A large part of the world’s population lives in cities, with growing estimates for the coming years. Many agglomerations are in areas of greater vulnerability, such as the coast. Demographic growth demands a larger area, with expansion of public services and more local infrastructure. Economic growth, usually confused with development, can increase the risks of epidemics and disasters, when people start to live in risk areas and there is inequality in the provision of basic services. This work, within the scope of the joint evolution of the health sector and sustainable development as strategies to reduce vulnerability, makes a methodological cut for the coast of the state of São Paulo - Brazil, with analyzes of the connections with socio-environmental disasters data. The municipalities in this study present a good structure for monitoring the risk of disasters, but it is not enough to promote a sustainable development.

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Despite all the knowledge, the cellular and molecular mechanisms involved in myeloproliferative neoplasm (MPN) pathophysiology remain unclear. Authors have shown galectin-1 (Gal-1) and 3 playing roles in tumour angiogenesis and fibrosis, which were correlated with poor prognosis in patients with MPN. In the present study LGALS1 and LGALS3 were differently expressed between polycythemia vera, essential thrombocythemia (ET) and primary myelofibrosis (PMF) diseases. Increased LGALS3 expression was associated with a negative JAK2 V617F status mutation in leucocytes from PMF but not in patients with ET without this mutation. However, a positive Janus kinase 2 (JAK2) V617F cell line established from patients with ET (SET-2 cells) when treated with JAK inhibitor presented high levels of LGALS3. Additionally, high LGALS1 expression was found in CD34(+) cells but not in leucocytes from patients with PMF, in absence of JAK2 V617F mutation, and also in SET-2 cells treated with JAK inhibitor. Thus, our findings indicate that differential expression of LGALS1 and/or LGALS3 in patients with MPN is linked with JAK2 V617F status mutation in these diseases and state of cell differentiation.

2022. ResumoDesde, pelo menos, as últimas quatro décadas, o cenário nosológico com o qual se defronta o campo da Saúde Pública, se mostra cada vez mais complexo e incerto diante da emergência, reemergência e recrudescência de doenças infecciosas. Isso é parte das mudanças sociais contemporâneas que se experiencia e estão sendo conformadas na interface entre natureza e sociedade. Compreende-se que o desenvolvimento tecnocientífico tem se mostrado ambivalente para lidar com essas doenças pois, se de um lado, a sociedade demanda e produz mais ciência e tecnologia (C&T) em saúde, de outro, um crescente número de situações de saúde não respondem às incorporações tecno-científicas ou mesmo foram criadas, reflexivamente, por essas práticas. Tomou-se como recorte empírico desta pesquisa o vírus e a doença zika, consideradas expressão das doenças infecciosas emergentes. O objetivo geral foi compreender a constituição sociobiológica destas doenças à luz da teoria da modernização reflexiva. Como abordagem teórico-metodológico elaborou-se uma articulação entre a teoria da modernização reflexiva e um enfoque construtivista dos fatos científicos. Compuseram os materiais de pesquisa um conjunto de artigos selecionados sobre o vírus e a doença zika e um conjunto de textos sobre o contexto sociopolítico de instauração de pesquisas médicocientíficas na África Oriental, onde se identificou pela primeira vez o vírus da zika. A partir disso elaborou-se a história da gênese sóciocientífica do vírus zika e da doença por ele causada para mostrar as interações entre humanos e não humanos envolvidas nas circunstâncias de expansão da modernidade industrial capitalista e das atividades científicas, nos primórdios e no meado do século XX, para o continente africano. Além disso, identificou-se que os métodos e técnicas científicos produziram condições para o surgimento de novas situações de doença. Compreende-se que essa análise lança um olhar sobre as doenças infecciosas emergentes no âmbito dos paradoxos e ambiguidades constitutivos da sociedade tecnocientífica contemporânea.

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5057 Background: Polycythaemia vera (PV) is a clonal disorder characterized by an accumulation of normal red and white cells, platelets, and their progenitors in absence of a definable stimulus. Despite the advances in PV diagnosis its physiopathology remains not well elucidated. Apoptosis deregulation seems to contribute to disease establishment. MicroRNAs are small noncoding RNAs, post transcriptional repressors of genes by deadenilation, which play relevant roles in regulation of apoptotic machinery. Here we investigate the relation of apoptosis deregulation and apoptomirs expression in PV patients. Aims: To quantify the apoptomirs −16, −21, −15a, −26a, 130b, 29c and let-7d expression in peripheral leukocytes and CD34+ hematopoietic stem cells (HSC) in Polycythemia Vera (PV) patients and to correlate with targets genes expression data. Subjects and Methods: 30 PV patients, 13 men and 17 women with a mean age (ma) of 64. 7y. 30 healthy subjects, 13 males and 17 females, ma=60. 2y and 23 bone marrow donors, 14 males and 9 females, ma=32. 6y. Peripheral leukocytes were obtained by Haes-Steril method and CD34+ hematopoietic stem cells were enriched by using the magnetically activated cell sorting, total RNA was extracted according to Trizol® method and High Capacity® Kit was used to synthesize cDNA. The microRNAs and apoptosis-related genes expression quantification was performed by real time PCR. Results were given as 2-ΔΔCt and statistical analyses were carried out by Mann-Whitney and Spearman tests. Western Blot was applied to detect Bcl-2 protein expression. Results: miR-16 and miR21 levels were increased in PV leukocytes (median= 3. 45 and 6. 97 respectively)) and CD34+ HSC (median= 3. 86 and 4. 07 respectively) in comparison to controls (control leukocytes median= 0. 483 and 0. 989 respectively) (CD34+ HSC median= 0. 978 and 1. 15, respectively) (p= 0. 0001 and 0. 0001 in leukocytes) and (p= 0. 0001 and 0. 0005 in CD34+ HSC, respectively). The Bcl-2 gene expression was decreased in PV leukocytes (m= 0.18) when compared to controls (m= 1. 03; p= 0. 019). In addition we found in CD34+ HSC negative correlation between miR-21 and anti-apoptotic gene Bcl-2 (r= −0. 417; p= 0. 033) and between miR16 and anti-apoptotic gene Bcl-2(r= −0. 384; p=0. 046). Bcl-2 western blot showed half expression in PV leukocytes when compared to controls. Conclusions: The results indicate the apoptomirs expression is linked to apoptosis deregulation in Polycythemia Vera physiopathology. Disclosures: No relevant conflicts of interest to declare.