Clinical specialty training in UK undergraduate medical schools: A retrospective observational study

Objectives: To determine if increased exposure to clinical specialties at medical school is associated with increased interest in pursuing that specialty as a career after foundation training. Design: A retrospective observational study. Setting: 31 UK medical schools were asked how much time students spend in each of the clinical specialties. We excluded two schools that were solely Graduate Entry, and two schools were excluded for insufficient information. Main outcome measures: Time spent on clinical placement from UK undergraduate medical schools, and the training destinations of graduates from each school. A general linear model was used to analyse the relationship between the number of weeks spent in a specialty at medical school and the percentage of graduates from that medical school entering each of the Core Training (CT1)/Specialty Training (ST1) specialties directly after Foundation Year 2 (FY2). Results: Students spend a median of 85 weeks in clinical training. This includes a median of 28 weeks on medical firms, 15 weeks in surgical firms, and 8 weeks in general practice (GP). In general, the number of training posts available in a specialty was proportionate to the number of weeks spent in medical school, with some notable exceptions including GP. Importantly, we found that the number of weeks spent in a specialty at medical school did not predict the percentage of graduates of that school training in that specialty at CT1/ST1 level (ß coefficient=0.061, p=0.228). Conclusions: This study found that there was no correlation between the percentage of FY2 doctors appointed directly to a CT1/ST1 specialty and the length of time that they would have spent in those specialties at medical school. This suggests that curriculum adjustments focusing solely on length of time spent in a specialty in medical school would be unlikely to solve recruitment gaps in individual specialties

Population Inversion in Monolayer and Bilayer Graphene

The recent demonstration of saturable absorption and negative optical conductivity in the Terahertz range in graphene has opened up new opportunities for optoelectronic applications based on this and other low dimensional materials. Recently, population inversion across the Dirac point has been observed directly by time- and angle-resolved photoemission spectroscopy (tr-ARPES), revealing a relaxation time of only ~ 130 femtoseconds. This severely limits the applicability of single layer graphene to, for example, Terahertz light amplification. Here we use tr-ARPES to demonstrate long-lived population inversion in bilayer graphene. The effect is attributed to the small band gap found in this compound. We propose a microscopic model for these observations and speculate that an enhancement of both the pump photon energy and the pump fluence may further increase this lifetime.Comment: 18 pages, 6 figure

Generating single photons at gigahertz modulation-speed using electrically controlled quantum dot microlenses

This article may be downloaded for personal use only. Any other use requires prior permission of the author and AIP Publishing. This article appeared in Appl. Phys. Lett. 108, 021104 (2016) and may be found at https://doi.org/10.1063/1.4939658.We report on the generation of single-photon pulse trains at a repetition rate of up to 1 GHz. We achieve this speed by modulating the external voltage applied on an electrically contacted quantum dot microlens, which is optically excited by a continuous-wave laser. By modulating the photoluminescence of the quantum dot microlens using a square-wave voltage, single-photon emission is triggered with a response time as short as (281 ± 19) ps, being 6 times faster than the radiative lifetime of (1.75 ± 0.02) ns. This large reduction in the characteristic emission time is enabled by a rapid capacitive gating of emission from the quantum dot, which is placed in the intrinsic region of a p-i-n-junction biased below the onset of electroluminescence. Here, since our circuit acts as a rectifying differentiator, the rising edge of the applied voltage pulses triggers the emission of single photons from the optically excited quantum dot. The non-classical nature of the photon pulse train generated at GHz-speed is proven by intensity autocorrelation measurements with g(2)(0) = 0.3 ± 0.1. Our results combine optical excitation with fast electrical gating and thus show promise for the generation of indistinguishable single photons at rates exceeding the limitations set by the intrinsic radiative lifetime.BMBF, 03V0630, Entwicklung einer Halbleiterbasierten Einzelphotonenquelle für die Quanteninformationstechnologie (QSOURCE)DFG, 43659573, SFB 787: Halbleiter - Nanophotonik: Materialien, Modelle, Bauelement

Stigma as a fundamental hindrance to the United States opioid overdose crisis response.

Alexander Tsai and co-authors discuss the role of stigma in responses to the US opioid crisis

IL-4 Mediated Resistance of BALB/c Mice to Visceral Leishmaniasis Is Independent of IL-4Rα Signaling via T Cells

Previous studies infecting global IL-4Rα-/-, IL-4-/-, and IL-13-/-mice on a BALB/c background with the visceralizing parasite Leishmania donovani have shown that the T helper 2 cytokines, IL-4, and IL-13, play influential but not completely overlapping roles in controlling primary infection. Subsequently, using macrophage/neutrophil-specific IL-4Rα deficient BALB/c mice, we demonstrated that macrophage/neutrophil unresponsiveness to IL-4 and IL-13 did not have a detrimental effect during L. donovani infection. Here we expand on these findings and show that CD4+ T cell-(Lckcre), as well as pan T cell-(iLckcre) specific IL-4Rα deficient mice, on a BALB/c background, unlike global IL-4Rα deficient mice, are also not adversely affected in terms of resistance to primary infection with L. donovani. Our analysis suggested only a transient and tissue specific impact on disease course due to lack of IL-4Rα on T cells, limited to a reduced hepatic parasite burden at day 30 post-infection. Consequently, the protective role(s) demonstrated for IL-4 and IL-13 during L. donovani infection are mediated by IL-4Rα-responsive cell(s) other than macrophages, neutrophils and T cells

Genetic liability to cannabis use disorder and COVID-19 hospitalization

BACKGROUND: Vulnerability to COVID-19 hospitalization has been linked to behavioral risk factors, including combustible psychoactive substance use (e.g., tobacco smoking). Paralleling the COVID-19 pandemic crisis have been increasingly permissive laws for recreational cannabis use. Cannabis use disorder (CUD) is a psychiatric disorder that is heritable and genetically correlated with respiratory disease, independent of tobacco smoking. We examined the genetic relationship between CUD and COVID-19 hospitalization. METHODS: We estimated the genetic correlation between CUD (case: RESULTS: Genetic vulnerability to COVID-19 was correlated with genetic liability to CUD ( CONCLUSIONS: Problematic cannabis use and vulnerability to serious COVID-19 complications share genetic underpinnings that are unique from common correlates. While CUD may plausibly contribute to severe COVID-19 presentations, causal inference models yielded no evidence of putative causation. Curbing excessive cannabis use may mitigate the impact of COVID-19

Experiments and Modeling of the Autoignition of Methyl-Cyclohexane at High Pressure

The autoignition delays of mixtures of methyl-cyclohexane (MCH), oxygen, nitrogen, and argon have been studied in a heated rapid compression machine under the conditions $P_C$ = 50 bar, $T_C$ = 690 - 910K. Three different mixture compositions were studied, with equivalence ratios ranging from $\phi$ = 0.5 - 1.5. The trends of the ignition delay measured at 50 bar were similar to the trends measured in earlier experiments at $P_C$ = 15.1 and 25.5 bar. The experimentally measured ignition delays were compared to a newly updated chemical kinetic model for the combustion of MCH. The model has been updated to include newly calculated reaction rates for much of the low-temperature chemistry. The agreement between the experiments and the model was substantially improved compared to a previous version of the model. Nevertheless, despite the encouraging improvements, work continues on further advances, e.g. in improving predictions of the first stage ignition delays.Comment: 8 pages, 8 figures, 1 table, presented at the 8th US National Combustion Meetin

DNA methylation partially mediates antidiabetic effects of metformin on HbA1c levels in individuals with type 2 diabetes

Aims: Despite metformin being used as first-line pharmacological therapy for type 2 diabetes, its underlying mechanisms remain unclear. We aimed to determine whether metformin altered DNA methylation in newlydiagnosed individuals with type 2 diabetes. Methods and Results: We found that metformin therapy is associated with altered methylation of 26 sites in blood from Scandinavian discovery and replication cohorts (FDR < 0.05), using MethylationEPIC arrays. The majority (88%) of these 26 sites were hypermethylated in patients taking metformin for ~ 3 months compared to controls, who had diabetes but had not taken any diabetes medication. Two of these blood-based methylation markers mirrored the epigenetic pattern in muscle and adipose tissue (FDR < 0.05). Four type 2 diabetes-associated SNPs were annotated to genes with differential methylation between metformin cases and controls, e.g., GRB10, RPTOR, SLC22A18AS and TH2LCRR. Methylation correlated with expression in human islets for two of these genes. Three metformin-associated methylation sites (PKNOX2, WDTC1 and MICB) partially mediate effects of metformin on follow-up HbA1c levels. When combining methylation of these three sites into a score, which was used in a causal mediation analysis, methylation was suggested to mediate up to 32% of metformin’s effects on HbA1c. Conclusion: Metformin-associated alterations in DNA methylation partially mediates metformin’s antidiabetic effects on HbA1c in newly-diagnosed individuals with type 2 diabetes