Os cuidados com a mistura de racoes na propriedade.

Tipos de misturadores; Como misturar as racoes na propriedade; Como determinar o tempo otimo de mistura de um misturador?; Metodologia; Outros cuidados importantes.bitstream/item/57936/1/CUsersPiazzonDocumentsCIT-19.pdf; bitstream/item/67821/1/CUsersPiazzonDocumentsProntosCNPSA-DOCUMENTOS-19-OS-CUIDADOS-COM-A-MISTURA-DE-RACOES-NA-PROPRIEDADE-FL-12801A.pd

Metodologia para a determinação da intensidade de coloração em grãos de milho.

bitstream/CNPSA/15614/1/cot260.pd

Applied genomics: the brazilian experience.

Projeto/Plano de Ação: 01.06.10602-03

Background suppression in massive TeO2_2 bolometers with Neganov-Luke amplified light detectors

Bolometric detectors are excellent devices for the investigation of neutrinoless double-beta decay (0$\nu\beta\beta$). The observation of such decay would demonstrate the violation of lepton number, and at the same time it would necessarily imply that neutrinos have a Majorana character. The sensitivity of cryogenic detectors based on TeO$_2$ is strongly limited by the alpha background in the region of interest for the 0$\nu\beta\beta$ of $^{130}$Te. It has been demonstrated that particle discrimination in TeO$_2$ bolometers is possible measuring the Cherenkov light produced by particle interactions. However an event-by-event discrimination with NTD-based light detectors has to be demonstrated. We will discuss the performance of a highly-sensitive light detector exploiting the Neganov-Luke effect for signal amplification. The detector, being operated with NTD-thermistor and coupled to a 750 g TeO$_2$ crystal, shows the ability for an event-by-event identification of electron/gamma and alpha particles. The extremely low detector baseline noise, RMS 19 eV, demonstrates the possibility to enhance the sensitivity of TeO$_2$-based 0$\nu\beta\beta$ experiment to an unprecedented level

Determinação do tempo ótimo de mistura de um misturador de rações.

bitstream/item/59510/1/CUsersPiazzonDocuments5.pd

Mapping quantitative trait loci in Gallus gallus using principal components.

Projeto/Plano de Ação: 01.06.10.602-03

Heritabilities and genetic correlations for reproductive traits in an F2 reciprocal cross chicken population.

Projeto: 01.06.01.003

Clinical and molecular characterization of HER2 amplified-pancreatic cancer

<p>Background: Pancreatic cancer is one of the most lethal and molecularly diverse malignancies. Repurposing of therapeutics that target specific molecular mechanisms in different disease types offers potential for rapid improvements in outcome. Although HER2 amplification occurs in pancreatic cancer, it is inadequately characterized to exploit the potential of anti-HER2 therapies.</p> <p>Methods: HER2 amplification was detected and further analyzed using multiple genomic sequencing approaches. Standardized reference laboratory assays defined HER2 amplification in a large cohort of patients (n = 469) with pancreatic ductal adenocarcinoma (PDAC).</p> <p>Results: An amplified inversion event (1 MB) was identified at the HER2 locus in a patient with PDAC. Using standardized laboratory assays, we established diagnostic criteria for HER2 amplification in PDAC, and observed a prevalence of 2%. Clinically, HER2- amplified PDAC was characterized by a lack of liver metastases, and a preponderance of lung and brain metastases. Excluding breast and gastric cancer, the incidence of HER2-amplified cancers in the USA is >22,000 per annum.</p> <p>Conclusions: HER2 amplification occurs in 2% of PDAC, and has distinct features with implications for clinical practice. The molecular heterogeneity of PDAC implies that even an incidence of 2% represents an attractive target for anti-HER2 therapies, as options for PDAC are limited. Recruiting patients based on HER2 amplification, rather than organ of origin, could make trials of anti-HER2 therapies feasible in less common cancer types.</p&gt

Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis

Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-offunction mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n¼40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC