Using recombinant and , cloned under different promoters, confirmed their TA nature, as expression was able to reverse growth inhibition by CptA in a dose-time dependent manner. Furthermore, transcriptional analysis of in clinical and standard strains demonstrated the downregulation of this system under oxidative and antibiotic stress. Combining in silico and studies confirmed the predicted TA nature of a -like system in . Transcriptional analysis suggests a possible role of in response to antibiotics and stress factors in , making it a promising drug target. Combining in silico and in vitro studies confirmed the predicted TA nature of a cptBA-like system in A. baumannii . Transcriptional analysis suggests a possible role of cptBA in response to antibiotics and stress factors in A. baumannii, making it a promising drug target. A population-specific genomic reference is important for research and clinical practice, yet it remains unavailable for Han Chinese (HC) in Taiwan. We report the first whole genome sequencing (WGS) database of HC (1000 Taiwanese genome (1KTW-WGS)) and demonstrate several applications to cardiovascular medicine. Whole genomes of 997 HC were sequenced to at least 30X depth. A total of 20,117 relatively healthy HC individuals were genotyped using a customized Axiom GWAS array. We performed a genome-wide genotype imputation technique using IMPUTE2. We identified 26.7 million single-nucleotide variants (SNVs) and 4.2 million insertions-deletions. Of the SNVs, 16.1% were novel relative to dbSNP (build 152), and 34.2% were novel relative to gnomAD. A total of 18,450 healthy HC individuals were genotyped using a customized Genome-Wide Association Study (GWAS) array. We identified hypertension-associated variants and developed a hypertension prediction model based on the correlation between the WGS data and GWAS data (combined clinical and genetic models, AUC 0.887), and also identified 3 novel hyperlipidemia-associated variants. Each individual carried an average of 16.42 (SD=3.72) disease-causing variants. Additionally, we established an online (an important cardiac gene) database that can be used to explore racial differences. Finally, pharmacogenetics studies identified HC population-specific SNVs in genes ( and ) involved in drug metabolism and blood clotting. This research demonstrates the benefits of constructing a population-specific genomic reference database for precision medicine. This research demonstrates the benefits of constructing a population-specific genomic reference database for precision medicine. Ovarian cancer (OC) is one of the most frequent gynecologic cancers among women, and high-accuracy risk prediction techniques are essential to effectively select the best intervention strategies and clinical management for OC patients at different risk levels. Current risk prediction models used in OC have low sensitivity, and few of them are able to identify OC patients at high risk of mortality, which would both optimize the treatment of high-risk patients and prevent unnecessary medical intervention in those at low risk. To this end, we have developed a bagging-based algorithm with GA-XGBoost models that predicts the risk of death from OC using gene expression profiles. Four gene expression datasets from public sources were used as training (n=1) or validation (n=3) sets. The performance of our proposed algorithm was compared with fine-tuning and other existing methods. Moreover, the biological function of selected genetic features was further interpreted, and the response to a panel of approved drugs was predicted for different risk levels. The proposed algorithm showed good sensitivity (74-100%) in the validation sets, compared with two simple models whose sensitivity only reached 47% and 60%. The prognostic gene signature used in this study was highly connected to , a key component of the PI3K/AKT/mTOR signaling pathway, which influences the tumorigenesis, proliferation, and progression of OC. These findings demonstrated an improvement in the sensitivity of risk classification of OC patients with our risk prediction models compared with other methods. Ongoing effort is needed to validate the outcomes of this approach for precise clinical treatment. These findings demonstrated an improvement in the sensitivity of risk classification of OC patients with our risk prediction models compared with other methods. Ongoing effort is needed to validate the outcomes of this approach for precise clinical treatment. The dermal papilla (DP) represents the major regulatory entity within the hair follicle (HF), inducing hair formation and growth through reciprocal interactions with epithelial cells. However, human DP cells rapidly lose their hair inductive ability when cultured in an epithelium-deficient environment. To determine if the conditioned medium collected from interfollicular keratinocytes (KCs-CM) is capable of improving DP cell native properties and inductive phenotype. DP cells were cultured with KCs-CM both in 2D and 3D culture conditions (spheroids). Further, the hair-inductive capacity of DP cells precultured with KCs-CM was tested in a hair reconstitution assay, after co-grafting with human keratinocytes in nude mice. We demonstrate that KCs-CM contributes to restore the inductivity of cultured human DP cells in a more effective mode than the conventional 3D-cultures. This is supported by the higher active alkaline phosphatase (ALP) levels in DP cells, the improved self-aggregative capacity and the es. The proposed strategy encourages future cell-based strategies for HF regeneration not only in the context of hair-associated disorders, but also in the management of wounds to aid in restoring critical skin regulatory appendages. As a member of annexin family proteins, annexin A3 (ANXA3) has 36-kDa and 33-kDa isoforms. https://www.selleckchem.com/products/SGX-523.html ANXA3 plays crucial roles in the tumorigenesis, aggressiveness and drug-resistance of cancers. However, previous studies mainly focused on the role of total ANXA3 in cancers without distinguishing the distinction between the two isoforms, the role of 33-kDa ANXA3 in cancer remains unclear. Current work aimed to investigate the function and regulation mechanism of 33-kDa ANXA3 in hepatocarcinoma. The expressions of ANXA3, CRKL, Rac1, c-Myc and pAkt were analyzed in hepatocarcinoma specimens by Western blotting. The biological function of 33-kDa ANXA3 in the growth, metastasis, apoptosis, angiogenesis, chemoresistance of hepatocarcinoma cells with the underlying molecular mechanism were investigated using gain-of-function strategy or . 33-kDa ANXA3 was remarkably upregulated in tumor tissues compared with corresponding normal liver tissues of hepatocarcinoma patients. Its stable knockdown decreased the tumor growing velocity and malignancy of hepatocarcinoma HepG2 cells transplanted in nude mice.