The venom of Colombian specimens of the rear-fanged snake Pseudoboa neuwiedii contains proteolytic and phospholipase A (PLA) activities, but is devoid of esterases. Mass spectrometric analysis of electrophoretic bands indicated that this venom contains C-type lectins (CTL), cysteine-rich secretory proteins (CRiSP), PLA, snake venom metalloproteinases (SVMP), and snake venom matrix metalloproteinases (svMMP). In this investigation, we extended our characterization of P.
View Article and Find Full Text PDFPestic Biochem Physiol
November 2024
Neonicotinoid insecticides (NNI) are agonists of insect nicotinic acetylcholine receptors (nAChR) that induce non-elucidate mechanisms of abnormal behavior in insects. In this work, we investigated the effects of sublethal doses of the neonicotinoid thiamethoxam (TMX) on neurochemical and physiological parameters in cockroaches. Sublethal doses of TMX (0.
View Article and Find Full Text PDFDespite the wide range of institutions that maintain venomous snakes in captivity in Brazil there are no comprehensive data on the occurrence of snakebites and envenomations in these places. We examined the range of native and exotic species of venomous snakes kept by Brazilian zoos and serpentaria (scientific and commercial) and assessed the frequency of snakebites in workers handling these snakes during a 10-year period (2012-2021). Twenty-two (73.
View Article and Find Full Text PDFFipronil, a pesticide widely used to control agricultural and household insect pests, blocks insect GABA and glutamate (GluCl) ionotropic receptors, resulting in uncontrolled hyperexcitation and paralysis that eventually leads to death. The use of fipronil is controversial because unintentional exposure to this compound may contribute to the ongoing global decline of insect pollinator populations. Although the sublethal effects of fipronil have been linked to aberrant behavior and impaired olfactory learning in insects, the precise mechanisms involved in these responses remain unclear.
View Article and Find Full Text PDFTumors typically lack canonical danger signals required to activate adaptive immunity and also frequently employ substantial immunomodulatory mechanisms that downregulate adaptive responses and contribute to escape from immune surveillance. Given the variety of mechanisms involved in shielding tumors from immune recognition, it is not surprising that single-agent immunomodulatory approaches have been largely unsuccessful in generating durable antitumor responses. Here we report a unique combination of immunomodulatory and cytostatic agents that recondition the tumor microenvironment and eliminate complex and/or poor-prognosis tumor types including the non-immunogenic 4T-1 model of TNBC, the aggressive MOC-2 model of HNSCC, and the high-risk MYCN-amplified model of neuroblastoma.
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