Educomunicação, Transformação Social e Desenvolvimento Sustentável

Esta publicação apresenta os principais trabalhos dos GTs do II Congresso Internacional de Comunicação e Educação nos temas Transformação social, com os artigos que abordam principalmente Educomunicação e/ou Mídia-Educação, no contexto de políticas de diversidade, inclusão e equidade; e, em Desenvolvimento Sustentável os artigos que abordam os avanços da relação comunicação/educação no contexto da educação ambiental e desenvolvimento sustentável

The Relationship between Injury Characteristics and Post-Traumatic Recovery after Diffuse Axonal Injury

Background: The diagnosis and prognosis of diffuse axonal injury (DAI) remain challenging. This research aimed to analyze the impact on activities of daily living (ADL), functional outcomes, quality of life (QoL), and the association between lesion severity and DAI location identified through imaging exams. Methods: This prospective cohort study included 95 patients diagnosed with DAI. Data were collected at admission, three, six, and twelve months post-injury. The associations between variables were evaluated using a mixed-effects model. Results: Functional recovery and QoL improved between three and twelve months after DAI. An interaction was observed between independence in performing ADL and subarachnoid hemorrhage (p = 0.043) and intraventricular hemorrhage (p = 0.012). Additionally, an interaction over time was observed between the Glasgow Outcome Scale (GOS) and DAI severity (p p = 0.014), and the Disability Rating Scale (DRS) with injury in brain hemispheres (p = 0.026) and Adams classification (p = 0.013). Interaction effects over time were observed with the general health perceptions and energy/vitality domains with intraventricular hemorrhage, and the social functioning domain with the obliteration of basal cisterns and Gentry’s classification. Conclusion: The use of CT in the acute phase of DAI is important for predicting outcomes. The severity and location of DAI are associated with functional outcomes, ADL, and QoL

Long-Term Outcomes in Severe Traumatic Brain Injury and Associated Factors: A Prospective Cohort Study

Objective: The presence of focal lesion (FL) after a severe traumatic brain injury is an important factor in determining morbidity and mortality. Despite this relevance, few studies show the pattern of recovery of patients with severe traumatic brain injury (TBI) with FL within one year. The objective of this study was to identify the pattern of recovery, independence to perform activities of daily living (ADL), and factors associated with mortality and unfavorable outcome at six and twelve months after severe TBI with FL. Methodology: This is a prospective cohort, with data collected at admission, hospital discharge, three, six, and twelve months after TBI. RESULTS: The study included 131 adults with a mean age of 34.08 years. At twelve months, 39% of the participants died, 80% were functionally independent by the Glasgow Outcome Scale Extended, 79% by the Disability Rating Scale, 79% were independent for performing ADLs by the Katz Index, and 53.9% by the Lawton Scale. Report of alcohol intake, sedation time, length of stay in intensive care (ICU LOS), Glasgow Coma Scale, trauma severity indices, hyperglycemia, blood glucose, and infection were associated with death. At six and twelve months, tachypnea, age, ICU LOS, trauma severity indices, respiratory rate, multiple radiographic injuries, and cardiac rate were associated with dependence. Conclusions: Patients have satisfactory functional recovery up to twelve months after trauma, with an accentuated improvement in the first three months. Clinical and sociodemographic variables were associated with post-trauma outcomes. Almost all victims of severe TBI with focal lesions evolved to death or independence

Unveiling the Intracellular Survival Gene Kit of Trypanosomatid Parasites

<div><p>Trypanosomatids are unicellular protozoans of medical and economical relevance since they are the etiologic agents of infectious diseases in humans as well as livestock. Whereas <i>Trypanosoma cruzi</i> and different species of <i>Leishmania</i> are obligate intracellular parasites, <i>Trypanosoma brucei</i> and other trypanosomatids develop extracellularly throughout their entire life cycle. After their genomes have been sequenced, various comparative genomic studies aimed at identifying sequences involved with host cell invasion and intracellular survival have been described. However, for only a handful of genes, most of them present exclusively in the <i>T. cruzi</i> or <i>Leishmania</i> genomes, has there been any experimental evidence associating them with intracellular parasitism. With the increasing number of published complete genome sequences of members of the trypanosomatid family, including not only different <i>Trypanosoma</i> and <i>Leishmania</i> strains and subspecies but also trypanosomatids that do not infect humans or other mammals, we may now be able to contemplate a slightly better picture regarding the specific set of parasite factors that defines each organism's mode of living and the associated disease phenotypes. Here, we review the studies concerning <i>T. cruzi</i> and <i>Leishmania</i> genes that have been implicated with cell invasion and intracellular parasitism and also summarize the wealth of new information regarding the mode of living of intracellular parasites that is resulting from comparative genome studies that are based on increasingly larger trypanosomatid genome datasets.</p></div

Common genes present exclusively in intracellular parasites.

<p>After identifying orthologous proteins, by performing an all-versus-all alignment between the amino acid sequences, the results of the pairwise alignments were used as input to the OrthoMCL software V1.4 with its default parameters. Specific OrthoMCL clusters of intracellular and extracellular/apathogenic trypanosomatids and functional enrichment analysis based in genome annotation were performed using in-house PERL scripts.</p

<i>T. cruzi</i> and <i>Leishmania</i> genes involved with host cell invasion and intracellular survival.

<p><i>T. cruzi</i> and <i>Leishmania</i> genes involved with host cell invasion and intracellular survival.</p

Surface proteins present in <i>Leishmania</i> and <i>T. cruzi</i>.

<p>The figure shows six different surface molecules known to be present in promastigote and amastigote forms of <i>Leishmania</i> (left) and trypomastigote and amastigote forms of <i>T. cruzi</i> (right). Each protein is represented by the symbols indicated below the figure.</p

The distinct life cycles of tritryp parasites.

<p>Panels A–C show the life cycles of <i>T. cruzi</i>, <i>Leishmania</i> spp, and <i>T. brucei</i>, respectively. In each panel, some of the parasite stages present in their insect vectors, <i>T. cruzi</i> epimastigotes, <i>Leishmania</i> promastigotes, and <i>T. brucei</i> procyclic forms, are shown on the left. Different sand fly species of the genera <i>Lutzomyia</i> and <i>Phlebotomus</i> are vectors for Leishmania. <i>Triatoma infestans</i> and <i>Rhodnius prolixus</i> are the most important vector species in the transmission of <i>T. cruzi</i> to man, whereas different species of <i>Glossina</i>, also known as tse-tse fly, are vectors of African trypanosomes. Leishmania and <i>T. brucei</i> parasites move from the fly midgut up to the mouthparts before being inoculated into the human host as metacyclic, infective forms. Although Leishmania promastigotes achieve their journey in sand flies by being regurgitated from the stomodeal valve to the mouthparts, <i>T. brucei</i> epimastigotes do not stay in the mouthparts, as they have to first migrate from the proventriculus to the salivary glands where they develop into metacyclic forms and are expelled with the insect saliva. In contrast, <i>T. cruzi</i> infective metacyclic trypomastigotes develop in the hindgut of the triatomine bug and, after being excreted with the insect feces, gain access to the mammalian host bloodstream through skin wounds or the mucous membranes. On the right side of each panel, parasite forms present in the mammalian host, <i>T. cruzi</i> trypomastigotes, and intracellular amastigotes, <i>Leishmania</i> intracellular amastigotes, and <i>T. brucei</i> bloodstream forms are shown. Whereas <i>Leishmania</i> promastigotes are internalized by host phagocytes and reside into the phagolysosome, <i>T. cruzi</i> trypomastigotes actively invade a variety of nonphagocytic cells and are able to escape from the phagocytic vacuole and multiply in the host cell cytoplasm. Although distinct developmental forms of <i>T. brucei</i> are found in the mammalian host, namely stumpy and slender trypomastigotes, they remain extracellular during the entire parasite life cycle and were represented here as bloodstream trypomastigotes. Panel D shows a phylogenetic analysis inferred from glycosomal glyceraldehyde 3-phosphate dehydrogenase (gapdh) nucleotide sequences from 16 trypanosomatid species, with the species that have an intracellular stage shown with a light blue color. The maximum likelihood tree was constructed with 849 nt (80% of gapdh coding sequences), using SeaView v.04 and rooted at the <i>Crithidia fasciculata</i>/<i>A. deanei</i> clade, with the bootstrap values for 1,000 replicates shown in the major basal nodes.</p

Amastin Knockdown in <i>Leishmania braziliensis</i> Affects Parasite-Macrophage Interaction and Results in Impaired Viability of Intracellular Amastigotes

<div><p>Leishmaniasis, a human parasitic disease with manifestations ranging from cutaneous ulcerations to fatal visceral infection, is caused by several <i>Leishmania</i> species. These protozoan parasites replicate as extracellular, flagellated promastigotes in the gut of a sandfly vector and as amastigotes inside the parasitophorous vacuole of vertebrate host macrophages. Amastins are surface glycoproteins encoded by large gene families present in the genomes of several trypanosomatids and highly expressed in the intracellular amastigote stages of <i>Trypanosoma cruzi</i> and <i>Leishmania</i> spp. Here, we showed that the genome of <i>L</i>. <i>braziliensis</i> contains 52 amastin genes belonging to all four previously described amastin subfamilies and that the expression of members of all subfamilies is upregulated in <i>L</i>. <i>braziliensis</i> amastigotes. Although primary sequence alignments showed no homology to any known protein sequence, homology searches based on secondary structure predictions indicate that amastins are related to claudins, a group of proteins that are components of eukaryotic tight junction complexes. By knocking-down the expression of δ-amastins in <i>L</i>. <i>braziliensis</i>, their essential role during infection became evident. δ-amastin knockdown parasites showed impaired growth after <i>in vitro</i> infection of mouse macrophages and completely failed to produce infection when inoculated in BALB/c mice, an attenuated phenotype that was reverted by the re-expression of an RNAi-resistant amastin gene. Further highlighting their essential role in host-parasite interactions, electron microscopy analyses of macrophages infected with amastin knockdown parasites showed significant alterations in the tight contact that is normally observed between the surface of wild type amastigotes and the membrane of the parasitophorous vacuole.</p></div