Explore the vast range of titles available.

There are two main factors explaining variation among species and the evolution of characters along phylogeny: adaptive change, including phenotypic and genetic responses to selective pressures, and phylogenetic inertia, or the resemblance between species due to shared phylogenetic history. Phenotype-habitat colour match, a classic Darwinian example of the evolution of camouflage (crypsis), offers the opportunity to test the importance of historical versus ecological mechanisms in shaping phenotypes among phylogenetically closely related taxa. To assess it, we investigated fur (phenotypic data) and habitat (remote sensing data) colourations, along with phylogenetic information, in the species-rich Gerbillus genus. Overall, we found a strong phenotype-habitat match, once the phylogenetic signal is taken into account. We found that camouflage has been acquired and lost repeatedly in the course of the evolutionary history of Gerbillus . Our results suggest that fur colouration and its covariation with habitat is a relatively labile character in mammals, potentially responding quickly to selection. Relatively unconstrained and substantial genetic basis, as well as structural and functional independence from other fitness traits of mammalian colouration might be responsible for that observation.

BackgroundThe deviation from perfect bilateral symmetry is defined as fluctuating asymmetry (FA) and is a common phenomenon among living organisms. This deviation from perfection is thought to reflect the environmental pressures experienced during development and, therefore, the FA represents an epigenetic measure of the environmental stress, which affects all living beings from conception, progressively affecting all aspects of life.Rinaldi and Fontani hypothesized that the FA morpho-functional changes are originated by an adaptive motor behavior determined by functional alterations in the cerebellum and neural circuits, not caused by a lesion, but induced by the experienced environmental stress. They identified in the asymmetric activation of symmetrical muscle groups, detectable even in healthy subjects, the expression of the dysfunctional adaptation state of the subject and named this clinical semeiotic phenomenon functional dysmetria (FD).On these premises, they developed the radio electric asymmetric conveyer (REAC) technology, a neuromodulation technology aimed at optimizing the best neuro-psycho-motor strategies in relation to environmental interaction. Neuro postural optimization (NPO) is a neurobiological stimulation treatment administered with the REAC technology and it has been specifically studied to treat the state of dysfunctional adaptation that is revealed through the presence of FD.AimThe purpose of this study was to verify whether a single administration of the REAC NPO treatment can trigger the improvement of the capacity of stress management and the quality of life in a population of children housed in a group home in Macapá, Brazil.Materials and methodsThe sample of this study consisted of nine children (six boys and three girls) in the age group of 6-11 years, which represented the totality of the children present in the structure. The children was investigated for the assessment of the presence of functional dysmetria and with the Pediatric Quality of Life Inventory TM 4.0 (PedsQL) before and one week after the administration of the REAC NPO.ResultsThe stable disappearance of FD was found in all children at follow-up. In addition, improvements were found in stress management and quality of life, in the physical, emotional, social, and scholastic aspects evaluated with PedsQL.ConclusionsIt was seen that the REAC NPO neurobiological modulation treatment induced the stable disappearance of FD and triggered the initial improvement of neurophysical aspects also in a population of children housed in a group home in the Amazon region of Macapá, Brazil.

Inflammatory pain can be triggered by different stimuli, such as trauma, radiation, antigen and infection. In a model of inflammatory pain caused by infection, injection in the mice paw of lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) agonist, produces mechanical hyperalgesia. We identify here the TLR4 linked signaling pathways that elicit this response. Firstly, LPS paw injection in wild type (WT) mice produced mechanical hyperalgesia that was not altered in TRIF-/- mice. On the other hand, this response was absent in TLR4 mutant and MyD88 null mice and reduced in TNFR1 null mice. Either an IL-1 receptor antagonist, anti-KC/CXCL1 antibody, indomethacin or guanethidine injection also lessened this response. Moreover, LPS-induced time dependent increases in TNF-α, KC/CXCL1 and IL-1β expression in the mice paw, which were absent in TLR4 mutant and MyD88 null mice. Furthermore, in TNFR1 deficient mice, the LPS-induced rises in KC/CXCL1 and IL-1β release were less than in their wild type counterpart. LPS also induced increase of myeloperoxidase activity in the paw skin, which was inhibited in TLR4 mutant and MyD88 null mice, and not altered in TRIF-/- mice. These results suggest that LPS-induced inflammatory pain in mice is solely dependent on the TLR4/MyD88 rather than the TLR4/TRIF signaling pathway. This pathway triggers pronociceptive cytokine TNF-α release that in turn mediates rises in KC/CXCL1 and IL-1β expression. Finally, these cytokines might be involved in stimulating production of directly-acting hyperalgesic mediators such as prostaglandins and sympathomimetic amine.

This study aimed to establish a protocol for in vitro embryo production using epididymal sperm (EP). Samples were obtained from ejaculated sperm (EJ) and the epididymis of 7 Gir bulls. First, the effect of heparin (+) on the viability, longevity (Experiment 1) and fertilization rates (Experiment 2) of the EP was evaluated. In experiment 2, a pool of EP and EJ sperm (n = 7) was coincubated with cumulus-oocyte complexes (COCs) for 0, 3, 6, 12 and 18 h, and the fertilization rate (FR) was evaluated. A third experiment was performed to test sperm treatments for IVP using the Percoll (P) or PureSperm (PS) gradients or a spTALP wash for sperm selection. Cleavage, blastocyst rate (BR) and embryo sex were evaluated. In experiment 4, embryos were produced using 6, 12, and 18 h of sperm-oocyte coincubation. The cleavage, BR, and total number and percentage of apoptotic cells were determined. Heparin affected EP viability, longevity and FR. After 6 h, 82% of the oocytes were fertilized in the EP+ group, a higher value (P<0.05) than that in the EJ (19%) and EP- (42%) groups. At 12 and 18 h, FR remained higher in the EP+ group, and a gradual increase in polyspermy was observed. The use of a P or PS gradient yielded a similar BR on D7 (54% and 52%), which was higher than the rate obtained using the washing method (37%). The embryos produced by EP and selected in a P or PS gradient resulted in a sex deviation in favor of male embryos (P>0.05). No differences (P>0.05) were observed among the groups that were coincubated for 6, 12 and 18 h with respect to embryo production, kinetics of development, total cell number and percentage of apoptotic cells. In conclusion, IVF time can be reduced to 6 h without affecting embryo production and quality. In addition, EP sperm selection can be performed by either a PS or P gradient.

Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. Methods Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers. Results DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro , which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I. Conclusions Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes.

SARS-CoV-2 is considered a global emergency, resulting in an exacerbated crisis in the health public in the world. Although there are advances in vaccine development, it is still limited for many countries. On the other hand, an immunological response that mediates protective immunity or indicates that predict disease outcome in SARS-CoV-2 infection remains undefined. This work aimed to assess the antibody levels, avidity, and subclasses of IgG to RBD protein, in symptomatic patients with severe and mild forms of COVID-19 in Brazil using an adapted in-house RBD-IgG ELISA. The RBD IgG-ELISA showed 100% of specificity and 94.3% of sensibility on detecting antibodies in the sera of hospitalized patients. Patients who presented severe COVID-19 had higher anti-RBD IgG levels compared to patients with mild disease. Additionally, most patients analyzed displayed low antibody avidity, with 64.4% of the samples of patients who recovered from the disease and 84.6% of those who died in this avidity range. Our data also reveals an increase of IgG1 and IgG3 levels since the 8th day after symptoms onset, while IgG4 levels maintained less detectable during the study period. Surprisingly, patients who died during 8–14 and 15–21 days also showed higher anti-RBD IgG4 levels in comparison with the recovered (P < 0.05), suggesting that some life-threatening patients can elicit IgG4 to RBD antibody response in the first weeks of symptoms onset. Our findings constitute the effort to clarify IgG antibodies' kinetics, avidity, and subclasses against SARS-CoV-2 RBD in symptomatic patients with COVID-19 in Brazil, highlighting the importance of IgG antibody avidity in association with IgG4 detection as tool laboratory in the follow-up of hospitalized patients with more significant potential for life-threatening.

Fructose 1,6-bisphosphate (FBP) is an endogenous intermediate of the glycolytic pathway. Exogenous administration of FBP has been shown to exert protective effects in a variety of ischemic injury models, which are attributed to its ability to sustain glycolysis and increase ATP production. Here, we demonstrated that a single treatment with FBP markedly attenuated arthritis, assessed by reduction of articular hyperalgesia, joint swelling, neutrophil infiltration and production of inflammatory cytokines, TNF and IL-6, while enhancing IL-10 production in two mouse models of arthritis. Our mechanistic studies showed that FBP reduces joint inflammation through the systemic generation of extracellular adenosine and subsequent activation of adenosine receptor A2a (A2aR). Moreover, we showed that FBP-induced adenosine generation requires hydrolysis of extracellular ATP through the activity of the ectonucleosides triphosphate diphosphohydrolase-1 (ENTPD1, also known as CD39) and ecto-5′-nucleotidase (E5NT, also known as CD73). In accordance, inhibition of CD39 and CD73 abolished anti-arthritic effects of FBP. Taken together, our findings provide a new insight into the molecular mechanism underlying the anti-inflammatory effect of FBP, showing that it effectively attenuates experimental arthritis by activating the anti-inflammatory adenosinergic pathway. Therefore, FBP may represent a new therapeutic strategy for treatment of rheumatoid arthritis (RA).

To evaluate if using a soft-tipped guidewire to cannulate the common bile duct may ameliorate development of post-ERCP pancreatitis and facilitate cannulation of the CBD. A single-center, blinded, randomized trial of conventional cannulation technique using sphinctertome and contrast injection versus guidewire cannulation technique. We prospectively randomized 300 patients to conventional cannulation (group I) or guidewire cannulation (group II) technique. Primary outcome measure was incidence of acute pancreatitis and secondary outcome measures were ease of cannulation of common bile duct (assessed by attempts required for common bile duct cannulation & rates of precut sphincterotomy) and overall complication rates. Guidewire cannulation was associated with significantly lower likelihood of post-ERCP pancreatitis (adjusted OR 0.43, 95% CI 0.21-0.89, P= 0.02). Twenty-five patients (16.6%) in group I and thirteen patients (8.6%) in group II developed acute pancreatitis, P= 0.037. All instances of pancreatitis were mild. There were more women in group II; 41 in group I and 59 in group II, P= 0.028. Otherwise the two groups were comparable for age, age under 35 yr, indication for ERCP, diagnosis, and number of patients with SOD. The number of patients requiring 0-3, 4-6, and 7-10 attempts for successful cannulation of the common bile duct were 87, 48, and 15 in group I and 117, 24, and 9 in group II, respectively, P= 0.001. A total of 33 patients in group I and 13 patients in group II required precut sphincterotomy, P= 0.007. Rates of accidental pancreatic duct cannulation were 21 in group I and 27 in group II, P= 0.34. Rates of overall complication were not significantly different in the two groups. Guidewire technique for bile duct cannulation lowers likelihood of post-ERCP pancreatitis by facilitating cannulation and reducing need for precut sphincterotomy.

EGFR and KRAS are the most frequently mutated genes in lung cancer, being active research topics in targeted therapy. The biopsy is the traditional method to genetically characterise a tumour. However, it is a risky procedure, painful for the patient, and, occasionally, the tumour might be inaccessible. This work aims to study and debate the nature of the relationships between imaging phenotypes and lung cancer-related mutation status. Until now, the literature has failed to point to new research directions, mainly consisting of results-oriented works in a field where there is still not enough available data to train clinically viable models. We intend to open a discussion about critical points and to present new possibilities for future radiogenomics studies. We conducted high-dimensional data visualisation and developed classifiers, which allowed us to analyse the results for EGFR and KRAS biological markers according to different combinations of input features. We show that EGFR mutation status might be correlated to CT scans imaging phenotypes; however, the same does not seem to hold for KRAS mutation status. Also, the experiments suggest that the best way to approach this problem is by combining nodule-related features with features from other lung structures.

A 2 3 full factorial design was used to identify the main effects and interactions of pH, collagen concentration and temperature on the degree of collagen hydrolysis (DH) by collagenase from Penicillium aurantiogriseum URM 4622. Increases in both pH and collagen concentration improved DH, and a positive interaction effect was observed for these variables. On the other hand, temperature had a negative main effect on DH. The maximum value of DH (4.65 μg/mL) was achieved at 7.5 mg/mL collagen concentration, pH 8.0 and 25 °C. The peptide profile showed several peptides with molecular weights lower than 2 kDa and exhibited antibacterial activity against Escherichia coli , Bacillus subtilis and Staphylococcus aureus . An antioxidant activity of 84.7 ± 0.24 % towards the radical ABTS• + was obtained with 50 mg/mL hydrolysates. This study demonstrated that collagen hydrolysed by P. aurantiogriseum URM 4622 collagenase possesses interesting antibacterial and antioxidant activities.