Oscillations of neutral B mesons systems

The oscillation phenomenon in the neutral B mesons systems is now well established. The motivations and principles of the measurements are given; then the most recent results from the LEP experiments, the CDF collaboration at Fermilab and the SLD collaboration at SLAC are reviewed. The present world average of the \bd meson oscillation frequency is \dmd = 0.471 \pm 0.016 \ps and the lower limit on the \bs oscillation frequency is \dms > 12.4 \ps at 95% CL.Comment: 9 page

Morphisms of pre-Calabi-Yau categories and morphisms of cyclic A∞A_{\infty}-categories

In this article we prove that there exists a relation between $d$-pre-Calabi-morphisms introduced by M. Kontsevich, A. Takeda and Y. Vlassopoulos and cyclic $A_{\infty}$-morphisms, extending a result proved by D. Fern\'andez and E. Herscovich. This leads to a functor between the category of $d$-pre-Calabi-Yau structures and the partial category of $A_{\infty}$-categories of the form $\mathcal{A}\oplus\mathcal{A}^*[d-1]$ with $\mathcal{A}$ a graded quiver and whose morphisms are the data of an $A_{\infty}$-structure on $\mathcal{A}\oplus\mathcal{B}^*[d-1]$ together with $A_{\infty}$-morphisms $\mathcal{A}[1]\oplus\mathcal{B}^*[d]\rightarrow \mathcal{A}[1]\oplus\mathcal{A}^*[d]$ and $\mathcal{A}[1]\oplus\mathcal{B}^*[d]\rightarrow \mathcal{B}[1]\oplus\mathcal{B}^*[d]$

Constraints on anomalous quartic gauge boson couplings from photon pair events from 189 GeV to 209 GeV

The analysis of acoplanar photon pair events with missing energy and transverse momentum measured in the ALEPH detector at centre-of-mass energies between 189 and 209 GeV, leads to constraints on anomalous quartic gauge couplings in the reaction $e^{+}e^{-} \rightarrow \nu \bar{\nu} \gamma \gamma$. From 1-parameter fits, and using only the cross-section variation in the low missing mass region, the following 95 % CL constraints are obtained on the anomalous parameters $a_{0}/ \Lambda^{2}$ and $a_{c}/ \Lambda^{2}$: $-0.029 GeV^{-2} < a_{0}/ \Lambda^{2} < 0.026 GeV^{-2}$, $-0.080 GeV^{-2} < a_{c}/ \Lambda^{2} < 0.075 GeV^{-2}$

Measuring Endocytosis During Proliferative Cell Quiescence

Quiescence (also called "G0") is the state in which cells have exited the cell cycle but are capable to reenter as required. Though poorly understood, it represents one of the most prevalent cell states across all life. Many biologically important cell types reside in quiescence including mature hepatocytes, endothelial cells, and dormant adult stem cells. Furthermore, the quiescence program occurs in both short- and long-term varieties, depending on the physiological environments. A barrier slowing our understanding of quiescence has been a scarcity of available in vitro model systems to allow for the exploration of key regulatory pathways, such as endocytosis. Endocytosis, the internalization of extracellular material into the cell, is a fundamental and highly regulated process that impacts many cell biological functions. Accordingly, we have developed an in vitro model of deep quiescence in hTERT-immortalized RPE1 cells, combining both long-term contact inhibition and mitogen removal, to measure endocytosis. In addition, we present an analytical approach employing automated high-throughput microscopy and image analysis that yields high-content data allowing for meaningful and statistically robust interpretation. Importantly, the methods presented herein provide a suitable platform that can be easily adapted to investigate other regulatory processes across the cell cycle

Clustered Intracellular Salmonella enterica Serovar Typhimurium blocks host cell cytokinesis

Several bacterial pathogens and viruses interfere with the cell cycle of their host cells to enhance virulence. This is especially apparent in bacteria that colonize the gut epithelium, where inhibition of the cell cycle of infected cells enhances the intestinal colonization. We found that intracellular Salmonella enterica serovar Typhimurium induced the binucleation of a large proportion of epithelial cells by 14 h postinvasion and that the effect was dependent on an intact Salmonella pathogenicity island 2 (SPI-2) type 3 secretion system. The SPI-2 effectors SseF and SseG were required to induce binucleation. SseF and SseG are known to maintain microcolonies of Salmonella-containing vacuoles close to the microtubule organizing center of infected epithelial cells. During host cell division, these clustered microcolonies prevented the correct localization of members of the chromosomal passenger complex and mitotic kinesin-like protein 1 and consequently prevented cytokinesis. Tetraploidy, arising from a cytokinesis defect, is known to have a deleterious effect on subsequent cell divisions, resulting in either chromosomal instabilities or cell cycle arrest. In infected mice, proliferation of small intestinal epithelial cells was compromised in an SseF/SseG-dependent manner, suggesting that cytokinesis failure caused by S. Typhimurium delays epithelial cell turnover in the intestine

Endocytosis in proliferating, quiescent and terminally differentiated cells

Endocytosis mediates nutrient uptake, receptor internalization and the regulation of cell signaling. It is also hijacked by many bacteria, viruses and toxins to mediate their cellular entry. Several endocytic routes exist in parallel, fulfilling different functions. Most studies on endocytosis have used transformed cells in culture. However, as the majority of cells in an adult body have exited the cell cycle, our understanding is biased towards proliferating cells. Here, we review the evidence for the different pathways of endocytosis not only in dividing, but also in quiescent, senescent and terminally differentiated cells. During mitosis, residual endocytosis is dedicated to the internalization of caveolae and specific receptors. In non-dividing cells, clathrin-mediated endocytosis (CME) functions, but the activity of alternative processes, such as caveolae, macropinocytosis and clathrin-independent routes, vary widely depending on cell types and functions. Endocytosis supports the quiescent state by either upregulating cell cycle arrest pathways or downregulating mitogen-induced signaling, thereby inhibiting cell proliferation. Endocytosis in terminally differentiated cells, such as skeletal muscles, adipocytes, kidney podocytes and neurons, supports tissue-specific functions. Finally, uptake is downregulated in senescent cells, making them insensitive to proliferative stimuli by growth factors. Future studies should reveal the molecular basis for the differences in activities between the different cell states