CrossRef 45 Agarwal S, Sairam RK, Srivastava GC, Meena RC: Chang

CrossRef 45. click here Agarwal S, Sairam RK, Srivastava GC, Meena RC: Changes in antioxidant enzymes activity and oxidative stress by abscisic acid and salicylic acid in wheat genotypes. Biologia Plantarum 2005,49(4):541–550.CrossRef 46. Mittler R, Vanderauwera S, Gollery M, Breusegem FV: Reactive oxygen gene network of plants. Trends Plant Sci 2004, 9:1360–1385.CrossRef 47. Lee S, Kim SG, Park CM: Salicylic acid promotes seed germination under high salinity by modulating antioxidant activity in Arabidopsis. New Phytol 2010, 188:626–637.PubMedCrossRef 48. Yuan S, Lin HH: Role of

salicylic acid in plant abiotic stress. Zeitschrift für Naturforschung 2008, 63:313–320.PubMed 49. Janda K, Hideg E, Szalai G, Kovács L, Janda T: Salicylic

acid may indirectly influence BV-6 mouse the photosynthetic electron transport. J Plant Physiol 2012. 50. Singh B, Usha K: Salicylic acid induced physiological and biochemical changes in wheat seedlings under water stress. Plant Growth Regul 2003, 39:137–141.CrossRef 51. Alonso-Ramirez A, Rodriguez D, Reyes D, Jimenez JA, Nicolas G, Lopez-Climent M: Evidence for a role of gibberellins in salicylic acid-modulated early plant responses to abiotic stress in Arabidopsis seeds. Plant Physiol 2009, 150:1335–1344.PubMedCrossRef Authors’ contributions ALK planned and undertaken the research project. ALK performed the experiments, analyzed the data and drafted the manuscript. MH, MW and IJL had undertaken the plant hormonal work. AA and AA helped in revision of the MS and statistical analysis. All Authors contributed in writing the manuscript and approved its selleck chemical Niclosamide final content.”
“Background Clostridium perfringens is

commonly found in the gastrointestinal (GI) tract of humans, animals, soils, freshwater sediments and sewage. It can cause various diseases in humans, including food poisoning, antibiotic-associated diarrhea, sporadic diarrhea, internal abscesses, and gas gangrene and also various animal diseases [1–5]. C. perfringens strains all are prolific toxin producers and are classified based on their toxin formation. Various C. perfringens toxins denature cellular components of mammalian cells and are implicated in virulence and pathogenicity. Among these toxins are α-toxin (phospholipase C, PLC) and θ-toxin (perfringolysin O, PFO), which are essential for gas gangrene pathogenesis. Other toxins or hydrolytic enzymes may be involved in destruction of connective tissue or spread of bacteria in infected tissues [4, 6, 7]. C. perfringens, although a commensal, can cause life threatening infections and is implicated in inflammatory bowel diseases [8–10]. In a survey of Clostridium species bacteremia, in a Canadian hospital between 2000–2006, C. perfringens was shown to have caused 42% of the cases, which was more than any other Clostridium species [11]. It causes nearly a million cases of food borne illness each year in the United States [1]. Bacteria from the GI tract, including C.

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