Cross-sectional studies showed an inverse association between serum 25-hydroxyvitamin D (25OHD) and white matter hyperintensities (WMHs) whereas the few longitudinal studies did not. The association between baseline 25OHD and WMHs at 10-year follow-up in the Heinz Nixdorf Recall Study plus 1000BRAINS was investigated.
 
  Data of 505 participants (49% women, 56.2±6.6years) with 25OHD at baseline (2000-2003) and WMH volume and grade of WMHs using the Fazekas classification at 10-year follow-up were analysed. The association between deseasonalized 25OHD and the base-10 logarithm of WMH volume was evaluated by multiple linear regression, adjusted for age, sex, education, smoking, alcohol consumption, sports, diabetes mellitus, systolic blood pressure and total cholesterol. β-estimators were transformed back (10
  ). Using multiple logistic regression, odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated to evaluate the association between deseasonalized 25OHD and Fazekas grades (0, absence and 1, punctate foci vs. 2, beginning and 3, large confluence).
 
  Mean 25OHD was 17.0±8.2ng/ml, and mean deseasonalized 25OHD was 16.9±7.5ng/ml. Mean WMH volume was 16.6±17.4ml, range 1-132ml. Most grade 2-3 WMHs were found to be periventricular (39% of the participants), parietal (32%) and frontal (31%) (temporal 6%, occipital 3%). The linear regression showed an inverse association between 25OHD and WMH volume. On average, a 25OHD increase of 1ng/ml was associated with a reduced WMH volume by a factor of 0.99 (95% CI 0.98; 1.00) (fully adjusted). There was also some indication for an inverse association between 25OHD and extent of periventricular (OR 0.98 [95% CI 0.96; 1.01]), frontal (0.99 [0.97; 1.02]) and parietal (0.98 [0.95; 1.00]) WMHs according to the Fazekas classification.
 
  Lower 25OHD may be a risk factor for the occurrence of WMHs.
 Lower 25OHD may be a risk factor for the occurrence of WMHs.Social media allows interventional cardiologists to disseminate and discuss research and clinical cases in real-time, to demonstrate and learn innovative techniques, to build professional networks, and to reach out to patients and the general public. Social media provides a democratic platform for all participants to influence the conversation and demonstrate their expertise. This review addresses the use of social media for these purposes in interventional cardiology, as well as respect for patient privacy, how to get started on social media, the creation of high-impact social media content, and the role of traditional journals in the age of social media. In the future, we hope that interventional cardiology fellowship programs will incorporate social media training into their curricula. In addition, professional societies may adapt to the rapid dissemination of data on social media by developing processes to update guidelines more rapidly and more frequently.Metal-organic frameworks (MOFs) hold great promise for biomedical applications owing to their unique properties. The porous structures make MOFs excellent candidates for the delivery of different drugs; the flexibility in choosing metal ions and organic ligands makes it feasible to prepare MOFs with intrinsic antitumor activities and further devise MOF-drug synergistic systems; many other types of antitumor agents could also be developed using MOFs as the precursors/templates. Thus, the past two decades have witnessed the great development of MOF-based drugs, especially in the antitumor field.  https://www.selleckchem.com/products/atezolizumab.html  This Minireview mainly focuses on the design and applications of MOF-based antitumor agents. Four aspects covering the whole field are introduced MOFs as carriers, MOFs as antitumor agents, MOF-drug synergistic systems, and MOF-derived antitumor agents. The challenges and opportunities of MOFs for clinical antitumor applications are also discussed.
  To analyse whether there is a difference in marginal bone levels (MBL) and the respective changes between cemented and screw-retained reconstructions at 3 and 5years of loading.
 
  Radiographic data from 14 prospective multicentre clinical trials following implant loading with fixed cemented (CEM) or screw-retained (SCREW) reconstructions with a 3- to 5-year follow-up were retrieved from a database. MBL and MBL changes were assessed at initiation of implant loading (BL), at 3 (FU-3) and 5years (FU-5) thereafter. The presence of peri-implantitis was also determined.
 
  Data from 1,672 implants at BL, 1,565 implants at FU-3 and 1,109 implants at FU-5 were available. The mean MBL amounted to 0.57mm (SD 0.87) at BL, 0.55mm (SD 0.86) at FU-3 and 0.65mm (SD 1.18) at FU-5. At FU-3, the mean MBL was 0.44mm (SD 0.65) in group CEM and 0.63mm (SD 0.99) in group SCREW showing a significant difference between the groups (intergroup <0.05). At FU-5, the mean MBL was 0.42mm (SD 0.77) in CEM and 0.80mm (SD 1.37) in SCREW,e respective changes between the two groups, however, appear to be clinically negligible.Osimertinib is a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that is effective in treating both naïve and T790M-mutated EGFR-TKI-resistant non-small cell lung cancer patients. The EGFR C797S mutation is the major osimertinib resistance mechanism. The present study monitored the EGFR C797S mutation during osimertinib treatment in Japanese patients using droplet digital PCR (ddPCR). In our first cohort, C797S detection was validated with tumor specimens and/or plasma samples from 26 patients using ddPCR with custom-designed probes detecting and discriminating T790M and C797S in cis and trans positions. In our second cohort, 18 patients with EGFR-T790M who were going to start osimertinib were analyzed using ddPCR by collecting the plasma samples every month from the beginning of the course of osimertinib. In the first cohort, C797S was detected in 15.4% of patients. C797S and T790M in cis and trans positions were distinguished using ddPCR. In the second cohort, serial cfDNA evaluation revealed that the rate of EGFR mutation changes with disease state. Increases of EGFR mutation were detected, including C797S several months before the diagnosis of disease progression. As with the first cohort, C797S and T790M in cis and trans position were distinguished by ddPCR at disease progression. Coincidentally, in the first cohort, next generation sequencing detected NRAS Q61K mutation and the resistance with NRAS Q61K mutation was overcome by trametinib. In the second cohort, serial cfDNA analysis was useful for evaluating bone oligo-progression and local radiation therapy.