Baxtervinding7354

Purpose To evaluate the refractive results and rotational stability of Eyecryl toric phakic intraocular lens (pIOL). Methods In this retrospective single-surgeon case series, manifest refraction, visual acuities, endothelial cell density (ECD), and pIOL rotation were evaluated over 6 months. Results 43 eyes from 23 patients were included. At 6 months, the SE was within ±0.50  D of emmetropia in 30 (70%) eyes and within ±1.00  D of emmetropia in 39 (91%) eyes. The efficacy and safety indices were 1.25 ± 0.38 and 1.41 ± 0.34, respectively. Mean ECD was 2719 ± 296 cells/mm2 at the preoperative visit and 2779.42 ± 422 cells/mm2 at the 6-month visit (p > 0.05). The mean value of absolute axis orientation error was 4.95 ± 5.28°. Mean absolute change in axis orientation between visits was less than 3° for all visit intervals. Ninety percent or more of lenses were found to rotate 5° or less between all visit intervals. None of the patients experienced a vision-threatening complication, and no patient required secondary IOL repositioning. Conclusion The pIOL appears to effectively reduce subjective manifest astigmatism and provide good visual acuity. MM3122 Its position was found to be stable throughout the follow-up. Copyright © 2020 Dilek Yaşa et al.Apoptosis is characterized by the destruction of essential cell organelles, including the cell nucleus. The nuclear envelope (NE) separates the nuclear interior from the cytosol. During apoptosis, the apoptotic machinery, in particular caspases, increases NE permeability by cleaving its proteins, such as those of the nuclear pore complex (NPC) and the nuclear lamina. This in turns leads to passive diffusion of cytosolic apoptogenic proteins, such as caspases and nucleases, through NPCs into the nucleus and the subsequent breakdown of the NE and destruction of the nucleus. However, NE leakiness at early stages of the apoptotic process can also occur in a caspase-independent manner, where Bax, by a non-canonical action, promotes transient and repetitive localized generation and subsequent rupture of nuclear protein-filled nuclear bubbles. This NE rupture leads to discharge of apoptogenic nuclear proteins from the nucleus to the cytosol, a process that can contribute to the death process. Therefore, the NE may play a role as mediator of cell death at early stages of apoptosis. The NE can also serve as a platform for assembly of complexes that regulate the death process. Thus, the NE should be viewed as both a mediator of the cell death process and a target. © The Author(s) 2020.lncRNA genes can be genic or "intergenic". "Genic" RNAs can be further divided into six biotypes. Through genome-wide analysis of a publicly available data set on corticogenesis, we found that the divergent lncRNA (XH) biotype, comprising the lncRNA and the coding gene being in opposite directions in a head-to-head manner, was most prominent during neural commitment. Within this biotype, a coding gene/divergent RNA pair of the BASP1 gene and the uncharacterized RNA loc285696 (hitherto referred as BASP1-AS1) formed a major HUB gene during neuronal differentiation. Experimental validation during the in vitro differentiation of human neural progenitor cells (hNPCs) showed that BASP1-AS1 regulates the expression of its adjacent coding gene, BASP1. Both transcripts increased sharply on the first day of neuronal differentiation of hNPCs, to fall steadily thereafter, reaching very low levels in differentiated neurons. BASP1-AS1 RNA and the BASP1 gene formed a molecular complex that also included the transcription factor TCF12. TCF12 is coded by the DYX1 locus, associated with inherited dyslexia and neurodevelopmental defects. Knockdown of BASP1-AS1, BASP1, or TCF12 impaired the neuronal differentiation of hNPCs, as seen by reduction in DCX and TUJ1-positive cells and by reduced neurite length. There was also increased cell proliferation. A common set of critical genes was affected by the three molecules in the complex. Our study thus identified the role of the XH biotype and a novel mediator of neuronal differentiation-the complex of BASP1-AS1, BASP1, and TCF12. It also linked a neuronal differentiation pathway to inherited dyslexia. © The Author(s) 2020.Glucose is a major requirement for biological life. Its concentration is constantly sensed at the cellular level, allowing for adequate responses to any changes of glucose availability. Such responses are mediated by key sensors and signaling pathway components that adapt cellular metabolism to glucose levels. One of the major hubs of these responses is mechanistic target of rapamycin (mTOR) kinase, which forms the mTORC1 and mTORC2 protein complexes. Under physiological glucose concentrations, mTORC1 is activated and stimulates a number of proteins and enzymes involved in anabolic processes, while restricting the autophagic process. Conversely, when glucose levels are low, mTORC1 is inhibited, in turn leading to the repression of numerous anabolic processes, sparing ATP and antioxidants. Understanding how mTORC1 activity is regulated by glucose is not only important to better delineate the biological function of mTOR, but also to highlight potential therapeutic strategies for treating diseases characterized by deregulated glucose availability, as is the case of cancer. In this perspective, we depict the different sensors and upstream proteins responsible of controlling mTORC1 activity in response to changes in glucose concentration. This includes the major energy sensor AMP-activated protein kinase (AMPK), as well as other independent players. The impact of such modes of regulation of mTORC1 on cellular processes is also discussed. © The Author(s) 2020.The lifespan of a neutrophil is short and limited by programmed cell death, followed by efferocytosis. When activated or exposed to insult, neutrophil death may be delayed to support neutrophil effector functions such as phagocytosis, cytokine release, and pathogen destruction by degranulation. However, neutrophils may also alter the type of cell death and thereby affect inflammatory responses and tissue remodeling. This review briefly introduces the various forms of neutrophil death including apoptosis, necrosis/necroptosis, and the formation of so-called "neutrophil extracellular traps" (NETs), and it summarizes the clearance of dead cells by efferocytosis. Importantly, distinct types of neutrophil death have been found to drive chronic inflammatory disorders and cancer. Thus, the tumor and its microenvironment can delay neutrophil apoptosis to exploit their pro-angiogenic and pro-metastatic properties. Conversely, neutrophils may enter rapid and suicidal cell death by forming extracellular traps, which are expelled DNA strands with neutrophil proteins. Components of these DNA-protein complexes such as histones, high-mobility group protein B1, or neutrophil elastase have been found to promote cancer cell proliferation, adhesion, migration, invasion, and thereby tumor metastasis. In other settings of chronic inflammatory disease such as gout, NETs have been found protective rather than detrimental, as they promoted the local degradation of pro-inflammatory cytokines by neutrophil proteases. Thus, the interaction of neutrophils with the tissue environment extends beyond the stage of the living cell and the type of neutrophil death shapes immune responses and tissue remodeling in health and disease. © The Author(s) 2020.Kinesin-7 CENP-E is an essential kinetochore motor required for chromosome alignment and congression. However, the specific functions of CENP-E in the spermatogenic cells during spermatogenesis remain unknown. In this study, we find that CENP-E proteins are expressed in the spermatogonia, spermatocytes, and the elongating spermatids. CENP-E inhibition by specific inhibitor GSK923295 results in the disruption of spermatogenesis and cell cycle arrest of spermatogenic cells. Both spermatogonia and spermatocytes are arrested in metaphase and several chromosomes are not aligned at the equatorial plate. We find that CENP-E inhibition leads to chromosome misalignment, the spindle disorganization, and the formation of the aneuploidy cells. Furthermore, the inhibition of CENP-E results in the defects in the formation of spermatids, including the sperm head condensation and the sperm tail formation. We have revealed that kinesin-7 CENP-E is essential for chromosome alignment and genome stability of the spermatogenic cells. © The Author(s) 2020.In order to harness the potential of pluripotent stem cells, we need to understand how to differentiate them to our target cell types. Here, we developed a protocol to differentiate mouse embryonic stem cells (ESCs) to renal progenitors in a step-wise manner. Microarrays were used to track the transcriptional changes at each stage of differentiation and we observed that genes associated with metanephros, ureteric bud, and blood vessel development were significantly upregulated as the cells differentiated towards renal progenitors. Priming the ESCs and optimizing seeding cell density and growth factor concentrations helped improve differentiation efficiency. Organoids were used to determine the developmental potential of the renal progenitor cells. Aggregated renal progenitors gave rise to organoids consisting of LTL+/E-cadherin+ proximal tubules, cytokeratin+ ureteric bud-derived tubules, and extracellular matrix proteins secreted by the cells themselves. Over-expression of key kidney developmental genes, Pax2, Six1, Eya1, and Hox11 paralogs, during differentiation did not improve differentiation efficiency. Altogether, we developed a protocol to differentiate mouse ESCs in a manner that recapitulates embryonic kidney development and showed that precise gene regulation is essential for proper differentiation to occur. © The Author(s) 2020.Green's one-step-late (OSL) algorithm is a popular image reconstruction algorithm in emission-data tomography, in spite of its convergence issues. One drawback of Green's algorithm is that the algorithm exhibits non-stationary regularization when the algorithm's projector and backprojector model the attenuation effects in single photon emission computed tomography (SPECT). This paper suggests a remedy to improve Green's OSL algorithm so that stationary regularization can be obtained. This paper also observes some similarities between the modified Green's OSL algorithm and the gradient descent algorithm.Head and neck squamous cell carcinoma (HNSCC) lacks predictive biomarkers for drug responses. By targeted sequencing, we identified two MAPK1 mutations in recurrent HNSCC, MAPK1p.D321N, and p.R135K. We previously reported an exceptional erlotinib responder with MAPK1p.E322K. Here, by in silico and drug studies, we determined functions of these two recurrence-associated MAPK1 mutations. Residues D321, R135, and E322 are in 3D proximity. MAPK1p.D321N drives marked in vivo erlotinib sensitivity, while p.R135K's effect is moderate. © The Author(s) 2020.Although there is a growing consensus about the positive relationship between prevention of overweight/obesity and academic performance in children, relevant studies targeting the relationship between underweight and academic performance are scarce. This study aimed to examine the longitudinal relationship of favorable weight change to academic performance in schoolchildren. We analyzed 2-year longitudinal data derived from 197 seventh-grade children aged 12-13 years. Academic performance was assessed using the total grade points of five academic subjects. Body mass index (BMI) was calculated as body weight (kg)/height (m2). A significant interaction effect of baseline BMI and BMI changes over 2 years (B = -0.10, SE B = 0.03, β = -0.40, t = -3.37, p  less then  0.001) was noted after controlling for confounders such as socioeconomic status, afterschool learning duration, screen time, exercise habits, and cardiorespiratory fitness. When the centered baseline BMI was outside the interval [-2.49, 3.21], the slope of the change in BMI was significant (p  less then  0.