Month: February 2020

Legacy data from natural history collections contain invaluable information about biodiversity in the recent past, providing a baseline for detecting change and forecasting future trends. In the case of plants, specimens have accumulated for hundreds of years in herbaria, and these may be used as the basis for identifying threatened or declining species, guiding future research and monitoring programs, and establishing conservation priorities. For instance, the IUCN Sampled Red List Index for plants was driven in its first iteration almost solely by herbarium specimen data. Data from herbaria are particularly important in poorly MK-0683 explored regions of the tropics, where the lack of continuous field-based botanical research has emphasized the pivotal role of herbaria in documenting plant diversity and species distributions. The interest in herbaria for undertaking conservation biology research has thus grown in recent years, though less than about 2% of the herbarium specimens have been used to answer biogeographical or environmental questions. Establishing baselines is particularly important for those tropical tree species that are exploited commercially and have come under increasing pressure from the global timber trade. Overexploitation has resulted in declining populations of the most valuable timber species and it is one of the foremost causes for the loss and degradation of tropical forests, with utmost negative consequences for the conservation of biodiversity and ecosystem services. In recent decades, efforts have been made to increase the sustainability of tropical timber exploitation, through for instance the outright ban on or severe restrictions to the trade of endangered species, or the implementation of certification schemes for timber harvested sustainably. These approaches face several problems, however, including uncertainties related to the conservation status of many exploited species due to insufficient knowledge of their distribution, abundance and population trends. Although this type of information has become increasingly available for tropical forests of Central and South America and Asia, data are still very limited for most African forests. Considering that Africa still holds some of the most important tropical forests in the world and that these have been increasingly exploited, information on the conservation status of its timber species is urgently required. Angola is one of the African countries for which basic data on timber tree species are most severely lacking, though the country has a forested area of about 40–60 million hectares largely administered by the government. Deforestation rates in Angola are among the highest in Sub-Saharan Africa, which is likely a consequence of wood extraction for firewood and charcoal, slash-and-burn cultivation, urban expansion, and logging. Illegal logging of valuable timber is considered one of the potential causes of forest degradation, but there is no information on the extent of this problem.

There are also a large number of avenin DNA sequences in Genbank, but not formally reported or analyzed in the literature, that have originated from both a variety of A. sativa cultivars and from other SB203580 species of Avena. These latter sequences were generated via PCR and represent an unknown coverage of the total avenin family. A recent report states, without details in the analysis or giving sequences, that there were eleven different avenin sequences found within the ESTs of a single oat cultivar. For the oat globulins, there has as yet been no complete oat globulin sequence family. Missing for both the oat avenins and globulins is such a detailed and comprehensive description. Although the best method of identifying complete gene sets is using a high-quality complete genome sequence, no such resource is currently available for oats, nor is likely to be available for some time. As a substitute, if sufficient high-quality ESTs are available, sets of active gene coding region sequences can be assembled. It is also best to use ESTs from single germplasms to avoid the complications of sorting out allelic sequences and differing gene set compositions. In the current report, ESTs for the oat cultivar CDC Dancer are used to assemble a proposed complete set of active oat avenin and globulin seed protein gene coding and derived amino acid sequences. Nine unique sequences are identified for the avenins and 24 for the globulins. The sequences of both classes generally agree with previously reported sequences. In addition, novel classes are reported. The composition and structure of the sequence families are analyzed and discussed along with evolutionary aspects of the families, relative representation of sequences in the EST resource, and issues in nomenclature within the grass prolamins. Individual contigs were examined for potential chimeric ESTs causing a truncation in contig assembly. Suspected chimeras were checked by BLAST analysis and ESTs with 59 or 39 sequence not matching avenins were removed. In cases where most of the EST sequence was UTR, the remaining coding sequence was too short for reliable assembling and such ESTs were also removed. The remaining ESTs were reassembled and the resulting contigs were divided into classes according to having five or more ESTs or fewer than five. The former were assembled together to find overlapping sequences not initially joined by the software. The resulting contigs were individually assembled with ESTs from the contigs with fewer than five ESTs and those matching exactly were merged into the larger contigs. Finally, each larger contig was manually inspected for ESTs apparently not matching the contig. These were removed and compared to the other contig consensus sequences and merged if found a match otherwise were left as unassigned. To check if ESTs might have been assigned incorrectly, possibly due to sequence similarity among avenin gene family members, the ESTs assigned to each final contig were assembled with the other eight contigs consensus sequences.

BPA enhances fear memory and increases serotonin metabolites 5hydroxyindoleacetic acid levels and 5-HIAA/serotonin in the hippocampus, striatum and midbrain in juvenile female mice, and delays perinatal chloride shift by significantly decreasing potassium chloride co-transporter 2 mRNA expression in developing rat, mouse, and human cortical neurons. BPA also AbMole BioScience kinase inhibitors causes adverse effects on neuronal morphology and functions as to interrupting neuronal dendritic and synaptic development in cultures of fetal rat hypothalamus cells at 10 and 100 nM. BPA suppresses neurite extension by inhibiting phosphorylation of mitogen activated protein kinase in rat pheochromocytoma PC12 cells differentiated neuronal-like cells. Furthermore, perinatal exposure to BPA causes GABAergic disinhibition and dopaminergic enhancement that is related to abnormal cortical basolateral amygdala synaptic transmission and plasticity; this effect may be responsible for hyperactivity and attention deficit in BPA-rats. Microarray analysis is an effective way to explore possible mechanisms and has been used to study the molecular pathway of reproductive toxicity of BPA exposure in animal models. However, few studies evaluated childhood neuronal development in exposure to BPA with human data. In human samples, umbilical cord blood is a postpartum placental remnant containing fetal blood which can be used as a surrogate for childhood study. In this study, we used meta-analysis of publicly available microarray datasets to find the neuronal target genes in exposure to BPA, and explored whether trans-placental BPA exposure in mothers would alter gene expression on their progeny in human umbilical cord blood and the potential underlying mechanism from gene network analysis to childhood neuronal development. Although some studies have found that BPA affects growth and development of reproductive organ, potential adverse effects of BPA on childhood neuronal development are not fully understood yet. In this study, we identified Sox2 and Pax6 as neuronal development biomarkers whose gene expression was appeared in response to trans-placental BPA exposure. Such a biomarker holds promise in assessing BPA exposure and acts as a clinically relevant predictor for neurogenesis in children underlying maternal BPA exposure. In general, it’s hard to explore the health effect of prenatal exposure in human subjects. A biomarker is found from a costly method because of the need for several gene chips with sufficient amount of samples; childhood neuronal development research takes time to prospectively follow up a cohort which generates additional challenges. The method described in this study offered an alternative strategy to examine the molecular effect of prenatal BPA exposure on child development. Candidate biomarkers were surveyed from the use of microarray meta-analysis and the gene expression of biomarkers were investigated in human samples from fetal umbilical cord blood for potential impact research.

The edaravone concentrations used were in the millimolar range similarly to another independent work on cultured human brain R428 endothelial cells. For long-lasting protection suprapharmacological concentration of edaravone was needed in our culture study. However, the applied methylglyoxal levels were also comparably high, as in other in vitro methylglyoxal studies. Although we use higher concentrations in cultured cells, importantly, the ratio of the methylglyoxal to edaravone used in our study is the same as the ratio of the pathological plasma methylglyoxal concentrations to clinical concentrations of edaravone. Originally, edaravone has been described as a drug to treat ischemic stroke by protecting against oxidative stress. Its antioxidant effect was observed in our experiment, too. In a recent independent study edaravone suppressed methyglyoxal-induced ROS production in human brain endothelial cells by two possible mechanisms. Pre-treatment with edaravone decreased methylglyoxal-induced AGE accumulation and activation of its receptor RAGE, and the subsequent production of ROS. Furthermore, edaravone inhibited protein-glycation by methylglyoxal in a cell free system, therefore, it decreased ROS generated as by-products during protein glycation. All these results together indicate that the antioxidant mechanisms induced by edaravone contribute to its protective effect against methylglyoxal-induced oxidative stress. However, it remained unanswered whether edaravone can also protect against methylglyoxal-induced barrier dysfunction in brain endothelial monolayers. Therefore, this study focused on the protective effect of edaravone against methylglyoxal-induced barrier damage. We found that co-treatment with edaravone restored barrier properties of endothelial cells and protected against methylglyoxalinduced decrease of resistance and increase in permeability for paracellular and transcellular markers. Moreover, we also demonstrated that edaravone treatment alone tightened the brain endothelial barrier. Our data expand and further support previous observations on barrier enhancing effect of edaravone. Increased endothelial permeability was coupled with disturbed localization of junctional proteins claudin-5 and b-catenin after incubation with methylglyoxal, while co-treatment with edaravone restored distribution of both proteins along the cell borders. Similar observation was made in a previous study, where edaravone treatment enhanced b-catenin at cell-cell contact area and the cortical arrangement for its linked protein, actin on half confluent endothelial monolayer. Our holographic phase contrast microscopic data are in accordance with these observations: edaravone completely prevented methylglyoxal-induced changes in cell morphology, no sign of detachment and cellular morphological change was observed, indicating there was no cytoskeletal rearrangement. Our results have answered the question that edaravone can protect against methylglyoxal-induced barrier dysfunction in brain endothelial cells.

Hence, we speculated that both CmCAD2 and CmCAD5 could be involved in fruit development. While CmCAD2 only belonged to group I as bona fide CADs, and may be likely main candidate gene for lignin biosynthesis in melon. However, little information is available on the role of CAD in relation to the lignification of melon flesh tissue during fruit development and ripening. These findings implied that melon CAD genes might also be involved in the lignification of flesh tissue, and there were difference in function among family members. There were significant expression differences between Carfilzomib 868540-17-4 CmCAD4 and other CmCADs in different tissues and during development and ripening. These observed differences could partly be explained by the amino acids differences at position 58–59. CmCAD4 had a KL motif, whereas other CmCADs had an either EW or DL/EL motif. Furthermore, based on our analysis of CmCADs, CmCAD4 had little key residues, and had a Ser123 instead of Asp123 which was suggested to be involved in determining the activity of all bona fide lignifying CADs; One mutation, D123S, resulted in a essentially inactive protein. On the basis of the above results, it appears that CmCAD4 is a pseudogene. But we used the expressed sequence tag database in NCBI as a source of mRNA sequence bioinformatics for CmCAD4, and we found that CmCAD4 showed the highest homology with a Cucumis melo cDNA clone , obtained from callus, from EST database of melon. Hence, It appears that CmCAD4 is specifically expressed in callus. Further researches are needed to confirm this speculation. We also studied the effect of ABA and IAA on CmCADs expression. ABA is extensively involved in the plant’s response to abiotic stresses, such as drought, low temperature and osmotic stress, and also regulates a variety of growth and developmental processes, and can regulate the expression of relevant genes to increase plant adaptability. ABA has been shown to induce CADs genes expression in sweet potato, ginkgo and tea after exposure to biotic or abiotic stresses. Real time qPCR and semi-quantitative PCR analysis of CmCADs in response of ABA suggested that ABA treatment increased the expressions of CmCAD1, 2, 3 and 5. Purportedly, ABAmediated plant responses to drought stress may be related to the regulation of relevant genes by the MYB transcription factor. However, to the best of our information, there were no reports on effect of ABA or IAA on ripening specific CADs. Promoter analysis of the five melon CADs suggested the presence of ABA responsive ABRE motif in the promoter of CmCAD1, 2,3 and 5, and the promoter of CmCAD1 and CmCAD5 contains response elements to IAA. Therefore, the ABAinduced these CmCADs expression observed in present study may be related to the upstream MYB response elements. However this speculation has to be demonstrated by further cloning and function analyses of the promoter of CmCADs. Auxin also plays a role in fruit development and ripening.