Local extinctions may be evidenced by the holes of the morphometric hypervolume in dung beetle communities

The body shape of a species is associated with its evolutionary history and can reflect behavioural peculiarities related to the ecological niche of each species. Morphology can characterise the morphometric niche of species and can be represented as body shape points within a morphometric universe. This information can be to calculate the morphometric diversity of communities through hypervolume metrics, and the hole sizes that remain in the morphometric hypervolume, which are empty areas with no species. Such holes may be ‘natural’ or caused by a local extinction. In this study, we evaluate the ecological community of dung beetles through the lens of morphometric diversity. We evaluated 38 dung beetle species from 30 subtropical communities in southern Brazil sampled in the summer of 2015, including 15 forest remnant communities from the Atlantic Forest and 15 communities from adjacent maize cultivations. The shape of 495 dung beetle specimens was measured using geometric morphometric and hypervolume techniques to calculate the morphometric diversity and the hole size of each of the 30 communities. We found that the taxonomic diversity positively correlated with the morphometric diversity and negatively correlated with the size of the holes. We also found that forest communities had higher values of morphometric diversity and smaller holes in the hypervolume than the maize cultivation communities, suggesting that local extinction may reduce community body shape spaces.     

Alterations of red cell membrane proteins and hemoglobin under natural and experimental oxidant stress

We compared on red cell membrane proteins and hemoglobin (Hb) the effects of (i) natural oxidant stress that has been suggested to occur in a variety of oxidative hemolytic anemias, and (ii) experimental stress induced by hydrogen peroxide. SDS-polyacrylamide gel electrophoresis was used for protein analysis. Under natural conditions (thalassemias, hemoglobinopathies with Hb unstability), a high molecular weight polymer (HMWP) and variable amounts of globin mono- and dimers became apparent. Furthermore, a major 12 kDa polypeptide, its dimer, and conspicuous spectrin degradation products in the band 2.2–2.6 region occurred in a patient carrying the highly unstable Hb Hammersmith. Under experimental conditions, incubation of erythrocyte ghosts with H₂O₂ in the presence of minimal concentration (25 μM) of Hb generated a HMWP at the expense of membrane proteins, mainly spectrin. Incubation of a diluted (200 μM) membrane-free hemolysate with H₂O₂ induced a HMWP, an array of globin oligomers and a 12 kDa polypeptide similar to that mentionned above. Therefore, the damage to the red cell membrane present in various oxidative hemolytic anemias, including polypeptide polymerisation and breakdown, can be produced by experimental oxidant stress. These observations support the view that the alterations described in the patients result directly from oxidative reactions. However, we did not observe in the patient the sharp breakdown of polyunsaturated fatty acids that was triggered in vitro by H₂O₂ in the presence of Hb acting as a catalyst. In most cases, oligo- and polymers were resistant to β-mercaptoethanol, and the chemical nature of the underlying cross-links is discussed. To our knowledge, the 12 kDa polypeptide, that we consider as arising from globin proteolysis, has never been reported under pathological conditions.     

High‐density lipoprotein cholesterol affects early endothelial progenitor cell number and endothelial function in obese women

Objective: In order to improve our understanding of high‐density lipoprotein cholesterol (HDL‐C) cardiovascular (CV) impact in obesity, the association of HDL‐C plasma level with circulating early endothelial progenitor cell (early‐EPC) number and endothelium‐dependent vasodilatation (EDV) in obese women with normal or high low‐density lipoprotein cholesterol (LDL‐C) plasma levels was evaluated. Design and Methods: One hundred thirteen obese female subjects and a control group of 78 healthy female subjects were recruited. Circulating early‐EPC were assessed by single‐ and two‐color flow cytometric analyses with a fluorescence activated cell sorting (FACScan) flow cytometer. EDV was evaluated as response to ischemia by strain gauge plethysmography. Results: Both early‐EPC number and EDV were significantly decreased in obese women compared with the control group. Obese women with low HDL‐C showed a further decrease of early‐EPC and EDV in the presence of both high or normal LDL‐C plasmatic levels. In the normal HDL‐C level subgroup, hypercholesterolemic and nonhypercholesterolemic subjects showed no difference in early‐EPC number, whereas slight EDV impairment was present in hypercholesterolemic subjects. Conclusion: In obese women, low HDL‐C is associated to decreased early‐EPC number and impaired EDV, suggesting the need to assess whether evaluation of early‐EPC and EDV may increase HDL‐C prognostic value in the stratification of CV risk.     

Microalga added to Bradyrhizobium inoculant improve soybean tolerance to salt stress

Journal of Applied Phycology - Addressing the growing challenges for food production imposed by abiotic stresses, the aim of this work was evaluate the effect and determine the ideal dose of the...     

Colorimetric microwell plate reverse-hybridization assay for Mycobacterium tuberculosis detection

Direct smear examination using Ziehl-Neelsen staining for pulmonary tuberculosis (PTB) diagnosis is inexpensive and easy to use, but has the major limitation of low sensitivity. Rapid molecular methods are becoming more widely available in centralized laboratories, but they depend on timely reporting of results and strict quality assurance obtainable only from costly commercial kits available in high burden nations. This study describes a pre-commercial colorimetric method, Detect-TB, for detecting Mycobacterium tuberculosis DNA in which an oligonucleotide probe is fixed onto wells of microwell plates and hybridized with biotinylated polymerase chain reaction amplification products derived from clinical samples. The probe is capable of hybridising with the IS6110 insertion element and was used to specifically recognise the M. tuberculosis complex. When combined with an improved silica-based DNA extraction method, the sensitivity of the test was 50 colony-forming units of the M. tuberculosis reference strain H37Rv. The results that were in agreement with reference detection methods were observed in 95.2% (453/476) of samples included in the analysis. Sensitivity and specificity for 301 induced sputum samples and 175 spontaneous sputum samples were 85% and 98%, and 94% and 100%, respectively. This colorimetric method showed similar specificity to that described for commercially available kits and may provide an important contribution for PTB diagnosis.     

Modification of the structural and redox properties of cytochrome c by heteropolytungstate binding

Complex formation between horse heart ferricytochrome c and large three-dimensional polyanions has been investigated, in order to study the influence of surface electrostatic interactions on the structural and redox properties of cytochrome c. Cytochrome c binds the large heteropolytungstates (NaSb9W21O86)18- and (KAs4W40O140)27- with a 1/1 polyanion/cytochrome c ratio, and the smaller ion (SiW11O39)8- with a 2/1 ratio. Upon complexation, cytochrome c undergoes structural changes that are dependent on the size and charge of the polyanion, and on the pH and ionic strength of the medium. Three different forms of complexed cytochrome c have been characterized by optical and EPR spectroscopies, in the pH range 6.5-8: an N form, close to the native structure, an A form, analogous to cytochrome c in acidic medium, and a novel B form in which the heme pocket is open but the iron remains low-spin. The redox potential of cytochrome c is lowered to 250-220 mV (vs. NHE) in the N form, and to 80 mV in the B form.     

Conditional deletion of Nbs1 in murine cells reveals its role in branching repair pathways of DNA double-strand breaks

NBS1 forms a complex with MRE11 and RAD50 (MRN) that is proposed to act on the upstream of two repair pathways of DNA double-strand break (DSB), homologous repair (HR) and non-homologous end joining (NHEJ). However, the function of Nbs1 in these processes has not fully been elucidated in mammals due to the lethal phenotype of cells and mice lacking Nbs1. Here, we have constructed mouse Nbs1-null embryonic fibroblasts and embryonic stem cells, through the Cre-loxP and sequential gene targeting techniques. We show that cells lacking Nbs1 display reduced HR of the single DSB in chromosomally integrated substrate, affecting both homology-directed repair (HDR) and single-stranded annealing pathways, and, surprisingly, increased NHEJ-mediated sequence deletion. Moreover, focus formation at DSBs and chromatin recruitment of the Nbs1 partners Rad50 and Mre11 as well as Rad51 and Brca1 are attenuated in these cells, whereas the NHEJ molecule Ku70 binding to chromatin is not affected. These data provide a novel insight into the function of MRN in the branching of DSB repair pathways.     

Acetylcholinesterase activity in the rat brain after pneumococcal meningitis

Pneumococcal meningitis is a life-threatening disease characterized by acute purulent infection of the meninges causing neuronal injury, cortical necrosis and hippocampal apoptosis. Cholinergic neurons and their projections are extensively distributed throughout the central nervous system. The aim of this study was to assess acetylcholinesterase activity in the rat brain after pneumococcal meningitis. In the hippocampus, frontal cortex and cerebrospinal fluid, acetylcholinesterase activity was found to be increased at 6, 12, 24, 48 and 96 hr without antibiotic treatment, and at 48 and 96 hr with antibiotic treatment. Our data suggest that acetylcholinesterase activity could be related to neuronal damage induced by pneumococcal meningitis.