditions, a successful cure of the disease seems to be obscure. New treatment plans, like immunotherapy and precision medicine, are being employed for different studies. Nevertheless, their actual benefits to the patients would be known only after the evaluation of clinical data over the next few years. Therefore, we need to look at few fundamental challenges that should be addressed in more depth before we could devise better, rigorous, and comprehensive treatment plans and may successfully reach a possible cure of the disease. This article aims at bringing attention towards some fundamental gaps in our approach towards the disease that leads to failure in devising successful therapeutics.Mitochondrial autophagy (mitophagy) is the selective clearance of damaged or incomplete mitochondria by autophagy, which is critical for the functional integrity of the entire mitochondrial network and cell survival. Because dysfunction of mitophagy is closely related to many diseases, it is important to study the specific molecular mechanism and pathophysiological significance of mitophagy. FUN14 domain-containing 1 (FUNDC1) is a newly identified mitochondrial outer membrane protein that induces receptor-mediated mitophagy by its interaction with LC3 during hypoxia. The expression, phosphorylation, regulation and significance of FUNDC1 are reviewed in the context of a large number of pathophysiological conditions. check details Emerging evidence has demonstrated that levels and phosphorylation states of FUNDC1 are closely related to occurrence, progression and prognosis of various diseases including heart diseases and cancers, indicating that FUNDC1 may serve as a promising biomarker and potential therapeutic target.