Consequências fisiológicas da dessecação em sementes de açaí (Euterpe oleracea Mart.).

O presente trabalho foi realizado com o objetivo de verificar os efeitos imediatos da desidratação sobre a qualidade fisiológica de sementes de açaí. Anteriormente à secagem das sementes da cultivar BRS Pará foi determinado o teor de água das mesmas e selecionado o lote daquelas que apresentavam o maior teor de água, que foi de 43,4%. As sementes foram submetidas à secagem, em equipamento com circulação forçada de ar (30±2ºC), até atingirem o teor de água de 37,4%, 30,3% 26,1%, 21,0%, 15,% e 11,9%, constituindo os demais tratamentos. O efeito da secagem sobre a qualidade das sementes foi avaliado por meio das determinações de germinação, tempo médio de germinação, velocidade de emergência, comprimento e massa da matéria seca de plântulas. A secagem até 37,4% de água não produz efeitos fisiológicos prejudiciais imediatos sobre as sementes de açaí, contudo, abaixo de 30,3% há redução progressiva da germinação e do vigor das sementes e ao atingirem 15,1% de teor de água, o desempenho fisiológico é anulado.Título em inglês: Physiological consequences of desiccation in Euterpe oleracea Mart. seeds. Disponível também on-line

Conservação de sementes de açaí (Euterpe oleracea Mart.).

Sementes de Euterpe oleracea são consideradas recalcitrantes e demandam ampliação do conhecimento sobre os fatores que interferem na sua conservação. Diante disso, o presente trabalho foi realizado com o objetivo de verificar os efeitos do teor de água da semente e da temperatura do ambiente na manutenção da qualidade das mesmas. Sementes da cultivar BRS Pará, com diferentes teores de água (43,4; 37,4; 30,3; 26,1; 21,0; 15,1 e 11,9%) e acondicionadas em sacos de polietileno foram armazenadas sob temperaturas de 20, 15 e 10 ºC durante 360 dias e submetidas a avaliações periódicas do teor de água, da germinação e do vigor. A secagem parcial até 37,4% de água não produz efeitos imediatos sobre a germinação e o vigor das sementes, a partir daí a secagem favorece, progressivamente, a deterioração das sementes e, ao atingirem 15,1% as sementes não germinam. Após o armazenamento, sementes com 21,0% de água ou menos não germinam independentemente da temperatura. A associação de 43,4% de água na semente e o armazenamento em ambiente a 20 ºC favorece a conservação das sementes por até 270 dias

Techonolgy of Qualea grandiflora Mart. (Vochysiaceae) seeds

Qualea grandiflora Mart. (Vochysiaceae), commonly known as "pau-terra", is an arborous species native to the Brazilian savannah which possess commercial interests, as it can be used either as an ornamental or as a medicinal plant. "Pau-terra" can also be used in the heterogeneous reforestation of areas which are destined for restoration of permanent preservation degraded areas. Propagation studies with this species are scarce, being necessary then further clarification regarding the factors that influences the germination process. In this context, the objective of this work was to evaluate the influence of different temperatures, substrates and light conditions on seed germination. We selected light brown seeds which were subjected to different interactions between temperatures (15-25, 20-30, 25 and 30°C), substrate (paper, sand and vermiculite) and light (light and dark). All seeds were later dry-incubated at 32°C for 3, 6 and 12 hours. After treatments, seeds were kept in BOD at 58% RH and the following parameters were calculated: germination (%G) and germination speed index (GSI); the formation of normal and abnormal seedlings and the number dead seeds. Interaction was observed for all variables. In the optimum temperature range, the seeds behaved as photoblastic neutral or indifferent. Under alternating temperatures, darkness enhanced the germination, especially when combined with the lower temperatures. We noted that the sowing in sand, at 25°C, allowed the maintenance of suitable combinations of germination and seedling development. With respect to desiccation tolerance, "pau-terra" seeds presented an orthodox behavior, with a linear increase of the vigor as function of drying

Functional Comparison of Innate Immune Signaling Pathways in Primates

Humans respond differently than other primates to a large number of infections. Differences in susceptibility to infectious agents between humans and other primates are probably due to inter-species differences in immune response to infection. Consistent with that notion, genes involved in immunity-related processes are strongly enriched among recent targets of positive selection in primates, suggesting that immune responses evolve rapidly, yet providing only indirect evidence for possible inter-species functional differences. To directly compare immune responses among primates, we stimulated primary monocytes from humans, chimpanzees, and rhesus macaques with lipopolysaccharide (LPS) and studied the ensuing time-course regulatory responses. We find that, while the universal Toll-like receptor response is mostly conserved across primates, the regulatory response associated with viral infections is often lineage-specific, probably reflecting rapid host–virus mutual adaptation cycles. Additionally, human-specific immune responses are enriched for genes involved in apoptosis, as well as for genes associated with cancer and with susceptibility to infectious diseases or immune-related disorders. Finally, we find that chimpanzee-specific immune signaling pathways are enriched for HIV–interacting genes. Put together, our observations lend strong support to the notion that lineage-specific immune responses may help explain known inter-species differences in susceptibility to infectious diseases

A genome-wide association study identifies new susceptibility loci for esophageal adenocarcinoma and Barrett's esophagus.

Esophageal adenocarcinoma is a cancer with rising incidence and poor survival. Most such cancers arise in a specialized intestinal metaplastic epithelium, which is diagnostic of Barrett's esophagus. In a genome-wide association study, we compared esophageal adenocarcinoma cases (n = 2,390) and individuals with precancerous Barrett's esophagus (n = 3,175) with 10,120 controls in 2 phases. For the combined case group, we identified three new associations. The first is at 19p13 (rs10419226: P = 3.6 × 10(-10)) in CRTC1 (encoding CREB-regulated transcription coactivator), whose aberrant activation has been associated with oncogenic activity. A second is at 9q22 (rs11789015: P = 1.0 × 10(-9)) in BARX1, which encodes a transcription factor important in esophageal specification. A third is at 3p14 (rs2687201: P = 5.5 × 10(-9)) near the transcription factor FOXP1, which regulates esophageal development. We also refine a previously reported association with Barrett's esophagus near the putative tumor suppressor gene FOXF1 at 16q24 and extend our findings to now include esophageal adenocarcinoma

Role of CCL3L1-CCR5 Genotypes in the Epidemic Spread of HIV-1 and Evaluation of Vaccine Efficacy

Polymorphisms in CCR5, the major coreceptor for HIV, and CCL3L1, a potent CCR5 ligand and HIV-suppressive chemokine, are determinants of HIV-AIDS susceptibility. Here, we mathematically modeled the potential impact of these genetic factors on the epidemic spread of HIV, as well as on its prevention.Ro, the basic reproductive number, is a fundamental concept in explaining the emergence and persistence of epidemics. By modeling sexual transmission among HIV+/HIV- partner pairs, we find that Ro estimates, and concordantly, the temporal and spatial patterns of HIV outgrowth are highly dependent on the infecting partners' CCL3L1-CCR5 genotype. Ro was least and highest when the infected partner possessed protective and detrimental CCL3L1-CCR5 genotypes, respectively. The modeling data indicate that in populations such as Pygmies with a high CCL3L1 gene dose and protective CCR5 genotypes, the spread of HIV might be minimal. Additionally, Pc, the critical vaccination proportion, an estimate of the fraction of the population that must be vaccinated successfully to eradicate an epidemic was <1 only when the infected partner had a protective CCL3L1-CCR5 genotype. Since in practice Pc cannot be >1, to prevent epidemic spread, population groups defined by specific CCL3L1-CCR5 genotypes might require repeated vaccination, or as our models suggest, a vaccine with an efficacy of >70%. Further, failure to account for CCL3L1-CCR5-based genetic risk might confound estimates of vaccine efficacy. For example, in a modeled trial of 500 subjects, misallocation of CCL3L1-CCR5 genotype of only 25 (5%) subjects between placebo and vaccine arms results in a relative error of approximately 12% from the true vaccine efficacy.CCL3L1-CCR5 genotypes may impact on the dynamics of the HIV epidemic and, consequently, the observed heterogeneous global distribution of HIV infection. As Ro is lowest when the infecting partner has beneficial CCL3L1-CCR5 genotypes, we infer that therapeutic vaccines directed towards reducing the infectivity of the host may play a role in halting epidemic spread. Further, CCL3L1-CCR5 genotype may provide critical guidance for optimizing the design and evaluation of HIV-1 vaccine trials and prevention programs

Overexpression of the Cytokine BAFF and Autoimmunity Risk

$\textbf{BACKGROUND}$: Genomewide association studies of autoimmune diseases have mapped hundreds of susceptibility regions in the genome. However, only for a few association signals has the causal gene been identified, and for even fewer have the causal variant and underlying mechanism been defined. Coincident associations of DNA variants affecting both the risk of autoimmune disease and quantitative immune variables provide an informative route to explore disease mechanisms and drug-targetable pathways. $\textbf{METHODS}$: Using case-control samples from Sardinia, Italy, we performed a genomewide association study in multiple sclerosis followed by TNFSF13B locus-specific association testing in systemic lupus erythematosus (SLE). Extensive phenotyping of quantitative immune variables, sequence-based fine mapping, cross-population and cross-phenotype analyses, and gene-expression studies were used to identify the causal variant and elucidate its mechanism of action. Signatures of positive selection were also investigated. $\textbf{RESULTS}$: A variant in TNFSF13B, encoding the cytokine and drug target B-cell activating factor (BAFF), was associated with multiple sclerosis as well as SLE. The disease-risk allele was also associated with up-regulated humoral immunity through increased levels of soluble BAFF, B lymphocytes, and immunoglobulins. The causal variant was identified: an insertion-deletion variant, GCTGT→A (in which A is the risk allele), yielded a shorter transcript that escaped microRNA inhibition and increased production of soluble BAFF, which in turn up-regulated humoral immunity. Population genetic signatures indicated that this autoimmunity variant has been evolutionarily advantageous, most likely by augmenting resistance to malaria. $\textbf{CONCLUSIONS}$: A TNFSF13B variant was associated with multiple sclerosis and SLE, and its effects were clarified at the population, cellular, and molecular levels. (Funded by the Italian Foundation for Multiple Sclerosis and others.).Supported by grants (2011/R/13 and 2015/R/09, to Dr. Cucca) from the Italian Foundation for Multiple Sclerosis; contracts (N01-AG-1-2109 and HHSN271201100005C, to Dr. Cucca) from the Intramural Research Program of the National Institute on Aging, National Institutes of Health (NIH); a grant (FaReBio2011 “Farmaci e Reti Biotecnologiche di Qualità,” to Dr. Cucca) from the Italian Ministry of Economy and Finance; a grant (633964, to Dr. Cucca) from the Horizon 2020 Research and Innovation Program of the European Union; a grant (U1301.2015/AI.1157.BE Prat. 2015-1651, to Dr. Cucca) from Fondazione di Sardegna; grants (“Centro per la ricerca di nuovi farmaci per malattie rare, trascurate e della povertà” and “Progetto collezione di composti chimici ed attività di screening,” to Dr. Cucca) from Ministero dell’Istruzione, dell’Università e della Ricerca; grants (HG005581, HG005552, HG006513, and HG007022, to Dr. Abecasis) from the National Human Genome Research Institute; a grant (9-2011-253, to Dr. Todd) from JDRF; a grant (091157, to Dr. Todd) from the Wellcome Trust; a grant (to Dr. Todd) from the National Institute for Health Research (NIHR); and the NIHR Cambridge Biomedical Research Centre. Dr. Idda was a recipient of a Master and Back fellowship from the Autonomous Region of Sardinia