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- Mazumder, D. N. G., et al.
(author)
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Bronchiectasis in persons with skin lesions resulting from arsenic in drinking water
- 2005
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In: Epidemiology. - : Ovid Technologies (Wolters Kluwer Health). - 1044-3983 .- 1531-5487. ; 16:6, s. 760-765
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Journal article (peer-reviewed)abstract
- Background: Arsenic is a unique human carcinogen in that it causes lung cancer by exposure through ingestion (in drinking water) as well as through inhalation. Less is known about nonmalignant pulmonary disease after exposure to arsenic in drinking water. Methods: We recruited 108 subjects with arsenic-caused skin lesions and 150 subjects without lesions from a population survey of over 7000 people in an arsenic-exposed region in West Bengal, India. Thirty-eight study participants who reported at least 2 years of chronic cough underwent high-resolution computed tomography (CT); these scans were read by investigators in India and the United States without knowledge of the presence or absence of skin lesions. Results: The mean ( +/- standard deviation) bronchiectasis severity score was 3.4 ( +/- 3.6) in the 27 participants with skin lesions and 0.9 ( +/- 1.6) in the 11 participants without these lesions. In subjects who reported chronic cough, CT evidence of bronchiectasis was found in 18 (67%) participants with skin lesions and 3 (27%) subjects without skin lesions. Overall, subjects with arsenic-caused skin lesions had a 10-fold increased prevalence of bronchiectasis compared with subjects who did not have skin lesions (adjusted odds ratio = 10; 95% confidence interval = 2.7-37). Conclusions: These results suggest that, in addition to being a cause of lung cancer, ingestion of high concentrations of arsenic in drinking water may be a cause of bronchiectasis.
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- Capeding, MR, et al.
(author)
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Immune persistence and response to booster dose of Vi-DT vaccine at 27.5 months post-first dose
- 2022
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In: NPJ vaccines. - : Springer Science and Business Media LLC. - 2059-0105. ; 7:1, s. 12-
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Journal article (peer-reviewed)abstract
- Vaccination with typhoid conjugate vaccines (TCV) is a major part of typhoid prevention. However, little is known about long-term immune persistence following vaccination with TCVs. In this phase-2, randomized double-blind trial (NCT03527355), 285 children aged 6–23 months were randomized to one of three groups: (1) the group that received a first dose of Vi polysaccharide conjugated to diphtheria-toxoid (Vi-DT) vaccine followed by an “early booster” at 24 weeks, (2) the group that which received a first dose of Vi-DT followed by a “late booster” at 96 or 110 weeks, and (3) comparator group. Safety and immunogenicity of anti-Vi IgG GMTs were assessed at weeks 0, 4, 24, 28, 60, 96, 110, and 114 since the first dose. Here, we describe persistence of immune responses at weeks 60, 96, 110, and 114 post first dose. The anti-Vi IgG seroconversion rate after 27.5 months of follow-up was 88.16% (95% CI: 79.00, 93.64) in late-booster and 94.76% (95% CI: 86.91, 97.88) in early booster Vi-DT groups (p = 0.081). Whereas anti-Vi IgG GMTs were significantly higher in the early booster group (11.95 [95% CI: 9.65, 14.81]) than prebooster GMTs in the late booster group (5.50 [95% CI: 4.44, 6.80], p < 0.0001). GMT in the late booster group significantly increased to 351.76 (95% CI: 265.01, 466.93) (p < 0.0001) when measured 4 weeks after they received their “late-booster” shot. In conclusion, late booster dosing with Vi-DT at 27.5 months post first dose was safe and elicited robust anti-Vi IgG immune responses. Anti-Vi IgG seroconversion rates were persistently comparable in early and late-booster Vi-DT groups.
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- Pander, Piotr, et al.
(author)
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Thermally activated delayed fluorescence in a deep red dinuclear iridium(iii) complex: a hidden mechanism for short luminescence lifetimes
- 2023
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In: Chemical Science. - : ROYAL SOC CHEMISTRY. - 2041-6520 .- 2041-6539. ; 14:47, s. 13934-13943
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Journal article (peer-reviewed)abstract
- The high luminescence efficiency of cyclometallated iridium(III) complexes, including those widely used in OLEDs, is typically attributed solely to the formally spin-forbidden phosphorescence process being facilitated by spin-orbit coupling with the Ir(III) centre. In this work, we provide unequivocal evidence that an additional mechanism can also participate, namely a thermally activated delayed fluorescence (TADF) pathway. TADF is well-established in other materials, including in purely organic compounds, but has never been observed in iridium complexes. Our findings may transform the design of iridium(III) complexes by including an additional, faster fluorescent radiative decay pathway. We discover it here in a new dinuclear complex, 1, of the form [Ir(N<^>C)(2)](2)(mu-L), where N<^>C represents a conventional N<^>C-cyclometallating ligand, and L is a bis-N<^>O-chelating bridging ligand derived from 4,6-bis(2-hydroxyphenyl)-pyrimidine. Complex 1 forms selectively as the rac diastereoisomer upon reaction of [Ir(N<^>C)(2)(mu-Cl)](2) with H2L under mild conditions, with none of the alternative meso isomer being separated. Its structure is confirmed by X-ray diffraction. Complex 1 displays deep-red luminescence in solution or in polystyrene film at room temperature (lambda(em) = 643 nm). Variable-temperature emission spectroscopy uncovers the TADF pathway, involving the thermally activated re-population of S-1 from T-1. At room temperature, TADF reduces the photoluminescence lifetime in film by a factor of around 2, to 1 mu s. The TADF pathway is associated with a small S-1-T-1 energy gap Delta E-ST of approximately 50 meV. Calculations that take into account the splitting of the T-1 sublevels through spin-orbit coupling perfectly reproduce the experimentally observed temperature-dependence of the lifetime over the range 20-300K. A solution-processed OLED comprising 1 doped into the emitting layer at 5 wt% displays red electroluminescence, lambda(EL) = 625 nm, with an EQE of 5.5% and maximum luminance of 6300 cd m(-2).
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