Population Dynamic, Anthelmintic Treatments and the Influence of Helminth Infections on Weight Gain in Water Buffalo Calves (Bubalus Bubalis)

The dynamics of gastrointestinal helminthiasis was studied in buffalo calves naturally exposed to helminth infection at two farms in Minas Gerais, Brazil. The effect of helminthiasis was evaluated with respect to weight gain of naturally infected untreated calves versus those which received anthelmintic treatment either with fenbendazole or ivermectin. The treated animals had significantly (p<0.05) higher weight gain. Strongyloides papillosus was diagnosed from 30 to 60 days after birth, and Toxocara vitulorum from 60 to 90 days. During spring, there was a rise in the eggs per gram (EPG) count of Trichostrongylidae. Severe infection of Paracooperia nodulosa was detected in few 9-month-old buffalo calves.The results of this study indicate efficacy of fenbendazole and ivermectin in different age group calves for better health and reduced probability of helminth resistance. This study also indicates the necessity for good nutritional management of buffalo calves to improve the efficacy of parasite control

Efficacy analysis of parasitic integrated control in buffaloes

Parasitic infestations are responsible for economic losses to buffalo farms. Using the scientific support of epidemiological and parasitic studies in this area, the present research aimed to evaluate the efficacy of an integrated control of parasitic disease purposed. The parasitic integrated control provides a schedule for optimize the drugs for parasitic control to reduce the number of treatments, reduce costs and the parasitic infestation impact in animal productions. In the experiment was used a total population of buffaloes reared in a farm located at Minas Gerais State, Brazil. The in the same day the calves, growing males and non lactation animals were treated with doramectin (200 mcg/ kg BW) and the lactation animals were treated with alfa-ciano-3fenoxibenzil-2, 2-dimetil-3-(2,2-diclorovinil)-ciclopropano carboxilaton solution. Calves positive to Eimeria bareillyi and Eimeria bovis oocysts were treated with toltrazuril. The lice population was eradicated and the average numbers of trichostrongylid eggs and Eimeria sp. oocysts were substantially reduced to acceptable account

Dinâmica de nematóides gastrointestinais e desempenho de bovinos de corte em sistema pastoril e silvipastoril.

Entre os modelos de produção para bovinos de corte, os sistemas extrativis¬tas foram a base da pecuária nacional ao longo de muitas décadas. Esses sistemas se caracterizam pelo baixo investimento tecnológico e pela estacio¬nalidade de produção, baseando-se, por exemplo, no monocultivo de pasta¬gens e em baixas taxas de lotação. Devido ao seu menor potencial produtivo e por serem menos sustentáveis, inclusive pelos seus eventuais impactos ambientais, esses sistemas têm sido substituídos gradativamente por mode¬los mais dinâmicos e rentáveis. Nesse contexto, a integração lavoura-pecuária-floresta (ILPF) tem sido con¬siderada como a terceira revolução verde. Em comparação com o processo de produção tradicional, os sistemas integrados apresentam características peculiares, tornando-os complexos, mas com grande potencial produtivo. Entre as várias estratégias que combinam agricultura, pecuária e silvicultu¬ra, os sistemas silvipastoris (SSP) destacam-se devido às suas condições microclimáticas mais favoráveis, principalmente em países de clima tropical, como o Brasil. Suas características proporcionam maior conforto para os bo¬vinos, favorecendo o bem-estar animal e a obtenção de maiores índices de produtividade.bitstream/item/188233/1/2018-cpamt-luciano-lopes-nematoide-bovino-corte-sistema-silvipastoril.pd

Neurosteroid Dehydroepiandrosterone Interacts with Nerve Growth Factor (NGF) Receptors, Preventing Neuronal Apoptosis

The neurosteroid dehydroepiandrosterone (DHEA), produced by neurons and glia, affects multiple processes in the brain, including neuronal survival and neurogenesis during development and in aging. We provide evidence that DHEA interacts with pro-survival TrkA and pro-death p75NTR membrane receptors of neurotrophin nerve growth factor (NGF), acting as a neurotrophic factor: (1) the anti-apoptotic effects of DHEA were reversed by siRNA against TrkA or by a specific TrkA inhibitor; (2) [3H]-DHEA binding assays showed that it bound to membranes isolated from HEK293 cells transfected with the cDNAs of TrkA and p75NTR receptors (KD: 7.4±1.75 nM and 5.6±0.55 nM, respectively); (3) immobilized DHEA pulled down recombinant and naturally expressed TrkA and p75NTR receptors; (4) DHEA induced TrkA phosphorylation and NGF receptor-mediated signaling; Shc, Akt, and ERK1/2 kinases down-stream to TrkA receptors and TRAF6, RIP2, and RhoGDI interactors of p75NTR receptors; and (5) DHEA rescued from apoptosis TrkA receptor positive sensory neurons of dorsal root ganglia in NGF null embryos and compensated NGF in rescuing from apoptosis NGF receptor positive sympathetic neurons of embryonic superior cervical ganglia. Phylogenetic findings on the evolution of neurotrophins, their receptors, and CYP17, the enzyme responsible for DHEA biosynthesis, combined with our data support the hypothesis that DHEA served as a phylogenetically ancient neurotrophic factor

Complete Phenotypic Recovery of an Alzheimer's Disease Model by a Quinone-Tryptophan Hybrid Aggregation Inhibitor

The rational design of amyloid oligomer inhibitors is yet an unmet drug development need. Previous studies have identified the role of tryptophan in amyloid recognition, association and inhibition. Furthermore, tryptophan was ranked as the residue with highest amyloidogenic propensity. Other studies have demonstrated that quinones, specifically anthraquinones, can serve as aggregation inhibitors probably due to the dipole interaction of the quinonic ring with aromatic recognition sites within the amyloidogenic proteins. Here, using in vitro, in vivo and in silico tools we describe the synthesis and functional characterization of a rationally designed inhibitor of the Alzheimer's disease-associated β-amyloid. This compound, 1,4-naphthoquinon-2-yl-L-tryptophan (NQTrp), combines the recognition capacities of both quinone and tryptophan moieties and completely inhibited Aβ oligomerization and fibrillization, as well as the cytotoxic effect of Aβ oligomers towards cultured neuronal cell line. Furthermore, when fed to transgenic Alzheimer's disease Drosophila model it prolonged their life span and completely abolished their defective locomotion. Analysis of the brains of these flies showed a significant reduction in oligomeric species of Aβ while immuno-staining of the 3rd instar larval brains showed a significant reduction in Aβ accumulation. Computational studies, as well as NMR and CD spectroscopy provide mechanistic insight into the activity of the compound which is most likely mediated by clamping of the aromatic recognition interface in the central segment of Aβ. Our results demonstrate that interfering with the aromatic core of amyloidogenic peptides is a promising approach for inhibiting various pathogenic species associated with amyloidogenic diseases. The compound NQTrp can serve as a lead for developing a new class of disease modifying drugs for Alzheimer's disease

Orally Administrated Cinnamon Extract Reduces β-Amyloid Oligomerization and Corrects Cognitive Impairment in Alzheimer's Disease Animal Models

An increasing body of evidence indicates that accumulation of soluble oligomeric assemblies of β-amyloid polypeptide (Aβ) play a key role in Alzheimer's disease (AD) pathology. Specifically, 56 kDa oligomeric species were shown to be correlated with impaired cognitive function in AD model mice. Several reports have documented the inhibition of Aβ plaque formation by compounds from natural sources. Yet, evidence for the ability of common edible elements to modulate Aβ oligomerization remains an unmet challenge. Here we identify a natural substance, based on cinnamon extract (CEppt), which markedly inhibits the formation of toxic Aβ oligomers and prevents the toxicity of Aβ on neuronal PC12 cells. When administered to an AD fly model, CEppt rectified their reduced longevity, fully recovered their locomotion defects and totally abolished tetrameric species of Aβ in their brain. Furthermore, oral administration of CEppt to an aggressive AD transgenic mice model led to marked decrease in 56 kDa Aβ oligomers, reduction of plaques and improvement in cognitive behavior. Our results present a novel prophylactic approach for inhibition of toxic oligomeric Aβ species formation in AD through the utilization of a compound that is currently in use in human diet

Opposing Effects of Sirtuins on Neuronal Survival: SIRT1-Mediated Neuroprotection Is Independent of Its Deacetylase Activity

Background: Growing evidence suggests that sirtuins, a family of seven distinct NAD-dependent enzymes, are involved in the regulation of neuronal survival. Indeed, SIRT1 has been reported to protect against neuronal death, while SIRT2 promotes neurodegeneration. The effect of SIRTs 3–7 on the regulation of neuronal survival, if any, has yet to be reported. Methodology and Principal Findings: We examined the effect of expressing each of the seven SIRT proteins in healthy cerebellar granule neurons (CGNs) or in neurons induced to die by low potassium (LK) treatment. We report that SIRT1 protects neurons from LK-induced apoptosis, while SIRT2, SIRT3 and SIRT6 induce apoptosis in otherwise healthy neurons. SIRT5 is generally localized to both the nucleus and cytoplasm of CGNs and exerts a protective effect. In a subset of neurons, however, SIRT5 localizes to the mitochondria and in this case it promotes neuronal death. Interestingly, the protective effect of SIRT1 in neurons is not reduced by treatments with nicotinamide or sirtinol, two pharmacological inhibitors of SIRT1. Neuroprotection was also observed with two separate mutant forms of SIRT1, H363Y and H355A, both of which lack deacetylase activity. Furthermore, LK-induced neuronal death was not prevented by resveratrol, a pharmacological activator of SIRT1, at concentrations at which it activates SIRT1. We extended our analysis to HT-22 neuroblastoma cells which can be induced to die by homocysteic acid treatment. While the effects of most of the SIRT proteins were similar to that observed in CGNs, SIRT6 was modestly protective against homocysteic acid toxicity in HT-22 cells. SIRT5 was generally localized in th

Ginkgo Biloba Extract Ameliorates Oxidative Phosphorylation Performance and Rescues Aβ-Induced Failure

Energy deficiency and mitochondrial failure have been recognized as a prominent, early event in Alzheimer's disease (AD). Recently, we demonstrated that chronic exposure to amyloid-beta (Abeta) in human neuroblastoma cells over-expressing human wild-type amyloid precursor protein (APP) resulted in (i) activity changes of complexes III and IV of the oxidative phosphorylation system (OXPHOS) and in (ii) a drop of ATP levels which may finally instigate loss of synapses and neuronal cell death in AD. Therefore, the aim of the present study was to investigate whether standardized Ginkgo biloba extract LI 1370 (GBE) is able to rescue Abeta-induced defects in energy metabolism