Continental drift: connecting Great Britain and Scandinavia

Institute of Transport and Logistics Studies. Faculty of Economics and Business. The University of Sydne

Yield of Photoperiod-sensitive Sorghum Hybrids Based on Guinea-race Germplasm under Farmers’ Field Conditions in Mali

The first sorghum [Sorghum bicolor (L.) Moench] hybrids based on West African Guinea-race-derived parents were created to enhance farmer’s food security and income through increased yields. To assess their performance, eight hybrids, six experimental pure-line cultivars, one pure-line check (Lata), and a highly adapted landrace cultivar (Tieble) were evaluated in 27 farmer-managed and two on-station yield trials in Mali, West Africa, from 2009 to 2011. The hybrids were confirmed to have photoperiod sensitivity similar to the well-adapted Guinea landrace check cultivar. Genotypic differences for on-farm grain yield were highly significant and genotype × environment crossover interactions were limited. The yield superiorities of individual hybrids, relative to the landrace check, ranged from 17 to 37% over the 27 on-farm trials. The three top yielding hybrids showed 30% yield advantages across productivity levels, with absolute yield advantages averaging 380 kg ha−1 under lower (1.0–1.5 t ha−1) and 660 kg ha−1 under higher (2.0–3.5 t ha−1) productivity conditions. A mean male-parent (better parent) heterosis of 26% was observed for the four hybrids having Lata as a male parent. As the hybrids studied here were obtained with a low intensity of selection using a limited number of parents, even greater yield superiorities may be attained with development of distinct parental pools and scaled-up hybrid breeding

SUCNR1-mediated chemotaxis of macrophages aggravates obesity-induced inflammation and diabetes

Contains fulltext : 174075.pdf (publisher's version ) (Open Access)AIMS/HYPOTHESIS: Obesity induces macrophages to drive inflammation in adipose tissue, a crucial step towards the development of type 2 diabetes. The tricarboxylic acid (TCA) cycle intermediate succinate is released from cells under metabolic stress and has recently emerged as a metabolic signal induced by proinflammatory stimuli. We therefore investigated whether succinate receptor 1 (SUCNR1) could play a role in the development of adipose tissue inflammation and type 2 diabetes. METHODS: Succinate levels were determined in human plasma samples from individuals with type 2 diabetes and non-diabetic participants. Succinate release from adipose tissue explants was studied. Sucnr1 -/- and wild-type (WT) littermate mice were fed a high-fat diet (HFD) or low-fat diet (LFD) for 16 weeks. Serum metabolic variables, adipose tissue inflammation, macrophage migration and glucose tolerance were determined. RESULTS: We show that hypoxia and hyperglycaemia independently drive the release of succinate from mouse adipose tissue (17-fold and up to 18-fold, respectively) and that plasma levels of succinate were higher in participants with type 2 diabetes compared with non-diabetic individuals (+53%; p < 0.01). Sucnr1 -/- mice had significantly reduced numbers of macrophages (0.56 +/- 0.07 vs 0.92 +/- 0.15 F4/80 cells/adipocytes, p < 0.05) and crown-like structures (0.06 +/- 0.02 vs 0.14 +/- 0.02, CLS/adipocytes p < 0.01) in adipose tissue and significantly improved glucose tolerance (p < 0.001) compared with WT mice fed an HFD, despite similarly increased body weights. Consistently, macrophages from Sucnr1 -/- mice showed reduced chemotaxis towards medium collected from apoptotic and hypoxic adipocytes (-59%; p < 0.05). CONCLUSIONS/INTERPRETATION: Our results reveal that activation of SUCNR1 in macrophages is important for both infiltration and inflammation of adipose tissue in obesity, and suggest that SUCNR1 is a promising therapeutic target in obesity-induced type 2 diabetes. DATA AVAILABILITY: The dataset generated and analysed during the current study is available in GEO with the accession number GSE64104, www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64104

Complement Activation in the Disease Course of Coronavirus Disease 2019 and Its Effects on Clinical Outcomes

BACKGROUND: Excessive activation of immune responses in coronavirus disease 2019 (COVID-19) is considered to be related to disease severity, complications, and mortality rate. The complement system is an important component of innate immunity and can stimulate inflammation, but its role in COVID-19 is unknown. METHODS: A prospective, longitudinal, single center study was performed in hospitalized patients with COVID-19. Plasma concentrations of complement factors C3a, C3c, and terminal complement complex (TCC) were assessed at baseline and during hospital admission. In parallel, routine laboratory and clinical parameters were collected from medical files and analyzed. RESULTS: Complement factors C3a, C3c, and TCC were significantly increased in plasma of patients with COVID-19 compared with healthy controls (P < .05). These complement factors were especially elevated in intensive care unit patients during the entire disease course (P < .005 for C3a and TCC). More intense complement activation was observed in patients who died and in those with thromboembolic events. CONCLUSIONS: Patients with COVID-19 demonstrate activation of the complement system, which is related to disease severity. This pathway may be involved in the dysregulated proinflammatory response associated with increased mortality rate and thromboembolic complications. Components of the complement system might have potential as prognostic markers for disease severity and as therapeutic targets in COVID-19