ATLANTIC EPIPHYTES: a data set of vascular and non-vascular epiphyte plants and lichens from the Atlantic Forest

Epiphytes are hyper-diverse and one of the frequently undervalued life forms in plant surveys and biodiversity inventories. Epiphytes of the Atlantic Forest, one of the most endangered ecosystems in the world, have high endemism and radiated recently in the Pliocene. We aimed to (1) compile an extensive Atlantic Forest data set on vascular, non-vascular plants (including hemiepiphytes), and lichen epiphyte species occurrence and abundance; (2) describe the epiphyte distribution in the Atlantic Forest, in order to indicate future sampling efforts. Our work presents the first epiphyte data set with information on abundance and occurrence of epiphyte phorophyte species. All data compiled here come from three main sources provided by the authors: published sources (comprising peer-reviewed articles, books, and theses), unpublished data, and herbarium data. We compiled a data set composed of 2,095 species, from 89,270 holo/hemiepiphyte records, in the Atlantic Forest of Brazil, Argentina, Paraguay, and Uruguay, recorded from 1824 to early 2018. Most of the records were from qualitative data (occurrence only, 88%), well distributed throughout the Atlantic Forest. For quantitative records, the most common sampling method was individual trees (71%), followed by plot sampling (19%), and transect sampling (10%). Angiosperms (81%) were the most frequently registered group, and Bromeliaceae and Orchidaceae were the families with the greatest number of records (27,272 and 21,945, respectively). Ferns and Lycophytes presented fewer records than Angiosperms, and Polypodiaceae were the most recorded family, and more concentrated in the Southern and Southeastern regions. Data on non-vascular plants and lichens were scarce, with a few disjunct records concentrated in the Northeastern region of the Atlantic Forest. For all non-vascular plant records, Lejeuneaceae, a family of liverworts, was the most recorded family. We hope that our effort to organize scattered epiphyte data help advance the knowledge of epiphyte ecology, as well as our understanding of macroecological and biogeographical patterns in the Atlantic Forest. No copyright restrictions are associated with the data set. Please cite this Ecology Data Paper if the data are used in publication and teaching events. © 2019 The Authors. Ecology © 2019 The Ecological Society of Americ

An Exploration Into Wastewater Surveillance Of Dengue Virus To Detect Outbreaks In A Community

INTRODUCTION: In the Americas, dengue disease which is associated with the Dengue virus has the highest incidence of all mosquito-borne viruses with cyclic epidemics every 3 to 5 years. It is estimated that the number of dengue cases is underreported globally as most cases of infection are asymptomatic, affecting both clinical surveillance and timeliness (Angelo et al., 2020). Wastewater-based epidemiology has recently gained much attention and has the potential to provide a snapshot view of community health (Irene Xagoraraki, 2019). Research into the feasibility of wastewater monitoring for the detection of viral outbreaks has been emerging. Detection of non-waterborne viruses including arboviruses Zika, West Nile virus, Dengue virus, and yellow fever virus in urine samples which suggests the concept of wastewater-based epidemiology could be used in the future (Irene Xagoraraki, 2019). AIM: In the current study, we investigate the concentration and presence of dengue virus nucleic acid in various fluids of infected patients. The hope is to further contribute to the growing data on the feasibility of the use of WBE to monitor DENV infections as a tool for community-level public health surveillance. METHODS: De-identified secondary data was obtained from a community-based enhanced surveillance study in Pau da Lima community, Salvador, Brazil and included the results of analysis of serum, oral fluid, and urine. Literature review and evidence gap mapping was completed to inform on existing research and gaps in knowledge. RESULTS: A total of 96 participants were confirmed positive for dengue virus in laboratory testing. Of these, 53 (55%) were positive in acute-phase serum, 5 (5%) in acute-phase urine, 2 (3.5%) in convalescent-phase urine, and 1 (2%) in acute-phase oral fluid. There were no observed statistically significant associations between demographic and clinical manifestations and positive nucleic test detection of dengue virus RNA in acute-phase urine. DISCUSSION: Testing of acute- and convalescent-phase urine resulted in an overall 7% positivity across all confirmed positive patients via serum. Higher frequencies of detection in urine were seen during the acute-phase (days 0-7 days) than in the convalescent-phase (days 10-40 days). Future research into detection rates and viral shedding in feces or the use other highly sensitive assays could provide valuable information for in the feasibility of wastewater surveillance

Endothelin A receptor inhibition increases nitric oxide-dependent vasodilation independent of superoxide in non-Hispanic Black young adults

Endothelin-1 A receptors (ETARs) have been shown to reduce endothelial function independently and through increased production of superoxide. We show that independent ETAR inhibition increases microvascular endothelial function in non-Hispanic Black young adults. However, administration of a superoxide dismutase mimetic alone and in combination with ETAR inhibition had no effect on microvascular endothelial function suggesting that, in the cutaneous microvasculature, the negative effects of ETAR in non-Hispanic Black young adults are independent of superoxide production. </jats:p

Prevalência da tuberculose no Maranhão

Objetivos: Descrever a prevalência de Tuberculose (TB) no Maranhão em relação à macrorregião Nordeste, observando a sua relevância dentre os estados, nos últimos 6 anos, assim como as variações das taxas de ocorrência. Metodologia: Trata-se de um estudo descritivo, analítico. Foram levantados os casos positivos para Tuberculose no Estado do Maranhão entre os anos 2009 e 2014. Os valores foram obtidos a partir dos dados disponibilizados pelo Ministério da Saúde e atualizados com o uso do Software BioEstat versão 5.3, com aplicação do Teste de G.Resultados: Dos resultados obtidos a partir dos registros da plataforma do MS, 115.334 ocorreram na região Nordeste do Brasil. Onde, 12.051 configuram os casos brutos de Tuberculose no Maranhão, com uma média anual de 2.008,5 casos.Foi constatada uma queda percentual de 18,38% nos índices de Tuberculose no estado, no período de 2009 – 2014.Conclusões: A diminuição dos casos de Tuberculose se deve aos programas de educação em saúde promovidos pelo Governo Federal em conjunto com as secretarias Estadual e Municipal de saúde do Estado do Maranhão, entre os anos de 2009/2014. Outrossim, uma melhor consciência populacional em relação ao agravo da doença e à manutenção do planejamento de tratamento, que é obrigatório em todo o território nacional.Palavras-chave: Tuberculose.Prevalência. Doença Transmissível.</jats:p

Presence of dengue virus RNA in urine and oral fluid of laboratory-confirmed dengue patients: Implications for wastewater surveillance

Introduction: Dengue cases in the Americas in 2024 have reached record highs, especially in Brazil. However, surveillance remains suboptimal and new methods are needed to monitor Dengue Virus (DENV) spread. To assess whether wastewater-based epidemiology would be a useful tool, we investigated the presence of DENV RNA in dengue patients’ urine and oral fluid from an endemic area to inform how shedding in these fluids occurs and provide insight for wastewater surveillance. Methods: We examined how often DENV RNA is detected in urine and oral fluid from dengue patients confirmed by serum RT-qPCR, NS1 ELISA or IgM seroconversion in Salvador, Brazil. Results: Of 88 confirmed cases, 9.1 % were positive for DENV RNA in urine (7/88) or oral fluid (1/88). Of 53 serum RT-qPCR-positive patients, 6 (11.3 %) showed detectable DENV RNA in acute- or convalescent-phase urine. Patients with RT-qPCR-positive urine had a lower frequency of DENV IgG in acute-phase serum (a proxy for secondary infection) (57 % vs. 74 %) and a lower median serum RT-qPCR cycle threshold than those with negative urine (21.8 vs. 23.9). Conclusion: The low presence of DENV RNA in urine suggests that additional research is needed to evaluate whether using wastewater-based epidemiology to monitor DENV transmission is possible

CREB3 gain of function variants protect against ALS

Abstract Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly evolving neurodegenerative disease that arises from the loss of glutamatergic corticospinal neurons (CSN) and cholinergic motoneurons (MN). The disease is mostly sporadic, but genetics is expected to highly contribute to disease onset and progression. Genome wide association studies identified a few genetic disease modifiers, mostly associated with a negative outcome, and demonstrated that ALS is primarily a disease of excitatory glutamatergic neurons. Here, we reasoned that at least a subpart of genetic disease modifiers may directly modulate the molecular pathways selectively activated in vulnerable neurons as the disease progresses, and concentrated on CSN for their selective vulnerability and glutamatergic identity. We implemented comparative cross-species transcriptomics using snRNAseq data from postmortem motor cortex of ALS patients and controls, and longitudinal RNAseq data from anatomically defined CSN purified from the Sod1 G86R mouse model of ALS. We report that disease vulnerable neuronal populations undergo ER stress and altered mRNA translation, and identify the transcription factor CREB3 and its regulatory network as a resilience marker of neuronal dysfunction in ALS. Using genetic and epidemiologic analyses we further identify the rare variant CREB3 R119G (rs11538707) as a new disease modifier in ALS. Through gain of function, CREB3 R119G decreases both the risk of developing ALS and the progression rate of ALS patients. This study reveals novel genetic variants that protect against ALS and highlights the benefice of combining transcriptomics and genetics to identify new disease modifiers and therapeutic targets

Toxic gain of function from mutant FUS protein is crucial to trigger cell autonomous motor neuron loss.

FUS is an RNA-binding protein involved in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS-containing aggregates are often associated with concomitant loss of nuclear FUS Whether loss of nuclear FUS function, gain of a cytoplasmic function, or a combination of both lead to neurodegeneration remains elusive. To address this question, we generated knockin mice expressing mislocalized cytoplasmic FUS and complete FUS knockout mice. Both mouse models display similar perinatal lethality with respiratory insufficiency, reduced body weight and length, and largely similar alterations in gene expression and mRNA splicing patterns, indicating that mislocalized FUS results in loss of its normal function. However, FUS knockin mice, but not FUS knockout mice, display reduced motor neuron numbers at birth, associated with enhanced motor neuron apoptosis, which can be rescued by cell-specific CRE-mediated expression of wild-type FUS within motor neurons. Together, our findings indicate that cytoplasmic FUS mislocalization not only leads to nuclear loss of function, but also triggers motor neuron death through a toxic gain of function within motor neurons

Toxic gain of function from mutant FUS protein is crucial to trigger cell autonomous motor neuron loss

International audienceFUS is an RNA-binding protein involved in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS-containing aggregates are often associated with concomitant loss of nuclear FUS Whether loss of nuclear FUS function, gain of a cytoplasmic function, or a combination of both lead to neurodegeneration remains elusive. To address this question, we generated knockin mice expressing mislocalized cytoplasmic FUS and complete FUS knockout mice. Both mouse models display similar perinatal lethality with respiratory insufficiency, reduced body weight and length, and largely similar alterations in gene expression and mRNA splicing patterns, indicating that mislocalized FUS results in loss of its normal function. However, FUS knockin mice, but not FUS knockout mice, display reduced motor neuron numbers at birth, associated with enhanced motor neuron apoptosis, which can be rescued by cell-specific CRE-mediated expression of wild-type FUS within motor neurons. Together, our findings indicate that cytoplasmic FUS mislocalization not only leads to nuclear loss of function, but also triggers motor neuron death through a toxic gain of function within motor neurons

Celecoxib pathways

Gong L, Thorn CF, Bertagnolli MM, Grosser T, Altman RB, Klein TE. Celecoxib pathways: pharmacokinetics and pharmacodynamics. Pharmacogenetics and Genomics. 2012;22(4):310-318