THE EFFECT OF ASSOCIATED SOIL MICROFLORA ON FUSARIUM UDUM BUTL., THE FUNGUS CAUSING WILT OF PIGEON-PEA (CAJANUS CAJAN (L.) MILLSP.)

Inoculation with Fusarium udum Butl. produced more wilt of pigeon-pea in sterilized than in unsterilized soils at the same pH. From unsterilized soils with low disease incidence, nine fungi, Bacillus subtilis and an Actinomyces were isolated. The number of isolations of a particular organism varied from month to month during the cropping season of pigeon-pea in Delhi. Interaction of Fusarium udum and other organisms isolated was studied. Aspergillus niger and A. terreus secreted inhibitory substances in potato-dextrose broth: Bacillus subtilis inhibited growth on solid medium and also produced a toxic substance in potato-dextrose broth. The nature of the medium employed and period of growth were important factors in the production of the inhibitory principle, which is thermostable. The low incidence of pigeon-pea wilt in unsterilized soils may result from the inhibitory activity of the associated microflora in the soil.     

The complement cascade in the regulation of neuroinflammation,nociceptive sensitization,and pain

The complement cascade is a key component of the innate immune system that is rapidly recruited through a cascade of enzymatic reactions to enable the recognition and clearance of pathogens and promote tissue repair. Despite its well-understood role in immunology, recent studies have highlighted new and unexpected roles of the complement cascade in neuroimmune interaction and in the regulation of neuronal processes during development, aging, and in disease states. Complement signaling is particularly important in directing neuronal responses to tissue injury, neurotrauma, and nerve lesions. Under physiological conditions, complement-dependent changes in neuronal excitability, synaptic strength, and neurite remodeling promote nerve regeneration, tissue repair, and healing. However, in a variety of pathologies, dysregulation of the complement cascade leads to chronic inflammation, persistent pain, and neural dysfunction. This review describes recent advances in our understanding of the multifaceted cross-communication that takes place between the complement system and neurons. In particular, we focus on the molecular and cellular mechanisms through which complement signaling regulates neuronal excitability and synaptic plasticity in the nociceptive pathways involved in pain processing in both health and disease. Finally, we discuss the future of this rapidly growing field and what we believe to be the significant knowledge gaps that need to be addressed.