The cultural activities and the classroom of the Herero/Helelo ethnic group in southern Angola(Mucubal and Muhimba subgroup)

O povo Herero/Helelo do Sul de Angola, ainda hoje, mantém suas tradições vivas no seu dia a dia. Por meio de entrevistas com os mais velhos e visitas ao grupo, bem como estudo das teorias do programa de Etnomatemática de Ubiratan D’Ambrosio é que o estudo se pauta. Foi possível por meio da observação dos subgrupos Mucubais e Himbas aliado à vontade de se manter as raízes do povo, pensar novos modos e maneiras do professor trabalhar saberes da escola de forma contextualizada e próxima a realidade dos grupos. Em especial, a enfâse foi dada pensando nas relações que envolvem a Arte, a Cultura e a Matemática que o professor pode criar e tecer a fim de aproximar a realidade escolar da realidade vivenciada pelos mais jovens. Nesse sentido, a pesquisa se justifica pela necessidade da apreensão de saberes da atualidade e do entorno do grupo, a fim de garantir a sua sobrevivência nos dias atuais sem perder a cultura

Atteinte hépatique au cours de la maladie de Rendu-Osler: à propos d’un cas et revue de la littérature

Patiente âgée de 48 ans était hospitalisée pour une cholestase asymptomatique hépatique. Elle rapportait une histoire personnelle et familiale d’épistaxis récidivante. Le bilan biologique révélait une anémie ferriprive et une cholestase modérée. Les sérologies virales ainsi que les anticorps anti tissu hépatique étaient négatifs. Le scanner abdominal objectivait de multiples shunts artério-veineux dans la région sous-capsulaire du foie. Le diagnostic d’une atteinte hépatique dans le cadre d’un Rendu Osler était retenu. Un traitement martial était prescrit et une surveillance biologique et morphologique du foie était entreprise.The Pan African Medical Journal 2016;2

Rare diseases in the elderly: a new perspective for the specialist in geriatrics

Rare diseases (RD) encompass a broad spectrum of highly heterogeneous illnesses characterized by a prevalence lower than 1: 2000 in general population. Although relatively uncommon, when considered as a whole, these pathologies represent a relevant public health problem. In light of their usual early onset and high severity and mortality, RD have been traditionally regarded as affecting mainly childhood or young adulthood, and considered to be excluded from filed of interest of geriatric specialists. However, more recent epidemiological studies, suggest that demographic changes, sometimes joined with advances in diagnostic and therapeutic strategies, are permitting longer survival of some persons affected by these conditions, thus making RD compatible with geriatric age. Hence, in the next future, specialists in geriatrics will be referred to by an increasing number of elderly subjects with RD seeking medical care. Geriatricians should be aware about the high management complexity of elderly patients with RD, characterized by considerable frailty status, related to both the primary RD and to the ageing-related condition

The perplexity of targeting genetic alterations in hepatocellular carcinoma

Genetic heterogeneity is a well-recognized feature of hepatocellular carcinoma (HCC). The coexistence of multiple genetic alterations in the same HCC nodule contributes to explain why gene-targeted therapy has largely failed. Targeting of early genetic alterations could theoretically be a more effective therapeutic strategy preventing HCC. However, the failure of most targeted therapies has raised much perplexity regarding the role of genetic alterations in driving cancer as the main paradigm. Here, we discuss the methodological and conceptual limitations of targeting genetic alterations and their products that may explain the limited success of the novel mechanism-based drugs in the treatment of HCC. In light of these limitations and despite the era of the so-called “precision medicine,” prevention and early diagnosis of conditions predisposing to HCC remain the gold standard approach to prevent the development of this type of cancer. Finally, a paradigm shift to a more systemic approach to cancer is required to find optimal therapeutic solutions to treat this disease

Vitamin C inhibits endothelial cell apoptosis in congestive heart failure

Background - Proinflammatory cytokines like tumor necrosis factor- and oxidative stress induce apoptotic cell death in endothelial cells (ECs). Systemic inflammation and increased oxidative stress in congestive heart failure (CHF) coincide with enhanced EC apoptosis and the development of endothelial dysfunction. Therefore, we investigated the effects of antioxidative vitamin C therapy on EC apoptosis in CHF patients. Methods and Results - Vitamin C dose dependently suppressed the induction of EC apoptosis by tumor necrosis factor- and angiotensin II in vitro as assessed by DNA fragmentation, DAPI nuclear staining, and MTT viability assay. The antiapoptotic effect of vitamin C was associated with reduced cytochrome C release from mitochondria and the inhibition of caspase-9 activity. To assess EC protection by vitamin C in CHF patients, we prospectively randomized CHF patients in a double-blind trial to vitamin C treatment versus placebo. Vitamin C administration to CHF patients markedly reduced plasma levels of circulating apoptotic microparticles to 32±8% of baseline levels, whereas placebo had no effect (87±14%, P<0.005). In addition, vitamin C administration suppressed the proapoptotic activity on EC of the serum of CHF patients (P<0.001). Conclusions - Administration of vitamin C to CHF patients suppresses EC apoptosis in vivo, which might contribute to the established functional benefit of vitamin C supplementation on endothelial function

Myocardial infarction in a low risk patient with hereditary hemorrhagic telangiectasia

We describe the case of a 57 year-old woman with NSTE ACS, a history of recurrent and prolonged epistaxis, and low prior cardiovascular risk. Additional findings revealed anemia and an aneurysm in her central nervous system. During her hospital stay, hereditary hemorrhagic telangiectasia (HHT) was diagnosed. After application of two antiplatelet drugs, the patient was scheduled for coronarography, followed by coronary artery bypass grafting. During her hospital stay, only a minor episode of epistaxis was observed. We conclude that anemization due to HTT may significantly accelerate the progress of ischemic heart disease, resulting in acute coronary syndrome. Moreover, coronarography preceded by routine application of two antiplatelet drugs seems not to increase the risk of hemorrhage in HHT patients complicated with myocardial infarction. (Cardiol J 2010; 17, 2: 189-191

Obesity, nonalcoholic fatty liver disease and adipocytokines network in promotion of cancer

Western populations are becoming increasingly sedentary and the incidence of nonalcoholic fatty liver disease (NAFLD) is increasing and becoming one of the most common causes of liver disease worldwide. Also, NAFLD is considered one the new emerging risk factors for development of tumors of the gastro-intestinal tract, particularly hepatocellular carcinoma (HCC). Visceral obesity is an important risk factor for the onset of NAFLD. An accumulation of ectopic fat, including visceral obesity and fatty liver leads to a dysfunction of the adipose tissue with impaired production of adipocytokines which, in turn, favor an increase in pro-inflammatory cytokines. In this review, we discuss how the obesity-related chronic state of low-grade inflammation and the presence of NAFLD lead to the emergence of a microenvironment favorable to the development of cancer

Identification of miR-9-5p as direct regulator of ABCA1 and HDL-driven reverse cholesterol transport in circulating CD14+ cells of patients with metabolic syndrome.

Aims: Metabolic syndrome (MS) is a cluster of cardio-metabolic risk factors associated with atherosclerosis and low-grade inflammation. Using unbiased expression screenings in peripheral blood mononuclear cells, we depict here a novel expression chart of 678 genes and 84 microRNAs (miRNAs) controlling inflammatory, immune and metabolic responses. In order to further elucidate the link between inflammation and the HDL cholesterol pathway in MS, we focussed on the regulation of the ATP-binding cassette transporter A1 (ABCA1), a key player in cholesterol efflux (CE). Methods and results: ABCA1 mRNA levels are suppressed in CD14+ cells of MS patients and are negatively correlated to body mass index (BMI), insulin-resistance (HOMA-IR) and cardiovascular risk, and positively to HDL cholesterol and CE. miRNA target in silico prediction identified a putative modulatory role of ABCA1 for the nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) target miR-9-5p, whose expression pattern was up-regulated in CD14+ cells of MS patients, positively correlated to BMI, HOMA-IR, and triglycerides, and negatively to ABCA1 mRNA levels, HDL cholesterol and CE. Ectopic gain and loss of miR-9-5p function in macrophages modulated ABCA1 mRNA and protein levels, ABCA1 miRNA 3'-untranslated region target sequence reporter assay, and CE into HDL, thus confirming ABCA1 as a target of miR-9-5p. Conclusions: We identified the NF-κB target miR-9-5p as a negative regulator of ABCA1 adding a novel target pathway in the relationship between inflammation and HDL-driven reverse cholesterol transport for prevention or treatment of atherosclerosis in MS.N/