Andrea Freschi
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View article: Typical Ramsey properties of the primes, abelian groups and other discrete structures
Typical Ramsey properties of the primes, abelian groups and other discrete structures Open
Given a matrix $A$ with integer entries, a subset $S$ of an abelian group and $r \in \mathbb N$, we say that $S$ is $(A,r)$-Rado if any $r$-colouring of $S$ yields a monochromatic solution to the system of equations $Ax=0$. A classical res…
View article: The induced saturation problem for posets
The induced saturation problem for posets Open
For a fixed poset P, a family F of subsets of [n] is induced P-saturated if F does not contain an induced copy of P, but for every subset S of [n] such that S ∉ F, P is an induced subposet of F ∪{S}. The size of the smallest such family F …
View article: A general bound for the induced poset saturation problem
A general bound for the induced poset saturation problem Open
For a fixed poset $P$, a family $\mathcal F$ of subsets of $[n]$ is induced $P$-saturated if $\mathcal F$ does not contain an induced copy of $P$, but for every subset $S$ of $[n]$ such that $ S\not \in \mathcal F$, then $P$ is an induced …
View article: An oriented discrepancy version of Dirac's theorem
An oriented discrepancy version of Dirac's theorem Open
The study of graph discrepancy problems, initiated by Erdős in the 1960s, has received renewed attention in recent years. In general, given a $2$-edge-coloured graph $G$, one is interested in embedding a copy of a graph $H$ in $G$ with lar…
View article: The induced saturation problem for posets
The induced saturation problem for posets Open
For a fixed poset $P$, a family $\mathcal F$ of subsets of $[n]$ is induced $P$-saturated if $\mathcal F$ does not contain an induced copy of $P$, but for every subset $S$ of $[n]$ such that $ S\not \in \mathcal F$, $P$ is an induced subpo…
View article: Dirac-type results for tilings and coverings in ordered graphs
Dirac-type results for tilings and coverings in ordered graphs Open
A recent paper of Balogh, Li and Treglown [3] initiated the study of Dirac-type problems for ordered graphs. In this paper, we prove a number of results in this area. In particular, we determine asymptotically the minimum degree threshold …
View article: The number of the CTCF binding sites of the <i>H19/IGF2</i>:IG-DMR correlates with DNA methylation and expression imprinting in a humanized mouse model
The number of the CTCF binding sites of the <i>H19/IGF2</i>:IG-DMR correlates with DNA methylation and expression imprinting in a humanized mouse model Open
The reciprocal parent of origin-specific expression of H19 and IGF2 is controlled by the H19/IGF2:IG-DMR (IC1), whose maternal allele is unmethylated and acts as a CTCF-dependent insulator. In humans, internal IC1 deletions are associated …
View article: Loss of Snord116 alters cortical neuronal activity in mice: a preclinical investigation of Prader–Willi syndrome
Loss of Snord116 alters cortical neuronal activity in mice: a preclinical investigation of Prader–Willi syndrome Open
Prader–Willi syndrome (PWS) is a neurodevelopmental disorder that is characterized by metabolic alteration and sleep abnormalities mostly related to rapid eye movement (REM) sleep disturbances. The disease is caused by genomic imprinting d…
View article: Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors
Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors Open
Imprinted genes are highly expressed in the hypothalamus; however, whether specific imprinted genes affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader-Willi syndrome (PWS), a neurodevelopm…
View article: Humanized H19/Igf2 locus reveals diverged imprinting mechanism between mouse and human and reflects Silver–Russell syndrome phenotypes
Humanized H19/Igf2 locus reveals diverged imprinting mechanism between mouse and human and reflects Silver–Russell syndrome phenotypes Open
Genomic imprinting is essential for mammalian development. Curiously, elements that regulate genomic imprinting, the imprinting control regions (ICRs), often diverge across species. To understand whether the diverged ICR sequence plays a s…
View article: The paternally imprinted gene<i>Snord116</i>regulates cortical neuronal activity
The paternally imprinted gene<i>Snord116</i>regulates cortical neuronal activity Open
Prader-Willi syndrome (PWS) is a neurodevelopmental disorder that is characterized by rapid eye movement (REM) sleep abnormalities. The disease is caused by genomic imprinting defects that are inherited through the paternal line. Among the…
View article: Tissue-specific and mosaic imprinting defects underlie opposite congenital growth disorders in mice
Tissue-specific and mosaic imprinting defects underlie opposite congenital growth disorders in mice Open
Differential DNA methylation defects of H19/IGF2 are associated with congenital growth disorders characterized by opposite clinical pictures. Due to structural differences between human and mouse, the mechanisms by which mutations of the H…
View article: Humanized <i>H19/Igf2</i> locus reveals diverged imprinting mechanism between mouse and human and reflects Silver–Russell syndrome phenotypes
Humanized <i>H19/Igf2</i> locus reveals diverged imprinting mechanism between mouse and human and reflects Silver–Russell syndrome phenotypes Open
Significance Genomic imprinting is essential for mammalian development. Curiously, elements that regulate genomic imprinting, the imprinting control regions (ICRs), often diverge across species. To understand whether the diverged ICR seque…
View article: Two maternal duplications involving the CDKN1C gene are associated with contrasting growth phenotypes
Two maternal duplications involving the CDKN1C gene are associated with contrasting growth phenotypes Open
We report two novel in cis microduplications encompassing part of the centromeric domain of the 11p15.5-p15.4 imprinted gene cluster and both including the growth inhibitor CDKN1C gene. Likely, as a consequence of the differential involvem…