Corn, a main feed ingredient in the livestock industry, is one of the most susceptible crops to fungal infection and aflatoxin contamination. Livestock feeding on aflatoxin (AF)-contaminated feed have been shown to experience feed refusal, and decreased growth rate, milk production, and feed efficiency. In poultry, AF poisoning causes weight loss, poor feed efficiency, and reduced egg production and egg weight. The present work therefore aimed to determine the prevalence of mycotoxigenic fungi and the occurrence of AF contamination along the integrated corn-based poultry feed supply chain in Malaysia. A total of 51 samples were collected from different points along the feed supply chain from integrated poultry feed companies. The samples were subjected to mycological analyses (fungal isolation, enumeration, identification), and AFs were quantified by high-performance liquid chromatography equipped with a fluorescence detector (HPLC-FLD).
 
  Samples collected from sampling point 1 (company A) and sampling point 9 (company B) yielded the highest total fungal load (>log 4 CFU g
  ). The prevalent fungal genera isolated were Aspergillus, Fusarium, and Penicillium spp. Aflatoxin B
  was detected in 8.3% of corn samples, and 7.4% of corn-based poultry feed samples along the feed supply chain, whereas AFs B
  , G
  , and G
  were not detected.
 
  The incidence of mycotoxigenic fungi along the integrated poultry feed supply chain warrant continuous monitoring of mycotoxin contamination to reduce the exposure risk of mycotoxin intake in poultry. © 2020 Society of Chemical Industry.
 The incidence of mycotoxigenic fungi along the integrated poultry feed supply chain warrant continuous monitoring of mycotoxin contamination to reduce the exposure risk of mycotoxin intake in poultry. © 2020 Society of Chemical Industry.Over the past two decades, liana density and basal area have been increasing in many tropical forests, which has profound consequences for forest diversity and functioning. One hypothesis to explain increasing lianas is elevated nutrient deposition in tropical forests resulting from fossil fuels, agricultural fertilizer, and biomass burning.  https://www.selleckchem.com/  We tested this hypothesis by surveying all lianas ≥1 cm in diameter (n = 3,967) in 32 plots in a fully factorial nitrogen (N), phosphorus (P), and potassium (K) addition experiment in a mature tropical forest in central Panama. We conducted the nutrient-addition experiment from 1998 until present and we first censused lianas in 2013 and then again in 2018. After 20 yr of nutrient addition (1998-2018), liana density, basal area, and rarefied species richness did not differ significantly among any of the nutrient-addition and control treatments. Moreover, nutrient addition in the most recent 5 yr of the experiment did not affect liana relative growth, recruitment, or mortality rates. From 2013 until 2018, liana density, basal area, and species richness increased annually by 1.6%, 1.4%, and 2.4%, respectively. Nutrient addition did not influence these increases. Our findings indicate that nutrient deposition does not explain increasing lianas in this tropical forest. Instead, increases in tree mortality and disturbance, atmospheric carbon dioxide, drought frequency and severity, and hunting pressure may be more likely explanations for the increase in lianas in tropical forests.Hidradenitis suppurativa (HS) is a chronic, inflammatory, recurrent and debilitating skin disease of the hair follicle unit that typically develops after puberty. The disorder is characterized by comedones, painful inflammatory nodules, abscesses, dermal tunnels and scarring, with a predilection for intertriginous areas of the body (axillae, inguinal and anogenital regions). Recruitment of neutrophils to HS lesion sites may play an essential role in the development of the painful inflammatory nodules and abscesses that characterize the disease. This is a review of the major mediators involved in the recruitment of neutrophils to sites of active inflammation, including bacterial components (endotoxins, exotoxins, capsule fragments, etc.), the complement pathway anaphylatoxins C3a and C5a, tumour necrosis factor-alpha, interleukin (IL)-17, IL-8 (CXCL8), IL-36, IL-1, lipocalin-2, leukotriene B4, platelet-activating factor, kallikreins, matrix metalloproteinases, and myeloperoxidase inhibitors. Pharmacological manipulation of the various pathways involved in the process of neutrophil recruitment and activation could allow for successful control and stabilization of HS lesions and the remission of active, severe flares.
  Muscle contractions increase protein synthesis in a mechanistic target of rapamycin (mTOR)-dependent manner, yet it is unclear which/how mTOR complexes regulate muscle protein synthesis. We investigated the requirement of mTOR Complex 2 (mTORC2) in contraction-stimulated muscle protein synthesis. mTORC2 inhibition by muscle-specific Rictor knockout (Rictor mKO) did not prevent contraction-induced muscle protein synthesis. Rapamycin prevented contraction-induced muscle protein synthesis in Rictor mKO but not wild-type mice.
 
  Protein synthesis increases following muscle contractions. Previous studies have shown that inhibition of the mechanistic target of rapamycin complex 1 (mTORC1) suppresses the early but not late muscle protein synthesis response, while inhibition of both mTORC1 and mTORC2 abolishes the two effects. Therefore, we hypothesized that mTORC2 regulates muscle protein synthesis following muscle contractions. To test this, we investigated the effect of mTORC2 inhibition by mouse muscle-specificn. Treatment of WT mice with rapamycin and Rictor mKO lowered protein synthesis in general, but the response to contractions was intact 3 h after contractions in both conditions. Rapamycin treatment in Rictor mKO mice prevented contraction-stimulated muscle protein synthesis. Notably, signalling traditionally associated with mTORC1 was increased by muscle contractions despite rapamycin treatment. In rapamycin-treated Rictor mKO mice, the same mTORC1 signalling was blocked following contractions. Our results indicate that although neither rapamycin-sensitive mTOR/mTORC1 nor mTORC2 is necessary for contraction-induced muscle protein synthesis, combined inhibition of rapamycin-sensitive mTOR/mTORC1 and mTORC2 synergistically inhibits contraction-induced muscle protein synthesis.