36 research outputs found

    Carcass yield and intestinal morphology of male rabbits fed diets supplemented with turmeric (Curcuma Longa) powder

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    Thirty-two (7-8 weeks old) male rabbits that weighed between 700 and 800 g were used to determine the effect of inclusion of Turmeric powder on carcass yield and intestinal morphology of rabbits. The rabbits were randomly allotted to four diets containing varying levels of turmeric powder (0, 5, 10 and 15 g) in a complete randomized design. Data were collected on carcass yield, duodenum, jejunum, ileum, crypt depth, mucosal thickness and analyzed using ANOVA. Significant (p<0.05) differences were obtained on bled and eviscerated weights, forelimbs, hind limbs, neck, tail and loin. Highest (p<0.05) duodenum crypt depth (111.50 μm) was obtained with buck fed diet containing 15 g turmeric inclusion while buck fed with diet containing 0 g turmeric had the least value of (67.67 μm). This was similar (p>0.05) with values obtained for buck fed diets containing 5 g turmeric (73.83 μm) and those fed with 10 g turmeric inclusion (79.33 μm). There was significant difference (P<0.05) of rabbit fed with diets with turmeric on jejunum villi height. There was significant difference (P<0.05) in jejunum crypt depth and mucosal thickness. However, 10 g inclusion could be assumed as economic inclusion level for carcass yield and intestinal increase in rabbit production

    Effect of turmeric, garlic, ginger powder and their blends on growth performance and carcass yield of rabbits

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    Phytogenic additives are natural growth promoters that can be used as potential alternatives for common artificial growth promoters like antibiotics. Thus, this study was conducted to evaluate the effect of turmeric garlic, ginger powder and their blends on growth performance and carcass yield of rabbits. Forty-eight (48) weaner rabbits (8 weeks old) were randomly allotted into eight dietary groups designated in a completely randomized design. The T1 contained 0g, T2- 3g of turmeric, T3- 3g of garlic, T4-3g of ginger, T5- 3g turmeric and 3g garlic, T6- 3g turmeric and 3g ginger, T7- 3g of garlic and 3g of ginger and T8- 2g turmeric, 2g garlic, 2g ginger. Data were collected for all the growth parameters and carcass yield. Result showed significant (p< 0.05) higher final body weight of the rabbits were recorded with rabbit fed diets containing 3g of Garlic and Ginger (2057.0g) while rabbit fed diets containing 6g Ginger (1339.5g) had lowest total weight gain. Rabbits fed 6g garlic had significant (p< 0.05) higher quantity of feed consumed per day (65.42g) while rabbit fed diet containing 3g turmeric and 3g garlic had the least value (55.05g). Rabbit group fed diet containing 3g turmeric and 3g garlic had significantly (p<0.05) lower value (0.10) of feed efficiency ratio while rabbits fed 3g garlic and 3g ginger utilized feed more efficiently (0.21). Rabbit fed diet with 6g garlic had highest (p<0.05) eviscerated and dressed weight of (1438.40g), (1204.7g) while lowest were recorded in rabbit fed 6g ginger (885.70g) and (733.3g) respectively. It was concluded that rabbits fed 3g of garlic and ginger blend had higher growth indices and carcass yield hence could be recommended for use by rabbit farmers

    Elimination of Falciparum Malaria and Emergence of Severe Dengue:An Independent or Interdependent Phenomenon?

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    The global malaria burden, including falciparum malaria, has been reduced by 50% since 2000, though less so in Sub-Saharan Africa. Regional malaria elimination campaigns beginning in the 1940s, up-scaled in the 1950s, succeeded in the 1970s in eliminating malaria from Europe, North America, the Caribbean (except Haiti), and parts of Asia and South- and Central America. Dengue has grown dramatically throughout the pantropical regions since the 1950s, first in Southeast Asia in the form of large-scale epidemics including severe dengue, though mostly sparing Sub-Saharan Africa. Globally, the WHO estimates 50 million dengue infections every year, while others estimate almost 400 million infections, including 100 million clinical cases. Curiously, despite wide geographic overlap between malaria and dengue-endemic areas, published reports of co-infections have been scarce until recently. Superimposed acute dengue infection might be expected to result in more severe combined disease because both pathogens can induce shock and hemorrhage. However, a recent review found no reports on more severe morbidity or higher mortality associated with co-infections. Cases of severe dual infections have almost exclusively been reported from South America, and predominantly in persons infected by Plasmodium vivax. We hypothesize that malaria infection may partially protect against dengue – in particular falciparum malaria against severe dengue – and that this inter-species cross-protection may explain the near absence of severe dengue from the Sub-Saharan region and parts of South Asia until recently. We speculate that malaria infection elicits cross-reactive antibodies or other immune responses that infer cross-protection, or at least partial cross-protection, against symptomatic and severe dengue. Plasmodia have been shown to give rise to polyclonal B-cell activation and to heterophilic antibodies, while some anti-dengue IgM tests have high degree of cross-reactivity with sera from malaria patients. In the following, the historical evolution of falciparum malaria and dengue is briefly reviewed, and we explore early evidence of subclinical dengue in high-transmission malaria areas as well as conflicting reports on severity of co-morbidity. We also discuss examples of other interspecies interactions

    Differential patterns of IgG subclass responses to <i>Plasmodium falciparum</i> antigens in relation to malaria protection and RTS,S vaccination

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    Naturally acquired immunity (NAI) to Plasmodium falciparum malaria is mainly mediated by IgG antibodies but the subclasses, epitope targets and effector functions have not been unequivocally defined. Dissecting the type and specificity of antibody responses mediating NAI is a key step toward developing more effective vaccines to control the disease. We investigated the role of IgG subclasses to malaria antigens in protection against disease and the factors that affect their levels, including vaccination with RTS,S/AS01E. We analyzed plasma and serum samples at baseline and 1 month after primary vaccination with RTS,S or comparator in African children and infants participating in a phase 3 trial in two sites of different malaria transmission intensity: Kintampo in Ghana and Manhiça in Mozambique. We used quantitative suspension array technology (qSAT) to measure IgG1-4 responses to 35 P. falciparum pre-erythrocytic and blood stage antigens. Our results show that the pattern of IgG response is predominantly IgG1 or IgG3, with lower levels of IgG2 and IgG4. Age, site and RTS,S vaccination significantly affected antibody subclass levels to different antigens and susceptibility to clinical malaria. Univariable and multivariable analysis showed associations with protection mainly for cytophilic IgG3 levels to selected antigens, followed by IgG1 levels and, unexpectedly, also with IgG4 levels, mainly to antigens that increased upon RTS,S vaccination such as MSP5 and MSP1 block 2, among others. In contrast, IgG2 was associated with malaria risk. Stratified analysis in RTS,S vaccinees pointed to novel associations of IgG4 responses with immunity mainly involving pre-erythrocytic antigens upon RTS,S vaccination. Multi-marker analysis revealed a significant contribution of IgG3 responses to malaria protection and IgG2 responses to malaria risk. We propose that the pattern of cytophilic and non-cytophilic IgG antibodies is antigen-dependent and more complex than initially thought, and that mechanisms of both types of subclasses could be involved in protection. Our data also suggests that RTS,S efficacy is significantly affected by NAI, and indicates that RTS,S vaccination significantly alters NAI

    Ferritin heavy chain supports stability and function of the regulatory T cell lineage

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    Regulatory T (TREG) cells develop via a program orchestrated by the transcription factor forkhead box protein P3 (FOXP3). Maintenance of the TREG cell lineage relies on sustained FOXP3 transcription via a mechanism involving demethylation of cytosine-phosphate-guanine (CpG)-rich elements at conserved non-coding sequences (CNS) in the FOXP3 locus. This cytosine demethylation is catalyzed by the ten-eleven translocation (TET) family of dioxygenases, and it involves a redox reaction that uses iron (Fe) as an essential cofactor. Here, we establish that human and mouse TREG cells express Fe-regulatory genes, including that encoding ferritin heavy chain (FTH), at relatively high levels compared to conventional T helper cells. We show that FTH expression in TREG cells is essential for immune homeostasis. Mechanistically, FTH supports TET-catalyzed demethylation of CpG-rich sequences CNS1 and 2 in the FOXP3 locus, thereby promoting FOXP3 transcription and TREG cell stability. This process, which is essential for TREG lineage stability and function, limits the severity of autoimmune neuroinflammation and infectious diseases, and favors tumor progression. These findings suggest that the regulation of intracellular iron by FTH is a stable property of TREG cells that supports immune homeostasis and limits the pathological outcomes of immune-mediated inflammation.peer-reviewe

    Bioenergetics of an Infected state

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    Illness-induced anorexia is an evolutionarily conserved response leading to the withdrawal from food during an infection. This behavior reduces the supply of metabolic substrates during infection; and if not countered by a metabolic response, anorexia can lead to starvation and death. We reasoned that the infected host relies on de novo synthesis of glucose via hepatic glucose production (HGP), and the mobilization of free fatty acids (FFAs) via adipose tissue lipolysis to provide energetic metabolites to sustain vital metabolic processes compatible with survival during infection

    Sickle cell trait is associated with controlled levels of haem and mild proinflammatory response during acute malaria infection

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    Summary The controlled induction of haemoxygenase-1 (HO-1), an enzyme that catabolizes haem, has been shown to reduce haem, preventing pathologies associated with haem toxicity. The hemoglobin genotype HbAS confers reduced susceptibility to severe complications of malaria by a mechanism that is not well understood. Using a longitudinal approach, we investigated the effect of baseline concentrations of HO-1 on the accumulation of haem during acute Plasmodium falciparum malaria in HbAS and HbAA genotypes. Plasma concentrations of haem, HO-1 and cytokines were quantified in venous blood obtained from children (9 months–5 years of age) during malaria infection, and at convalescence (baseline levels). Parasitaemia was determined during malaria infection. In patients with the HbAA genotype, there was a significant elevation in the plasma concentration of haem (P = 0.002), and a consequent increased induction of HO-1 (P &amp;lt; 0.001) during falciparum malaria compared with levels at convalescence. Contrary to HbAA, plasma concentration of haem did not change in the HbAS genotypical group (P = 0·110), and the induction of HO-1 was reduced during malaria compared with levels at convalescence (P = 0·006). Higher plasma levels of haem were observed in HbAS compared with HbAA at convalescence (P = 0·010), but this difference did not affect the levels of HO-1 within each genotype (P = 0·450). Relatively milder proinflammatory responses were observed in HbAS children during malaria infection compared to HbAA children. Our findings suggest that a mechanism of reduced susceptibility to severe malaria pathologies by the HbAS genotype may involve the control of haem, leading to controlled levels of HO-1 and milder proinflammatory responses during acute malaria.</jats:p

    Patterns of inflammatory responses and parasite tolerance vary with malaria transmission intensity

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    Abstract Background In individuals living in malaria-endemic regions, parasitaemia thresholds for the onset of clinical symptoms vary with transmission intensity. The mechanisms that mediate this relationship are however, unclear. Since inflammatory responses to parasite infection contribute to the clinical manifestation of malaria, this study investigated inflammatory cytokine responses in children with malaria from areas of different transmission intensities (ranging from low to high). Methods Blood samples were obtained from children confirmed with malaria at community hospitals in three areas with differing transmission intensities. Cytokine levels were assessed using the Luminex®-based magnetic bead array system, and levels were compared across sites using appropriate statistical tests. The relative contributions of age, gender, parasitaemia and transmission intensity on cytokine levels were investigated using multivariate regression analysis. Results Parasite density increased with increasing transmission intensity in children presenting to hospital with symptomatic malaria, indicating that the parasitaemia threshold for clinical malaria increases with increasing transmission intensity. Furthermore, levels of pro-inflammatory cytokines, including tumour necrosis factor alpha (TNF-α), interferon-gamma (IFN-γ), interleukin (IL)-1β, IL-2, IL-6, IL-8, and IL-12, decreased with increasing transmission intensity, and correlated significantly with parasitaemia levels in the low transmission area but not in high transmission areas. Similarly, levels of anti-inflammatory cytokines, including IL-4, IL-7, IL-10 and IL-13, decreased with increasing transmission intensity, with IL-10 showing strong correlation with parasitaemia levels in the low transmission area. Multiple linear regression analyses revealed that transmission intensity was a stronger predictor of cytokine levels than age, gender and parasitaemia. Conclusion Taken together, the data demonstrate a strong relationship between the prevailing transmission intensity, parasitaemia levels and the magnitude of inflammatory responses induced during clinical malaria
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