Integration of gender considerations in climate-smart agriculture R4D in South Asia: Useful research questions

Aimed at researchers working with climate-smart agriculture in South Asia, this resource suggests a set of issues to consider in relation to the integration of gender in climate-smart agricultural research for development. Climate change often exacerbates the problems and inequities that poor rural women face. The feminization of agriculture underscores the need to ensure that both men and women are able to learn about, try out, take up, and benefit from improved agricultural technologies, including climate-smart practices

HtrA chaperone activity contributes to host cell binding in Campylobacter jejuni

<p>Abstract</p> <p>Background</p> <p>Acute gastroenteritis caused by the food-borne pathogen <it>Campylobacter jejuni </it>is associated with attachment of bacteria to the intestinal epithelium and subsequent invasion of epithelial cells. In <it>C. jejuni</it>, the periplasmic protein HtrA is required for efficient binding to epithelial cells. HtrA has both protease and chaperone activity, and is important for virulence of several bacterial pathogens.</p> <p>Results</p> <p>The aim of this study was to determine the role of the dual activities of HtrA in host cell interaction of <it>C. jejuni </it>by comparing an <it>htrA </it>mutant lacking protease activity, but retaining chaperone activity, with a Δ<it>htrA </it>mutant and the wild type strain. Binding of <it>C</it>. <it>jejuni </it>to both epithelial cells and macrophages was facilitated mainly by HtrA chaperone activity that may be involved in folding of outer membrane adhesins. In contrast, HtrA protease activity played only a minor role in interaction with host cells.</p> <p>Conclusion</p> <p>We show that HtrA protease and chaperone activities contribute differently to <it>C. jejuni</it>'s interaction with mammalian host cells, with the chaperone activity playing the major role in host cell binding.</p

Psychotropic prescribing after hospital discharge in survivors of critical illness, a retrospective cohort study (2012–2019)

Background:Many people survive critical illness with the burden of new or worsened mental health issues and sleep disturbances. We examined the frequency of psychotropic prescribing after critical illness, comparing critical care to non-critical care hospitalised survivors, and whether this varied in important subgroups.Methods:This retrospective cohort study included 23,340 critical care and 367,185 non-critical care hospitalised adults from 2012 through 2019 in Lothian, Scotland, who survived to discharge.Results:One-third of critical care survivors (32 7527/23,340) received a psychotropic prescription within 90 days after hospital discharge (25 14hypnotics; 4mania medicines). In contrast, 1554,589/367,185) of non-critical care survivors received a psychotropic prescription (12 5hypnotics; 2mania medicines). Among patients without psychotropic prescriptions within 180 days prior to hospitalisation, after hospital discharge, the critical care group had a higher incidence of psychotropic prescription (10.3 1610/15,609) compared with the non-critical care group (3.2 9743/307,429); unadjusted hazard ratio (HR) 3.39, 95 3.22–3.57. After adjustment for potential confounders, the risk remained elevated (adjusted HR 2.03, 95 1.91–2.16), persisted later in follow-up (90–365 days; adjusted HR 1.38, 95 1.30–1.46), and was more pronounced in those without recorded comorbidities (adjusted HR 3.49, 95 3.22–3.78).Conclusions:Critical care survivors have a higher risk of receiving psychotropic prescriptions than hospitalised patients, with a significant proportion receiving benzodiazepines and other hypnotics. Future research should focus on the requirement for and safety of psychotropic medicines in survivors of critical illness, to help guide policy for clinical practice

Can vitamin D3 supplementation prevent bone loss in persons with MS? A placebo-controlled trial

Multiple sclerosis (MS) is a possible cause of secondary osteoporosis. In this phase II trial we assessed whether a weekly dose of 20,000 IU vitamin D3 prevents bone loss in ambulatory persons with MS age 18–50 years. ClinicalTrials.gov ID NCT00785473. All patients managed at the University Hospital of North Norway who fulfilled the main inclusion criteria were invited to participate in this double-blinded trial. Participants were randomised to receive 20,000 IU vitamin D3 or placebo once a week and 500 mg calcium daily for 96 weeks. The primary outcome was the effect of the intervention on percentage change in bone mineral density (BMD) at the hip, the spine, and the ultradistal radius over the study period. Of 71 participants randomised, 68 completed. Mean serum 25-hydroxyvitamin D [25(OH)D] levels in the intervention group increased from 55 nmol/L at baseline to 123 nmol/L at week 96. After 96 weeks, percentage change in BMD did not differ between groups at any site. BMD decreased at the hip, by 1.4% in the placebo group (95% CI −2.3 to −0.4, SD 2.7, p = 0.006) and by 0.7% in the treatment group (−1.6 to 0.2, 2.7, p = 0.118), difference 0.7% (−1.9 to 0.7, p = 0.332). Findings were not altered by adjustment for sex or serum 25(OH)D. Supplementation with 20,000 IU vitamin D3 a week did not prevent bone loss in this small population. Larger studies are warranted to assess the effect of vitamin D on bone health in persons with MS

The heme sensing response regulator HssR in Staphylococcus aureus but not the homologous RR23 in Listeria monocytogenes modulates susceptibility to the antimicrobial peptide plectasin

<p>Abstract</p> <p>Background</p> <p>Host defence peptides (HDPs), also known as antimicrobial peptides (AMPs), have emerged as potential new therapeutics and their antimicrobial spectrum covers a wide range of target organisms. However, the mode of action and the genetics behind the bacterial response to HDPs is incompletely understood and such knowledge is required to evaluate their potential as antimicrobial therapeutics. Plectasin is a recently discovered HDP active against Gram-positive bacteria with the human pathogen, <it>Staphylococcus aureus </it>(<it>S. aureus</it>) being highly susceptible and the food borne pathogen, <it>Listeria monocytogenes </it>(<it>L. monocytogenes</it>) being less sensitive. In the present study we aimed to use transposon mutagenesis to determine the genetic basis for <it>S. aureus </it>and <it>L. monocytogenes </it>susceptibility to plectasin.</p> <p>Results</p> <p>In order to identify genes that provide susceptibility to plectasin we constructed bacterial transposon mutant libraries of <it>S. aureus </it>NCTC8325-4 and <it>L. monocytogenes </it>4446 and screened for increased resistance to the peptide. No resistant mutants arose when <it>L. monocytogenes </it>was screened on plates containing 5 and 10 fold Minimal Inhibitory Concentration (MIC) of plectasin. However, in <it>S. aureus</it>, four mutants with insertion in the heme response regulator (<it>hssR</it>) were 2-4 fold more resistant to plectasin as compared to the wild type. The <it>hssR </it>mutation also enhanced resistance to the plectasin-like defensin eurocin, but not to other classes of HDPs or to other stressors tested. Addition of plectasin did not influence the expression of <it>hssR </it>or <it>hrtA</it>, a gene regulated by HssR. The genome of <it>L. monocytogenes </it>LO28 encodes a putative HssR homologue, RR23 (in <it>L. monocytogenes </it>EGD-e lmo2583) with 48% identity to the <it>S. aureus </it>HssR, but a mutation in the <it>rr23 </it>gene did not change the susceptibility of <it>L. monocytogenes </it>to plectasin.</p> <p>Conclusions</p> <p><it>S. aureus </it>HssR, but not the homologue RR23 from <it>L. monocytogenes</it>, provides susceptibility to the defensins plectasin and eurocin. Our data suggest that a functional difference between response regulators HssR and RR23 is responsible for the difference in plectasin susceptibility observed between <it>S. aureus </it>and <it>L. monocytogenes</it>.</p