Pancreatic Stromal Tumor of Nerve Sheath Origin Treated by Pancreatoduodenectomy

A pancreatic sarcoma of nerve sheath origin is reported in a 28-year-old female patient, who presented with melaena. Preoperative imaging showed an 8.5 cm diameter mass in the head of pancreas. There was bleeding from the papilla of Vater at endoscopy and a highly vascular lesion on arteriography. The patient was submitted to proximal pancreatoduodenectomy and remains symptom-free at 1 year follow-up

Liver Resections for Metastases from Intraabdominal Leiomyosarcoma

This paper discusses liver resection for intraabdominal leiomyosarcoma metastases as a therapy for carefully selected patients. Of the 83 hepatectomies performed from 1992 to 1996, five were resections for liver metastases due to intraabdominal leiomyosarcoma, in 3 patients. The surgical indication was single liver metastases, without any evidence of extrahepatic disease. No mortality occurred during surgery and the longest survival was 38 months. We concluded that liver resection for leiomyosarcoma metastases can be performed, allowing a long term survival in an occasional patient

Components of partial resistance in Hevea clones to rubber tree leaf blight, caused by Microcyclus ulei.

Varios componentes de resistencia que reduzem a taxa do mal-das-folhas em seringueira foram avaliados. O periodo de susceptibilidade do foliolo, o periodo de geracao do patogeno e o numero de geracoes do patogeno por lancamento foliar, bem como o diametro das lesoes e a producao de esporos nas lesoes, diferem fortemente entre os clones de seringueira estudados. Esses fatores podem ser utilizados para reduzir o desenvolvimento epidemico do mal-das-folhas em seringais de cultivo. Algumas recomendacoes para a utilizacao desses fatores no melhoramento da seringuera visando resistencia ao Microcyclus ulei sao discutidas

Componentes de resistência de clones de seringueira ao Microcyclus ulei.

Analisou-se a resistencia da seringueira ao mal-das-folhas, inoculando-se, nos clones, isolados de Microcyclus ulei que se mostraram mais agressivos em testes anteriores. Os componentes de resistencia analisados foram: periodo de incubacao medio (PI) e periodo de geracao medio (PG) do M. ulei, periodo de suscetibilidade do foliolo (PSF), numero de geracoes do patogeno por fluxo foliar (NGPF)=PS:PG, frequencia de infeccao (FI), diametro medio das lesoes (DL), producao de esporos nas lesoes (PEL) e tolerancia a queda de folhas (TOF).Resumo apresentado no XXI Congresso Brasileiro de Fitopatologia, Salvador, 1988. Resumo 157

Crescimento de estabilidade genotípica em progênies de Pinus taeda L. em três localidades do Estado de São Paulo.

Este trabalho teve como objetivo avaliar progênies de P. taeda L., provenientes de pomar clonal da África do Sul, estabelecidas pelo Instituto Florestal do Estado de São Paulo em três localidades: Angatuba, Campos do Jordão e Itararé

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

Cigarette smoke induces miR-132 in Th17 cells that enhance osteoclastogenesis in inflammatory arthritis

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint destruction and severe morbidity. Cigarette smoking (CS) can exacerbate the incidence and severity of RA. Although Th17 cells and the Aryl hydrocarbon receptor (AhR) have been implicated, the mechanism by which CS induces RA development remains unclear. Here, using transcriptomic analysis, we show that microRNA-132 is specifically induced in Th17 cells in the presence of either AhR agonist or CS-enriched medium. miRNA-132 thus induced is packaged into extracellular vesicles produced by Th17 and acts as a proinflammatory mediator increasing osteoclastogenesis through the down-regulation of COX2. In vivo, articular knockdown of miR-132 in murine arthritis models reduces the number of osteoclasts in the joints. Clinically, RA patients express higher levels of miR-132 than do healthy individuals. This increase is further elevated by cigarette smoking. Together, these results reveal a hitherto unrecognized mechanism by which CS could exacerbate RA and further advance understanding of the impact of environmental factors on the pathogenesis of chronic inflammatory diseases

Secreted Human Amyloid Precursor Protein Binds Semaphorin 3a and Prevents Semaphorin-Induced Growth Cone Collapse

The amyloid precursor protein (APP) is well known for giving rise to the amyloid-β peptide and for its role in Alzheimer's disease. Much less is known, however, on the physiological roles of APP in the development and plasticity of the central nervous system. We have used phage display of a peptide library to identify high-affinity ligands of purified recombinant human sAPPα695 (the soluble, secreted ectodomain from the main neuronal APP isoform). Two peptides thus selected exhibited significant homologies with the conserved extracellular domain of several members of the semaphorin (Sema) family of axon guidance proteins. We show that sAPPα695 binds both purified recombinant Sema3A and Sema3A secreted by transfected HEK293 cells. Interestingly, sAPPα695 inhibited the collapse of embryonic chicken (Gallus gallus domesticus) dorsal root ganglia growth cones promoted by Sema3A (Kd≤8·10−9 M). Two Sema3A-derived peptides homologous to the peptides isolated by phage display blocked sAPPα binding and its inhibitory action on Sema3A function. These two peptides are comprised within a domain previously shown to be involved in binding of Sema3A to its cellular receptor, suggesting a competitive mechanism by which sAPPα modulates the biological action of semaphorins