Contributions to the functional morphology of caudate skulls: kinetic and akinetic forms
A strongly ossified and rigid skull roof, which prevents parietal kinesis, has been reported for the adults of all amphibian clades. Our μ-CT investigations revealed that the Buresch’s newt (Triturus ivanbureschi) possess a peculiar cranial construction. In addition to the typical amphibian pleurokinetic articulation between skull roof and palatoquadrate associated structures, we found flexible connections between nasals and frontals (prokinesis), vomer and parasphenoid (palatokinesis), and between frontals and parietals (mesokinesis). This is the first description of mesokinesis in urodelans. The construction of the skull in the Buresch’s newts also indicates the presence of an articulation between parietals and the exocipitals, discussed as a possible kind of metakinesis. The specific combination of pleuro-, pro-, meso-, palato-, and metakinetic skull articulations indicate to a new kind of kinetic systems unknown for urodelans to this date. We discuss the possible neotenic origin of the skull kinesis and pose the hypothesis that the kinesis in T. ivanbureschi increases the efficiency of fast jaw closure. For that, we compared the construction of the skull in T. ivanbureschi to the akinetic skull of the Common fire salamander Salamandra salamandra. We hypothesize that the design of the skull in the purely terrestrial living salamander shows a similar degree of intracranial mobility. However, this mobility is permitted by elasticity of some bones and not by true articulation between them. We comment on the possible relation between the skull construction and the form of prey shaking mechanism that the species apply to immobilize their victims.
Natchev et al. (2016) Contributions to the functional morphology of caudate skulls: kinetic and akinetic forms. PeerJ 4:e2392 https://doi.org/10.7717/peerj.2392
Are sites with multiple single nucleotide variants in cancer genomes a consequence of drivers, hypermutable sites or sequencing errors?
Across independent cancer genomes it has been observed that some sites have been recurrently hit by single nucleotide variants (SNVs). Such recurrently hit sites might be either (i) drivers of cancer that are postively selected during oncogenesis, (ii) due to mutation rate variation, or (iii) due to sequencing and assembly errors. We have investigated the cause of recurrently hit sites in a dataset of >3 million SNVs from 507 complete cancer genome sequences. We find evidence that many sites have been hit significantly more often than one would expect by chance, even taking into account the effect of the adjacent nucleotides on the rate of mutation. We find that the density of these recurrently hit sites is higher in non-coding than coding DNA and hence conclude that most of them are unlikely to be drivers. We also find that most of them are found in parts of the genome that are not uniquely mappable and hence are likely to be due to mapping errors. In support of the error hypothesis, we find that recurently hit sites are not randomly distributed across sequences from different laboratories. We fit a model to the data in which the rate of mutation is constant across sites but the rate of error varies. This model suggests that ∼4% of all SNVs are errors in this dataset, but that the rate of error varies by thousands-of-fold between sites.
Smith et al. (2016) Are sites with multiple single nucleotide variants in cancer genomes a consequence of drivers, hypermutable sites or sequencing errors?. PeerJ 4:e2391 https://doi.org/10.7717/peerj.2391
A ‘post-honeymoon’ measles epidemic in Burundi: mathematical model-based analysis and implications for vaccination timing
Using a mathematical model with realistic demography, we analyze a large outbreak of measles in Muyinga sector in rural Burundi in 1988–1989. We generate simulated epidemic curves and age × time epidemic surfaces, which we qualitatively and quantitatively compare with the data. Our findings suggest that supplementary immunization activities (SIAs) should be used in places where routine vaccination cannot keep up with the increasing numbers of susceptible individuals resulting from population growth or from logistical problems such as cold chain maintenance. We use the model to characterize the relationship between SIA frequency and SIA age range necessary to suppress measles outbreaks. If SIAs are less frequent, they must expand their target age range.
Corey et al. (2016) A ‘post-honeymoon’ measles epidemic in Burundi: mathematical model-based analysis and implications for vaccination timing. PeerJ 4:e2476 https://doi.org/10.7717/peerj.2476
Integrated analysis of ischemic stroke datasets revealed sex and age difference in anti-stroke targets
Ischemic stroke is a common neurological disorder and the burden in the world is growing. This study aims to explore the effect of sex and age difference on ischemic stroke using integrated microarray datasets. The results showed a dramatic difference in whole gene expression profiles and influenced pathways between males and females, and also in the old and young individuals. Furthermore, compared with old males, old female patients showed more serious biological function damage. However, females showed less affected pathways than males in young subjects. Functional interaction networks showed these differential expression genes were mostly related to immune and inflammation-related functions. In addition, we found ARG1 and MMP9 were up-regulated in total and all subgroups. Importantly, IL1A, ILAB, IL6 and TNF and other anti-stroke target genes were up-regulated in males. However, these anti-stroke target genes showed low expression in females. This study found huge sex and age differences in ischemic stroke especially the opposite expression of anti-stroke target genes. Future studies are needed to uncover these pathological mechanisms, and to take appropriate pre-prevention, treatment and rehabilitation measures.
Li et al. (2016) Integrated analysis of ischemic stroke datasets revealed sex and age difference in anti-stroke targets. PeerJ 4:e2470 https://doi.org/10.7717/peerj.2470
Bcl-2 homologue Debcl enhances α-synuclein-induced phenotypes in Drosophila
Background Parkinson disease (PD) is a debilitating movement disorder that afflicts 1–2% of the population over 50 years of age. The common hallmark for both sporadic and familial forms of PD is mitochondrial dysfunction. Mammals have at least twenty proapoptotic and antiapoptotic Bcl-2 family members, in contrast, only two Bcl-2 family genes have been identified in Drosophila melanogaster, the proapoptotic mitochondrial localized Debcl and the antiapoptotic Buffy. The expression of the human transgene α-synuclein, a gene that is strongly associated with inherited forms of PD, in dopaminergic neurons (DA) of Drosophila, results in loss of neurons and locomotor dysfunction to model PD in flies. The altered expression of Debcl in the DA neurons and neuron-rich eye and along with the expression of α-synuclein offers an opportunity to highlight the role of Debcl in mitochondrial-dependent neuronal degeneration and death. Results The directed overexpression of Debcl using the Ddc-Gal4 transgene in the DA of Drosophila resulted in flies with severely decreased survival and a premature age-dependent loss in climbing ability. The inhibition of Debcl resulted in enhanced survival and improved climbing ability whereas the overexpression of Debcl in the α-synuclein-induced Drosophila model of PD resulted in more severe phenotypes. In addition, the co-expression of Debcl along with Buffy partially counteracts the Debcl-induced phenotypes, to improve the lifespan and the associated loss of locomotor ability observed. In complementary experiments, the overexpression of Debcl along with the expression of α-synuclein in the eye, enhanced the eye ablation that results from the overexpression of Debcl. The co-expression of Buffy along with Debcl overexpression results in the rescue of the moderate developmental eye defects. The co-expression of Buffy along with inhibition of Debcl partially restores the eye to a roughened eye phenotype. Discussion The overexpression of Debcl in DA neurons produces flies with shortened lifespan and impaired locomotor ability, phenotypes that are strongly associated with models of PD in Drosophila. The co-expression of Debcl along with α-synuclein enhanced the PD-like phenotypes. The co-expression of Debcl along with Buffy suppresses these phenotypes. Complementary experiments in the Drosophila eye show similar trends during development. Taken all together these results suggest a role for Debcl in neurodegenerative disorders.
M’Angale et al. (2016) Bcl-2 homologue Debcl enhances α-synuclein-induced phenotypes in Drosophila. PeerJ 4:e2461 https://doi.org/10.7717/peerj.2461
Progesterone influences cytoplasmic maturation in porcine oocytes developing in vitro
Progesterone (P4), an ovarian steroid hormone, is an important regulator of female reproduction. In this study, we explored the influence of progesterone on porcine oocyte nuclear maturation and cytoplasmic maturation and development in vitro. We found that the presence of P4 during oocyte maturation did not inhibit polar body extrusions but significantly increased glutathione and decreased reactive oxygen species (ROS) levels relative to that in control groups. The incidence of parthenogenetically activated oocytes that could develop to the blastocyst stage was higher (p < 0.05) when oocytes were exposed to P4 as compared to that in the controls. Cell numbers were increased in the P4-treated groups. Further, the P4-specific inhibitor mifepristone (RU486) prevented porcine oocyte maturation, as represented by the reduced incidence (p < 0.05) of oocyte first polar body extrusions. RU486 affected maturation promoting factor (MPF) activity and maternal mRNA polyadenylation status. In general, these data show that P4 influences the cytoplasmic maturation of porcine oocytes, at least partially, by decreasing their polyadenylation, thereby altering maternal gene expression.
Yuan et al. (2016) Progesterone influences cytoplasmic maturation in porcine oocytes developing in vitro. PeerJ 4:e2454 https://doi.org/10.7717/peerj.2454
Muscle size explains low passive skeletal muscle force in heart failure patients
Background Alterations in skeletal muscle function and architecture have been linked to the compromised exercise capacity characterizing chronic heart failure (CHF). However, how passive skeletal muscle force is affected in CHF is not clear. Understanding passive force characteristics in CHF can help further elucidate the extent to which altered contractile properties and/or architecture might affect muscle and locomotor function. Therefore, the aim of this study was to investigate passive force in a single muscle for which non-invasive measures of muscle size and estimates of fiber force are possible, the soleus (SOL), both in CHF patients and age- and physical activity-matched control participants. Methods Passive SOL muscle force and size were obtained by means of a novel approach combining experimental data (dynamometry, electromyography, ultrasound imaging) with a musculoskeletal model. Results We found reduced passive SOL forces (∼30%) (at the same relative levels of muscle stretch) in CHF vs. healthy individuals. This difference was eliminated when force was normalized by physiological cross sectional area, indicating that reduced force output may be most strongly associated with muscle size. Nevertheless, passive force was significantly higher in CHF at a given absolute muscle length (non length-normalized) and likely explained by the shorter muscle slack lengths and optimal muscle lengths measured in CHF compared to the control participants. This later factor may lead to altered performance of the SOL in functional tasks such gait. Discussion These findings suggest introducing exercise rehabilitation targeting muscle hypertrophy and, specifically for the calf muscles, exercise that promotes muscle lengthening.
Panizzolo et al. (2016) Muscle size explains low passive skeletal muscle force in heart failure patients. PeerJ 4:e2447 https://doi.org/10.7717/peerj.2447
Functional, size and taxonomic diversity of fish along a depth gradient in the deep sea
Biodiversity is well studied in ecology and the concept has been developed to include traits of species, rather than solely taxonomy, to better reflect the functional diversity of a system. The deep sea provides a natural environmental gradient within which to study changes in different diversity metrics, but traits of deep-sea fish are not widely known, hampering the application of functional diversity to this globally important system. We used morphological traits to determine the functional richness and functional divergence of demersal fish assemblages along the continental slope in the Northeast Atlantic, at depths of 300–2,000 m. We compared these metrics to size diversity based on individual body size and species richness. Functional richness and size diversity showed similar patterns, with the highest diversity at intermediate depths; functional divergence showed the opposite pattern, with the highest values at the shallowest and deepest parts of the study site. Species richness increased with depth. The functional implications of these patterns were deduced by examining depth-related changes in morphological traits and the dominance of feeding guilds as illustrated by stable isotope analyses. The patterns in diversity and the variation in certain morphological traits can potentially be explained by changes in the relative dominance of pelagic and benthic feeding guilds. All measures of diversity examined here suggest that the deep areas of the continental slope may be equally or more diverse than assemblages just beyond the continental shelf.
Mindel et al. (2016) Functional, size and taxonomic diversity of fish along a depth gradient in the deep sea. PeerJ 4:e2387 https://doi.org/10.7717/peerj.2387
The evidence of porcine hemagglutinating encephalomyelitis virus induced nonsuppurative encephalitis as the cause of death in piglets
An acute outbreak of porcine hemagglutinating encephalomyelitis virus (PHEV) infection in piglets, characterized with neurological symptoms, vomiting, diarrhea, and wasting, occurred in China. Coronavirus-like particles were observed in the homogenized tissue suspensions of the brain of dead piglets by electron microscopy, and a wild PHEV strain was isolated, characterized, and designated as PHEV-CC14. Histopathologic examinations of the dead piglets showed characteristics of non-suppurative encephalitis, and some neurons in the cerebral cortex were degenerated and necrotic, and neuronophagia. Similarly, mice inoculated with PHEV-CC14 were found to have central nervous system (CNS) dysfunction, with symptoms of depression, arched waists, standing and vellicating front claws. Furthmore, PHEV-positive labeling of neurons in cortices of dead piglets and infected mice supported the viral infections of the nervous system. Then, the major structural genes of PHEV-CC14 were sequenced and phylogenetically analyzed, and the strain shared 95%–99.2% nt identity with the other PHEV strains available in GenBank. Phylogenetic analysis clearly proved that the wild strain clustered into a subclass with a HEV-JT06 strain. These findings suggested that the virus had a strong tropism for CNS, in this way, inducing nonsuppurative encephalitis as the cause of death in piglets. Simultaneously, the predicted risk of widespread transmission showed a certain variation among the PHEV strains currently circulating around the world. Above all, the information presented in this study can not only provide good reference for the experimental diagnosis of PHEV infection for pig breeding, but also promote its new effective vaccine development.
Li et al. (2016) The evidence of porcine hemagglutinating encephalomyelitis virus induced nonsuppurative encephalitis as the cause of death in piglets. PeerJ 4:e2443 https://doi.org/10.7717/peerj.2443
Emotion recognition using Kinect motion capture data of human gaits
Automatic emotion recognition is of great value in many applications, however, to fully display the application value of emotion recognition, more portable, non-intrusive, inexpensive technologies need to be developed. Human gaits could reflect the walker’s emotional state, and could be an information source for emotion recognition. This paper proposed a novel method to recognize emotional state through human gaits by using Microsoft Kinect, a low-cost, portable, camera-based sensor. Fifty-nine participants’ gaits under neutral state, induced anger and induced happiness were recorded by two Kinect cameras, and the original data were processed through joint selection, coordinate system transformation, sliding window gauss filtering, differential operation, and data segmentation. Features of gait patterns were extracted from 3-dimentional coordinates of 14 main body joints by Fourier transformation and Principal Component Analysis (PCA). The classifiers NaiveBayes, RandomForests, LibSVM and SMO (Sequential Minimal Optimization) were trained and evaluated, and the accuracy of recognizing anger and happiness from neutral state achieved 80.5% and 75.4%. Although the results of distinguishing angry and happiness states were not ideal in current study, it showed the feasibility of automatically recognizing emotional states from gaits, with the characteristics meeting the application requirements.
Li et al. (2016) Emotion recognition using Kinect motion capture data of human gaits. PeerJ 4:e2364 https://doi.org/10.7717/peerj.2364