Proposal for a radiation shielding study aiming the implantation of neutrons beam shutter in the J-9 radiation channel of the Argonauta reactor of the Nuclear Engineering Institute.

Argonauta, the only nuclear research reactor situated in Rio de Janeiro, located at the Institute of Nuclear Engineering (IEN), regularly serves a network of users focused on research and development, and also provides its infrastructure for experimental classes and completion work course. Due to increasing demand for non-destructive thermal neutron assays and production of radioisotopes, there is a search for new procedures and/or devices that optimize users' exposure to neutrons. The implementation of mechanisms that allow access to the irradiation channels without the reactor being turned off and with a shielding configuration that limits the occupational doses at this location is very useful for the operation of the reactor. In order to achieve this, the present work proposes the establishment of a neutron beam shutter of the J-9 irradiation channel of the IEN’s Argonauta reactor. In a first step, experimental measurements were made in the irradiation channel of the reactor using a BF3 detector, which is coupled to a spectrometer. In this phase, the neutron beam was aligned to the spectrometer, and different materials were used as shields, aiming the attenuation of the beam. To validate and/or change the configuration of the barrier that best meets the material irradiation needs, a second planned phase is involving the neutron flux simulation of the reactor and the various shields with different boundary conditions using the particle transport code, Monte Carlo N-Particle Extended (MCNP- X)

An activating mutation in the CRHR1 gene is rarely associated with pituitary-dependent hyperadrenocorticism in poodles

OBJECTIVES: Pituitary-dependent hyperadrenocorticism is the most common cause of naturally occurring hypercortisolism in dogs. CRHR1 expression in human and dog corticotrophinomas suggested that this gene affects pituitary tumorigenesis. The present study aimed to investigate mutations in the CRHR1 coding region in poodles with pituitary-dependent hyperadrenocorticism. METHODS: Fifty poodles with pituitary-dependent hyperadrenocorticism and 50 healthy poodles were studied. Genomic DNA was amplified by PCR and analyzed by Sanger sequencing. RESULTS: The novel CRHR1 p.V97M mutation was identified in one dog. This valine residue, located in the amino-terminal extracellular domain, exhibits high affinity for its corticotropin-releasing hormone (CRH) ligand. Bioinformatic analysis revealed structural rearrangements in the mutant protein, with a 17% increase in the surface binding affinity between CRHR1 and CRH. In vitro functional studies showed that mutant CRHR1 induced higher ACTH secretion than the wild type after stimulation with human CRH. CONCLUSION: These results suggest that germline activating mutations in CRHR1 may be a rare cause of pituitary hyperadrenocorticism in poodles

Characteristics of two conditioning regimens cyclophosphamide plus antithymocyte globulin versus cyclophosphamide plus busulfan in allogeneic stem cell transplantation for severe aplastic anemia

Universidade Federal de São Paulo, São Paulo, BrazilHosp Santa Marcelina, São Paulo, BrazilUniversidade Federal de São Paulo, São Paulo, BrazilWeb of Scienc

Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells.

Background: Epidemiologic studies have highlighted the association of environmental factors with the development and progression of autoimmune and chronic inflammatory diseases. Among the environmental factors, smoking has been associated with increased susceptibility and poor prognosis in rheumatoid arthritis (RA). However, the immune and molecular mechanism of smoking-induced arthritis aggravation remains unclear. The transcription factor aryl hydrocarbon receptor (AHR) regulates the generation of Th17 cells, CD4 T cells linked the development of autoimmune diseases. AHR is activated by organic compounds including polycyclic aromatic hydrocarbons (PAHs), which are environmental pollutants that are also present in cigarette smoke. In this study, we investigated the role of AHR activation in the aggravation of experiment arthritis induced by exposure to cigarette smoke. Methods: Mice were exposed to cigarette smoke during the developmental phase of antigen-induced arthritis and collagen-induced arthritis to evaluate the effects of smoking on disease development. Aggravation of articular inflammation was assessed by measuring neutrophil migration to the joints, increase in articular hyperalgesia and changes in the frequencies of Th17 cells. In vitro studies were performed to evaluate the direct effects of cigarette smoke and PAH on Th17 differentiation. We also used mice genetically deficient for AHR (Ahr KO) and IL-17Ra (Il17ra KO) to determine the in vivo mechanism of smoking-induced arthritis aggravation. Results: We found that smoking induces arthritis aggravation and increase in the frequencies of Th17 cells. The absence of IL-17 signaling (Il17ra KO) conferred protection to smoking-induced arthritis aggravation. Moreover, in vitro experiments showed that cigarette smoke can directly increase Th17 differentiation of T cells by inducing AHR activation. Indeed, Ahr KO mice were protected from cigarette smoke-induced arthritis aggravation and did not display increase in TH17 frequencies, suggesting that AHR activation is an important mechanism for cigarette smoke effects on arthritis. Finally, we demonstrate that PAHs are also able to induce arthritis aggravation. Conclusions: Our data demonstrate that the disease-exacerbating effects of cigarette smoking are AHR dependent and environmental pollutants with AHR agonist activity can induce arthritis aggravation by directly enhancing Th17 cell development

Differential Behavior of Non-albicans Candida Species in the Central Nervous System of Immunocompetent and Immunosuppressed Mice

The genus Candida includes commensal fungi that can cause local and systemic infections, frequently involving vital organs as the central nervous system (CNS). Candida spp. occupy the fourth place among infections that affect the CNS. Although the incidence of Candida albicans is decreasing among patients under immunosuppressive therapies, the incidence of non-albicans Candida is increasing. In this context, the objective of this work was to evaluate the ability of non-albicans Candida species to spread to the CNS of immunocompetent and immunosuppressed mice. Adult female C57BL/6 mice were treated with prednisolone, intravenously infected with Candida glabrata, Candida krusei and Candida parapsilosis yeasts and then evaluated at the 3rd and 14th days after infection. All Candida species disseminated to the brain from immunocompetent animals and induced local inflammation at the third day post-infection. The immunosuppression resulted in body weight loss, leukopenia and reduced IL-2 production by spleen cell cultures. Higher fungal loads were recovered from the CNS of immunosuppressed mice. Inflammatory infiltration associated to a Th1 subset profile was higher in brain samples from C. krusei immunosuppressed mice compared with immunocompetent ones. Additionally, C. krusei was able to transform into pseudohypha inside microglia in vitro infected cells and also to induce elevated nitric oxide production. Altogether, these results indicate that C. glabrata, C. krusei and C. parapsilosis are able to disseminate to the CNS and promote local inflammation in both immunocompetent and immunosuppressed mice. C. krusei displayed a distinct behavior at the CNS triggering a local Th1 profile. The possible contribution of these non-albicans Candida species to other CNS pathologies as multiple sclerosis, Parkinson’s and Alzheimer’s diseases deserves further attention

Retalho de padrão axial ilíaco circunflexo empregado após ressecção de hemangiopericitoma em cão - relato de caso

Os hemangiopericitomas fazem parte dos sarcomas de tecido mole, e correspondem a 14% das neoplasias mesenquimais em cães e gatos. Apresenta etiologia desconhecida, crescimento lento, aspecto infiltrativo e não metastático. Acometem principalmente animais de raças grandes, de meia idade a idosos e não apresenta predileção por raça e sexo. Os tratamentos mais indicados são a amputação, ressecção local associada à radioterapia e cirurgias reconstrutivas. O uso de técnicas cirúrgicas reconstrutivas, permite que o animal retorne sua rotina normal com maior rapidez e com resultados estéticos satisfatórios. O presente trabalho tem como objetivo relatar o emprego de retalho de padrão axial da artéria ilíaca circunflexa profunda após a ressecção de hemangiopericitoma em região de membro pélvico esquerdo de um cão. Esta modalidade de tratamento empregada no presente relato, juntamente com quimioterapia mostraram resultados satisfatórios, mantendo a funcionalidade do membro e qualidade de vida da paciente. Palavras-chave: cirurgia reconstrutiva, neoplasia, quimioterapia, canino