Good neighbours: distribution of black-tufted marmoset (Callithrix penicillata) in an urban environment

Context Primates are one of the most charismatic and widely studied vertebrate groups. However, the study of new world primates in green patches within urban areas has been neglected. Such primates have been viewed as a source of human–animal conflict; however, their ecological importance to urban ecosystems and their role in human well being is poorly understood. Aims To increase understanding of both ecological and socioeconomical factors affecting the distribution, density and group sizes of urban marmosets in a large Brazilian city (Belo Horizonte). Methods A map of vegetation cover and land use was produced and employed to investigate the distribution of marmosets. An online questionnaire was extensively publicised, which permitted the public to report the occurrence or not of marmosets near their residences. For sites with low salary levels and low internet availability, face-to-face interviews were conducted. Additionally, field surveys were conducted in 120 green areas identified by spatial analysis as potential areas of occurrence. The human population density, salary levels and green areas were posteriorly correlated with marmoset distribution. Key results Despite the urbanisation and high human population density, green fragments within the city still housed marmoset groups. However, the presence of green areas did not always indicate primate presence. Group presence was significantly related to the size of parks or green areas and negatively related to built-up areas, and human density. Salary levels were related to more forested streets and possibly tolerance. Marmosets were classified as urban utilisers. Conclusions The human–wildlife conflict with marmoset species was relatively low, owing to marmoset avoidance of built-up areas. The interaction of marmoset species and city dwellers was mainly limited to borders of forest fragments and inside city parks, and appeared to be human motivated. Implications This study showed the importance of public involvement in wildlife studies in urban environments; clarifying the interaction between city dwellers and wild species is essential to mitigate negative interactions

Trabalho educativo do enfermeiro na Estratégia Saúde da Família: dificuldades e perspectivas de mudanças

Este estudo objetivou conhecer as dificuldades e perspectivas de mudanças que os enfermeiros identificam no desenvolvimento das ações educativas na Estratégia Saúde da Família (ESF). Trata-se de uma pesquisa qualitativa descritivo-exploratória. Os dados foram coletados junto a 20 enfermeiros que atuam na ESF, no âmbito da 10ª Regional de Saúde do Paraná, por meio de entrevistas semiestruturadas, no mês de abril de 2010, as quais foram submetidas à análise de conteúdo. Os resultados demonstraram que os enfermeiros enfrentam dificuldades no desenvolvimento da educação em saúde junto aos usuários, à equipe, aos gestores e quanto à falta de recursos físicos, materiais e financeiros. Mas, a partir das dificuldades sentidas, buscam alternativas diversificadas para superá-las e sugerem modificações visando à melhoria na atenção primária à saúde da população, principalmente, no que tange ao trabalho educativo

Impact of rare variants in ARHGAP29 to the etiology of oral clefts: role of loss-of-function vs missense variants

Non-syndromic cleft lip with or without cleft palate (NSCL/P) is a prevalent, complex congenital malformation. Genome-wide association studies (GWAS) on NSCL/P have consistently identified association for the 1p22 region, in which ARHGAP29 has emerged as the main candidate gene. ARHGAP29 re-sequencing studies in NSCL/P patients have identified rare variants; however, their clinical impact is still unclear. In this study we identified 10 rare variants in ARHGAP29, including five missense, one in-frame deletion, and four loss-of-function (LoF) variants, in a cohort of 188 familial NSCL/P cases. A significant mutational burden was found for LoF (Sequence Kernel Association Test, p = 0.0005) but not for missense variants in ARHGAP29, suggesting that only LoF variants contribute to the etiology of NSCL/P. Penetrance was estimated as 59%, indicating that heterozygous LoF variants in ARHGAP29 confer a moderate risk to NSCL/P. The GWAS hits in IRF6 (rs642961) and 1p22 (rs560426 and rs4147811) do not seem to contribute to the penetrance of the phenotype, based on co-segregation analysis. Our data show that rare variants leading to haploinsufficiency of ARHGAP29 represent an important etiological clefting mechanism, and genetic testing for this gene might be taken into consideration in genetic counseling of familial cases

Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli

Background: Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.  Methodology/Principal Findings: The T. rangeli haploid genome is ,24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heatshock proteins.  Conclusions/Significance: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets

IL6 and CRP haplotypes are associated with COPD risk and systemic inflammation: a case-control study

<p>Abstract</p> <p>Background</p> <p>Elevated circulating levels of C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen (FG) have been repeatedly associated with many adverse outcomes in patients with chronic obstructive pulmonary disease (COPD). To date, it remains unclear whether and to what extent systemic inflammation is primary or secondary in the pathogenesis of COPD.</p> <p>The aim of this study was to examine the association between haplotypes of <it>CRP</it>, <it>IL6 </it>and <it>FGB </it>genes, systemic inflammation, COPD risk and COPD-related phenotypes (respiratory impairment, exercise capacity and body composition).</p> <p>Methods</p> <p>Eighteen SNPs in three genes, representing optimal haplotype-tagging sets, were genotyped in 355 COPD patients and 195 healthy smokers. Plasma levels of CRP, IL-6 and FG were measured in the total study group. Differences in haplotype distributions were tested using the global and haplotype-specific statistics.</p> <p>Results</p> <p>Raised plasma levels of CRP, IL-6 and fibrinogen were demonstrated in COPD patients. However, COPD population was very heterogeneous: about 40% of patients had no evidence of systemic inflammation (CRP < 3 mg/uL or no inflammatory markers in their top quartile). Global test for haplotype effect indicated association of <it>CRP </it>gene and CRP plasma levels (P = 0.0004) and <it>IL6 </it>gene and COPD (P = 0.003). Subsequent analysis has shown that <it>IL6 </it>haplotype H2, associated with an increased COPD risk (p = 0.004, OR = 4.82; 1.64 to 4.18), was also associated with very low CRP levels (p = 0.0005). None of the genes were associated with COPD-related phenotypes.</p> <p>Conclusion</p> <p>Our findings suggest that common genetic variation in <it>CRP </it>and <it>IL6 </it>genes may contribute to heterogeneity of COPD population associated with systemic inflammation.</p