Publications by authors named "Luis Roberto C Goncalves"

In recent years, extensive research has delved into the pathophysiology of local reactions triggered by snake venoms. Even though antivenom works well at reducing death and systemic effects, it is still not very effective in treating local reactions because it cannot counteract damage that has already been triggered. This limitation might be attributed to certain molecules that amplify the venom-induced innate response.

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Alzheimer's disease (AD) is the main type of dementia, caused by the accumulation of amyloid plaques, formed by amyloid peptides after being processed from amyloid precursor protein (APP) by - and -secretases (BACE-1). Although amyloid peptides have been well established for AD, they have been found in other neurodegenerative diseases, such as Parkinson's disease, Lewy body dementia, and amyotrophic lateral sclerosis. Inhibitors of BACE-1 have been searched and developed, but clinical trials failed due to lack of efficacy or toxicity.

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Contact with Lonomia caterpillars can cause severe envenomation with hemorrhagic syndrome, consumptive coagulopathy, acute renal failure, and death. In Brazil, an antivenom was produced using extracts from L. obliqua caterpillar bristles as antigen and has been used in other countries in South America to treat envenomation caused by distinct species of Lonomia.

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Crotoxin (CTX) is a neurotoxin that is isolated from the venom of Crotalus durissus terrificus, which displays immunomodulatory, anti-inflammatory, and anti-tumoral effects. Previous research has demonstrated that CTX promotes the adherence of leukocytes to the endothelial cells in blood microcirculation and the high endothelial venules of lymph nodes, which reduces the number of blood cells and lymphocytes. Studies have also shown that these effects are mediated by lipoxygenase-derived mediators.

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Snake venom metalloproteinases (SVMP) are involved in local inflammatory reactions observed after snakebites. Based on domain composition, they are classified as PI (pro-domain + proteolytic domain), PII (PI + disintegrin-like domains), or PIII (PII + cysteine-rich domains). Here, we studied the role of different SVMPs domains in inducing the expression of adhesion molecules at the microcirculation of the cremaster muscle of mice.

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Snake venom metalloproteinases (SVMPs) are key toxins involved in local inflammatory reactions after snakebites. This study aimed to investigate the effect of SVMP domains on the alterations in leukocyte-endothelium interactions in the microcirculation of mouse cremaster muscle. We studied three toxins: BnP1, a PI-toxin isolated from Bothrops neuwiedi venom, which only bears a catalytic domain; Jararhagin (Jar), a PIII-toxin isolated from Bothrops jararaca venom with a catalytic domain, as well as ECD-disintegrin and cysteine-rich domains; and Jar-C, which is produced from the autolysis of Jar and devoid of a catalytic domain.

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Article Synopsis
  • - In South America, contact with certain caterpillars, especially those from the Lonomia genus, can cause serious health issues, including hemorrhagic syndromes and even death due to venom that disrupts blood clotting mechanisms.
  • - The only effective treatment for these envenomations is the Lonomia Antivenom (LAV) manufactured in Brazil; however, its efficacy against other Lonomia species, apart from L. obliqua, had not been experimentally tested before this study.
  • - This research demonstrated that LAV effectively restores normal blood clotting in rats injected with venom from Lonomia casanarensis and Lonomia orientoandensis, confirming its potential as a treatment for envenomation by these cater
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We have investigated the mechanisms involved in the genesis of edema and nociception induced by venom (PpV) injected into the footpad of mice. PpV induced dose-related edema and nociceptive effects. Pretreatment of mice with cyclooxygenase inhibitor (indomethacin), but not with cyclooxygenase 2 inhibitor (celecoxib) markedly inhibited both effects.

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In this study, we evaluated the effect of the Crotalus durissus terrificus (Cdt) venom on the chronic paw edema induced by the injection of bacillus Calmette-Guérin (BCG) into the footpad of mice. The BCG injection evoked chronic edema, which was significantly diminished in animals treated subcutaneously (s.c.

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Various toxins isolated from Bothrops snake venoms induce inflammatory reactions and have been claimed to contribute to the severity of local symptoms present in this envenomation. Notwithstanding, the relative participation of serine proteases, metalloproteases and phospholipases A(2) in the inflammatory reaction produced by crude Bothrops venoms is poorly understood. Herein, crude Bothrops jararaca venom was treated with phenylmethanesulfonyl fluoride (PMSF), 1,10-phenanthroline (oPhe), or p-bromophenacyl-bromide (p-BPB) to inhibit those classes of enzymes, respectively, and inflammatory parameters were evaluated and compared to those induced by the control crude venom.

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Article Synopsis
  • Bothrops antivenom was found to affect leukocyte-endothelial interactions (LEI) in mice, similar to the effects of B. jararaca venom.
  • The antivenom caused symptoms like tremors and breathing difficulties, attributed to phenol used as a preservative.
  • Phenol-free antivenom successfully neutralized venom effects on LEI, indicating that while the antivenom is effective, its preservative can lead to unwanted side effects.
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Large number of accidents caused by contact with Lonomia obliqua caterpillars, with hemorrhagic complications, have occurred in southern Brazil. Based on Venezuelan expertise to treat Lonomia achelous envenomation, the use of the antifibrinolytic drug epsilon-aminocaproic acid (EACA) has been indicated to treat L. obliqua envenomation, although no evidence has been presented to justify its use.

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Hemostatic disturbances are frequent findings in human accidents caused by Lonomia obliqua caterpillars in the southern region of Brazil. In severe envenomation, patients may present life-threatening bleedings. Such disturbances may be mimicked in rats, which also develop intravascular hemolysis.

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