TRY plant trait database - enhanced coverage and open access

Plant traits-the morphological, anatomical, physiological, biochemical and phenological characteristics of plants-determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait-based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits-almost complete coverage for 'plant growth form'. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait-environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Stress-Induced Reinstatement of Drug Seeking: 20 Years of Progress

In human addicts, drug relapse and craving are often provoked by stress. Since 1995, this clinical scenario has been studied using a rat model of stress-induced reinstatement of drug seeking. Here, we first discuss the generality of stress-induced reinstatement to different drugs of abuse, different stressors, and different behavioral procedures. We also discuss neuropharmacological mechanisms, and brain areas and circuits controlling stress-induced reinstatement of drug seeking. We conclude by discussing results from translational human laboratory studies and clinical trials that were inspired by results from rat studies on stress-induced reinstatement. Our main conclusions are (1) The phenomenon of stress-induced reinstatement, first shown with an intermittent footshock stressor in rats trained to self-administer heroin, generalizes to other abused drugs, including cocaine, methamphetamine, nicotine, and alcohol, and is also observed in the conditioned place preference model in rats and mice. This phenomenon, however, is stressor specific and not all stressors induce reinstatement of drug seeking. (2) Neuropharmacological studies indicate the involvement of corticotropin-releasing factor (CRF), noradrenaline, dopamine, glutamate, kappa/dynorphin, and several other peptide and neurotransmitter systems in stress-induced reinstatement. Neuropharmacology and circuitry studies indicate the involvement of CRF and noradrenaline transmission in bed nucleus of stria terminalis and central amygdala, and dopamine, CRF, kappa/dynorphin, and glutamate transmission in other components of the mesocorticolimbic dopamine system (ventral tegmental area, medial prefrontal cortex, orbitofrontal cortex, and nucleus accumbens). (3) Translational human laboratory studies and a recent clinical trial study show the efficacy of alpha-2 adrenoceptor agonists in decreasing stress-induced drug craving and stress-induced initial heroin lapse

Social factors related to the clinical severity of influenza cases in Spain during the A(H1N1)2009 virus pandemic

Background During the 2009 influenza pandemic, a change in the type of patients most often affected by influenza was observed. The objective of this study was to assess the role of individual and social determinants in hospitalizations due to influenza A (H1N1) 2009 infection. Methods We studied hospitalized patients (cases) and outpatients (controls) with confirmed influenza A (H1N1) 2009 infection. A standardized questionnaire was used to collect data. Variables that might be related to the hospitalization of influenza cases were compared by estimation of the odds ratio (OR) and 95% confidence intervals (CI) and the variables entered into binomial logistic regression models. Results Hospitalization due to pandemic A (H1N1) 2009 influenza virus infections was associated with non-Caucasian ethnicity (OR: 2.18, 95% CI 1.17 − 4.08), overcrowding (OR: 2.84, 95% CI 1.20 − 6.72), comorbidity and the lack of previous preventive information (OR: 2.69, 95% CI: 1.50 − 4.83). Secondary or higher education was associated with a lower risk of hospitalization (OR 0.56, 95% CI: 0.36 − 0.87) Conclusions In addition to individual factors such as comorbidity, other factors such as educational level, ethnicity or overcrowding were associated with hospitalization due to A (H1N1) 2009 influenza virus infections

Genome-wide analysis of differential transcriptional and epigenetic variability across human immune cell types

Abstract Background A healthy immune system requires immune cells that adapt rapidly to environmental challenges. This phenotypic plasticity can be mediated by transcriptional and epigenetic variability. Results We apply a novel analytical approach to measure and compare transcriptional and epigenetic variability genome-wide across CD14+CD16− monocytes, CD66b+CD16+ neutrophils, and CD4+CD45RA+ naïve T cells from the same 125 healthy individuals. We discover substantially increased variability in neutrophils compared to monocytes and T cells. In neutrophils, genes with hypervariable expression are found to be implicated in key immune pathways and are associated with cellular properties and environmental exposure. We also observe increased sex-specific gene expression differences in neutrophils. Neutrophil-specific DNA methylation hypervariable sites are enriched at dynamic chromatin regions and active enhancers. Conclusions Our data highlight the importance of transcriptional and epigenetic variability for the key role of neutrophils as the first responders to inflammatory stimuli. We provide a resource to enable further functional studies into the plasticity of immune cells, which can be accessed from: http://blueprint-dev.bioinfo.cnio.es/WP10/hypervariability

Extensive and coordinated transcription of noncoding RNAs within cell-cycle promoters

Transcription of long noncoding RNAs (lncRNAs) within gene regulatory elements can modulate gene activity in response to external stimuli, but the scope and functions of such activity are not known. Here we use an ultrahigh-density array that tiles the promoters of 56 cell-cycle genes to interrogate 108 samples representing diverse perturbations. We identify 216 transcribed regions that encode putative lncRNAs, many with RT-PCR–validated periodic expression during the cell cycle, show altered expression in human cancers and are regulated in expression by specific oncogenic stimuli, stem cell differentiation or DNA damage. DNA damage induces five lncRNAs from the CDKN1A promoter, and one such lncRNA, named PANDA, is induced in a p53-dependent manner. PANDA interacts with the transcription factor NF-YA to limit expression of pro-apoptotic genes; PANDA depletion markedly sensitized human fibroblasts to apoptosis by doxorubicin. These findings suggest potentially widespread roles for promoter lncRNAs in cell-growth control.National Institutes of Health (U.S.)National Institute of Arthritis and Musculoskeletal and Skin Diseases (U.S.) (NIAMS) (K08-AR054615))National Cancer Institute (U.S.) (NIH/(NCI) (R01-CA118750))National Cancer Institute (U.S.) (NIH/(NCI) R01-CA130795))Juvenile Diabetes Research Foundation InternationalAmerican Cancer SocietyHoward Hughes Medical Institute (Early career scientist)Stanford University (Graduate Fellowship)National Science Foundation (U.S.) (Graduate Research Fellowship)United States. Dept. of Defense (National Defense Science and Engineering Graduate Fellowship

Teste de Morisky-Green e Brief Medication Questionnaire para avaliar adesão a medicamentos

OBJETIVO: Analisar a confiabilidade e o desempenho da versão em português de instrumentos de avaliação da adesão ao tratamento anti-hipertensivo. MÉTODOS: Pacientes hipertensos atendidos de janeiro a setembro de 2010 em uma unidade de atenção primária em Porto Alegre, RS, foram selecionados aleatoriamente (n = 206). Na avaliação da adesão foram utilizadas versões em português do Teste de Morisky-Green (TMG) e do Brief Medication Questionnaire (BMQ). Foram analisados consistência interna, estabilidade temporal e desempenho com relação a três padrões-ouro: controle inadequado da pressão arterial (&gt; 140/90 mmHg); taxa insuficiente de retirada de medicação na farmácia da Unidade Básica de Saúde (< 80%); e a combinação de ambos. RESULTADOS: Dos pacientes avaliados, 97 utilizavam medicamentos dispensados somente pela farmácia da Unidade Básica de Saúde. Os testes apresentaram boa consistência interna: BMQ &#945; de Cronbach de 0,66 (IC95% 0,60;0,73) e o TMG 0,73 (IC95% 0,67;0,79). O desempenho do BMQ no domínio regime apresentou sensibilidade de 77%, especificidade de 58% e área sob a curva ROC de 0,70 (IC95% 0,55;0,86), e o TMG sensibilidade de 61%, especificidade de 36% e área sob a curva ROC de 0,46 (IC95% 0,30;0,62). A correlação entre o BMQ e o TMG foi de r = 0,28, p &gt; 0,001. A baixa adesão ao BMQ está associada a maiores níveis tensionais quando comparada com pacientes aderentes (148,4 [dp 20,1] vs 128,8 [dp 17,8], p < 0,001), mas não para o TMG. CONCLUSÕES: O BMQ apresentou melhor desempenho que o TMG, com maiores sensibilidade e especificidade. A avaliação da adesão pode auxiliar o clinico na discriminação entre uso inadequado da medicação e esquema terapêutico insuficiente.OBJETIVO: Analizar la confiabilidad y el desempeño de la versión en portugués de instrumentos de evaluación de la adherencia al tratamiento antihipertensivo. MÉTODOS: Pacientes hipertensos atendidos de enero a septiembre de 2010 en una unidad de atención primaria en Porto Alegre, Sur de Brasil, fueron seleccionados aleatoriamente (n=206). En la evaluación de la adherencia fueron utilizadas versiones en portugués de la Prueba de Morisky-Green (TMG) y del Brief Medication Questionnarie (BMQ). Se analizaron consistencia interna, estabilidad temporal y desempeño con relación a tres patrones-oro: control inadecuado de la presión arterial (&gt; 140/90 mmHg); tasa insuficiente de retirada de medicación en la farmacia de la Unidad Básica de Salud (< 80%) y la combinación de ambos. RESULTADOS: De los pacientes evaluados, 97 utilizaban medicamentos dispensados solamente por la farmacia de la Unidad Básica de Salud. Las pruebas presentaron buena consistencia interna: BMQ &#945; de Cronbach de 0,66 (IC95% 0,60;0,73) y el TMG 0,73 (IC95% 0,67;0,79). El desempeño del BMQ en el dominio régimen presentó sensibilidad de 77%, especificidad de 58%, y área bajo la curva ROC de 0,70 (IC95% 0,55;0,86) y el TMG sensibilidad de 61%, especificidad de 36% y área bajo la curva ROC de 0,46 (IC95% 0,30;0,62). La correlación entre el BMQ y el TMG fue de r=0,28, p&gt;0,001. La baja adherencia al BMQ está asociada a mayores niveles tensionales al compararlo con pacientes adherentes 148,4 [de 0,1] vs 128,8 [de 17,8], pOBJECTIVE: To analyze the reliability and performance of the Portuguese version of questionnaires used to evaluate adherence to hypertensive treatment. METHODS: Hypertensive patients attending a primary healthcare unit in Porto Alegre, Southern Brazil, from January to September 2010, were randomly selected (n = 206). To evaluate adherence, Portuguese versions of the Morisky-Green test (MGT) and the Brief Medication Questionnaire (BMQ) were used. The analysis considered internal consistency, temporal stability and performance compared to three gold standards, which are: inadequate control of blood pressure (BP &gt; 140/90 mmHg); insufficient rate of medication acquisition at the institution's pharmacy

Reactive Oxygen Species Production and Mitochondrial Dysfunction Contribute to Quercetin Induced Death in Leishmania amazonensis

BACKGROUND: Leishmaniasis, a parasitic disease caused by protozoa of the genus Leishmania, affects more than 12 million people worldwide. Quercetin has generated considerable interest as a pharmaceutical compound with a wide range of therapeutic activities. One such activity is exhibited against the bloodstream parasite Trypanosoma brucei and amastigotes of Leishmania donovani. However, the mechanism of protozoan action of quercetin has not been studied. METHODOLOGY/PRINCIPAL FINDINGS: In the present study, we report here the mechanism for the antileishmanial activity of quercetin against Leishmania amazonensis promastigotes. Quercetin inhibited L. amazonensis promastigote growth in a dose- and time- dependent manner beginning at 48 hours of treatment and with maximum growth inhibition observed at 96 hours. The IC(50) for quercetin at 48 hours was 31.4 µM. Quercetin increased ROS generation in a dose-dependent manner after 48 hours of treatment. The antioxidant GSH and NAC each significantly reduced quercetin-induced cell death. In addition, quercetin caused mitochondrial dysfunction due to collapse of mitochondrial membrane potential. CONCLUSIONS/SIGNIFICANCE: The effects of several drugs that interfere directly with mitochondrial physiology in parasites such as Leishmania have been described. The unique mitochondrial features of Leishmania make this organelle an ideal drug target while minimizing toxicity. Quercetin has been described as a pro-oxidant, generating ROS which are responsible for cell death in some cancer cells. Mitochondrial membrane potential loss can be brought about by ROS added directly in vitro or induced by chemical agents. Taken together, our results demonstrate that quercetin eventually exerts its antileishmanial effect on L. amazonensis promastigotes due to the generation of ROS and disrupted parasite mitochondrial function

Epidemiology of Concomitant Infection Due to Loa loa and Mansonella perstans in Gabon

Loa loa and Mansonella perstans are blood filarial parasites, endemic in the central and western African forest block, and transmitted by chrysops and culicoides flies, respectively. Loa loa is pathogenic and represents a major obstacle to the control of co-endemic filariae. Treatment of individuals with >8000 Loa loa microfilariae/ml can result in severe adverse reactions. M. perstans is prevalent in the tropics, with undefined clinical symptoms. We screened 4392 individuals for these infections in 212 Gabonese villages. The overall prevalence rates were 22.4% for Loa loa microfilariae, 10.2% for M. perstans, and 3.2% for mixed infection. These rates varied across the different ecosystems: forest, savannah, Lakeland, river (Ogouée), and equator. A correlation was found between the prevalence and intensity of microfilariae, while a negative relationship was found between clinical symptoms (pruritis, Calabar swelling) and the prevalence of Loa loa microfilaremia. This study confirms the spatial uniformity of the relationship between parasitological indices, and provides a map and baseline data for implementation of mass chemotherapy for these infections

RNA-interference in rice against Rice tungro bacilliform virus results in its decreased accumulation in inoculated rice plants

Rice tungro is a viral disease seriously affecting rice production in South and Southeast Asia. Tungro is caused by the simultaneous infection in rice of Rice tungro bacilliform virus (RTBV), a double-stranded DNA virus and Rice tungro spherical virus (RTSV), a single-stranded RNA virus. To apply the concept of RNA-interference (RNAi) for the control of RTBV infection, transgenic rice plants expressing DNA encoding ORF IV of RTBV, both in sense as well as in anti-sense orientation, resulting in the formation of double-stranded (ds) RNA, were raised. RNA blot analysis of two representative lines indicated specific degradation of the transgene transcripts and the accumulation of small molecular weight RNA, a hallmark for RNA-interference. In the two transgenic lines expressing ds-RNA, different resistance responses were observed against RTBV. In one of the above lines (RTBV-O-Ds1), there was an initial rapid buildup of RTBV levels following inoculation, comparable to that of untransformed controls, followed by a sharp reduction, resulting in approximately 50-fold lower viral titers, whereas the untransformed controls maintained high levels of the virus till 40 days post-inoculation (dpi). In RTBV-O-Ds2, RTBV DNA levels gradually rose from an initial low to almost 60% levels of the control by 40 dpi. Line RTBV-O-Ds1 showed symptoms of tungro similar to the untransformed control lines, whereas line RTBV-O-Ds2 showed extremely mild symptoms