Kumarcarlsson8864

Mechanistically, PDGFRβ overexpression induced the activation of FAK and Src leading to cell migration and invasion. Orthotopic xenograft transplantation of stable breast cancer cells and CSCs with PDGFRβ overexpression in nude mice led to a significant increase in tumorigenesis, and metastasis to lung and liver as depicted by the significant increase in human gene-specific PDGFRβ and CD44 expression, and colocalization along with an expression of human-specific Alu sequences which were perturbed with stable silencing of PDGFRβ in breast CSCs. Thus, PDGFRβ plays a crucial role in inducing breast cancer tumorigenesis and metastasis that can be a plausible therapeutic target to treat TNBC patients.

Low skeletal muscle mass (SMM) is an emerging risk factor of cardiovascular disease (CVD). We investigated the association between SMM and coronary artery calcification (CAC).

We enrolled 19,728 adults free of CVD who underwent computed tomographic estimation of Agatston CAC scores for cross-sectional analysis. Among them, 5,401 subjects who had two and more follow-up CAC scores were included in longitudinal analysis. Relative SMM is presented using the skeletal muscle mass index [SMI (%) = total appendicular muscle mass (kg)/body weight (kg) x 100]. CAC presence and incidence were defined as CAC score>0, and CAC progression was defined as √CAC score (follow-up) -√CAC score (baseline)>2.5.

Among all the subjects (mean 53.4 years, 80.8% of men), the prevalence of CAC was 36.7%. The incidence of CAC was 17.4% during mean of 3.6 years, and the progression of CAC was 49.9% during mean 2.3 years. The lowest SMI quartile was significantly associated with an increased risk of CAC presence (adjusted odds ratio=2.75, 95% confidence interval [CI]= 2.45-3.05; P<0.001), incidence (adjusted hazard ratio [AHR]=1.99, 95% CI = 1.36-2.91; P<0.001) and progression (AHR 1.48, 95% CI=1.25-1.77; P<0.001), compared to the highest quartile. learn more SMI as a continuous value was also significantly, inversely associated with CAC. SMI was the best parameter to be related to CAC among other quantitative indices such as height- or BMI- adjusted.

Low SMM is significantly associated with an elevated risk of CAC, independent of other cardiometabolic parameters.

Low SMM is significantly associated with an elevated risk of CAC, independent of other cardiometabolic parameters.RecQ4, a member of the RecQ helicase family, is required for the maintenance of genome integrity. RecQ4 has been shown to promote the following two DNA double-strand break (DSB) repair pathways non-homologous end joining (NHEJ) and homologous recombination (HR). However, its molecular function has not been fully elucidated. In the present study, we aimed to investigate the role of RecQ4 in NHEJ using Xenopus egg extracts. The N-terminal 598 amino acid region of Xenopus RecQ4 (N598), which lacks a central helicase domain and a downstream C-terminal region, was added to the extracts and its effect on the joining of DNA ends was analyzed. We found that N598 inhibited the joining of linearized DNA ends in the extracts. In addition, N598 inhibited DSB-induced chromatin binding of Ku70, which is essential for NHEJ, while the DSB-induced chromatin binding of the HR-associated proteins, replication protein A (RPA) and Rad51, increased upon the addition of N598. These results suggest that RecQ4 possibly influences the choice of the DSB repair pathway by influencing the association of the Ku heterodimer with the DNA ends.Obtaining detectable knockout phenotypes in the G0 generation is essential for gene function studies. Although CRISPR/Cas9-mediated gene editing has been employed to knock out molluscan genes, detectable phenotypes in the G0 generation have not been reported in these animals. In this study, we determined the knockout phenotype of a cilium-related gene, calaxin, using CRISPR/Cas9 technology in the gastropod mollusk Lottia goshimai. Injections with the Cas9-sgRNA complex caused approximately 30-80% of the injected larvae to exhibit a short-cilia phenotype characteristic of shortened cilia and decreased motility in the larvae. This phenotype was detectable in the G0 generation and was consistent for two independent sgRNAs. Genotyping of the injected larvae revealed various types of deletions and insertions in the target gene, which occurred in all sequences from the short-cilia larvae. This result indicated that the short-cilia phenotype was indeed caused by calaxin knockout. This possibility was supported by an RNAi assay targeting calaxin, which produced a highly similar short-cilia phenotype. We observed that a single SNP in the target sequences of the sgRNAs could show varied effects on the efficiency of mutagenesis. These results help to establish a foundation for future studies on molluscan gene editing using the CRISPR/Cas9 technique and contribute to the body of knowledge on molluscan ciliary functions.

To perform a systematic review of reported terminologies, surgical techniques, preoperative diagnostic measures, and geographic differences in the treatment of core muscle injury (CMI)/athletic pubalgia/inguinal disruption.

A systematic review was performed by searching PubMed, the Cochrane Library, and Embase to identify clinical studies or articles that described a surgical technique to treat CMI refractory to nonoperative treatment. The search phrase used was "core muscle injury" OR "sports hernia" OR "athletic pubalgia" OR "inguinal disruption." The diagnostic terminology, country of publication, preoperative diagnostic measures, surgical technique, and subspecialty of the operating surgeons described in each article were extracted and reported.

Thirty-one studies met the inclusion and exclusion criteria, including 3 surgical technique articles and 28 clinical articles (2 Level I evidence, 1 Level II, 4 Level III, and 21 Level IV). A total of 1,571 patients were included. The most common terminologyguinal disruption. These procedures are performed by orthopaedic and/or general surgeons, with the procedures performed differing on the basis of surgeon subspecialty and geographic location.

Level V, systematic review of Level I to V studies.

Level V, systematic review of Level I to V studies.