Aflatoxin B1 as a complicit in intestinal damage caused by Eimeria ovinoidalis in lambs: Novel insights to reveal parasite-gut battle.

Mycotoxins, unavoidable contaminants in feed and feed ingredients, have the potential to influence the incidence and severity of various diseases upon ingestion. Sheep coccidiosis is an enteric disease caused by protozoa of Eimeria spp. However, the extent to which the presence of aflatoxin b1 (AFB1) synergistically exacerbates damage to intestinal health in lambs with Eimeria remains unclear. 50-day-old female lambs were randomly assigned to a 2 × 2 factorial arrangement of treatments for 15 days to assess the impact of AFB1 exposure on lambs with or without Eimeria (E.) ovinoidalis infection. Our findings reveal that AFB1 synergistically intensifies damage to intestinal health in lambs challenged by E. ovinoidalis. This is evidenced by disruptions to the intestinal microbiota and reductions in the production of short-chain fatty acids. AFB1 further aggravates damage to the cecal mechanical barrier. Additionally, AFB1 contributes to the entry of lipopolysaccharide into the bloodstream, activating the inflammatory response. Interestingly, AFB1 exposure history results in an early peak of oocyst excretion and a decreased number of oocyst excretion in E. ovinoidalis infected lambs. This may be closely linked to the destruction of the intestinal epithelial cell structure and its apoptosis, as indicated by a decreased ratio of Bcl-2 to Bax and increased caspase-3 levels. Mechanistically, proteomics analysis identified mitochondrial dysfunction (inhibition of the oxidative phosphorylation pathway) as the primary factor intensifying intestinal epithelial cell destruction caused by coccidia, exacerbated by AFB1 through the inhibiting the conversion of NADH to NAD+ in the cecum of lambs via down-regulation of the PGC-1α/NRF1/TFAM pathway. Overall, these results offer novel insights into the AFB1 complicity in accelerating intestinal damage caused by E. ovinoidalis in lambs. Targeting the mitochondrial oxidative phosphorylation pathway of the intestine may represent a new therapeutic strategy against the detrimental effects of mycotoxin and coccidia.

Calcineurin and CK2 Reciprocally Regulate Synaptic AMPA Receptor Phenotypes via α2δ-1 in Spinal Excitatory Neurons.

Calcineurin inhibitors, such as cyclosporine and tacrolimus (FK506), are commonly used immunosuppressants for preserving transplanted organs and tissues. However, these drugs can cause severe and persistent pain. GluA2-lacking, calcium-permeable AMPA receptors (CP-AMPARs) are implicated in various neurological disorders, including neuropathic pain. It is unclear whether and how constitutive calcineurin, a Ca2+/calmodulin protein phosphatase, controls synaptic CP-AMPARs. In this study, we found that blocking CP-AMPARs with IEM-1460 markedly reduced the amplitude of AMPAR-EPSCs in excitatory neurons expressing vesicular glutamate transporter-2 (VGluT2), but not in inhibitory neurons expressing vesicular GABA transporter, in the spinal cord of FK506-treated male and female mice. FK506 treatment also caused an inward rectification in the current-voltage relationship of AMPAR-EPSCs specifically in VGluT2 neurons. Intrathecal injection of IEM-1460 rapidly alleviated pain hypersensitivity in FK506-treated mice. Furthermore, FK506 treatment substantially increased physical interaction of α2δ-1 with GluA1 and GluA2 in the spinal cord and reduced GluA1/GluA2 heteromers in endoplasmic reticulum-enriched fractions of spinal cords. Correspondingly, inhibiting α2δ-1 with pregabalin, Cacna2d1 genetic knock-out, or disrupting α2δ-1-AMPAR interactions with an α2δ-1 C terminus peptide reversed inward rectification of AMPAR-EPSCs in spinal VGluT2 neurons caused by FK506 treatment. In addition, CK2 inhibition reversed FK506 treatment-induced pain hypersensitivity, α2δ-1 interactions with GluA1 and GluA2, and inward rectification of AMPAR-EPSCs in spinal VGluT2 neurons. Thus, the increased prevalence of synaptic CP-AMPARs in spinal excitatory neurons plays a major role in calcineurin inhibitor-induced pain hypersensitivity. Calcineurin and CK2 antagonistically regulate postsynaptic CP-AMPARs through α2δ-1-mediated GluA1/GluA2 heteromeric assembly in the spinal dorsal horn.

Development of End-to-End Artificial Intelligence Models for Surgical Planning in Transforaminal Lumbar Interbody Fusion.

Transforaminal lumbar interbody fusion (TLIF) is a commonly used technique for treating lumbar degenerative diseases. In this study, we developed a fully computer-supported pipeline to predict both the cage height and the degree of lumbar lordosis subtraction from the pelvic incidence (PI-LL) after TLIF surgery, utilizing preoperative X-ray images. The automated pipeline comprised two primary stages. First, the pretrained BiLuNet deep learning model was employed to extract essential features from X-ray images. Subsequently, five machine learning algorithms were trained using a five-fold cross-validation technique on a dataset of 311 patients to identify the optimal models to predict interbody cage height and postoperative PI-LL. LASSO regression and support vector regression demonstrated superior performance in predicting interbody cage height and postoperative PI-LL, respectively. For cage height prediction, the root mean square error (RMSE) was calculated as 1.01, and the model achieved the highest accuracy at a height of 12 mm, with exact prediction achieved in 54.43% (43/79) of cases. In most of the remaining cases, the prediction error of the model was within 1 mm. Additionally, the model demonstrated satisfactory performance in predicting PI-LL, with an RMSE of 5.19 and an accuracy of 0.81 for PI-LL stratification. In conclusion, our results indicate that machine learning models can reliably predict interbody cage height and postoperative PI-LL.

Constitutive KCC2 Cell- and Synapse-Specifically Regulates NMDA Receptor Activity in the Spinal Cord.

K+-Cl- cotransporter-2 (KCC2) critically controls neuronal chloride homeostasis and maintains normal synaptic inhibition by GABA and glycine. Nerve injury diminishes synaptic inhibition in the spinal cord via KCC2 impairment. However, how KCC2 regulates nociceptive input to spinal excitatory and inhibitory neurons remains elusive. Here, we show that basal GABA reversal potentials were significantly more depolarized in vesicular GABA transporter (VGAT)-expressing inhibitory neurons than those in vesicular glutamate transporter-2 (VGluT2)-expressing excitatory neurons in spinal cords of male and female mice. Strikingly, inhibiting KCC2 with VU0463271 increased currents elicited by puff NMDA and the NMDAR-mediated frequency of mEPSCs in VGluT2, but not in VGAT, dorsal horn neurons. Notably, VU0463271 had no effect on EPSCs monosynaptically evoked from the dorsal root in VGluT2 neurons. Furthermore, VU0463271 augmented α2δ-1-NMDAR interactions and their protein levels in spinal cord synaptosomes. In Cacna2d1 KO mice, VU0463271 had no effect on puff NMDA currents or the mEPSC frequency in dorsal horn neurons. Disrupting α2δ-1-NMDAR interactions with α2δ-1 C-terminus mimicking peptide diminished VU0463271-induced potentiation in the mEPSC frequency and puff NMDA currents in VGluT2 neurons. Additionally, intrathecal injection of VU0463271 reduced mechanical and thermal thresholds in wild-type mice, but not in Cacna2d1 KO mice. VU0463271-induced pain hypersensitivity in mice was abrogated by co-treatment with the NMDAR antagonist, pregabalin (an α2δ-1 inhibitory ligand), or α2δ-1 C-terminus mimicking peptide. Our findings suggest that KCC2 controls presynaptic and postsynaptic NMDAR activity specifically in excitatory dorsal horn neurons. KCC2 impairment preferentially potentiates nociceptive transmission between spinal excitatory interneurons via α2δ-1-bound NMDARs.Significance statementImpaired function of potassium-chloride cotransporter-2 (KCC2), a key regulator of neuronal inhibition, in the spinal cord plays a major role in neuropathic pain. This study unveils that KCC2 controls spinal nociceptive synaptic strength via NMDA receptors in a cell type- and synapse type-specific manner. KCC2 inhibition preferentially augments presynaptic and postsynaptic NMDA receptor activity in spinal excitatory interneurons via α2δ-1 (previously known as a calcium channel subunit). Importantly, spinal KCC2 impairment triggers pain hypersensitivity through α2δ-1-coupled NMDA receptors. These findings pinpoint the cell and molecular substrates for the reciprocal relationship between spinal synaptic inhibition and excitation in chronic neuropathic pain. Targeting both KCC2 and α2δ-1­NMDA receptor complexes could be an effective strategy in managing neuropathic pain conditions.

Mathematical Aspects of a New Synergy Theory Applicable to Malstressor-Dominated Mixtures which Include Damage-Ameliorating Countermeasures.

In radiobiology, and throughout translational biology, synergy theories for multi-component agent mixtures use 1-agent dose-effect relations (DERs) to calculate baseline neither synergy nor antagonism mixture DERs. The most used synergy theory, simple effect additivity, is not self-consistent when curvilinear 1-agent DERs are involved, and many alternatives have been suggested. In this paper we present the mathematical aspects of a new alternative, generalized Loewe additivity (GLA). To the best of our knowledge, generalized Loewe additivity is the only synergy theory that can systematically handle mixtures of agents that are malstressors (tend to produce disease) with countermeasures - agents that oppose malstressors and ameliorate malstressor damage. In practice countermeasures are often very important, so generalized Loewe additivity is potentially far-reaching. Our paper is a proof-of-principle preliminary study. Unfortunately, generalized Loewe additivity's scope is restricted, in various unwelcome but perhaps unavoidable ways. Our results illustrate its strengths and its weaknesses. One area where our methodology has potentially important applications is analyzing counter-measure mitigation of galactic cosmic ray damage to astronauts during interplanetary travel.

Effect of Porosity and Heat Treatment on Mechanical Properties of Additive Manufactured CoCrMo Alloys.

To minimize the stress shielding effect of metallic biomaterials in mimicking bone, the body-centered cubic (bcc) unit cell-based porous CoCrMo alloys with different, designed volume porosities of 20, 40, 60, and 80% were produced via a selective laser melting (SLM) process. A heat treatment process consisting of solution annealing and aging was applied to increase the volume fraction of an ε-hexagonal close-packed (hcp) structure for better mechanical response and stability. In the present study, we investigated the impact of different, designed volume porosities on the compressive mechanical properties in as-built and heat-treated CoCrMo alloys. The elastic modulus and yield strength in both conditions were dramatically decreased with increasing designed volume porosity. The elastic modulus and yield strength of the CoCrMo alloys with a designed volume porosity of 80% exhibited the closest match to those of bone tissue. Different strengthening mechanisms were quantified to determine their contributing roles to the measured yield strength in both conditions. The experimental results of the relative elastic modulus and yield strength were compared to the analytical and simulation modeling analyses. The Gibson-Ashby theoretical model was established to predict the deformation behaviors of the lattice CoCrMo structures.

MiniBooNE and MicroBooNE Combined Fit to a 3+1 Sterile Neutrino Scenario.

This Letter presents the results from the MiniBooNE experiment within a full "3+1" scenario where one sterile neutrino is introduced to the three-active-neutrino picture. In addition to electron-neutrino appearance at short baselines, this scenario also allows for disappearance of the muon-neutrino and electron-neutrino fluxes in the Booster Neutrino Beam, which is shared by the MicroBooNE experiment. We present the 3+1 fit to the MiniBooNE electron-(anti)neutrino and muon-(anti)neutrino data alone and in combination with MicroBooNE electron-neutrino data. The best-fit parameters of the combined fit with the exclusive charged-current quasielastic analysis (inclusive analysis) are Δm^{2}=0.209 eV^{2}(0.033 eV^{2}), |U_{e4}|^{2}=0.016(0.500), |U_{µ4}|^{2}=0.500(0.500), and sin^{2}(2θ_{µe})=0.0316(1.0). Comparing the no-oscillation scenario to the 3+1 model, the data prefer the 3+1 model with a Δχ^{2}/d.o.f.=24.7/3(17.3/3), a 4.3σ(3.4σ) preference assuming the asymptotic approximation given by Wilks's theorem.

Systematic analysis of the MAPK signaling network reveals MAP3K-driven control of cell fate.

The classic network of mitogen-activated protein kinases (MAPKs) is highly interconnected and controls a diverse array of biological processes. In multicellular eukaryotes, the MAPKs ERK, JNK, and p38 control opposing cell behaviors but are often activated simultaneously, raising questions about how input-output specificity is achieved. Here, we use multiplexed MAPK activity biosensors to investigate how cell fate control emerges from the connectivity and dynamics of the MAPK network. Through chemical and genetic perturbation, we systematically explore the outputs and functions of all the MAP3 kinases encoded in the human genome and show that MAP3Ks control cell fate by triggering unique combinations of MAPK activity. We show that these MAPK activity combinations explain the paradoxical dual role of JNK signaling as pro-apoptotic or pro-proliferative kinase. Overall, our integrative analysis indicates that the MAPK network operates as a unit to control cell fate and shifts the focus from MAPKs to MAP3Ks to better understand signaling-mediated control of cell fate.

First Leptophobic Dark Matter Search from the Coherent-CAPTAIN-Mills Liquid Argon Detector.

We report the first results of a search for leptophobic dark matter (DM) from the Coherent-CAPTAIN-Mills (CCM) liquid argon (LAr) detector. An engineering run with 120 photomultiplier tubes (PMTs) and 17.9×10^{20} protons on target (POT) was performed in fall 2019 to study the characteristics of the CCM detector. The operation of this 10-ton detector was strictly light based with a threshold of 50 keV and used coherent elastic scattering off argon nuclei to detect DM. Despite only 1.5 months of accumulated luminosity, contaminated LAr, and nonoptimized shielding, CCM's first engineering run has already achieved sensitivity to previously unexplored parameter space of light dark matter models with a baryonic vector portal. With an expected background of 115 005 events, we observe 115 005+16.5 events which is compatible with background expectations. For a benchmark mediator-to-DM mass ratio of m_{V_{B}}/m_{χ}=2.1, DM masses within the range 9 MeV≲m_{χ}≲50 MeV are excluded at 90% C. L. in the leptophobic model after applying the Feldman-Cousins test statistic. CCM's upgraded run with 200 PMTs, filtered LAr, improved shielding, and 10 times more POT will be able to exclude the remaining thermal relic density parameter space of this model, as well as probe new parameter space of other leptophobic DM models.

Tracking neural markers of template formation and implementation in attentional inhibition under different distractor consistency.

Performing visual search tasks requires optimal attention deployment to promote targets and inhibit distractors. Rejection templates based on the distractor's feature can be built to constrain the search process. We measured electroencephalography (EEG) of human participants of both sexes when they performed a visual search task in conditions where the distractor cues were constant within a block (fixed-cueing) or changed on a trial-by-trial basis (varied-cueing). In the fixed-cueing condition, sustained decoding of the cued colors could be achieved during the retention interval and the participants with higher decoding accuracy showed larger suppression benefits of the distractor cueing in the search period. In the varied-cueing condition, the cued color could only be transiently decoded after its onset and the higher decoding accuracy was observed from the participants who demonstrated lower suppression benefit. The differential neural representations of the to-be-ignored color in the two cueing conditions as well as their reverse associations with behavioral performance implied that rejection templates were formed in the fixed-cueing condition but not in the varied-cueing condition. Additionally, we observed stronger posterior alpha lateralization and mid-frontal theta/beta power during the retention interval of the varied-cueing condition, indicating the cognitive costs in template formation caused by the trialwise change of distractor colors. Taken together, our findings revealed the neural markers associated with the critical roles of distractor consistency in linking template formation to successful inhibition.Significance StatementHow do we strategically build a rejection template based on distractor features to filter out matched items when performing visual search tasks? Previous studies have suggested that the consistency of the to-be-ignored feature may play a significant role in this process. We recorded scalp EEG when human participants searched for a target among distractors. Capitalized on multivariate decoding technique and time-frequency analysis, we revealed the neural markers of the rejection template under different distractor consistencies. Being able to track these processes in visual search could help us to understand the connection between template formation and successful distractor inhibition. Our findings may also benefit future EEG-based interventions on individuals with deficits in attentional control.

CREB inactivation by HDAC1/PP1γ contributes to dopaminergic neurodegeneration in Parkinson's disease.

Understanding the pathogenesis of nigral dopaminergic neurodegeneration is critical for developing mechanism-based treatments for Parkinson's disease (PD). In the nigral dopaminergic neurons of postmortem human PD brains, we found that CREB, a well-recognized pro-survival transcription factor in neurons, was inactivated by dephosphorylation at Ser133. CREB dephosphorylation correlated with decreased expression of NURR1, one of its target genes crucial for dopaminergic neuron survival, confirming that CREB function was impaired in nigral dopaminergic neurons in PD. An MPTP mouse model was used to further elucidate the mechanism underlying CREB dephosphorylation. Protein phosphatase 1γ (PP1γ), which dephosphorylates CREB, was constitutively associated with histone deacetylase 1 (HDAC1). HDAC1 promotes CREB Ser133 dephosphorylation via a stable interaction with PP1γ. We found that CREB interacted with the HDAC1/PP1γ complex during dopaminergic neurodegeneration. Importantly, increased CREB/HDAC1 interaction occurred in the nigral dopaminergic neurons of PD patients as demonstrated using a proximity ligation assay. Disrupting CREB/HDAC1 interaction via either overexpression of GAL4 M1, a CREB mutant, or administration of trichostatin A, a pan-HDAC inhibitor, restored the expression levels of phospho-CREB (Ser133) and NURR1, and protected nigral dopaminergic neurons in the MPTP-treated mice brain. Collectively, our results demonstrated that HDAC1/PP1γ-mediated CREB inactivation contributed to dopaminergic neuronal degeneration. Disruption of CREB/HDAC1 interaction has the potential as a new approach for PD therapy.Significance StatementPD is the most common movement disorder attributed to the progressive loss of dopaminergic neurons in the substantia nigra. Understanding the pathogenesis of nigral dopaminergic neurodegeneration is critical for developing mechanism-based treatments for PD. We found in nigral dopaminergic neurons of postmortem human PD brains that CREB, a well-recognized pro-survival transcription factor in neurons, was inactivated by dephosphorylation at Ser133. HDAC1, constitutively associated with PP1γ, interacted with CREB to mediate its dephosphorylation during dopaminergic degeneration. Disrupting CREB/HDAC1 interaction restored CREB activity and protected nigral dopaminergic neurons in the MPTP mouse brains. This work suggests that disruption of the CREB/HDAC1 interaction to restore CREB activity may be a potential therapeutic approach in PD.

Visualizing the valence states of europium ions in Eu-doped BaAl2O4 using X-ray nanoprobe mapping.

This study develops and successfully demonstrates visualization methods for the characterization of europium (Eu)-doped BaAl2O4 phosphors using X-ray nanoprobe techniques. X-ray fluorescence (XRF) mapping not only gives information on the elemental distributions but also clearly reveals the valence state distributions of the Eu2+ and Eu3+ ions. The accuracy of the estimated valence state distributions was examined by performing X-ray absorption spectroscopy (XAS) across the Eu L3-edge (6.977 keV). The X-ray excited optical luminescence (XEOL) spectra exhibit different emission lines in the selected local areas. Their corresponding emission distributions can be obtained via XEOL mapping. The emission properties can be understood through correlation analysis. The results demonstrate that the main contribution to the luminescence intensity of the Eu-doped BaAl2O4 comes from the Eu2+ activator and the emission intensity will not be influenced by the concentration of Eu2+ or Eu3+ ions. It is anticipated that X-ray nanoprobes will open new avenues with significant characterization ability for unravelling the emission mechanisms of phosphor materials.

Microstructural Evolution and Mechanical Properties of Non-Equiatomic (CoNi)74.66Cr17Fe8C0.34 High-Entropy Alloy.

In this study, we manufactured a non-equiatomic (CoNi)74.66Cr17Fe8C0.34 high-entropy alloy (HEA) consisting of a single-phase face-centered-cubic structure. We applied in situ neutron diffraction coupled with electron backscattered diffraction (EBSD) and transmission electron microscopy (TEM) to investigate its tensile properties, microstructural evolution, lattice strains and texture development, and the stacking fault energy. The non-equiatomic (CoNi)74.66Cr17Fe8C0.34 HEA revealed a good combination of strength and ductility in mechanical properties compared to the equiatomic CoNiCrFe HEA, due to both stable solid solution and precipitation-strengthened effects. The non-equiatomic stoichiometry resulted in not only a lower electronegativity mismatch, indicating a more stable state of solid solution, but also a higher stacking fault energy (SFE, ~50 mJ/m2) due to the higher amount of Ni and the lower amount of Cr. This higher SFE led to a more active motion of dislocations relative to mechanical twinning, resulting in severe lattice distortion near the grain boundaries and dislocation entanglement near the twin boundaries. The abrupt increase in the strain hardening rate (SHR) at the 1~3% strain during tensile deformation might be attributed to the unusual stress triaxiality in the {200} grain family. The current findings provide new perspectives for designing non-equiatomic HEAs.

Transient Phase-Driven Cyclic Deformation in Additively Manufactured 15-5 PH Steel.

The present work extends the examination of selective laser melting (SLM)-fabricated 15-5 PH steel with the 8%-transient-austenite-phase towards fully-reversed strain-controlled low-cycle fatigue (LCF) test. The cyclic-deformation response and microstructural evolution were investigated via in-situ neutron-diffraction measurements. The transient-austenite-phase rapidly transformed into the martensite phase in the initial cyclic-hardening stage, followed by an almost complete martensitic transformation in the cyclic-softening and steady stage. The compressive stress was much greater than the tensile stress at the same strain amplitude. The enhanced martensitic transformation associated with lower dislocation densities under compression predominantly governed such a striking tension-compression asymmetry in the SLM-built 15-5 PH.

Longitudinal Cognitive Decline in Patients With Mild Cognitive Impairment or Dementia Due to Alzheimer's Disease.

Sensitive cognitive assessments accurately detect and track cognitive decline in Alzheimer's disease. The Cogstate battery was used to measure cognitive change in cognitively normal participants and in individuals with mild cognitive impairment and mild Alzheimer's disease enrolled in the Australian Imaging, Biomarker and Lifestyle Rate of Change Substudy. Over 18 months, verbal episodic memory performance declined for mild cognitive impairment and mild Alzeheimer's disease groups when compared to cognitively normal participants. Frequent assessments of episodic memory may facilitate early detection of cognitive decline due to Alzheimer's disease.

Investigation of Left Ventricular Strain and Its Morphological Basis During Different Stages of Diastolic and Systolic Dysfunction in Spontaneously Hypertensive Rat.

BACKGROUND: Myocardial fibrosis plays an important role in the pathogenesis of hypertensive cardiac dysfunction, and myocardial strain could detect early systolic abnormalities when left ventricular ejection fraction (LVEF) is preserved. The aim of this study was to investigate the characteristics of left ventricular multidirectional strain during different stages of heart dysfunction and the possible morphological basis in spontaneously hypertensive rats (SHRs). METHODS: SHRs and Wistar-Kyoto (WKY) rats were randomly divided into cages and observed for 3-25 months. Echocardiographic measurements, LV + dp/dtmax and left ventricular end-diastolic pressure (LVEDP), and histological collagen volume fraction (CVF) were observed in all rats. RESULTS: According to LVEF and LVEDP, SHRs were divided into normal cardiac function group (group A), diastolic dysfunction group (group B1), and systolic dysfunction group (group B2). In group A, myocardial strain and CVF showed no difference compared with the control group. In group B1, global longitudinal strain (GLS) and endocardial longitudinal strain (SL-endo) were lower than those in group A CVF-endo was increased (all P < 0.05). In group B2, global and layer-specific strain decreased significantly, along with the increased CVF-endo and CVF-epi (all P < 0.05). The decrease of GLS and SL-endo was moderately correlated with the increase of CVF-endo. The reduction of LVEF was correlated with the decrease of SC-endo (r = 0.65, P < 0.01). CONCLUSIONS: Pathological myocardial fibrosis associated with hypertension develops from the inner to outer layer of myocardium, which is coincident with the impairment of myocardial deformation, where longitudinal strain is involved firstly and LVEF declines when all directions of strain are reduced.

Novel Genomic Insights into Body Size Evolution in Cetaceans and a Resolution of Peto's Paradox.

AbstractCetaceans (whales, dolphins, and porpoises) have undergone a radical transformation from the typical terrestrial mammalian body plan to a streamlined body, while exhibiting dramatic interspecific size differences. However, the molecular mechanisms underlying the diversification of cetacean body size are largely unknown. Here, by using genomic and phenotypic data for 22 cetaceans, we performed phylogenetic genome-body size analysis and explored the genetic basis of the high diversity of body size in cetaceans. A functional enrichment analysis showed that body size-related genes in cetaceans are enriched in pathways associated with immunity, cell growth, and metabolism, suggesting that they contributed to body size diversification. Genes showing correlated evolution with body size were mainly involved in immune surveillance, tumor suppression function, and development of hypertumors. The role of these genes in tumor control resolves Peto's paradox (i.e., the lack of a correspondence between an expansion in body size and, thereby, cell number and an increased cancer incidence). Our results provide novel insights into the evolution of substantial body size variation in cetaceans.

In-Situ Synchrotron SAXS and WAXS Investigation on the Deformation of Single and Coaxial Electrospun P(VDF-TrFE)-Based Nanofibers.

Coaxial core/shell electrospun nanofibers consisting of ferroelectric P(VDF-TrFE) and relaxor ferroelectric P(VDF-TrFE-CTFE) are tailor-made with hierarchical structures to modulate their mechanical properties with respect to their constituents. Compared with two single and the other coaxial membranes prepared in the research, the core/shell-TrFE/CTFE membrane shows a more prominent mechanical anisotropy between revolving direction (RD) and cross direction (CD) associated with improved resistance to tensile stress for the crystallite phase stability and good strength-ductility balance. This is due to the better degree of core/shell-TrFE-CTFE nanofiber alignment and the crystalline/amorphous ratio. The coupling between terpolymer P(VDF-TrFE-CTFE) and copolymer P(VDF-TrFE) is responsible for phase stabilization, comparing the core/shell-TrFE/CTFE with the pristine terpolymer. Moreover, an impressive collective deformation mechanism of a two-length scale in the core/shell composite structure is found. We apply in-situ synchrotron X-ray to resolve the two-length scale simultaneously by using the small-angle X-ray scattering to characterize the nanofibers and the wide-angle X-ray diffraction to identify the phase transformations. Our findings may serve as guidelines for the fabrication of the electrospun nanofibers used as membranes-based electroactive polymers.