Almost all types of learning involve, to some degree, the ability to encode regularities across time and space. Although statistical learning (SL) research initially focused on offering a viable alternative to rule-based grammars and specialized mechanisms for word learning (e.g. [1,2]), the processing of regularities embedded in sensory input extends well beyond language. SL, therefore, was taken to offer a comprehensive theory of information processing, holding the promise of advancing knowledge across various domains of cognition including visual and auditory perception, multimodal integration, motor learning, segmentation, categorization and generalization, to name a few.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5124073/?report=classic
Di-(2-ethylhexyl) phthalate (DEHP) and its metabolite, mono-(2-ethylhexyl) phthalate (MEHP), are reproductive toxicants. However, disruptive effects of MEHP at low concentrations on the oocyte and developing blastocyst are unknown. Previously, we detected low levels of MEHP in follicular fluid aspirated from DEHP-treated cows associated with reduced estradiol levels. Moreover, the MEHP concentrations found were similar to those reported for follicular fluid aspirated from women who have undergone IVF cycles. In the current study, we used an in vitro embryo production model to examine the effect of MEHP at low levels on oocyte developmental competence. We set up several experiments to mimic the follicular fluid content, i.e., low MEHP level and low estradiol. For all experiments, cumulus oocyte complexes (COCs) were aspirated from bovine ovaries, then matured in vitro in standard oocyte maturation medium (OMM) supplemented with: MEHP at a range levels (20–1000nM) or with estradiol at a range levels (0–2000ng/ml). Then, oocytes were fertilized and cultured for an additional 7days to allow blastocyst development. Findings revealed that MEHP at low levels impairs oocyte developmental competence in a dose-dependent manner (P<0.05) and that estradiol by itself does not impair it. Accordingly, in another set of experiments, COCs were matured in vitro with MEHP at two choosen concentrations (20 or 1000nM) with or without estradiol, fertilized and cultured for 7days. Samples of mature oocytes and their derived blastocysts were subjected to quantitative real-time PCR to examine the profiles of selected genes (CYC1, MT-CO1, ATP5B, POU5F1, SOX2 and DNMT3b). Maturation of COCs with MEHP (20 or 1000nM) affected gene expression in the mature oocyte. Maturation of COCs with MEHP (20 or 1000nM) in the absence of estradiol reduced oocyte developmental competence (P<0.05). A differential carryover effect on transcript abundance was recorded in blastocysts developed from MEHP-treated oocytes. In the presence of estradiol, increased expression was recorded for CYC1, ATP5B, SOX2 and DNMT3b. In the absence of estradiol, decreased expression was recorded, with a significant effect for 1000nM MEHP (P<0.05). Taken together, the findings suggest that low levels of phthalate must be taken into consideration in risk assessments.
Based on the idea of defect migration as the principal mechanism in the dielectric relaxation of ice I-h, the concept of low-temperature dynamic crossover was proposed. It is known that at high temperatures, the diffusion of Bjerrum and ionic defects is high and their movement may be considered to be independent. Simple switching between these two mechanisms leads to a dynamic crossover at similar to 235 K. By introducing coupling between the Bjerrum and ionic defects, it is possible to describe the smooth bend in the relaxation time at low temperatures in ice Ih. However, because the mobility of Bjerrum orientation defects slows down at low temperatures, they may create blockages for proton hopping. The trapping of ionic defects by L-D defects for a long period of time leads to an increase in the relaxation time and causes a low-temperature crossover. This model was validated by experimental dielectric measurements using various temperature protocols.
Necrotizing Enterocolitis (NEC) is a severe inflammatory disorder leading to high morbidity and mortality rates. A growing body of evidence demonstrate the key role of the Toll like receptor 4 (TLR4) in NEC. This membranal receptor recognizes lipopolysaccharides (LPS) from the bacterial wall and triggers an inflammatory response. The aim of the present study was to elucidate the effect of LPS on paracellular permeability known to be severely affected in NEC. IEC-18 cells were treated with LPS and the effects on morphology, paracellular permeability and their associated gene and protein expressions were measured. Our results show that LPS down regulated the expression of occludin and ZO-1 mRNAs while up regulating Cdkn1a. In addition LPS caused a significant increase in paracellular permeability and epithelial barrier damage. Finally ZO-1 protein was found to be spatially disarrayed in the intercellular junctions in response to LPS. We conclude that LPS adversely affected the functionality of the intestinal epithelial barrier suggesting a new mechanism by which bacterial infection may contribute to the development of NEC. J. Cell. Physiol. 232: 381-390, 2017. (c) 2016 Wiley Periodicals, Inc.
It is well established that in ruminants, and in other species with estrous cycles, luteal regression is stimulated by the episodic release of prostaglandin F2$\alpha$ (PGF2$\alpha$) from the uterus, which reaches the corpus luteum (CL) through a countercurrent system between the uterine vein and the ovarian artery. Because of their luteolytic properties, PGF2$\alpha$ and its analogues are routinely administered to induce CL regression and synchronization of estrus, and as such, it is the basis of protocols for synchronizing ovulation. Luteal regression is defined as the loss of steroidogenic function (functional luteolysis) and the subsequent involution of the CL (structural luteolysis). During luteolysis, the CL undergoes dramatic changes in its steroidogenic capacity, vascularization, immune cell activation, ECM composition, and cell viability. Functional genomics and many other studies during the past 20 years elucidated the mechanism underlying PGF2$\alpha$ actions, substantially revising old concepts. PGF2$\alpha$ acts directly on luteal steroidogenic and endothelial cells, which express PGF2$\alpha$ receptors (PTGFR), or indirectly on immune cells lacking PTGFR, which can be activated by other cells within the CL. Accumulating evidence now indicates that the diverse processes initiated by uterine or exogenous PGF2$\alpha$, ranging from reduction of steroid production to apoptotic cell death, are mediated by locally produced factors. Data summarized here show that PGF2$\alpha$ stimulates luteal steroidogenic and endothelial cells to produce factors such as endothelin-1, angiopoietins, nitric oxide, fibroblast growth factor 2, thrombospondins, transforming growth factor-B1, and plasminogen activator inhibitor-B1, which act sequentially to inhibit progesterone production, angiogenic support, cell survival, and ECM remodeling to accomplish CL regression.
Recent years have seen an explosion of immunotherapies and a better understanding of the dynamics of immune response, especially in the context of treating disease. T cells and B cells, both key immune actors, upon stimulation activate and follow a programmed response: an initial proliferative burst before returning to quiescence and eventually dying. Therapeutically, evidence suggests that the more potent the T‐cell proliferative potential, the more successful the treatment.1 Therefore, to optimize such therapies, we need to fully understand what controls the lymphocyte division program, ultimately aiming to control immune response. In a recent publication in Nature Immunology, Heinzel2 scrutinizes how many divisions, also called division destiny (DD), lymphocytes undergo before returning to quiescence. Surprisingly, we learn that DD is controlled by an inheritable, actively regulated clock, determined by the expression of the Myc proto‐oncogene.
Magic size III–V semiconductor nanoclusters were synthesized. Non-continuous transition of the absorption spectra upon mild heating of the reaction solution is observed, indicating transformation between differently sized clusters. Further manipulation of the clusters is demonstrated for an InP MSC by growing a ZnS and ZnSe shell aiming at blue fluorescence. The quantum yield is limited due to formation of interfacial defects for thick ZnS shells.
M. I Tsindlekht, Genkin, V. M, Felner, I. , Zeides, F. , Katz, N. , Gazi, S. , Chromik, S. , Dobrovolskiy, O. V, Sachser, R. , ו Huth, M.. 2017. “Magnetic Moment Jumps In Flat And Nanopatterned Nb Thin-Walled Cylinders”. Physica C-Superconductivity And Its Applications, 533, Pp. 101-104. doi:10.1016/j.physc.2016.06.016.
