Patients' and relatives' assessment of clozapine treatment

Published version: http://journals.cambridge.org/action/displayJournal?jid=PS

Quantum dot nonlinearity through cavity-enhanced feedback with a charge memory

In an oxide apertured quantum dot (QD) micropillar cavity-QED system, we found strong QD hysteresis effects and lineshape modifications even at very low intensities corresponding to less than 0.001 intracavity photons. We attribute this to the excitation of charges by the intracavity field; charges that get trapped at the oxide aperture, where they screen the internal electric field and blueshift the QD transition. This in turn strongly modulates light absorption by cavity QED effects, eventually leading to the observed hysteresis and lineshape modifications. The cavity also enables us to observe the QD dynamics in real time, and all experimental data agrees well with a power-law charging model. This effect can serve as a novel tuning mechanism for quantum dots.Comment: 7 pages, 6 figure

Cavity induced modifications to the resonance fluorescence and probe absorption of a laser-dressed V atom

A cavity-modified master equation is derived for a coherently driven, V-type three-level atom coupled to a single-mode cavity in the bad cavity limit. We show that population inversion in both the bare and dressed-state bases may be achieved, originating from the enhancement of the atom-cavity interaction when the cavity is resonant with an atomic dressed-state transition. The atomic populations in the dressed state representation are analysed in terms of the cavity-modified transition rates. The atomic fluorescence spectrum and probe absorption spectrum also investigated, and it is found that the spectral profiles may be controlled by adjusting the cavity frequency. Peak suppression and line narrowing occur under appropriate conditions.Comment: 12 pages, 10 postscript figures, to be appeared in Phys. Rev.

Conditional inactivation of the Men1 gene leads to pancreatic and pituitary tumorigenesis but does not affect normal development of these tissues

Mutations of the MEN1 gene, encoding the tumor suppressor menin, predispose individuals to the cancer syndrome multiple endocrine neoplasia type 1, characterized by the development of tumors of the endocrine pancreas and anterior pituitary and parathyroid glands. We have targeted the murine Men1 gene by using Cre recombinase-loxP technology to develop both total and tissue-specific knockouts of the gene. Conditional homozygous inactivation of the Men1 gene in the pituitary gland and endocrine pancreas bypasses the embryonic lethality associated with a constitutional Men1(-/-) genotype and leads to beta-cell hyperplasia in less than 4 months and insulinomas and prolactinomas starting at 9 months. The pituitary gland and pancreas develop normally in the conditional absence of menin, but loss of this transcriptional cofactor is sufficient to cause beta-cell hyperplasia in some islets; however, such loss is not sufficient to initiate pituitary gland tumorigenesis, suggesting that additional genetic events are necessary for the latter

Formation of Giant Quasibound Cold Diatoms by Strong Atom-Cavity Coupling

We show that giant quasi-bound diatomic complexes, whose size is typically hundreds of nm, can be formed by intra-cavity cold diatom photoassociation or photodissociation in the strong atom-cavity coupling regime.Comment: 4 pages, 3 figure

Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis

Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-offunction mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n¼40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC

Evolution of a periodic eight-black-hole lattice in numerical relativity

The idea of black-hole lattices as models for the large-scale structure of the universe has been under scrutiny for several decades, and some of the properties of these systems have been elucidated recently in the context of the problem of cosmological backreaction. The complete, three-dimensional and fully relativistic evolution of these system has, however, never been tackled. We explicitly construct the first of these solutions by numerically integrating Einstein's equation in the case of an eight-black-hole lattice with the topology of S3.Comment: 21 pages, 13 figures. Corrected and clarified discussio

Magnetic Behavior of a Mixed Ising Ferrimagnetic Model in an Oscillating Magnetic Field

The magnetic behavior of a mixed Ising ferrimagnetic system on a square lattice, in which the two interpenetrating square sublattices have spins +- 1/2 and spins +-1,0, in the presence of an oscillating magnetic field has been studied with Monte Carlo techniques. The model includes nearest and next-nearest neighbor interactions, a crystal field and the oscillating external field. By studying the hysteretic response of this model to an oscillating field we found that it qualitatively reproduces the increasing of the coercive field at the compensation temperature observed in real ferrimagnets, a crucial feature for magneto-optical applications. This behavior is basically independent of the frequency of the field and the size of the system. The magnetic response of the system is related to a dynamical transition from a paramagnetic to a ferromagnetic phase and to the different temperature dependence of the relaxation times of both sublattices.Comment: 10 figures. To be published in Phys.Rev

Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling

Large brain size is one of the defining characteristics of modern humans. Seckel syndrome (MIM 210600), a disorder of markedly reduced brain and body size, is associated with defective ATR-dependent DNA damage signaling. Only a single hypomorphic mutation of ATR has been identified in this genetically heterogeneous condition. We now report that mutations in the gene encoding pericentrin (PCNT)--resulting in the loss of pericentrin from the centrosome, where it has key functions anchoring both structural and regulatory proteins--also cause Seckel syndrome. Furthermore, we find that cells of individuals with Seckel syndrome due to mutations in PCNT (PCNT-Seckel) have defects in ATR-dependent checkpoint signaling, providing the first evidence linking a structural centrosomal protein with DNA damage signaling. These findings also suggest that other known microcephaly genes implicated in either DNA repair responses or centrosomal function may act in common developmental pathways determining human brain and body size