Chromatin-mediated cortical granule redistribution is responsible for the formation of the cortical granule-free domain in mouse eggs

AbstractA cortical granule-free domain (CGFD) overlies the metaphase chromatin in fully mature mouse eggs. Although a chromatin-induced localized release of cortical granules (CG) during maturation is thought to be a major contributing factor to its formation, there are indications that CG redistribution may also be involved in generating the CGFD. We performed experiments to determine the relative contributions of CG exocytosis and redistribution in generating the CGFD. We found that the CGFD-inducing activity was not specific to female germ cell chromatin and was heat stable but sensitive to DNase and protease treatment. Surprisingly, chelation of egg intracellular Ca2+ levels did not prevent CGFD formation in response to microinjection of exogenous chromatin, suggesting that development of the CGFD was not a result of CG exocytosis. This finding was confirmed by the lack of CG exudate on the plasma membrane surface of the injected eggs and the absence of conversion of ZP2 to ZP2f during formation of the new CGFD. Moreover, clamping intracellular Ca2+ did not prevent the formation of the CGFD during oocyte maturation, but did inhibit the maturation-associated release of CGs between metaphase I and II. Results of these experiments suggest that CG redistribution is the dominant factor in formation of the CGFD

Theory of Banana Liquid Crystal Phases and Phase Transitions

We study phases and phase transitions that can take place in the newly discovered banana (bow-shaped or bent-core) liquid crystal molecules. We show that to completely characterize phases exhibited by such bent-core molecules a third-rank tensor $T^{ijk}$ order parameter is necessary in addition to the vector and the nematic (second-rank) tensor order parameters. We present an exhaustive list of possible liquid phases, characterizing them by their space-symmetry group and order parameters, and catalog the universality classes of the corresponding phase transitions that we expect to take place in such bent-core molecular liquid crystals. In addition to the conventional liquid-crystal phases such as the nematic phase, we predict the existence of novel liquid phases, including the spontaneously chiral nematic $(N_T + 2)^*$ and chiral polar $(V_T + 2)^*$ phases, the orientationally-ordered but optically isotropic tetrahedratic $T$ phase, and a novel nematic $N_T$ phase with $D_{2d}$ symmetry that is neither uniaxial nor biaxial. Interestingly, the Isotropic-Tetrahedratic transition is {\em continuous} in mean-field theory, but is likely driven first-order by thermal fluctuations. We conclude with a discussion of smectic analogs of these phases and their experimental signatures.Comment: 28 pgs. RevTex, 32 eps figures, submitted to Phys. Rev.

Spontaneous parity and charge-conjugation violations at real isospin and imaginary baryon chemical potentials

The phase structure of two-flavor QCD is investigated at real isospin and imaginary quark chemical potentials by using the Polyakov-loop extended Nambu--Jona-Lasinio model. In the region, parity symmetry is spontaneously broken by the pion superfluidity phase transition, whereas charge-conjugation symmetry is spontaneously violated by the Roberge-Weiss transition. The chiral (deconfinement) crossover at zero isospin and quark chemical potentials is a remnant of the parity (charge-conjugation) violation. The interplay between the parity and charge-conjugation violations are analyzed, and it is investigated how the interplay is related to the correlation between the chiral and deconfinement crossovers at zero isospin and quark chemical potentials.Comment: 12 pages, 18 figures. Typos were revised. Symbols /P and /C were added in Figures 8a and 8b. Colors of the figures were changed. Some sentences were added and revise

No association between polymorphisms in the BDNF gene and age at onset in Huntington disease

BACKGROUND: Recent evidence suggests that brain-derived neurotrophic factor (BDNF) is an attractive candidate for modifying age at onset (AO) in Huntington disease (HD). In particular, the functional Val66Met polymorphism appeared to exert a significant effect. Here we evaluate BDNF variability with respect to AO of HD using markers that represent the entire locus. METHODS: Five selected tagging polymorphisms were genotyped across a 65 kb region comprising the BDNF gene in a well established cohort of 250 unrelated German HD patients. RESULTS: Addition of BDNF genotype variations or one of the marker haplotypes to the effect of CAG repeat lengths did not affect the variance of the AO. CONCLUSION: We were unable to verify a recently reported association between the functional Val66Met polymorphism in the BDNF gene and AO in HD. From our findings, we conclude that neither sequence variations in nor near the gene contribute significantly to the variance of AO

Relevance of pepsinogen, gastrin, and endoscopic atrophy in the diagnosis of autoimmune gastritis

Simple objective modalities are required for evaluating suspected autoimmune gastritis (AIG). This cross-sectional study aimed to examine whether pepsinogen, gastrin, and endoscopic findings can predict AIG. The diagnostic performance of endoscopic findings and serology in distinguishing AIG was evaluated. AIG was diagnosed in patients (N = 31) with anti-parietal cell antibody and/or intrinsic factor antibody positivity and histological findings consistent with AIG. Non-AIG patients (N = 301) were seronegative for anti-parietal cell antibodies. Receiver operating characteristic curve analysis of the entire cohort (N = 332) identified an endoscopic atrophic grade cutoff point of O3 on the Kimura–Takemoto classification (area under the curve [AUC]: 0.909), while those of pepsinogen-I, I/II ratio, and gastrin were 20.1 ng/mL (AUC: 0.932), 1.8 (AUC: 0.913), and 355 pg/mL (AUC: 0.912), respectively. In severe atrophy cases (≥ O3, N = 58, AIG/control; 27/31), the cutoff values of pepsinogen-I, I/II ratio, and gastrin were 9.8 ng/mL (AUC: 0.895), 1.8 (AUC: 0.86), and 355 pg/mL (AUC: 0.897), respectively. In conclusion, endoscopic atrophy is a predictor of AIG. High serum gastrin and low pepsinogen-I and I/II ratio are predictors even in the case of severe atrophy, suggesting their usefulness when the diagnosis of AIG is difficult or as serological screening tests