(Un)conditioned open dynamics in quantum optics

The study of the dynamics of open quantum systems sheds light on dissipative processes in quantum mechanics. Any system under continuous measurement is open and the act of measuring induces abrupt changes of the system’s state (collapses). The evolution conditioned to measurement records generates the so-called quantum trajectories. A continuous (unconditioned) evolution of the system is recovered by averaging over a large number of trajectories. Historically this kind of evolution has been the main focus of theoretical investigations. In this dissertation we consider both conditional and unconditional dynamics of quantum optical systems. Unconditioned dynamics is studied through the collision model paradigm. The formalism is described in detail and used for describing generic systems featuring many quantum emitters coupled to a usually one-dimensional field. The negligible-delay regime is widely explored. Collision models are used to unveil the mechanisms underlying the decoherence-free evolution regime typical of these systems, which has received considerable attention in the last years. Then we investigate conditioned dynamics by broadening the study of statistics of quantum trajectories. Specifically, we exploit the information about the emission’s full-counting statistics from large deviations to define a nonclassicality witness. Finally we come back to collision models in order to extend the theory of biased quantum trajectories from Lindblad-like dynamics to sequences of arbitrary dynamical maps, providing at once a transparent physical interpretation

Richer than you since 1895? A study of socioeconomic diversity at LSE

Original survey data is used to assess the degree of socioeconomic diversity at LSE in regard to student household income and parent educational attainment, finding significant variation between countries of origin and academic departments

The effect of residential urban greenness on allergic respiratory diseases in youth: A narrative review

Background: Environmental exposures across the life course may be a contributor to the increased worldwide prevalence of respiratory and allergic diseases occurring in the last decades. Asthma and rhinoconjunctivitis especially contribute to the global burden of disease. Greenness has been suggested to have beneficial effects in terms of reduction of occurrence of allergic respiratory diseases. However, the available evidence of a relationship between urban greenness and childhood health outcomes is not yet conclusive. The current review aimed at investigating the current state of evidence, exploring the relationship between children's exposure to residential urban greenness and development of allergic respiratory diseases, jointly considering health outcomes and study design. Methods: The search strategy was designed to identify studies linking urban greenness exposure to asthma, rhinoconjunctivitis, and lung function in children and adolescents. This was a narrative review of literature following PRISMA guidelines performed using electronic search in databases of PubMed and Embase (Ovid) from the date of inception to December 2018. Results: Our search strategy identified 2315 articles; after exclusion of duplicates (n = 701), 1614 articles were screened. Following review of titles and abstracts, 162 articles were identified as potentially eligible. Of these, 148 were excluded following full-text evaluation, and 14 were included in this review. Different methods for assessing greenness exposure were found; the most used was Normalized Difference Vegetation Index. Asthma, wheezing, bronchitis, rhinoconjunctivitis, allergic symptoms, lung function, and allergic sensitization were the outcomes assessed in the identified studies; among them, asthma was the one most frequently investigated. Conclusions: The present review showed inconsistencies in the results mainly due to differences in study design, population, exposure assessment, geographic region, and ascertainment of outcome. Overall, there is a suggestion of an association between urban greenness in early life and the occurrence of allergic respiratory diseases during childhood, although the evidence is still inconsistent. It is therefore hard to draw a conclusive interpretation, so that the understanding of the impact of greenness on allergic respiratory diseases in children and adolescents remains difficult

Isolated Subtle Neurological Abnormalities in Mild Cognitive Impairment Types

Background: Isolated, subtle neurological abnormalities (ISNA) are commonly seen in aging and have been related to cerebral small vessel disease (SVD) and subcortical atrophy in neurologically and cognitively healthy aging subjects. Objective: To investigate the frequency of ISNA in different mild cognitive impairment (MCI) types and to evaluate for each MCI type, the crosssectional relation between ISNA and white matter hyperintensities (WMH), lacunes, caudate atrophy, and ventricular enlargement. Methods: One thousand two hundred fifty subjects with different MCI types were included in the analysis and underwent brain magnetic resonance imaging. WMHs were assessed through two visual rating scales. Lacunes were also rated. Atrophy of the caudate nuclei and ventricular enlargement were assessed through the bicaudate ratio (BCr) and the lateral ventricles to brain ratio (LVBr), respectively. Apolipoprotein E (APOE) genotypes were also assessed. The routine neurological examination was used to evaluate ISNAs that were clustered as central-based signs, cerebellar-based signs, and primitive reflexes. The items of Part-III of the Unified Parkinson’s Disease Rating Scale were used to evaluate ISNAs that were clustered as mild parkinsonian signs. Associations of ISNAs with imaging findings were determined through logistic regression analysis. Results: The ISNAs increase with the age and are present in all MCI types, particularly in those multiple domains, and carrying the APOE ϵ4 allele, and are associated with WMH, lacunes, BCr, and LVBr. Conclusion: This study demonstrates that cortical and subcortical vascular and atrophic processes contribute to ISNAs. Long prospective population-based studies are needed to disentangle the role of ISNAs in the conversion from MCI to dementia

Mispositioned Neurokinin-1 Receptor-Expressing Neurons Underlie Heat Hyperalgesia in Disabled-1 Mutant Mice.

Reelin (Reln) and Disabled-1 (Dab1) participate in the Reln-signaling pathway and when either is deleted, mutant mice have the same spinally mediated behavioral abnormalities, increased sensitivity to noxious heat and a profound loss in mechanical sensitivity. Both Reln and Dab1 are highly expressed in dorsal horn areas that receive and convey nociceptive information, Laminae I-II, lateral Lamina V, and the lateral spinal nucleus (LSN). Lamina I contains both projection neurons and interneurons that express Neurokinin-1 receptors (NK1Rs) and they transmit information about noxious heat both within the dorsal horn and to the brain. Here, we ask whether the increased heat nociception in Reln and dab1 mutants is due to incorrectly positioned dorsal horn neurons that express NK1Rs. We found more NK1R-expressing neurons in Reln-/- and dab1-/- Laminae I-II than in their respective wild-type mice, and some NK1R neurons co-expressed Dab1 and the transcription factor Lmx1b, confirming their excitatory phenotype. Importantly, heat stimulation in dab1-/- mice induced Fos in incorrectly positioned NK1R neurons in Laminae I-II. Next, we asked whether these ectopically placed and noxious-heat responsive NK1R neurons participated in pain behavior. Ablation of the superficial NK1Rs with an intrathecal injection of a substance P analog conjugated to the toxin saporin (SSP-SAP) eliminated the thermal hypersensitivity of dab1-/- mice, without altering their mechanical insensitivity. These results suggest that ectopically positioned NK1R-expressing neurons underlie the heat hyperalgesia of Reelin-signaling pathway mutants, but do not contribute to their profound mechanical insensitivity

DNA demethylation caused By 5-Aza-2'-Deoxycytidine induces mitotic alterations and aneuploidy

Aneuploidy, the unbalanced number of chromosomes in a cell, is considered a prevalent form of genetic instability and is largely acknowledged as a condition implicated in tumorigenesis. Epigenetic alterations like DNA hypomethylation have been correlated with cancer initiation/progression. Furthermore, a growing body of evidence suggests the involvement of epigenome-wide disruption as a cause of global DNA hypomethylation in aneuploidy generation. Here, we report that the DNA hypomethylating drug 5-aza-2'-deoxycytidine (DAC), affects the correct ploidy of nearly diploid HCT-116 human cells by altering the methylation pattern of the chromosomes. Specifically, we show that a DACinduced reduction of 5-Methyl Cytosine at the pericentromeric region of chromosomes correlates with aneuploidy and mitotic defects. Our results suggest that DNA hypomethylation leads to aneuploidy by altering the DNA methylation landscape at the centromere that is necessary to ensure proper chromosomes segregation by recruiting the proteins necessary to build up a functional kinetochore