Effect of salt on germination of samphire species

Nine Halosarcia plant species from Lake Carey, Western Australia, were tested to determine the effect of salt on seed germination. These species were Halosarcia \u27Angel Fish Island\u27 (B. Davey 4) Halosarcia calyptrata Paul G. Wilson, Halosarcia halocnemoides (Nees) Paul G. Wilson, Halosarcia peltata Paul G. Wilson, Halosarcia pergranulata (J. M. Black) Paul G. Wilson, Halosarcia undulata Paul G. Wilson. All species were subjected to salt concentrations of 0, 10, 20 and 30 g/l NaCl both in the laboratory in Petri dishes and under outdoor conditions, wither buried or on the surface of soil from the lake margin. The nine species were also tested for their ability to recover, the seeds were germinated in fresh water. For the majority of species, increased NaCl concentrations resulted in decreased germination percentages both in the laboratory and outdoors. In contrast, H. halocnemoides showed a slight increase in germination percentages at higher NaCl concentrations. In laboratory trials, the greatest reduction in germination percentage was 81% for H. \u27Angel Fish Island\u27; the average reduction was 37% across all species. In outdoor experiments, germination only reached a maximum of 25% which could have been due to lack of moisture, scarification of seeds, or temperature. Averaged across all the species, there was an increase of 58% in germination of the remaining seeds once salt was removed by flushing with fresh water

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Plastic Surgeons’ Perceptions of Financial Conflicts of Interest and the Sunshine Act

Background:. It is unknown whether recent legislation known as the Physician Payments Sunshine Act has affected plastic surgeons’ views of conflicts of interest (COI). The purpose of this study was to evaluate plastic surgeons’ beliefs about COI and their comprehension of the government-mandated Sunshine Act. Methods:. Plastic surgeon members of the American Society of Plastic Surgeons were invited to complete an electronic survey. The survey contained 27 questions that assessed respondents’ past and future receipt of financial gifts from industry, awareness of the Sunshine Act, and beliefs surrounding the influence of COI on surgical practice. Results:. A total of 322 individuals completed the survey. A majority had previously accepted gifts from industry (n = 236; 75%) and would accept future gifts (n = 181; 58%). Most respondents believed that COI would affect their colleagues’ medical practice (n = 190; 61%) but not their own (n = 165; 51%). A majority was aware of the Sunshine Act (n = 272; 89%) and supported data collection on surgeon COI (n = 224; 73%). A larger proportion of young surgeons believed patients would benefit from knowing their surgeon’s COI (P = 0.0366). Surgeons who did not expect COI in the future believed financial COI could affect their own clinical practice (P = 0.0221). Conclusions:. Most plastic surgeons have a history of accepting industry gifts but refute their influence on personal clinical practice. Surgeon age and anticipation of future COI affected beliefs about the benefits of COI disclosure to patients and the influence of COI on surgical practice

Break-induced ATR and Ddb1-Cul4(Cdt)² ubiquitin ligase-dependent nucleotide synthesis promotes homologous recombination repair in fission yeast

Nucleotide synthesis is a universal response to DNA damage, but how this response facilitates DNA repair and cell survival is unclear. Here we establish a role for DNA damage-induced nucleotide synthesis in homologous recombination (HR) repair in fission yeast. Using a genetic screen, we found the Ddb1–Cul4(Cdt2) ubiquitin ligase complex and ribonucleotide reductase (RNR) to be required for HR repair of a DNA double-strand break (DSB). The Ddb1–Cul4(Cdt2) ubiquitin ligase complex is required for degradation of Spd1, an inhibitor of RNR in fission yeast. Accordingly, deleting spd1(+) suppressed the DNA damage sensitivity and the reduced HR efficiency associated with loss of ddb1(+) or cdt2(+). Furthermore, we demonstrate a role for nucleotide synthesis in postsynaptic gap filling of resected ssDNA ends during HR repair. Finally, we define a role for Rad3 (ATR) in nucleotide synthesis and HR through increasing Cdt2 nuclear levels in response to DNA damage. Our findings support a model in which break-induced Rad3 and Ddb1–Cul4(Cdt2) ubiquitin ligase-dependent Spd1 degradation and RNR activation promotes postsynaptic ssDNA gap filling during HR repair

Expert perspectives on global biodiversity loss and its drivers and impacts on people

Despite substantial progress in understanding global biodiversity loss, major taxonomic and geographic knowledge gaps remain. Decision makers often rely on expert judgement to fill knowledge gaps, but are rarely able to engage with sufficiently large and diverse groups of specialists. To improve understanding of the perspectives of thousands of biodiversity experts worldwide, we conducted a survey and asked experts to focus on the taxa and freshwater, terrestrial, or marine ecosystem with which they are most familiar. We found several points of overwhelming consensus (for instance, multiple drivers of biodiversity loss interact synergistically) and important demographic and geographic differences in specialists’ perspectives and estimates. Experts from groups that are underrepresented in biodiversity science, including women and those from the Global South, recommended different priorities for conservation solutions, with less emphasis on acquiring new protected areas, and provided higher estimates of biodiversity loss and its impacts. This may in part be because they disproportionately study the most highly threatened taxa and habitats. Front Ecol Environ 2022;

Expert perspectives on global biodiversity loss and its drivers and impacts on people

Despite substantial progress in understanding global biodiversity loss, major taxonomic and geographic knowledge gaps remain. Decision makers often rely on expert judgement to fill knowledge gaps, but are rarely able to engage with sufficiently large and diverse groups of specialists. To improve understanding of the perspectives of thousands of biodiversity experts worldwide, we conducted a survey and asked experts to focus on the taxa and freshwater, terrestrial, or marine ecosystem with which they are most familiar. We found several points of overwhelming consensus (for instance, multiple drivers of biodiversity loss interact synergistically) and important demographic and geographic differences in specialists’ perspectives and estimates. Experts from groups that are underrepresented in biodiversity science, including women and those from the Global South, recommended different priorities for conservation solutions, with less emphasis on acquiring new protected areas, and provided higher estimates of biodiversity loss and its impacts. This may in part be because they disproportionately study the most highly threatened taxa and habitats. Front Ecol Environ 2022;

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease