Polarization dependence of emission spectra of multiexcitons in self-assembled quantum dots

We have investigated the polarization dependence of the emission spectra of p-shell multiexcitons of a quantum dot when the single particle level spacing is larger than the characteristic energy of the Coulomb interactions. We find that there are many degenerate multiexciton states. The emission intensities depend on the number of degenerate initial and final states of the optical transitions. However, unlike the transition energies, they are essentially independent of the strength of the Coulomb interactions. In the presence of electron-hole symmetry the independence is exact.Comment: 7 pages, 5 figures, published in Solid State Commu

Pumping in quantum dots and non-Abelian matrix Berry phases

We have investigated pumping in quantum dots from the perspective of non-Abelian (matrix) Berry phases by solving the time dependent Schr{\"o}dinger equation exactly for adiabatic changes. Our results demonstrate that a pumped charge is related to the presence of a finite matrix Berry phase. When consecutive adiabatic cycles are performed the pumped charge of each cycle is different from the previous ones

The global burden of cancer attributable to risk factors, 2010–19: a systematic analysis for the Global Burden of Disease Study 2019

BACKGROUND: Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. METHODS: The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk–outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. FINDINGS: Globally, in 2019, the risk factors included in this analysis accounted for 4·45 million (95% uncertainty interval 4·01–4·94) deaths and 105 million (95·0–116) DALYs for both sexes combined, representing 44·4% (41·3–48·4) of all cancer deaths and 42·0% (39·1–45·6) of all DALYs. There were 2·88 million (2·60–3·18) risk-attributable cancer deaths in males (50·6% [47·8–54·1] of all male cancer deaths) and 1·58 million (1·36–1·84) risk-attributable cancer deaths in females (36·3% [32·5–41·3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20·4% (12·6–28·4) and DALYs by 16·8% (8·8–25·0), with the greatest percentage increase in metabolic risks (34·7% [27·9–42·8] and 33·3% [25·8–42·0]). INTERPRETATION: The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden

IL-32γ Inhibits Acetaminophen-Induced Acute Hepatotoxicity through Inactivation of NF-κB and Stat1 Signals

Although several studies have shown physiological functions of interleukin (IL)-32, the role of IL-32 in liver has not yet been reported. This study was initiated to examine the effects of IL-32γ on APAP-induced acute hepatic failure in IL-32γ transgenic mice. IL-32Γ overexpressing and non-transgenic mice received 500 mg/kg Acetoaminophen (APAP) intraperitoneally. Serum alanine transaminase and aspartate transaminase were significantly lower in the APAP treated IL-32γ overexpressing mice compared with those APAP-treated non-transgenic. IL-32γ markedly reduced a restricted area of the necrosis and inflammation. APAP-induced reduced glutathione depletion, induction of nitric oxide and lipid peroxidation, and cytochrome P4502E1 expression was significantly lowered in the IL-32γ overexpressing mice. Elevation of Kupffer cells and natural killer cells by APAP were reduced in the IL-32γ overexpressing mice. The expression of IL-1α, IL-1rα, macrophage inflammatory protein-2, C-C motif chemokine ligand 5 and tissue inhibitor of metalloproteinase-1 was increased by APAP in non-transgenic mice, and were lowered in the IL-32γ overexpressing mice. Moreover, APAP-induced nuclear transcription factor-kappa B (NF-κB) and signal transducers and activators of transcription 1 (STAT1) activities were greatly lowered in the IL-32γ overexpressing mice. The results indicate that IL-32γ could effectively inhibit drug-induced hepatic failure, and reduce the number of cytotoxic immune cells and pro-inflammatory cytokine production through reduced activities of NF-κB and STAT1. This might be attributable to lowering APAP-induced liver toxicity in IL-32γ overexpressing mice