Paid employment and common mental disorders in 50–64-year olds: analysis of three cross-sectional nationally representative survey samples in 1993, 2000 and 2007

Associations between employment status and mental health are well recognised, but evidence is sparse on the relationship between paid employment and mental health in the years running up to statutory retirement ages using robust mental health measures. In addition, there has been no investigation into the stability over time in this relationship: an important consideration if survey findings are used to inform future policy. The aim of this study is to investigate the association between employment status and common mental disorder (CMD) in 50–64-year old residents in England and its stability over time, taking advantage of three national mental health surveys carried out over a 14-year period. Data were analysed from the British National Surveys of Psychiatric Morbidity of 1993, 2000 and 2007. Paid employment status was the primary exposure of interest and CMD the primary outcome – both ascertained identically in all three surveys (CMD from the revised Clinical Interview Schedule). Multivariable logistic regression models were used. The prevalence of CMD was higher in people not in paid employment across all survey years; however, this association was only present for non-employment related to poor health as an outcome and was not apparent in those citing other reasons for non-employment. Odds ratios for the association between non-employment due to ill health and CMD were 3.05 in 1993, 3.56 in 2000, and 2.80 in 2007, after adjustment for age, gender, marital status, education, social class, housing tenure, financial difficulties, smoking status, recent physical health consultation and activities of daily living impairment. The prevalence of CMD was higher in people not in paid employment for health reasons, but was not associated with non-employment for other reasons. Associations had been relatively stable in strength from 1993 to 2007 in those three cross-sectional nationally representative samples

A CMOS silicon spin qubit

Silicon, the main constituent of microprocessor chips, is emerging as a promising material for the realization of future quantum processors. Leveraging its well-established complementary metal-oxide-semiconductor (CMOS) technology would be a clear asset to the development of scalable quantum computing architectures and to their co-integration with classical control hardware. Here we report a silicon quantum bit (qubit) device made with an industry-standard fabrication process. The device consists of a two-gate, p-type transistor with an undoped channel. At low temperature, the first gate defines a quantum dot (QD) encoding a hole spin qubit, the second one a QD used for the qubit readout. All electrical, two-axis control of the spin qubit is achieved by applying a phase-tunable microwave modulation to the first gate. Our result opens a viable path to qubit up-scaling through a readily exploitable CMOS platform.Comment: 12 pages, 4 figure

Pauli spin blockade in CMOS double quantum dot devices

Silicon quantum dots are attractive candidates for the development of scalable, spin-based qubits. Pauli spin blockade in double quantum dots provides an efficient, temperature independent mechanism for qubit readout. Here we report on transport experiments in double gate nanowire transistors issued from a CMOS process on 300 mm silicon-on-insulator wafers. At low temperature the devices behave as two few-electron quantum dots in series. We observe signatures of Pauli spin blockade with a singlet-triplet splitting ranging from 0.3 to 1.3 meV. Magneto-transport measurements show that transitions which conserve spin are shown to be magnetic-field independent up to B = 6 T.Comment: 5 pages , 4 figure

Study of the human hypoglossal nucleus: normal development and morpho-functional alterations in sudden unexplained late fetal and infant death

This study evaluated the development and the involvement in sudden perinatal and infant death of the medullary hypoglossal nucleus, a nucleus that, besides to coordinate swallowing, chewing and vocalization, takes part in inspiration. Through histological, morphometrical and immunohistochemical methods in 65 cases of perinatal and infant victims (29 stillbirths, 7 newborns and 29 infants), who died of both unknown and known cause, the authors observed developmental anomalies of the hypoglossal nucleus (HGN) in high percentage of sudden unexplained fetal and infant deaths. In particular, HGN hypoplasia, hyperplasia, positive expression of somatostatin and absence of interneurons were frequently found particularly in infant deaths, with a significant correlation with maternal smoking

Tizanidine does not affect the linear relation of stretch duration to the long latency M2 response of m. flexor carpi radialis

The long latency M2 electromyographic response of a suddenly stretched active muscle is stretch duration dependent of which the nature is unclear. We investigated the influence of the group II afferent blocker tizanidine on M2 response characteristics of the m. flexor carpi radialis (FCR). M2 response magnitude and eliciting probability in a group of subjects receiving 4 mg of tizanidine orally were found to be significantly depressed by tizanidine while tizanidine did not affect the significant linear relation of the M2 response to stretch duration. The effect of tizanidine on the M2 response of FCR is supportive of a group II afferent contribution to a compound response of which the stretch duration dependency originates from a different mechanism, e.g., rebound Ia firing

Brain iron accumulation in unexplained fetal and infant death victims with smoker mothers-The possible involvement of maternal methemoglobinemia

<p>Abstract</p> <p>Background</p> <p>Iron is involved in important vital functions as an essential component of the oxygen-transporting heme mechanism. In this study we aimed to evaluate whether oxidative metabolites from maternal cigarette smoke could affect iron homeostasis in the brain of victims of sudden unexplained fetal and infant death, maybe through the induction of maternal hemoglobin damage, such as in case of methemoglobinemia.</p> <p>Methods</p> <p>Histochemical investigations by Prussian blue reaction were made on brain nonheme ferric iron deposits, gaining detailed data on their localization in the brainstem and cerebellum of victims of sudden death and controls. The Gless and Marsland's modification of Bielschowsky's was used to identify neuronal cell bodies and neurofilaments.</p> <p>Results</p> <p>Our approach highlighted accumulations of blue granulations, indicative of iron positive reactions, in the brainstem and cerebellum of 33% of victims of sudden death and in none of the control group. The modified Bielschowsky's method confirmed that the cells with iron accumulations were neuronal cells.</p> <p>Conclusions</p> <p>We propose that the free iron deposition in the brain of sudden fetal and infant death victims could be a catabolic product of maternal methemoglobinemia, a biomarker of oxidative stress likely due to nicotine absorption.</p