Surface modification of poly(ether ether ketone) (PEEK) aimed at applying it as a bone implant material aroused the unflagging interest of the research community. In view of the development of implantology and the growing demand for new biomaterials, increasing biocompatibility and improving osseointegration are becoming the primary goals of PEEK surface modifications. The main aim of this review is to summarize the use of polymerization methods and various monomers applied for surface modification of PEEK to increase its bioactivity, which is a critical factor for successful applications of biomedical materials. In addition, the future directions of PEEK surface modifications are suggested, pointing to low-ppm surface-initiated atom transfer radical polymerization (SI-ATRP) as a method with unexplored capacity for flat surface modifications.Abstract The human oral cavity is home to an abundant and diverse microbial community (i.e., the oral microbiome), whose composition and roles in health and disease have been the focus of intense research in recent years. Thanks to developments in sequencing-based approaches, such as 16S ribosomal RNA metabarcoding, whole metagenome shotgun sequencing, or meta-transcriptomics, we now can efficiently explore the diversity and roles of oral microbes, even if unculturable. Recent sequencing-based studies have charted oral ecosystems and how they change due to lifestyle or disease conditions. As studies progress, there is increasing evidence of an important role of the oral microbiome in diverse health conditions, which are not limited to diseases of the oral cavity. This, in turn, opens new avenues for microbiome-based diagnostics and therapeutics that benefit from the easy accessibility of the oral cavity for microbiome monitoring and manipulation. Yet, many challenges remain ahead. STSinhibitor In this review, we survey the main sequencing-based methodologies that are currently used to explore the oral microbiome and highlight major findings enabled by these approaches. Finally, we discuss future prospects in the field.Active vitamin D (calcitriol, or 1.25 (OH) 2 D) is associated with muscle weakness, falls, and fracture in community-dwelling older people. This study aimed to investigate the relationship between a serum active vitamin D level and lower extremity muscle strength in elderly patients with pre-dialysis chronic kidney disease (CKD). This cross-sectional study included 231 patients with CKD treated conservatively as outpatients. We analyzed patient background factors, including age, sex, body mass index (BMI), intact parathyroid hormone (PTH), phosphorus, calcium, albumin, serum calcitriol level as an indicator of active vitamin D, and estimated glomerular filtration rate (eGFR) collected from medical records. As an index of lower extremity muscle strength, the isometric knee extension muscle strength-to-weight ratio (kgf/kg) was calculated. The mean patient age was 75.9 ± 6.1 years (68.8% male), and the BMI was 24.1 ± 3.8 kg/m2. A significant correlation was observed between knee extensor muscle strength and serum calcitriol level (r = 0.32, p less then 0.01), age (r = -0.30, p less then 0.01), BMI (r = -0.31, p less then 0.01), intact PTH (r = -0.22, p less then 0.01), phosphorus (r = -0.29, p less then 0.01), albumin (r = -0.28, p less then 0.01), and eGFR (r = 0.25, p less then 0.01). Multiple regression analysis showed calcitriol to be significantly associated with knee extensor muscle strength (β 0.14, 95% confidence interval 0-0.002, p = 0.04) after adjustment for covariates. These results suggest that the serum active vitamin D level is associated with lower extremity muscle strength in older adults with pre-dialysis CKD. It is necessary to verify whether vitamin D supplementation increases lower extremity muscle strength in pre-dialysis CKD patients.Multidrug resistance (MDR) due to P-glycoprotein (P-gp) overexpression is a major obstacle to successful leukemia chemotherapy. The combination of anticancer chemotherapy with a chemosensitizer of P-gp inhibitor is promising to overcome MDR, generate synergistic effects, and maximize the treatment effect. Herein, we co-encapsulated a chemotherapeutic drug of mitoxantrone (MTO) and a P-gp inhibitor of β-elemene (βE) in solid lipid nanoparticles (MTO/βE-SLNs) for reversing MDR in leukemia. The MTO/βE-SLNs with about 120 nm particle size possessed good colloidal stability and sustained release behavior. For the cellular uptake study, doxorubicin (DOX) was used as a fluorescence probe to construct SLNs. The results revealed that MTO/βE-SLNs could be effectively internalized by both K562/DOX and K562 cells through the pathway of caveolate-mediated endocytosis. Under the optimized combination ratio of MTO and βE, the in vitro cytotoxicity study indicated that MTO/βE-SLNs showed a better antitumor efficacy in both K562/DOX and K562 cells than other MTO formulations. The enhanced cytotoxicity of MTO/βE-SLNs was due to the increased cellular uptake and blockage of intracellular ATP production and P-gp efflux by βE. More importantly, the in vivo studies revealed that MTO/βE-SLNs could significantly prolong the circulation time and increase plasma half-life of both MTO and βE, accumulate into tumor and exhibit a much higher anti-leukemia effect with MDR than other MTO formulations. These findings suggest MTO/βE-SLNs as a potential combined therapeutic strategy for overcoming MDR in leukemia.The diabetic heart is characterized by a shift in substrate utilization from glucose to lipids, which may ultimately lead to contractile dysfunction. This substrate shift is facilitated by increased translocation of lipid transporter CD36 (SR-B2) from endosomes to the sarcolemma resulting in increased lipid uptake. We previously showed that endosomal retention of CD36 is dependent on the proper functioning of vacuolar H+-ATPase (v-ATPase). Excess lipids trigger CD36 translocation through inhibition of v-ATPase function. Conversely, in yeast, glucose availability is known to enhance v-ATPase function, allowing us to hypothesize that glucose availability, via v-ATPase, may internalize CD36 and restore contractile function in lipid-overloaded cardiomyocytes. Increased glucose availability was achieved through (a) high glucose (25 mM) addition to the culture medium or (b) adenoviral overexpression of protein kinase-D1 (a kinase mediating GLUT4 translocation). In HL-1 cardiomyocytes, adult rat and human cardiomyocytes cultured under high-lipid conditions, each treatment stimulated v-ATPase re-assembly, endosomal acidification, endosomal CD36 retention and prevented myocellular lipid accumulation.