This paper summarises current progress in BC fibre manufacturing, its downfalls and also gives a future perspective on how the landscape should change to allow BC to be utilised in wound care in the current environment. Vitamin D deficiency has been widely reported among pregnant women and infants around the world. Women with low sun exposure, high BMI, low vitamin D intakes and socioeconomic disadvantage with poor quality diets are at greatest risk of vitamin D deficiency, leading to very low serum concentrations of 25-hydroxyvitamin D (25(OH)D) in their offspring and an increased risk of nutritional rickets. Many observational studies, supported by compelling in vitro and in vivo data, have generated evidence suggesting that low vitamin D status in pregnancy may also contribute to the risk of adverse perinatal outcomes including hypertensive disorders (e.g., preeclampsia), fetal growth restriction, and preterm birth. However, the few large randomized controlled trials (RCTs) conducted to date have generated conflicting evidence for a role of vitamin D supplementation in improving perinatal outcomes. Vitamin D supplementation policies during pregnancy and implementation of policies vary within and between jurisdictions. Regulatory authorities have cited insufficient evidence to establish pregnancy-specific targets for serum 25(OH)D concentrations or prenatal vitamin D intake that effectively reduce the risks of adverse perinatal and infant outcomes. This paper arises from a Debate on Vitamin D Requirements during Pregnancy, held at the 22nd Vitamin D Workshop, 2019. From varied perspectives, our objectives were to evaluate the evidence for vitamin D metabolism in pregnancy and the prevalence of gestational vitamin D deficiency worldwide; the translation of laboratory research findings to clinical studies on the role of vitamin D in perinatal health; the challenges of designing and conducting clinical trials to establish prenatal vitamin D requirements; and results to date of major large RCTs of prenatal vitamin D supplementation. Lastly, we explored potential next steps towards generating robust clinical data in this field to address both public health protection and patient care. PURPOSE The aim of this study is to compare the efficacy of MSC exosomes with hyaluronic acid (HA) against HA alone for functional cartilage regeneration in a rabbit osteochondral defect model. METHODS Critical-size osteochondral defects (4.5-mm diameter and 1.5-mm depth) were created on the trochlear grooves in the knees of eighteen rabbits and were randomly allocated to two treatment groups (1) Exosomes and HA combination and (2) HA alone. Three 1-ml injections of either exosomes and HA or HA alone were administered intra-articularly immediately after surgery and thereafter at 7 and 14 days after surgery. At 6 and 12 weeks, gross evaluation, histological and immunohistochemical analysis, and scorings were performed. The functional biomechanical competence of the repaired cartilage was also evaluated. RESULTS Compared to defects treated with HA, defects treated with exosomes and HA showed significant improvements in macroscopic scores (P=0.032; P=0.001) and histological scores (P=0.005; P0.05). In contrast, HA-treated defects showed some repair at 6 weeks, but this was not sustained, as evidenced by significant deterioration of histological scores (P=0.002) and a plateau in mechanical properties from 6 to 12 weeks. CONCLUSIONS This study shows that the combination of MSC exosomes and HA administered at a clinically acceptable frequency of three intra-articular injections can promote sustained and functional cartilage repair in a rabbit post-traumatic cartilage defect model, when compared to HA alone. CLINICAL RELEVANCE Human MSC exosomes and HA administered in combination promote functional cartilage repair, and may represent a promising cell-free therapy for cartilage repair in patients. Sporadic Alzheimer's disease (SAD) is the most common form of dementia, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most frequent hereditary ischemic small vessel disease of the brain. Relevant biomarkers or specific metabolic signatures could provide powerful tools to manage these diseases. Therefore, the main goal of this study was to compare the postmortem frontal cortex gray matter, white matter and cerebrospinal fluid (CSF) between a cognitively healthy group and CADASIL and SAD groups. We evaluated 352 individual lipids, belonging to 13 lipid classes/subclasses, using mass spectrometry, and the lipid profiles were subjected to multivariate analysis to discriminate between the dementia groups (CADASIL and SAD) and healthy controls.  https://www.selleckchem.com/products/rin1.html  The main lipid molecular species showing greater discrimination by partial least squares-discriminant analysis (PLS-DA) and a higher significance multivariate correlation (sMC) index were as follows phosphatidylserine (PS) PS(447) and lysophosphatidylethanolamine (LPE) LPE(182) in gray matter (GM); phosphatidylethanolamine (PE) PE(322) and phosphatidylcholine PC PC(446) in white matter (WM), and ether PE (ePE) ePE(382) and ether PC (ePC) ePC(343) in CSF. Common phospholipid molecular species were obtained in both dementias, such as PS(447) and lyso PC (LPC) LPC(225) in GM, PE(322) in WM and phosphatidic acid (PA) PA(385) and PC(427) in CFS. Our exploratory study suggests that phospholipids (PLs) involved in neurotransmission alteration, connectivity impairment and inflammation response in GM, WM and CSF are a transversal phenomenon affecting dementias such as CADASIL and SAD independent of the etiopathogenesis, thus providing a possible common prodromal phospholipidic biomarker of dementia. V.Subarachnoid hemorrhage (SAH) is a severe acute cerebrovascular disease with high rates of disability and death. In recent years, a large number of studies has shown that early brain injury (EBI) may be a crucial cause of the poor prognosis of SAH and that microglia-mediated neuroinflammation is an important pathological process in EBI. Previous studies have indicated that tumor necrosis factor receptor-associated factor 6 (TRAF6) is involved in microglia-mediated neuroinflammation after SAH. In addition, it has been reported that cerebral cavernous malformation 3/mammalian sterile20-like kinase 4 (CCM3/MST4) directly phosphorylates TRAF6 to inhibit its ubiquitination and to limit inflammatory responses. However, the association between CCM3/MST4 and SAH has not been reported. In our present study, we established a SAH model in adult male rats through injecting autologous arterial blood into the prechiasmatic cistern. Additionally, BV-2 cells, as well as primary microglial cultures from rats treated with oxygen hemoglobin (OxyHb) for 24 h, were used as in vitro models of SAH.