Echinococcus granulosus sensu stricto (G1) and Echinococcus ortleppi (G5) are haplotypes of the parasite formerly known as Echinococcus granulosus sensu lato, which in its larval stage causes cystic hydatid disease, endemic in Southern Brazil. Epidemiological and molecular knowledge about the haplotypes occurring in a region is essential to control the spread of the disease. The aim of this work was to analyze the haplotype frequency and fertility of hydatid cysts in cattle from the state of Rio Grande do Sul. Cysts were collected and classified according to their fertility status. DNA was extracted from protoscoleces and germinal layers and then used as template for the amplification of the cytochrome c oxidase subunit 1 gene by PCR. Amplicons were purified and sequenced, and the sequences were analyzed for haplotype identification. A total of 638 fertile cysts collected in the last ten years were genotyped. On average, G1 (56.6%) was more frequent than G5 (43.4%). In lungs, the G5 haplotype exhibited a higher parasite load (52.8%), whereas in the liver, G1 was more frequent (90.4%). The analysis revealed an increase in the frequency of G5 haplotype cysts during the period of sampling, and an increase in the abundance of fertile cysts has also been observed in the last several years. Most infertile cysts were genotyped as G1. The possible factors involved in the increase in the proportion of E. ortleppi (G5) and the consequences of this increase are discussed. This study suggests that the proportion of E. ortleppi (G5) loads in cattle may be increasing overtime.

Background/Aim: Extracellular vesicles (EVs) can mediate drug resistance within the tumor microenvironment by delivering bioactive molecules, including proteins. Here, we performed a comparative proteomic analysis of EVs secreted by A549 lung cancer cells and their cisplatin-resistant counterparts in order to identify proteins involved in drug resistance. Materials and Methods: Cells were co-cultivated using a transwell system to evaluate EV exchange. EVs were isolated by ultracentrifugation and analyzed using microscopy and nanoparticle tracking. EV proteome was analyzed by mass spectrometry. Results: EV-mediated communication was observed between co-cultured A549 and A549/CDDP cells. EVs isolated from both cells were mainly exosome-like structures. Extracellular matrix components, cell adhesion proteins, complement factors, histones, proteasome subunits and membrane transporters were found enriched in the EVs released by cisplatin-resistant cells. Conclusion: Proteins identified in this work may have a relevant role in modulating the chemosensitivity of the recipient cells and could represent useful biomarkers to monitor cisplatin response in lung cancer.Lung cancer is the most common cancer worldwide and the leading cause of cancer death in both men and women (1). Nonsmall cell lung cancer (NSCLC) is the most prevalent type of lung cancer, accounting for approximately 85% of all lung cancer cases (2). Most patients with NSCLC have non operable, advanced-stage disease at the time of diagnosis and platinumbased chemotherapy is the first-line treatment for these patients (3). However, the high incidence of tumor chemoresistance limits treatment success (4). Although numerous mechanisms have been associated with cisplatin (CDDP) resistance in lung cancer (5, 6), the cellular events within the tumor microenvironment that facilitate the acquisition and maintenance of chemoresistance are still poorly understood.Recently, extracellular vesicles (EVs) have emerged as key players for cell-cell communication in the tumor microenvironment (7). EVs are a heterogeneous group of membrane-bound structures secreted by cells into the extracellular space. Based on their size and biogenesis, EVs can be broadly classified into two main categories: exosomes and microvesicles (8). Exosomes are small membrane vesicles (30-100 nm in diameter) formed as intraluminal vesicles within endosomal multivesicular bodies (MVBs), and secreted upon the fusion of MVBs with the plasma membrane. Microvesicles (MVs) range in size from 50 nm to 1000 nm in diameter, but the cancer-derived MV population termed oncosomes can be much larger (up to 10 μm) (9). MVs are generated by the outward budding and fission of the plasma membrane.EVs mediate cellular crosstalk by transporting bioactive cargo between cells, including proteins, lipids, and nucleic acids (10). The EV cargo composition determine its biological effects and varies depending on the cell type and physiological/pathological state (11). In the tumor microenvironment, EVs have been shown to med...