On Saturated kk-Sperner Systems

Given a set $X$, a collection $\mathcal{F}\subseteq\mathcal{P}(X)$ is said to be $k$-Sperner if it does not contain a chain of length $k+1$ under set inclusion and it is saturated if it is maximal with respect to this property. Gerbner et al. conjectured that, if $|X|$ is sufficiently large with respect to $k$, then the minimum size of a saturated $k$-Sperner system $\mathcal{F}\subseteq\mathcal{P}(X)$ is $2^{k-1}$. We disprove this conjecture by showing that there exists $\varepsilon>0$ such that for every $k$ and $|X| \geq n_0(k)$ there exists a saturated $k$-Sperner system $\mathcal{F}\subseteq\mathcal{P}(X)$ with cardinality at most $2^{(1-\varepsilon)k}$. A collection $\mathcal{F}\subseteq \mathcal{P}(X)$ is said to be an oversaturated $k$-Sperner system if, for every $S\in\mathcal{P}(X)\setminus\mathcal{F}$, $\mathcal{F}\cup\{S\}$ contains more chains of length $k+1$ than $\mathcal{F}$. Gerbner et al. proved that, if $|X|\geq k$, then the smallest such collection contains between $2^{k/2-1}$ and $O\left(\frac{\log{k}}{k}2^k\right)$ elements. We show that if $|X|\geq k^2+k$, then the lower bound is best possible, up to a polynomial factor.Comment: 17 page

Saturation in the Hypercube and Bootstrap Percolation

Let $Q_d$ denote the hypercube of dimension $d$. Given $d\geq m$, a spanning subgraph $G$ of $Q_d$ is said to be $(Q_d,Q_m)$-saturated if it does not contain $Q_m$ as a subgraph but adding any edge of $E(Q_d)\setminus E(G)$ creates a copy of $Q_m$ in $G$. Answering a question of Johnson and Pinto, we show that for every fixed $m\geq2$ the minimum number of edges in a $(Q_d,Q_m)$-saturated graph is $\Theta(2^d)$. We also study weak saturation, which is a form of bootstrap percolation. A spanning subgraph of $Q_d$ is said to be weakly $(Q_d,Q_m)$-saturated if the edges of $E(Q_d)\setminus E(G)$ can be added to $G$ one at a time so that each added edge creates a new copy of $Q_m$. Answering another question of Johnson and Pinto, we determine the minimum number of edges in a weakly $(Q_d,Q_m)$-saturated graph for all $d\geq m\geq1$. More generally, we determine the minimum number of edges in a subgraph of the $d$-dimensional grid $P_k^d$ which is weakly saturated with respect to `axis aligned' copies of a smaller grid $P_r^m$. We also study weak saturation of cycles in the grid.Comment: 21 pages, 2 figures. To appear in Combinatorics, Probability and Computin

Bcl-xL-mediated remodeling of rod and cone synaptic mitochondria after postnatal lead exposure: electron microscopy, tomography and oxygen consumption.

PurposePostnatal lead exposure produces rod-selective and Bax-mediated apoptosis, decreased scotopic electroretinograms (ERGs), and scotopic and mesopic vision deficits in humans and/or experimental animals. Rod, but not cone, inner segment mitochondria were considered the primary site of action. However, photoreceptor synaptic mitochondria were not examined. Thus, our experiments investigated the structural and functional effects of environmentally relevant postnatal lead exposure on rod spherule and cone pedicle mitochondria and whether Bcl-xL overexpression provided neuroprotection.MethodsC57BL/6N mice pups were exposed to lead only during lactation via dams drinking water containing lead acetate. The blood [Pb] at weaning was 20.6±4.7 µg/dl, which decreased to the control value by 2 months. To assess synaptic mitochondrial structural differences and vulnerability to lead exposure, wild-type and transgenic mice overexpressing Bcl-xL in photoreceptors were used. Electron microscopy, three-dimensional electron tomography, and retinal and photoreceptor synaptic terminal oxygen consumption (QO(2)) studies were conducted in adult control, Bcl-xL, lead, and Bcl-xL/lead mice.ResultsThe spherule and pedicle mitochondria in lead-treated mice were swollen, and the cristae structure was markedly changed. In the lead-treated mice, the mitochondrial cristae surface area and volume (abundance: measure correlated with ATP (ATP) synthesis) were decreased in the spherules and increased in the pedicles. Pedicles also had an increased number of crista segments per volume. In the lead-treated mice, the number of segments/crista and fraction of cristae with multiple segments (branching) similarly increased in spherule and pedicle mitochondria. Lead-induced remodeling of spherule mitochondria produced smaller cristae with more branching, whereas pedicle mitochondria had larger cristae with more branching and increased crista junction (CJ) diameter. Lead decreased dark- and light-adapted photoreceptor and dark-adapted photoreceptor synaptic terminal QO(2). Bcl-xL partially blocked many of the lead-induced alterations relative to controls. However, spherules still had partially decreased abundance, whereas pedicles still had increased branching, increased crista segments per volume, and increased crista junction diameter. Moreover, photoreceptor and synaptic QO(2) were only partially recovered.ConclusionsThese findings reveal cellular and compartmental specific differences in the structure and vulnerability of rod and cone inner segment and synaptic mitochondria to postnatal lead exposure. Spherule and pedicle mitochondria in lead-exposed mice displayed complex and distinguishing patterns of cristae and matrix damage and remodeling consistent with studies showing that synaptic mitochondria are more sensitive to Ca(2+) overload, oxidative stress, and ATP loss than non-synaptic mitochondria. The lead-induced decreases in QO(2) likely resulted from the decreased spherule cristae abundance and smaller cristae, perhaps due to Bax-mediated effects as they occurred in apoptotic rod inner segments. The increase in pedicle cristae abundance and CJ diameter could have resulted from increased Drp1-mediated fission, as small mitochondrial fragments were observed. The mechanisms of Bcl-xL-mediated remodeling might occur via interaction with formation of CJ protein 1 (Fcj1), whereas the partial protection of synaptic QO(2) might result from the enhanced efficiency of energy metabolism via Bcl-xL's direct interaction with the F1F0 ATP synthase and/or regulation of cellular redox status. These lead-induced alterations in photoreceptor synaptic terminal mitochondria likely underlie the persistent scotopic and mesopic deficits in lead-exposed children, workers, and experimental animals. Our findings stress the clinical and scientific importance of examining synaptic dysfunction following injury or disease during development, and developing therapeutic treatments that prevent synaptic degeneration in retinal and neurodegenerative disorders even when apoptosis is blocked

On saturated k-Sperner systems

Given a set X , a collection F ⊆ P (X) is said to be k-Sperner if it does not contain a chain of length k + 1 under set inclusion and it is saturated if it is maximal with respect to this property. Gerbner et al. [11] conjectured that, if |X| is sufficiently large with respect to k, then the minimum size of a saturated k-Sperner system F ⊆ P (X) is 2k-1 . We disprove this conjecture by showing that there exists ε > 0 such that for every k and |X| > n0 (k) there exists a saturated k-Sperner system F ⊆P (X) with cardinality at most 2 (1- ε)k. A collection F ⊆ P (X) is said to be an oversaturated k-Sperner system if, for every S∈P (X) \ F, F∪{ S } contains more chains of length k +1 than F. Gerbner et al. [11] proved that, if |X| > k, then the smallest such collection contains between 2k/2-1 and O (log k k 2 k) elements. We show that if |X| > k2 + k, then the lower bound is best possible, up to a polynomial factor

Maternal thyroid function and child educational attainment: prospective cohort study

Objective: To determine if first trimester maternal thyroid dysfunction is a critical determinant of child scholastic performance and overall educational attainment. Design: Prospective cohort study. Setting: Avon Longitudinal Study of Parents and Children cohort in the UK. Participants: 4615 mother-child pairs with an available first trimester sample (median 10 weeks gestation, interquartile range 8-12). Exposures: Free thyroxine, thyroid stimulating hormone, and thyroid peroxidase antibodies assessed as continuous measures and the seven clinical categories of maternal thyroid function. Main outcome measures: Five age-specific national curriculum assessments in 3580 children at entry stage assessment at 54 months, increasing up to 4461 children at their final school assessment at age 15. Results: No strong evidence of clinically meaningful associations of first trimester free thyroxine and thyroid stimulating hormone levels with entry stage assessment score or Standard Assessment Test scores at any of the key stages was found. Associations of maternal free thyroxine or thyroid stimulating hormone with the total number of General Certificates of Secondary Education (GCSEs) passed (range 0-16) were all close to the null: free thyroxine, rate ratio per pmol/L 1.00 (95% confidence interval 1.00 to 1.01); and thyroid stimulating hormone, rate ratio 0.98 (0.94 to 1.02). No important relationship was observed when more detailed capped scores of GCSEs allowing for both the number and grade of pass or when language, mathematics, and science performance were examined individually or when all educational assessments undertaken by an individual from school entry to leaving were considered. 200 (4.3%) mothers were newly identified as having hypothyroidism or subclinical hypothyroidism and 97 (2.1%) subclinical hyperthyroidism or hyperthyroidism. Children of mothers with thyroid dysfunction attained an equivalent number of GCSEs and equivalent grades as children of mothers with euthyroidism. Conclusions: Maternal thyroid dysfunction in early pregnancy does not have a clinically important association with impaired child performance at school or educational achievement