Kelleherharvey7653

The remaining 5 studies that included 1422 patients (SR group=559, TACE group=863) were studied for the meta-analysis. The median OS was longer in the SR group (8.2-64 months in SR vs. 6.6-32 months in TACE), proving that SR offered survival benefits. Moreover, the HR for the OS in the TACE group was 1.64 (95% CI, 1.43-1.88) compared to SR group, depicting that TACE was a less favorable option compared to SR.

There is evidence that SR may be a better viable option for advanced HCC with PVTT.

There is evidence that SR may be a better viable option for advanced HCC with PVTT.Enhancing motivation is a crucial issue in pediatric obesity interventions, as behavioral changes related to food intake and physical exercise are difficult to carry out with an insufficient level of motivation. In the treatment setting, low motivation towards change may lead to early termination or inadequate treatment outcomes. This paper reviews widely-used models of motivation, including the transtheoretical model of change, self-determination theory, and motivational interviewing (MI). We introduce useful strategies based on each theoretical model to enhance motivation, such as an importance and confidence scale and a decisional balance technique. A review of recent MI interventions in children and adolescents is presented to discuss the efficacy of MI-based interventions and considerations for applying MI in pediatric obesity.Chronic diseases in postmenopausal women are caused by rapid changes in hormones and are accompanied by rapid changes in body composition (muscle, bone, and fat). In an aging society, the health of postmenopausal women is a social issue, and people's interest in ingesting high-quality protein is increasing in order to maintain a healthy body composition. This review aims to summarize the efficacy of soy foods and their impact on body composition. The soy protein and isoflavones contained in soy foods can improve muscle and bone density quality and reduce body weight. It is considered a breakthrough in preventing osteosarcopenia and obesity that may occur after menopause.Renal cell carcinoma (RCC) is likely to metastasize to other organs, and is often resistant to conventional chemotherapies. Thymoquinone (TQ), a phytochemical derived from the seeds of Nigella sativa, has been shown to inhibit migration and metastasis in various cancers. In this study, we assessed the effect of TQ on the migratory activity of human RCC Caki-1 cells. We found that treatment with TQ reduced the proteolytic activity of matrix metalloproteinase-9 (MMP-9) in Caki-1 cells. TQ significantly repressed prostaglandin E2 (PGE2) production, its EP2 receptor expression as well as the activation of Akt and p38, the wellknown upstream signal proteins of MMP-9. Perhexiline In addition, treatment with butaprost, a PGE2 agonist, also induced MMP-9 activity and migration/invasion in Caki-1 cells. Moreover, pharmacological inhibitors of PI3K/Akt and p38 remarkably attenuated butaprostinduced Caki-1 cell migration and invasion, implying that activation of PI3K/Akt and p38 is a bridge between the PGE2-EP2 axis and MMP-9-dependent migration and invasion. Taken together, these data suggest that TQ is a promising anti-metastatic drug to treat advanced and metastatic RCC.

The angiogenesis post myocardial infarction (MI) is compromised in diabetes. MiR-144-3p is reported to be highly expressed in circulating exosomes of diabetic patients, implying its role in diabetic complications. However, whether circulating exosomes and enriched miR-144-3p are involved in the impaired neovascularization in diabetes and the underlying mechanism is unclear.

DMexo and miR-144-3p mimic-treated MSCs had elevated miR-144-3p levels and decreased MMP9, Ets1 and PLG expression. The percentage of EPCs were relatively lower in DMexo-treated or agomir-treated MI mice compared with MI mice. Finally, the luciferase assay confirmed the direct binding between miR-144-3p and Ets1.

Exosomal miR-144-3p could impair the mobilization ability of EPCs, which was associated with impaired ischemia-induced neovascularization.

Circulating exosomes were isolated from Streptozotocin (STZ)-induced mice.

, mesenchymal stem cells (MSCs) were incubated with exosomes from diabetic mice (DMexo), and miR-144-3p mimic or inhibitor. miR-144-3p, and MMP9 pathway were measured using qPCR and immunoblotting.

, MI mice induced by left anterior descending ligation were treated with DMexo, as well as miR-144-3p agomir. Flow cytometry was used to profile endothelial progenitor cells (EPCs) in peripheral blood and bone marrow post 24 hours respectively.

Circulating exosomes were isolated from Streptozotocin (STZ)-induced mice. In vitro, mesenchymal stem cells (MSCs) were incubated with exosomes from diabetic mice (DMexo), and miR-144-3p mimic or inhibitor. miR-144-3p, and MMP9 pathway were measured using qPCR and immunoblotting. In vivo, MI mice induced by left anterior descending ligation were treated with DMexo, as well as miR-144-3p agomir. Flow cytometry was used to profile endothelial progenitor cells (EPCs) in peripheral blood and bone marrow post 24 hours respectively.The Rho-kinases (ROCK) inhibitor Y-27632 has been shown to promote the growth of epidermal cells, however, its potential effects on human dermal fibroblasts (HDFs) need to be clarified. Here we show that prolonged treatment of HDFs with Y-27632 decreased their growth by inducing senescence, which was associated with induction of the senescence markers p16 and p21, and downmodulation of the ERK pathways. The senescent HDFs induced by Y-27632 acquired a cancer-associated-fibroblast (CAF)-like phenotype to promote squamous cell carcinoma (SCC) cell growth in vitro. Expression of a newly identified target of Y-27632 by RNA-seq, insulin growth factor binding protein 5 (IGFBP-5), was dramatically increased after 24 h of treatment with Y-27632. Adding recombinant IGFBP-5 protein to the culture medium produced similar phenotypes of HDFs as did treatment with Y-27632, and knockdown of IGFBP-5 blocked the Y-27632-induced senescence. Furthermore, Y-27632 induced the expression of an IGFBP-5 upstream gene, GATA4, and knockdown of GATA4 also reduced the Y-27632-induced senescence.