Myerslawrence1944

Human and mouse oocytes' developmental potential can be predicted by their mechanical properties. Their development into blastocysts requires a specific stiffness window. In this study, we combine live-cell and computational imaging, laser ablation, and biophysical measurements to investigate how deregulation of cortex tension in the oocyte contributes to early developmental failure. We focus on extra-soft cells, the most common defect in a natural population. Using two independent tools to artificially decrease cortical tension, we show that chromosome alignment is impaired in extra-soft mouse oocytes, despite normal spindle morphogenesis and dynamics, inducing aneuploidy. The main cause is a cytoplasmic increase in myosin-II activity that could sterically hinder chromosome capture. We describe here an original mode of generation of aneuploidies that could be very common in oocytes and could contribute to the high aneuploidy rate observed during female meiosis, a leading cause of infertility and congenital disorders.Human spiral ganglion (HSG) cell bodies located in the bony cochlea depend on a rich vascular supply to maintain excitability. These neurons are targeted by cochlear implantation (CI) to treat deafness, and their viability is critical to ensure successful clinical outcomes. The blood supply of the HSG is difficult to study due to its helical structure and encasement in hard bone. The objective of this study was to present the first three-dimensional (3D) reconstruction and analysis of the HSG blood supply using synchrotron radiation phase-contrast imaging (SR-PCI) in combination with histological analyses of archival human cochlear sections. Twenty-six human temporal bones underwent SR-PCI. Data were processed using volume-rendering software, and a representative three-dimensional (3D) model was created to allow visualization of the vascular anatomy. Histologic analysis was used to verify the segmentations. Results revealed that the HSG is supplied by radial vascular twigs which are separate from the rest of the inner ear and encased in bone. Unlike with most organs, the arteries and veins in the human cochlea do not follow the same conduits. There is a dual venous outflow and a modiolar arterial supply. This organization may explain why the HSG may endure even in cases of advanced cochlear pathology.To evaluate and compare the stability, quantity and quality of bone augmentation at maxillary sinus elevation sites by non-grafted transcrestal sinus floor elevation (TSFE) and platelet concentration grafted transcrestal sinus floor elevation (PC-TSFE). A complete literature search was performed up to April 2019. Clinical controlled trials, retrospective cohort studies, and prospective cohort studies were selected based on inclusion criteria. The clinical outcomes were implant survival rate (ISR), marginal/crestal bone loss (MBL/CBL) and endo-sinus bone gain (ESBG). Meta-analysis was conducted on these 1-year based values. Furthermore, another meta-analysis on 1-year ISR value was conducted among studies with different residual bone heights (RBH) within the non-grafted TSFE group. A total of 18 studies were included 13 in TSFE group and 5 in PC-TSFE group. No significant differences were displayed between the 1-year ISR of TSFE (97%, 95%CI = 0.96-0.99) and PC-TSFE group (99%, 95%CI = 0.97-1.00). Among the various studies with different RBH within TSFE group, no significant differences in 1-year ISR were displayed. The 1-year MBL/CBL value of PC-TSFE group (0.73 mm, 95%CI = 0.43-1.13 mm) did not show significant difference as compared to TSFE group (0.60 mm, 95%CI = 0.10-1.10 mm). Furthermore, no significant enhancement was observed on 1-year ESBG value on PC-TSFE group (3.51 mm, 95%CI = 2.31-4.71 mm) in comparison with the TSFE group (2.87 mm, 95%CI = 2.18m-3.55 mm). Grafting platelet concentrations around dental implants at TSFE sites did not significantly enhance the adjacent bone regeneration. Moreover, TSFE was shown to be a reliable therapeutic option for implant sites that need simultaneous maxillary sinus augmentation, even under limited RBH.Our understanding regarding the influence of intensive agricultural practices, including cover cropping and tillage, on communities of arbuscular mycorrhizal fungi (AMF) is lacking. This would prove to be an obstacle in the improvement of current maize (Zea mays L.) production. Therefore, using amplicon sequencing, we aimed to clarify how AMF communities and their diversity in maize roots vary under different cover cropping systems and two types of tillage (rotary and no tillage). Two kinds of cover crops (hairy vetch and brown mustard) and fallow treatments were established with rotary or no tillage in rotation with maize crops. Tillage and no tillage yielded a set of relatively common AMF operational taxonomic units (OTUs) in the maize crops, representing 78.3% of the total OTUs. The percentage of maize crop OTUs that were specific to only tillage and no tillage were 9.6% and 12.0%, respectively. We found that tillage system significantly altered the AMF communities in maize roots. However, the AMF communities of maize crops among cover cropping treatments did not vary considerably. Our findings indicate that compared with cover cropping, tillage may shape AMF communities in maize more strongly.The XPD helicase is a central component of the general transcription factor TFIIH which plays major roles in transcription and nucleotide excision repair (NER). Here we present the high-resolution crystal structure of the Arch domain of XPD with its interaction partner MAT1, a central component of the CDK activating kinase complex. The analysis of the interface led to the identification of amino acid residues that are crucial for the MAT1-XPD interaction. More importantly, mutagenesis of the Arch domain revealed that these residues are essential for the regulation of (i) NER activity by either impairing XPD helicase activity or the interaction of XPD with XPG; (ii) the phosphorylation of the RNA polymerase II and RNA synthesis. Selleckchem Ertugliflozin Our results reveal how MAT1 shields these functionally important residues thereby providing insights into how XPD is regulated by MAT1 and defining the Arch domain as a major mechanistic player within the XPD scaffold.