Paroxysmal atrial fibrillation (pAF) is a major risk factor for ischemic stroke, but challenging to detect with routine short-term monitoring methods. In this pilot study, we present a novel method for prolonged ECG and screening for pAF in patients with a recent embolic stroke of unknown source (ESUS). Fifteen patients aged≥50years with a recent ESUS were assigned to wear an external electrode belt-based 1-lead ECG device (Beat2Phone) continuously for 2weeks (wear time). The device was operated via a mobile phone application in nonhospital conditions. The primary outcome was patient adherence to monitoring. Secondary outcomes were incidence of new pAF, quality-wise comparison to Holter, and usability of the novel ECG monitoring method with Systems Usability Scale (SUS). We also performed a 24- to 48-hr comparison between simultaneous Beat2Phone ECG and a standard Holter in 6 patients. Wear time of Beat2Phone device was over 80% in 5 (33.3%) patients, 50%-80% in 7 (46.6%) patients, and less than 50% in 3 (20%) patients. We detected pAF≥30s in 1 patient (6.7%). In the simultaneous monitoring with Beat2Phone and Holter, there were a total of 817 (out of 1979) analyzable periods of sinus rhythm or premature atrial or ventricular beats (Cohen's Kappa coefficient 0.92±0.02 between Beat2Phone and Holter), and no pAF events. Beat2Phone ECG showed remarkable SUS scores in user evaluations (average score 81.4 out of 100 on SUS). Beat2Phone device was easy to use among ESUS patients and in optimal conditions provided high-quality 1-lead ECG signal for diagnosing pAF. The study was not registered, as it was a nonrandomized single-arm pilot study.The study was not registered, as it was a nonrandomized single-arm pilot study.Dexamethasone (DEX) is a glucocorticoid commonly used as an in vitro osteogenic inducer of mesenchymal stem/progenitor cells (abbreviated MSCs). However, several studies investigating the effects of glucocorticoids on bone regeneration through systemic injections have demonstrated negative impacts of the drugs at high concentration on the healing of hard tissues. These contrasting evidences suggest that application of glucocorticoids should be limited to low dosages but at the same time a long enough treatment period is preferred, which prompted us to evaluate the effects of different local release systems of DEX on MSC differentiation and bone repair. Two types of DEX-loaded β-cyclodextrin (CD) complexes, including CD/DEX and CD/AD-DEX, were fabricated via host-guest interactions and characterized by FTIR, 1H-NMR, MS-ESI, and UV-vis. The results demonstrated that these CD-based assemblies released DEX in differentiated profiles, with CD/DEX releasing significantly faster than CD/AD-DEX. Although CD/DEX were slightly more powerful than CD/AD-DEX in inducing rat bone marrow MSCs (rBMSCs) into osteogenic lineage in vitro, CD/AD-DEX was advantageous over CD/DEX in accelerating bone regeneration over a time period of 4 weeks in a rat tibia defect model. DSP5336 The results suggest that DEX-loaded assemblies via host-guest interactions are flexible in modulating DEX release patterns and have great potential in bone tissue engineering.Microglia activation toward M1 pro-inflammatory phenotype represents one of the earliest events of neurological disorders. Therefore, reducing microglia activation should inhibit neuroinflammation, thereby delaying the progression of neurodegeneration. Recently, we pointed out the role of STAT1 signaling in hypoxia-induced M1 activation and proposed STAT1 as a suitable molecular target for the prevention and treatment of neurodegeneration. Myricetin (MYR) is a natural flavonoid that exhibits a specific anti-STAT1 activity correlated with its direct interaction with STAT1 protein itself. Herein, we investigated the anti-inflammatory effect of MYR and its ability to protect neurons from death in an in vitro model of neurotoxicity using the neuroblast-like SH-SY5Y cells that were exposed to conditioned media from hypoxia-activated microglia BV2 cells. We demonstrate that MYR pretreatment is able to switch off hypoxia-induced M1 microglia polarization through the inhibition of STAT1 signaling. The analysis of the molecular mechanism suggests that the direct interaction of MYR with STAT1 impairs its S-glutathionylation and phosphorylation. Moreover, treatment of SH-SY5Y cells with conditioned medium from hypoxia-activated microglia pretreated with MYR produced a significant reduction in neuronal viability. Our data indicate that MYR may represent a promising candidate for prevention and treatment of neuroinflammation in neurodegenerative disorders.Preterm birth prevention is multifaceted and produces many nuanced questions. This review addresses six important clinical questions about preterm birth prevention as voted for by members of the UK Preterm Clinical Network. The questions cover the following areas preterm birth prevention in 'low-risk' populations; screening for asymptomatic genital tract infection in women at high risk of preterm birth; cervical length screening with cerclage or vaginal pessary in situ; cervical shortening whilst using progesterone; use of vaginal progesterone in combination with cervical cerclage; and optimal advice about intercourse for women at high risk of preterm birth.Senescence refers to a cellular state featuring a stable cell-cycle arrest triggered in response to stress. This response also involves other distinct morphological and intracellular changes including alterations in gene expression and epigenetic modifications, elevated macromolecular damage, metabolism deregulation and a complex pro-inflammatory secretory phenotype. The initial demonstration of oncogene-induced senescence in vitro established senescence as an important tumour-suppressive mechanism, in addition to apoptosis. Senescence not only halts the proliferation of premalignant cells but also facilitates the clearance of affected cells through immunosurveillance. Failure to clear senescent cells owing to deficient immunosurveillance may, however, lead to a state of chronic inflammation that nurtures a pro-tumorigenic microenvironment favouring cancer initiation, migration and metastasis. In addition, senescence is a response to post-therapy genotoxic stress. Therefore, tracking the emergence of senescent cells becomes pivotal to detect potential pro-tumorigenic events.