Aging is a fundamental biological process accompanied by a general decline in tissue function. Indeed, as the lifespan increases, age-related dysfunction, such as cognitive impairment or dementia, will become a growing public health issue. Aging is also a great risk factor for many age-related diseases. Nowadays, people want not only to live longer but also healthier. Therefore, there is a critical need in understanding the underlying cellular and molecular mechanisms regulating aging that will allow us to modify the aging process for healthy aging and alleviate age-related disease. Here, we reviewed the recent breakthroughs in the mechanistic understanding of biological aging, focusing on the adenosine monophosphate-activated kinase (AMPK), Sirtuin 1 (SIRT1) and mammalian target of rapamycin (mTOR) pathways, which are currently considered critical for aging. We also discussed how these proteins and pathways may potentially interact with each other to regulate aging. We further described how the knowledge of these pathways may lead to new interventions for antiaging and against age-related disease.Vetiver grass [Vetiveria zizanioides (L.) Nash] without seeds, suitable for growing on coastal saline land, has attracted attention because of oil extraction from its roots and industrial and agricultural use. In this study, a pot experiment with different NaCl contents was used to investigate the influence of water salinity levels on vetiver, salt tolerance, and the feasibility of transferring it to coastal saline regions. The results indicated that the fresh weight of roots and shoots increased initially and then gradually decreased with an increase in NaCl content, and the maximum was attributed to a water salinity of 0.3%. The vetiver can tolerate a maximum saline content of up to 2%. The promotion of vetiver growth under water salinity could be attributed to the acceleration of nutrient uptake-induced saline, including K, N, and Cl. The growth of vetiver was insignificantly inhibited with 0.5% water salinity (mild stress), significantly inhibited with 1.0% water salinity (moderate stress biomass decrease), and severe inhibited with >1.5% water salinity (intense stress biomass decrease). The salt tolerance of vetiver was due to osmotic regulation by reducing sugars under mild stress and of proline under intense stress, and Na+ sequestration in roots and the transformation of Cl- away from sensitive roots. The vetiver could be cultivated in slightly coastal saline soil (0.1-0.2% soil salinity) and even moderately saline coastal soil (0.2-0.4% soil salinity) under irrigation with low salt water during transplanting.Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of two superoxide anions (O2·-) into hydrogen peroxide (H2O2) and oxygen (O2) and is generally known to protect against oxidative stress. Angiotensin II (AngII) causes vascular hypertrophic remodeling which is associated with H2O2 generation. The aim of this study is to investigate the role of cytosolic SOD (SOD1) in AngII-induced vascular hypertrophy. We employed C57/BL6 mice (WT) and SOD1 deficient mice (SOD1-/-) with the same background. They received a continuous infusion of saline or AngII (3.2 mg/kg/day) for seven days. The blood pressures were equally elevated at 1.5 times with AngII, however, vascular hypertrophy was blunted in SOD1-/- mice compared to WT mice (WT mice 91.9 ± 1.13 µm versus SOD1-/- mice 68.4 ± 1.41 µm p less then 0.001). The elevation of aortic interleukin 6 (IL-6) and phosphorylation of pro-inflammatory STAT3 due to AngII were also blunted in SOD1-/- mice's aortas. In cultured rat vascular smooth muscle cells (VSMCs), reducing expression of SOD1 with siRNA decreased AngII induced IL-6 release as well as phosphorylation of STAT3. Pre-incubation with polyethylene glycol (PEG)-catalase also attenuated phosphorylation of STAT3 due to AngII. These results indicate that SOD1 in VSMCs plays a role in vascular hypertrophy due to increased inflammation caused by AngII, probably via the production of cytosolic H2O2.An Ugi three-component reaction using preformed α-phosphorated N-tosyl ketimines with different isocyanides in the presence of a carboxylic acid affords tetrasubstituted α-aminophosphonates. Due to the high steric hindrance, the expected acylated amines undergo a spontaneous elimination of the acyl group. The reaction is applicable to α-aryl ketimines bearing a number of substituents and several isocyanides. In addition, the densely substituted α-aminophosphonate substrates showed in vitro cytotoxicity, inhibiting the growth of carcinoma human tumor cell line A549 (carcinomic human alveolar basal epithelial cell).Molecular alterations in cancer genes and associated signaling pathways are used to inform new treatments for precision medicine in cancer. Small molecule inhibitors and monoclonal antibodies directed at relevant cancer-related proteins have been instrumental in delivering successful treatments of some blood malignancies (e.g., imatinib with chronic myelogenous leukemia (CML)) and solid tumors (e.g., tamoxifen with ER positive breast cancer and trastuzumab for HER2-positive breast cancer). However, inherent limitations such as drug toxicity, as well as acquisition of de novo or acquired mechanisms of resistance, still cause treatment failure. Here we provide an up-to-date review of the successes and limitations of current targeted therapies for cancer treatment and highlight how recent technological advances have provided a new level of understanding of the molecular complexity underpinning resistance to cancer therapies. We also raise three basic questions concerning cancer drug discovery based on molecular markers and alterations of selected signaling pathways, and further discuss how combination therapies may become the preferable approach over monotherapy for cancer treatments. Finally, we consider novel therapeutic developments that may complement drug delivery and significantly improve clinical response and outcomes of cancer patients.Because of preservation of proximal femoral bone stock and minimized soft tissue trauma, short-stem implants are becoming increasingly important in total hip arthroplasty (THA).  https://www.selleckchem.com/products/phtpp.html  The postulated advantage regarding the functional outcome has not been verified. We hypothesized an increased abductor muscle strength by the use of a short-stem design. Seventy consecutive patients of a randomized clinical trial were included. Of these, 67 patients met the inclusion criteria after 12 months. Thirty-five patients received a standard straight stem and 32 patients a short-stem femoral component. All surgeries were performed by a modified direct lateral approach. Isometric muscle strength of the hip abductors was evaluated preoperatively 3 and 12 months after surgery. Harris hip score (HHS) and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores were evaluated. After three months, there were no differences between the two groups; the abductor force was comparable to the preoperative initial values.