Can forest management based on natural disturbances maintain ecological resilience?

Given the increasingly global stresses on forests, many ecologists argue that managers must maintain ecological resilience: the capacity of ecosystems to absorb disturbances without undergoing fundamental change. In this review we ask: Can the emerging paradigm of natural-disturbance-based management (NDBM) maintain ecological resilience in managed forests? Applying resilience theory requires careful articulation of the ecosystem state under consideration, the disturbances and stresses that affect the persistence of possible alternative states, and the spatial and temporal scales of management relevance. Implementing NDBM while maintaining resilience means recognizing that (i) biodiversity is important for long-term ecosystem persistence, (ii) natural disturbances play a critical role as a generator of structural and compositional heterogeneity at multiple scales, and (iii) traditional management tends to produce forests more homogeneous than those disturbed naturally and increases the likelihood of unexpected catastrophic change by constraining variation of key environmental processes. NDBM may maintain resilience if silvicultural strategies retain the structures and processes that perpetuate desired states while reducing those that enhance resilience of undesirable states. Such strategies require an understanding of harvesting impacts on slow ecosystem processes, such as seed-bank or nutrient dynamics, which in the long term can lead to ecological surprises by altering the forest's capacity to reorganize after disturbance

UK Eutrophying and Acidifying Atmospheric Pollutants Monitoring networks UKEAP

In 2012 the complete dataset from the Defra funded UK Eutrophying and Acidifying Atmospheric Pollutants National Ammonia MOnitoring Network and the Acid Gas and aerosol network was prepared and submitted to EMEP for publication in the EMEP database. The talk gave an overview of the measurements being made and the scientific purpose of them

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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

Photoperiodic and ovarian steroid regulation of histone deacetylase 1, 2, and 3 in Siberian hamster (Phodopus sungorus) reproductive tissues

Epigenetic modifications in reproductive tissues have predominantly focused on pathological conditions, such as ovarian and uterine cancers. The contribution of DNA methylation and histone acetylation to the timing and control of fertility is not well described. Siberian hamsters provide an important model to investigate the relatively short-term regulation of fertility (e.g. estrous) as well as long-term timing of breeding (e.g. seasonal). Recent work has shown that DNA methyltransferase 3a (dnmt3a) expression is associated with reproductive involution. Here, the objectives were to identify the impact of photoperiod on hdac1–3 expression in hamster testicular, ovarian and uterine tissue. Then, we assessed the effect of E2P4 and estrous cycling on hdac1–3 expression in uterine tissue. Testicular expression of hdac1 was significantly reduced, whereas hdac3 increased in reproductively photoregressed male hamsters; hdac2 expression did not significantly change across photoperiod conditions. There was no significant photoperiodic effect on ovarian expression of hdac1–3. Uterine expression of hdac3 expression was greater in long day hamsters; exposure to short days significantly reduced uterine hdac2 expression. Ovariectomized hamsters administered a single bolus injection of oil were found to have elevated uterine hdac2 compared to E2P4 treated females 12 h and 24 h post injection. Uterine hdac1–3 expression was relatively constant across the estrous cycle. Altogether these data indicate tissue-dependent photoperiodic regulation of hdac1–3 expression and that E2P4 may inhibit uterine hdac2 over long-term breeding cycles

The Effect of Metformin and Standard Therapy versus Standard Therapy alone in Nondiabetic Patients with Insulin Resistance and Nonalcoholic Steatohepatitis (NASH): A Pilot Trial

Nonalcoholic steatohepatitis (NASH) is increasing in prevalence and is related to underlying insulin resistance. The aim of this study was to assess the efficacy of metformin on the characteristic histopathologic lesions of NASH. This was a 12-month prospective, randomized, placebo-controlled trial comparing diet and exercise alone to diet, exercise and metformin in nondiabetic patients with insulin resistance and NASH. Patients were randomized to either group A or B. Group A received placebo, dietary counseling, recommendations for weight loss and exercise four times per week. Group B received long-acting metformin 500 mg daily (titrated to 1000 mg daily) plus dietary counseling, recommendations for weight loss and exercise four times per week. Histopathology was assessed at 12 months and biopsies were scored by two pathologists who were blinded to all data. Twenty-three subjects were screened and 19 were randomized to either group A (n ¼10) or group B (n¼ 9). Seven of the 10 subjects in group A completed the study including repeat liver biopsy while all patients in group B completed the study. Body mass index improved in both groups decreasing by 1.7 kg/m2 in group A and 0.9 kg/m2 in group B (not significant, control versus treatment). Homeostasis model assessment of insulin resistance scores improved in both groups decreasing by 1.14 in group A and 1.58 in group B (not significant, control versus treatment). No significant difference in histopathology was seen between groups on follow-up liver biopsy. Metformin appeared to have little effect in improvement in liver function tests or liver histology in nondiabetic patients with insulin resistance and NASH. Decrease in BMI through diet and exercise significantly improved HOMA-IR scores, serum aminotransferases and liver histology

Apparent specific volumes and tastes of cyclamates, other sulfamates, saccharins and acesulfame sweeteners

Measurements of apparent specific volume (ASV) for a series of alternative sweeteners (cyclamates, sulfamates, saccharins, acesulfames and anilinomethanesulfonates) have been made. Taste data have been obtained for many of the new compounds unless the toxicity of the associated metals precluded this. Apparent molar volume (AMV), isentropic specific (IASC) and isentropic molar (IAMC) compressibilities were also measured. Sixteen metallic cyclamates cyc-C6H11NHSO3M and two phenylsulfamates ArNHSO3Na, namely 3.5-dimethyl- and 3,4-dimethoxyphenylsulfamates have been examined. When the ASVs for these are combined with those for 15 aliphatic, aromatic and alicyclic sulfamates from a previous study, many of the values are seen to fall into the region that was previously identified as being the "sweet area", i.e. the ASVs lay between similar to0.5 and similar to0.7 (a few sweet compounds fall below this range and it is suggested that it could be extended slightly to accommodate these). Interestingly, the anilinomethanesulfonates, ArNHCH2SO3Na (Ar = C6H5-, 3-MeC6H4- and 3-ClC6H4-) lie clearly in the sweet region but only one of them shows slight sweetness showing that the molecular structural change made (compared with the 'parent' sulfamate-NHSO3-) cannot be accommodated at the receptor site. (C) 2003 Elsevier Ltd. All rights reserved