SINALIZAÇÃO TURÍSTICA: UMA PROPOSTA DE USO TURÍSTICO PARA A SERRA DO TEPEQUÉM

A sinalização turística, componente de infraestrutura turística, oferece facilidade de orientação aos visitantes para se direcionarem com segurança aos destinos pretendidos e contribui para o planejamento e a melhoria do desenvolvimento turístico da localidade, além de valorizar o patrimônio natural e cultural da região. Com o aumento da procura dos atrativos da Serra do Tepequém, localizada no município do Amajari, a 213 quilômetros da capital do estado de Roraima, Boa Vista, tornou-se necessário promover ações para atender às necessidades da demanda turística e da comunidade, principalmente no que se refere à infraestrutura. Dessa forma, propôs-se o planejamento da implantação de sinalização turística na Serra do Tepequém, de acordo com os objetivos e princípios básicos do Guia Brasileiro de Sinalização Turística, visando o desenvolvimento sustentável da região. O método determinado para orientação geral da pesquisa foi o Estudo de caso. Dentre os resultados obtidos tem-se a elaboração do Plano Funcional de Sinalização Turística da Serra do Tepequém.

Relação umidade: proteína em genótipos de frangos de corte.

2016

Quantificação dos teores de óleo e proteína em grãos de genótipos de soja submetidos a diferentes regimes hídricos sob condições de campo.

2016

An envirogenomic signature is associated with risk of IBD-related surgery in a population-based Crohn’s Disease cohort

BACKGROUND AND AIMS: Crohn's disease (CD) is an inflammatory bowel disease (IBD) caused by a combination of genetic, clinical, and environmental factors. Identification of CD patients at high risk of requiring surgery may assist clinicians to decide on a top-down or step-up treatment approach. METHODS: We conducted a retrospective case-control analysis of a population-based cohort of 503 CD patients. A regression-based data reduction approach was used to systematically analyse 63 genomic, clinical and environmental factors for association with IBD-related surgery as the primary outcome variable. RESULTS: A multi-factor model was identified that yielded the highest predictive accuracy for need for surgery. The factors included in the model were the NOD2 genotype (OR = 1.607, P = 2.3 × 10(-5)), having ever had perianal disease (OR = 2.847, P = 4 × 10(-6)), being post-diagnosis smokers (OR = 6.312, P = 7.4 × 10(-3)), being an ex-smoker at diagnosis (OR = 2.405, P = 1.1 × 10(-3)) and age (OR = 1.012, P = 4.4 × 10(-3)). Diagnostic testing for this multi-factor model produced an area under the curve of 0.681 (P = 1 × 10(-4)) and an odds ratio of 3.169, (95 % CI P = 1 × 10(-4)) which was higher than any factor considered independently. CONCLUSIONS: The results of this study require validation in other populations but represent a step forward in the development of more accurate prognostic tests for clinicians to prescribe the most optimal treatment approach for complicated CD patients.

Progesterone activates multiple innate immune pathways inChlamydia trachomatis-Infected endocervical cells

Problem Susceptibility to Chlamydia trachomatis infection is increased by oral con- traceptives and modulated by sex hormones. We therefore sought to determine the effects of female sex hormones on the innate immune response to C. trachomatis infection. Method of study ECC-1 endometrial cells, pre-treated with oestradiol or progesterone, were infected with C. trachomatis and the host transcriptome analysed by Illumina Sentrix HumanRef-8 microarray. Primary endocervical epithe- lial cells, prepared at either the proliferative or secretory phase of the menstrual cycle, were infected with C. trachomatis and cytokine gene expression determined by quantitative RT-PCR analysis. Results Chlamydia trachomatis yield from progesterone-primed ECC-1 cells was significantly reduced compared with oestradiol-treated cells. Genes upregulated in progesterone-treated and Chlamydia-infected cells only included multiple CC and CXC chemokines, IL-17C, IL-29, IL-32, TNF-a, DEFB4B, LCN2, S100A7-9, ITGAM, NOD2, JAK1, IL-6ST, type I and II interferon receptors, numerous interferon-stimulated genes and STAT6. CXCL10, CXCL11, CX3CL1 and IL-17C, which were also upregu- lated in infected secretory-stage primary cells, and there was a trend towards higher levels of immune mediators in infected secretory-phase compared with proliferative-phase cells. Conclusion Progesterone treatment primes multiple innate immune pathways in hormone-responsive epithelial cells that could potentially increase resis- tance to chlamydial infection.

Non-major-histocompatibility-complex genetics of ankylosing spondylitis

There is strong evidence from twin and family studies indicating that a substantial proportion of the heritability of susceptibility to ankylosing spondylitis (AS) and its clinical manifestations is encoded by non-major-histocompatibility-complex genes. Efforts to identify these genes have included genomewide linkage studies and candidate gene association studies. One region, the interleukin (IL)-1 gene complex on chromosome 2, has been repeatedly associated with AS in both Caucasians and Asians. It is likely that more than one gene in this complex is involved in AS, with the strongest evidence to date implicating IL-1A. Identifying the genes underlying other linkage regions has been difficult due to the lack of obvious candidates and the low power of most studies to date to identify genes of the small to moderate magnitude that are likely to be involved. The field is moving towards genomewide association analysis, involving much larger datasets of unrelated cases and controls. Early successes using this approach in other diseases indicates that it is likely to identify genes in common diseases like AS, but there remains the risk that the common-variant, common-disease hypothesis will not hold true in AS. Nonetheless, it is appropriate for the field to be cautiously optimistic that the next few years will bring great advances in our understanding of the genetics of this condition.

Molecular basis of colorectal cancer predisposition

Colorectal cancer (CRC) is one of the most frequent malignancies in Western countries. Inherited factors have been suggested to be involved in 35% of CRCs. The hereditary CRC syndromes explain only ~6% of all CRCs, indicating that a large proportion of the inherited susceptibility is still unexplained. Much of the remaining genetic predisposition for CRC is probably due to undiscovered low-penetrance variations. This study was conducted to identify germline and somatic changes that contribute to CRC predisposition and tumorigenesis. MLH1 and MSH2, that underlie Hereditary non-polyposis colorectal cancer (HNPCC) are considered to be tumor suppressor genes; the first hit is inherited in the germline and somatic inactivation of the wild type allele is required for tumor initiation. In a recent study, frequent loss of the mutant allele in HNPCC tumors was detected and a new model, arguing against the two-hit hypothesis, was proposed for somatic HNPCC tumorigenesis. We tested this hypothesis by conducting LOH analysis on 25 colorectal HNPCC tumors with a known germline mutation in the MLH1 or MSH2 genes. LOH was detected in 56% of the tumors. All the losses targeted the wild type allele supporting the classical two-hit model for HNPCC tumorigenesis. The variants 3020insC, R702W and G908R in NOD2 predispose to Crohn s disease. Contribution of NOD2 to CRC predisposition has been examined in several case-control series, with conflicting results. We have previously shown that 3020insC does not predispose to CRC in Finnish CRC patients. To expand our previous study the variants R702W and G908R were genotyped in a population-based series of 1042 Finnish CRC patients and 508 healthy controls. Association analyses did not show significant evidence for association of the variants with CRC. Single nucleotide polymorphism (SNP) rs6983267 at chromosome 8q24 was the first CRC susceptibility variant identified through genome-wide association studies. To characterize the role of rs6983267 in CRC predisposition in the Finnish population, we genotyped the SNP in the case-control material of 1042 cases and 1012 controls and showed that G allele of rs6983267 is associated with the increased risk of CRC (OR 1.22; P=0.0018). Examination of allelic imbalance in the tumors heterozygous for rs6983267 revealed that copy number increase affected 22% of the tumors and interestingly, it favored the G allele. By utilizing a computer algorithm, Enhancer Element Locator (EEL), an evolutionary conserved regulatory motif containing rs6983267 was identified. The SNP affected the binding site of TCF4, a transcription factor that mediates Wnt signaling in cells, and has proven to be crucial in colorectal neoplasia. The preferential binding of TCF4 to the risk allele G was showed in vitro and in vivo. The element drove lacZ marker gene expression in mouse embryos in a pattern that is consistent with genes regulated by the Wnt signaling pathway. These results suggest that rs6983267 at 8q24 exerts its effect in CRC predisposition by regulating gene expression. The most obvious target gene for the enhancer element is MYC, residing ~335 kb downstream, however further studies are required to establish the transcriptional target(s) of the predicted enhancer element.

Novel Insights into the Molecular Genetic Background of Colorectal Tumors

Many of the genes predisposing to highly penetrant colorectal cancer (CRC) syndromes, including hereditary non-polyposis colorectal cancer (MLH1, MSH2, MSH6, PMS2), familial adenomatous polyposis (APC), Peutz-Jeghers syndrome (LKB1), juvenile polyposis (SMAD4, BMPR1A), MYH-associated polyposis (MYH), and Cowden syndrome (PTEN) have already been discovered. Identification of these genes has allowed a more precise classification of the hereditary CRC syndromes and provided a means for predictive genetic testing and surveillance. Some of the genes are also involved in sporadic cancer forms, and therefore the investigation of the rare CRC syndromes has been a breakthrough for general cancer research. Despite the accumulating knowledge on hereditary cancer syndromes, a significant number of familial CRCs remain molecularly unexplained after genetic testing, reflecting the possibility of other predisposing genes or existence of novel syndromes. Moreover, genetic variants conferring low-penetrance risk are still largely unknown. In this study, we examined the role of some new high- and low-penetrance alleles on CRC predisposition. We identified disease causing MYH mutations in a subset (9%) of patients with APC and AXIN2 mutation negative adenomatous polyposis. Due to differences in the pattern of inheritance and clinical manifestation, screening for mutations in MYH is beneficial in view of genetic counselling and surveillance. A novel functionally deficient MYH founder mutation A459D was identified in the Finnish population, and this finding had immediate clinical implications for genetic counselling of at risk families. Many patients with hamartomatous polyposis remain without molecular diagnosis due to atypical phenotypes. We therefore sought to classify 49 patients with unexplained hamartomatous or hyperplastic/mixed polyposis by extensive molecular analyses of PTEN, LKB1, BMPR1A, SMAD4, ENG, BRAF, MYH, and BHD along with revision of polyp histology. Mutations were identified in 11/49 (22%) of the patients. In 6 cases the molecular diagnosis was re-classified guiding surveillance and decisions for prophylactic surgery. Re-evaluation of polyp histology with subsequent more accurate selection of candidate gene analyses is beneficial and can be recommended for patients with unexplained polyposis. Furthermore, germline mutations in ENG underlying juvenile polyposis were described for the first time, characterizing a possible novel genetically defined form of hereditary CRC. Association analyses on two putative low-penetrance alleles, NOD2 3020insC and MDM2 SNP309 were performed in a population-based series of 1042 Finnish CRC patients and in cancer-free controls. In contrast to previous results, NOD2 3020insC did not associate with CRC or age at disease onset in the Finnish population. These data suggest that NOD2 3020insC alone might not be sufficient for CRC predisposition. MDM2 SNP309 was as common in the CRC cohort as in the healthy controls. Interesting trends, however, were observed, which after correction for multiple testing did not reach statistical significance. SNP309 was more common in female CRC patients and a trend towards an earlier age at disease onset was observed in women with SNP309. Subsequent studies have supported this observation and SNP309 could affect gender- or hormone-related tumorigenesis. Finally, a large-scale unbiased effort was designed to characterize the complete mutatome of CRC with microsatellite instability (MSI). Using an approach combining expression microarray and genome database searches, we were able to identify putative MSI target genes. Further characterization of one of the genes suggested that it might play a role also in microsatellite stable CRC and Peutz-Jeghers syndrome pathogenesis.

Smoking behaviour modifies IL23r-associated disease risk in patients with Crohn's disease

Background and Aim The etiology of Crohn's disease (CD) implicates both genetic and environmental factors. Smoking behavior is one environmental risk factor to play a role in the development of CD. The study aimed to assess the contribution of the interleukin 23 receptor (IL23R) in determining disease susceptibility in two independent cohorts of CD, and to investigate the interactions between IL23R variants, smoking behavior, and CD-associated genes, NOD2 and ATG16L1. Methods Ten IL23R single-nucleotide polymorphisms (SNPs) were genotyped in 675 CD cases, and 1255 controls from Brisbane, Australia (dataset 1). Six of these SNPs were genotyped in 318 CD cases and 533 controls from Canterbury, New Zealand (dataset 2). Case–control analysis of genotype and allele frequencies, and haplotype analysis for all SNPs was conducted. Results We demonstrate a strong increased CD risk for smokers in both datasets (odds ratio 3.77, 95% confidence interval 2.88–4.94), and an additive interaction between IL23R SNPs and cigarette smoking. Ileal involvement was a consistent marker of strong SNP–CD association (P ≤ 0.001), while the lowest minor allele frequencies for location were found in those with colonic CD (L2). Three haplotype blocks were identified across the 10 IL23R SNPs conferring different risk of CD. Haplotypes conferred no further risk of CD when compared with single SNP analyses. Conclusion IL23R gene variants determine CD susceptibility in the Australian and New Zealand population, particularly ileal CD. A strong additive interaction exists between IL23R SNPs and smoking behavior resulting in a dramatic increase in disease risk depending upon specific genetic background.

Genetic Variation and Clinical Manifestations in Inflammatory Bowel Disease

Crohn s disease (CD) and ulcerative colitis (UC), collectively known as inflammatory bowel disease (IBD), are characterised by chronic inflammation of the gastrointestinal tract. IBD prevalence in Finland is approximately 3-4 per 1000 inhabitants with a peak incidence in adolescence. The symptoms of IBD include diarrhoea, abdominal pain, fever, and weight loss. The precise aetiology of IBD is unknown but interplay of environmental risk factors and immunologic changes trigger the disease in a genetically susceptible individual. Twin and family studies have provided strong evidence for genetic factors in IBD susceptibility, and genetic factors may be more prominent in CD than UC. The first CD susceptibility gene was identified in 2001. Three common mutations R702W, G908R, and 1007fs of the CARD15/NOD2 gene are shown to associate independently with CD but the magnitude of association varies between different populations. The present study aimed at identifying mutations and genetic variations in IBD susceptibility and candidate genes. In addition, correlation to phenotype was also assessed. One of the main objectives of this study was to evaluate the role of CARD15 in a Finnish CD cohort. 271 CD patients were studied for the three common mutations and the results showed a lower mutation frequency than in other Caucasian populations. Only 16% of the patients carried one of the three mutations. Ileal location as well as stricturing and penetrating behaviour of the disease were associated with occurrence of the mutations. The whole protein coding region of CARD15 was screened for possible Finnish founder mutations. In addition to several sequence variants, five novel mutations (R38M, W355X, P727L, W907R, and R1019X) were identified in five patients. Functional consequences of these novel variants were studied in vitro, and these studies demonstrated a profound impairment of MDP response. Investigation of CARD15 mutation frequency in healthy people across three continents showed a large geographic fluctuation. No simple correlation between mutation frequency and disease incidence was seen in populations studied. The occurrence of double mutant carriers in healthy controls suggested that the penetrance of risk alleles is low. Other main objectives aimed at identifying other genetic variations that are involved in the susceptibility to IBD. We investigated the most plausible IBD candidate genes including TRAF6, SLC22A4, SLC22A5, DLG5, TLR4, TNFRSF1A, ABCB1/MDR1, IL23R, and ATG16L1. The marker for a chromosome 5 risk haplotype and the rare HLA-DRB1*0103 allele were also studied. The study cohort consisted of 699 IBD patients (240 CD and 459 UC), of which 23% had a first-degree relative with IBD. Of the several candidate genes studied, IL23R was associated with CD susceptibility, and TNFRSF1A as well as the HLA-DRB1*0103 allele with UC susceptibility. IL23R variants also showed association with the stricturing phenotype and longer disease duration in CD patients. In addition, TNFRSF1A variants were more common among familial UC and ileocolonic CD. In conclusion, the common CARD15 mutations were shown to account for 16% of CD cases in Finland. Novel CARD15 variants identified in the present study are most likely disease-causing mutations, as judged by the results of in vitro studies. The present study also confirms the IL23R association with CD susceptibility and, in addition, TNFRSF1A and HLA-DRB1*0103 allele association with UC of specific clinical phenotypes.

Efecto de tres periodos de suministro de alimento de retiro en broilers en la Empresa Tip-Top industrial, S.A.

En el presente estudio se evaluaron tres periodos de alimento de retiro o acabado en broilers (o, 3, 6 y 9 días antes de la matanza) el cual contiene 3,225 kcal EM/kg de alimento y 19% de proteína, ajustándose a los requerimientos nutricionales recomendados por Arbor Acres Farm Inc., (1992), en especial a la proporción energia-proteina. La evaluación tuvo lugar en la Granja Buenos Aires propiedad de la Empresa Tip-Top Industrial, S.A., con una duración de 42 días, en donde se utilizaron 800 pollos de engorde sin sexar (mixtos) de la línea Peterson-Arbor Acres de un día de edad, dichos pollos fueron distribuidos aleatoriamente en cuatro tratamientos: T1 suministro de alimento de retiro por nueve días), T2 suministro de alimento de retiro por seis días), T3, (Suministro de alimento de retiro por tres días) y T4 (testigo, con cero días de alimento de retiro), con cuatro repeticiones cada uno, distribuidos en un Diseño completamente al Azar sometidos a la prueba de rangos múltiples de Duncan. Las variables estudiadas fueron: consumo de alimento, peso vivo, ganancia de peso, conversión alimenticia, mortalidad vs viabilidad, rendimiento en la canal, análisis económico. No se encontraron diferencias significativas (P<0.05) entre los tratamientos al final del ensayo para el consumo de alimento, conversión alimenticia y costo de alimento, pero no así ara peso vivo y ganancia de peso. El porcentaje de mortalidad acumulada total fue de 2.5% y los rendimientos de la canal fueron: (90.74)T1 (88.98)T2, (85.86)T3,y (90.31)T4, Se corolo que el periodo de suministro de alimento de retiro que permitió los mejores pesos vivos, ganancias de pesos y conversiones alimenticias fue el periodo de tres días (T3), sin embargo, obtuvo el mayor consumo total para generar un peso promedio en la canal de 3.34 lbs, además, presentó el mayor costo alimenticio entre los tratamientos experimentales (T1, T2, T3) y bajo rendimiento en la canal, contrario al T1 que aunque los parámetros productivos fueron menores que el T3 obtuvo el mayor rendimiento en la canal con un menor costo alimenticio. El alimento de retiro no ejerció efecto sobre las variables estudiadas lo que demuestra que dicho alimento pueda ser una alternativa viable para disminuir costo alimenticio.

Estudio sobre la conservación del subproducto del camarón con dos niveles de inclusión [5 10] de ácido sulfúrico

Nicaragua produce 147,000 lb/mes de subproducto de la pesca del camarón y del pescado los cuales son destinados a la basura. Con e l objetivo de proporcionar un método de conservación que conlleve a utilizar estos desperdicios en la alimentación animal se realizó el presente estudio que consistió camarón, en elaborar tratados microensilajes con subproducto con ácido sulfúrico (5%, del 10%) volumen/peso utilizando de 2 Kg cada uno. 20 microsilos de PVC con capacidad se dividieron en 2 tratamientos evaluándolos a diferentes periodos de tiempo (7, 15, 30, 45 y 60 días), realizándose un DCA con arreglo unifactorial, análisis bromatológicos, determinación de AGV y pH. Todos los ensilados presentaron predominancia de la fermentación láctica, los contenidos de proteína bruta variaron en un rango de 40.70 a 50.20% según los tratamientos. Todos los ensilajes se pueden utilizar a los 7 días después de ensilarse. El tratamiento de menor costo resulto ser el T1 (5% H2so4 ) con 0.56 USA/Kg.

Composición quimica y digestibilidad in situ de los pastos angleton (Dichantium aristatum, poir.), Colonial (Panicum maximum, Jacq.) y Taiwan (Pennisetum purpureum, Schum)

Se determinó la digestibilidad de los pastos Angleton, Colonial y Taiwan mediante el método in situ, disponiendo para ello de tres novillos de la raza criolla Reyna cuya edad oscilaba entre 12 y 18 meses y con un peso promedio de 261 kg, los cuales estuvieron provistos de una fístula ruminal. El objetivo propuesto fue obtener y comparar los estimados cuantitativos relativos a la degradación ruminal a diferentes tiempos de incubación (24,48 y 72 horas} tanto de materia seca como de proteína bruta. Los pastos fueron cosechados a los 35 días después del rebrote y se analizaron químicamente según procedimientos de la A.O.A.C (1984) para materia seca (MS), proteína bruta (PB), extracto etéreo (EE), extracto libre de nitrógeno (ELN), fibra bruta (FB) y cenizas (C) (Weende), y según el método de Van Soest (CATIE, 1987) para fibra neutro detergente (FND)y fibra ácido detergente (FAD), así como Hemicelulosa (HC). Se incubaron 10 gr de las muestras de cada uno de los pastos en bolsas de nylon. Para analizar estadísticamente los valores de degradación obtenidos, se utilizaron análisis de varianza dentro de un DCA para determinar la significancia entre pastos en los tiempos medidos y prueba de rango múltiple de Duncan para comparar medias de los pastos dentro de cada tiempo, obteniéndose diferencias altamente significativas entre ellos (P <0.01), y al observar la separación de medias se manifestó la superioridad del Taiwan en todos los tiempos de incubación, sin embargo el Colonial, no presentó diferencias significativas con el Taiwan y el Angleton en el tiempo de 72 horas. Se concluye como resultado de este estudio, que a una edad de rebrote de 35 días, el. Taiwán es superior al Angleton y al Colonial en lo que respecta a solubilidad de materia seca v proteína bruta al mismo tiempo el Colonial. mostró superioridad ante el Angl.eton debido a su mayor solubilidad de materia seca. Las mayores degradaciones de materia seca se presentaron en el. período de 0 a 24 horas de fermentación para los tres pastos; en cambio para proteína bruta ocurrieron para el. Angleton y el Taiwán entra 1as 24 y 48 horas y para e1 Colonia1 entre O y 24 horas. En qenera1, a través de la dinámica de digestión de 1os pastos se observó la influencia negativa que ejerce proporcionalmente a su contenido, la fracción de fibra (fibra neutro detergente y fibra acido detergente).

Sustitución de la fuente proteica en dietas para camarón en etapa juvenil (Litopenaeus vannamei), utilizando harina de carne y hueso como sustituto parcial de la harina de pescado

Sustitución de la fuente proteica en dietas para camarón en etapa juvenil ( Litopenaeus vannamci ), . utilizando harina de carne y hueso como sustituto parcial de la harina de pescado. Con el objetivo de determinar el efecto dé cuatro niveles de sustitución de la fuente proteica de la harina de pescado, por la harina de carne y hueso se realizó el presente experimento a través de un diseño completamente aleatorio con 5 tratamientos, 0, 15, 25, 35 y .45 % de proteína bruta de sustitución para los tratamientos T0, T1, T2, T3 y T4 respectivamente, compuesto de 3 repeticiones para cada uno de ellos. Las raciones fueron isoproteica e isocalóricas y se estudiaron las siguientes variables: Tasa de crecimiento, tasa de consumo de alimento, tasa de conversión alimenticia, tasa de sobrevivencia y análisis costo beneficios. La tasa de crecimiento obtenida fueron de: 0.18, 0.20, 0.21, 0.16 y 0.13 gr/semana. Los resultados mostraron que existe diferencia significativa en la tasa de crecimiento entre los tratamientos Tl, T2 vs. T4. Encontrándose que los que pueden sustituir parcialmente la harina de pescado son los tratamientos Tl y T2, con 15 y 25% de sustitución de la proteína bruta de la harina de pescado por la harina de carne y hueso y con peso de 0.20 y 0.21 gr/semana, el que presento mayor consumo de alimento fue el tratamiento T1, con 0.58 gr, siguiéndole en orden de importancia los tratamientos T0, T2. T3 y T4, con 055 gr: 0.52 gr: 0.51 gr y 0.46 gr respectivamente, no existiendo diferencia significativa contra el T0. La conversión alimenticia obtenidas en los diferentes tratamientos fueron de: 3.41; 3.35; 2.96; 3.52 y 3.81 para los tratamientos T0. T1, T2, T3 y T4 respectivamente. no encontrándose diferencia significativa entre ellos. La sobrevivencia obtenida fue de 85.56%. El análisis económico encontró que la dieta más barata fue la del tratamiento T4, Con un costo de C$0.03425 centavos de córdobas por gramos de alimentos y con una utilidad de C$0.41.

Inclusión de la harina de larva de mosca doméstica (Musca doméstica) en la dieta de pollos de engorde

El presente trabajo experimental "Inclusión de harina de Larva de Mosca Doméstica (Musca domestica) en la dieta de pollos de engorde, es un estudio que se efectuó en El Instituto Politécnico Agroindustrial del Norte (IPADEN) "Naciones Unidas", ubicado en el kilómetro 114 1/2 carretera panamericana, (San Isidro, Matagalpa) por un periodo de siete meses. Este se desarrollo en dos etapas: 1. Producción de larva de mosca doméstica, donde se obtuvo una producción d 13.202 Kg de harina de larva de mosca seca, obtenida de una producción aproximada de 24.23 g de harina de larva de mosca seca (promedio) por Kg de estiércol de cerdo, aportando el 60.93% de proteína bruta. 2- inclusión de la harina de larva de mosca doméstica seca en la dieta de pollos, llevándose a cabo por un periodo de seis semanas. En el estudio se evaluaron dos tratamientos TI 16.34% de inclusión de HMLS y T2 0% de inclusión de HMLS, donde le utilizaron 56 pollos de engorde, sin sexar ( Mixtos ) ,de la línea Petter Hubbard de un día de edad y con un promedio de 60 g. Cada tratamiento estuvo conformado por cuatro repeticiones y 7 Pollos por cada repetición. El análisis estadístico empleado fue el Diseño Completamente al Azar (DCA) donde se evaluaron las variables, Consumo, ganancia media diaria, conversión alimenticia y peso vivo final, obteniendo una GMD de 31.63 g y 23.96 g. no encontrando diferencia significativa al P>0.05 respectivamente, además se constató una utilidad económica de los tratamientos donde el T2 obtuvo la mejor utilidad con respecto al Tl.