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The effect of genetic crossing and nutritional management on weight gain and the concentration of minerals and trace elements in the carcass, blood, leather, and viscera of sheep were evaluated. Several statistical strategies were used to evaluate the different elemental composition characteristics of pure breed animals, i.e., White Dorper (ODO), Ile de France (OIF), Texel (OTX), and Santa Ines (OSI), as well as their crossbreeds 1/2 White Dorper and 1/2 Santa Ines (ODS), 1/2 Ile de France, and 1/2 Santa Ines (OIS), 1/2 Texel × 1/2 Santa Ines (OTS). Three different diets were evaluated AL (ad libitum), R75, and R63 (75 and 63 g of dry matter/kg of the animal metabolic weight, respectively). Levels of Ca, Cu, Fe, K, Mg, Mn, P, S, and Zn were determined by inductively coupled plasma optical emission spectrometry (ICP OES). The concentration of inorganic elements in the different body components was not affected by the diet (P > 0.05), and OTX and OTS were the breeds with the highest weight gain. Random forest importance models demonstrated that Zn in the carcass, K, Ca, and Zn in blood, and K in leather are most associated with separating the different evaluated sheep’s breeds. Crossbreeding the native Santa Ines breed with sheep of exotic breeds produces animals well adapted to confinement.

Langerhans cell histiocytosis is a rare disease in the adult, predominates in the pediatric age and is more common in men than in women. The sites of greater affection are the long bones, followed by the bones of the skull. Patients usually have symptoms related to the site of affection, usually polyostotic lesions, monostotic lesions occur less frequently. The study of choice and treatment depends on the site affected, in the skull the main one is the magnetic resonance and the treatment is the surgical excision of the lesion.A 29-year-old female patient who entered the hospital due to a non-painful, rapidly growing, progressive tumor on the frontal region of the skull. Physical examination revealed a rounded mass of approximately 5 cm in diameter in the left, non-painful, non-painful, left-frontoparietal region. Magnetic resonance imaging of the skull showed a lytic lesion in the frontal bone. It was surgically excised with clean edges; titanium plate was placed. Histopathological diagnosis was histiocytosis of Langerhans cells.It is a rare case, with a patient of an uncommon age of presentation, absence of metastasis by means of study protocol and due to the monostotic presentation improves the prognosis for this patient.la histiocitosis de células de Langerhans es una enfermedad rara en el adulto, que predomina en la edad pediátrica, y es más común en los hombres que en las mujeres. Los sitios de mayor afectación son los huesos largos, seguidos de los huesos del cráneo. Suele cursar con sintomatología relacionada con el sitio de afectación. Por lo general son lesiones poliostóticas; las lesiones monostóticas se presentan con menor frecuencia. El estudio de elección y el tratamiento dependen del sitio afectado; en el cráneo, el principal es la resonancia magnética, y el tratamiento es la escisión quirúrgica de la lesión.Mujer de 29 años que ingresó al hospital debido a una tumoración no dolorosa de crecimiento rápido y progresivo sobre la región frontal del cráneo. A la exploración física se observó una masa redondeada, de aproximadamente 5 cm de diámetro, en la región frontoparietal izquierda, no dolorosa, de consistencia blanda, no móvil. La resonancia magnética de cráneo mostró una lesión lítica en el hueso frontal. Se extirpó quirúrgicamente con bordes limpios y se colocó una malla de titanio. El diagnóstico histopatológico fue de histiocitosis de células de Langerhans.Se trata de un caso poco frecuente, en una paciente de una edad no común de presentación, con ausencia de metástasis por medio de protocolo de estudio, y debido a la presentación monostótica mejora el pronóstico para esta paciente.

Introduction: Molecular heterogeneity occurs in Hepatocellular carcinoma (HCC), but its implications in clinical decision-making are unknown. The clonal evolution model explains that trunk alterations arise at early stages and are shared by all malignant cells, whereas branch alterations occur in subclonal tumoral cells. We aim to characterize the genomic landscape of HCC through the identification of trunk driver alterations and the study of its distribution in intra- and inter-tumor heterogeneity. Methods: 153 HCC samples representing the multiple steps of hepatocarcinogenesis were analyzed by deep targeted-sequencing covering exonic and promoter regions of the most frequently mutated drivers in HCC. Genes mutated in early lesions [39 dysplastic nodules and 54 early HCCs (eHCC) defined as 4cm (2-3 regions/tumor); and 2) inter-tumor heterogeneity cohort: 39 tumors from 17 patients with multinodular lesions (2-3 nodules/patient). Transcriptome and copy-number variations (CNVs) were analyzed using expression and SNP arrays, respectively. Results: A total of 46 mutations were identified in the cohort of early lesions. Average number of mutations and CNV aberrations were higher in eHCCs than in dysplastic nodules [1.1 vs 0.5, mutations/patient (p=0.03), and 8% vs 0.6% of aberrant chromosomal arms (p Conclusions: TERT, TP53 and CTNNB1 are trunk drivers mutated in early HCC tumors that remained as trunk aberrations across different regions of the same tumor and between primary and metastatic nodules. These mutations are early trunk drivers that can be captured with single biopsies and could represent ideal therapeutic targets in the future. Citation Format: Sara Torrecilla, Daniela Sia, Andrew N. Harrington, Zhongyang Zhang, Genis Camprecios, Agrin Moeini, Toffanin Sara, Isabel Fiel, Ke Hao, Monica Higuera, Laia Cabellos, Helena Cornella, Milind Mahajan, Yujin Hoshida, Augusto Villanueva, Sander Florman, Myron Schwartz, Josep Llovet. Characterization of molecular heterogeneity in hepatocellular carcinoma: Trunk and branch drivers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3944. doi:10.1158/1538-7445.AM2017-3944

Changes in mineral metabolism have recently been described in AIDS patients. To determine whether such changes affect bone turnover and bone mass, we studied 16 HIV-seropositive patients, classified according to Centers for Disease Control criteria, and 27 healthy controls. Biochemical markers of bone turnover and bone mineral density were analyzed. Serum concentrations of osteocalcin were abnormally low (0.5 +/- 1.3 ng/ml) in HIV-seropositive patients, in comparison with the control group (2.98 +/- 1.6 ng/ml) (p0.05). Urinary calcium/creatinine ratio was also decreased in HIV-positive patients (0.10 +/- 0.09 vs 0.14 +/- 0.09) (p0.05). In addition, bone mass was slightly lower in HIV-seropositive patients, although the difference was not statistically significant. The pathogenic mechanism of these alterations and their clinical relevance still remain unclear, and several factors may be implicated.

Pyomyositis is an acute bacterial infection of striated muscle. It is common in the tropics, but rarely reported in temperate climates. We present two cases in patients with the acquired immune deficiency syndrome (AIDS), one an active homosexual, and one an intravenous drug user. A brief review of the clinical findings and diagnostic procedures is included. We conclude that pyomyositis should be included in the list of locations of pyogenic infections that can occur in AIDS patients.

Program (HEPCAR, reference no. 667273-2); US Department of Defense(CA150272P3); an Accelerator Award (CRUCK, AECC, AIRC) (HUNTER,reference no. C9380/A26813), NCI Cancer Center Support Grant, National Cancer Institute; Tisch Cancer Institute (P30-CA196521); Samuel Waxman Cancer Research Foundation; Spanish National Health Institute (SAF2016-76390); and the Generalitat de Catalunya/AGAUR (SGR-1358). Agrin Moeini is supported by Spanish National Health Institute. Sara Torrecilla and Judit Peix are funded by Centro de Investigación Biomedica en Red de Enfermedades Hepáticas y Digestivas (Ciberehd-ISCIII). Carla Montironi is a recipient of Josep Font grant. Carmen Andreu-Oller is supported by "la Caixa" INPhINIT Fellowship Grant (LCF/BQ/IN17/11620024). Roser Pinyol is supported by HEPCAR and AECC. Daniela Sia is supported by the Gilead Sciences Research Scholar Program in Liver Disease. Scott L. Friedman is supported by the National Institutes of Health Research project grant (R01,DK5662) and US Department of Defense (CA150272P3). Mathias Heikenwälder was supported by an ERC Consolidator grant (HepatoMetaboPath), the SFBTR 209, 1335 and SFBTR179. Background & Aims: Cirrhosis and chronic inflammation precede development of hepatocellular carcinoma (HCC) in approximately 80% of cases. We investigated immune-related gene expression patterns in liver tissues surrounding early-stage HCCs and chemopreventive agents that might alter these patterns to prevent liver tumorigenesis. Methods: We analyzed gene expression profiles of nontumor liver tissues from 392 patients with early-stage HCC (training set, N = 167 and validation set, N = 225) and liver tissue from patients with cirrhosis without HCC (N = 216, controls) to identify changes in expression of genes that regulate the immune response that could contribute to hepatocarcinogenesis. We defined 172 genes as markers for this deregulated immune response, which we called the immune-mediated cancer field (ICF). We analyzed the expression data of liver tissues from 216 patients with cirrhosis without HCC and investigated the association between this gene expression signature and development of HCC and outcomes of patients (median follow-up, 10 years). Human liver tissues were also analyzed by histology. C57BL/6J mice were given a single injection of diethylnitrosamine (DEN) followed by weekly doses of carbon tetrachloride to induce liver fibrosis and tumorigenesis. Mice were then orally given the multiple tyrosine inhibitor nintedanib or vehicle (controls); liver tissues were collected and histology, transcriptome, and protein analyses were performed. We also analyzed transcriptomes of liver tissues collected from mice on a choline-deficient high-fat diet, which developed chronic liver inflammation and tumors, orally given aspirin and clopidogrel or the anti-inflammatory agent sulindac vs mice on a chow (control) diet. Results: We found the ICF gene expression pattern in 50% of liver tissues from patients with cirrhosis without HCC and in 60% of nontumor liver tissues from patients with early-stage HCC. The liver tissues with the ICF gene expression pattern had 3 different features: increased numbers of effector T cells; increased expression of genes that suppress the immune response and activation of transforming growth factor β signaling; or expression of genes that promote inflammation and activation of interferon gamma signaling. Patients with cirrhosis and liver tissues with the immunosuppressive profile (10% of cases) had a higher risk of HCC (hazard ratio, 2.41; 95% confidence interval, 1.21-4.80). Mice with chemically induced fibrosis or diet-induced steatohepatitis given nintedanib or aspirin and clopidogrel down-regulated the ICF gene expression pattern in liver and developed fewer and smaller tumors than mice given vehicle. Conclusions: We identified an immune-related gene expression pattern in liver tissues of patients with early-stage HCC, called the ICF, that is associated with risk of HCC development in patients with cirrhosis. Administration of nintedanib or aspirin and clopidogrel to mice with chronic liver inflammation caused loss of this gene expression pattern and development of fewer and smaller liver tumors. Agents that alter immune regulatory gene expression patterns associated with carcinogenesis might be tested as chemopreventive agents in patients with cirrhosis.