68 research outputs found

    21st Century Skills for 21st Century Jobs

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    Joint Agency Report21stCenturySkillsJobs.pdf: 8198 downloads, before Oct. 1, 2020

    Towards Poisson noise limited optical pump soft X-ray probe NEXAFS spectroscopy using a laser-produced plasma source

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    We present a laboratory setup for near edge X-ray absorption spectroscopy (NEXAFS) in the soft X-ray regime between 284 eV to 1303 eV with a resolving power of up to 1370. Based on a laser-produced plasma source, a pair of identical reflection zone plates and an X-ray CCD camera, the setup is intended for optical pump X-ray probe NEXAFS measurements with a detectable change in absorption of the excited sample down to 10−4 and 500 ps time resolution. Because of the high stability of the source the statistical error only depends on the detector response and the number of photons detected and can reach the detector noise limit after a couple of thousands single shots. Thus, structure-function relationship investigations of bio-molecules are rendered feasible in the laboratory.DFG, 313838950, Neuartiges Laborspektrometer für Pump-Probe NEXAFS-Untersuchungen an Biomolekülen in wässriger Lösun

    Age at Menopause and the Risk of Stroke: Observational and Mendelian Randomization Analysis in 204 244 Postmenopausal Women

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    BACKGROUND: Observational studies have shown that women with an early menopause are at higher risk of stroke compared with women with a later menopause. However, associations with stroke subtypes are inconsistent, and the causality is unclear. METHODS AND RESULTS: We analyzed data of the UK Biobank and EPIC-CVD (European Prospective Investigation Into Cancer and Nutrition-Cardiovascular Diseases) study. A total of 204 244 postmenopausal women without a history of stroke at baseline were included (7883 from EPIC-CVD [5292 from the subcohort], 196 361 from the UK Biobank). Pooled mean baseline age was 58.9 years (SD, 5.8), and pooled mean age at menopause was 47.8 years (SD, 6.2). Over a median follow-up of 12.6 years (interquartile range, 11.8–13.3), 6770 women experienced a stroke (5155 ischemic strokes, 1615 hemorrhagic strokes, 976 intracerebral hemorrhages, and 639 subarachnoid hemorrhages). In multivariable adjusted observational Cox regression analyses, the pooled hazard ratios per 5 years younger age at menopause were 1.09 (95% CI, 1.07–1.12) for stroke, 1.09 (95% CI, 1.06–1.13) for ischemic stroke, 1.10 (95% CI, 1.04–1.16) for hemorrhagic stroke, 1.14 (95% CI, 1.08–1.20) for intracerebral hemorrhage, and 1.00 (95% CI, 0.84–1.20) for subarachnoid hemorrhage. When using 2-sample Mendelian randomization analysis, we found no statistically significant association between genetically proxied age at menopause and risk of any type of stroke. CONCLUSIONS: In our study, earlier age at menopause was related to a higher risk of stroke. We found no statistically significant association between genetically proxied age at menopause and risk of stroke, suggesting no causal relationship

    Mitochondrial physiology

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    As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

    Mitochondrial physiology

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    As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

    Estimating dose—response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and revised Mendelian randomization analyses

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    Background Randomised trials of vitamin D supplementation for cardiovascular disease and all-cause mortality have generally reported null findings. However, generalisability of results to individuals with low vitamin D status is unclear. We aimed to characterise dose-response relationships between 25-hydroxyvitamin D (25[OH]D) concentrations and risk of coronary heart disease, stroke, and all-cause mortality in observational and Mendelian randomisation frameworks. Methods Observational analyses were undertaken using data from 33 prospective studies comprising 500 962 individuals with no known history of coronary heart disease or stroke at baseline. Mendelian randomisation analyses were performed in four population-based cohort studies (UK Biobank, EPIC-CVD, and two Copenhagen population-based studies) comprising 386 406 middle-aged individuals of European ancestries, including 33 546 people who developed coronary heart disease, 18 166 people who had a stroke, and 27 885 people who died. Primary outcomes were coronary heart disease, defined as fatal ischaemic heart disease (International Classification of Diseases 10th revision code I20-I25) or non-fatal myocardial infarction (I21-I23); stroke, defined as any cerebrovascular disease (I60-I69); and all-cause mortality. Findings Observational analyses suggested inverse associations between incident coronary heart disease, stroke, and all-cause mortality outcomes with 25(OH)D concentration at low 25(OH)D concentrations. In population-wide genetic analyses, there were no associations of genetically predicted 25(OH)D with coronary heart disease (odds ratio [OR] per 10 nmol/L higher genetically-predicted 25(OH)D concentration 0·98, 95% CI 0·95–1·01), stroke (1·01, [0·97–1·05]), or all-cause mortality (0·99, 0·95–1·02). Null findings were also observed in genetic analyses for cause-specific mortality outcomes, and in stratified genetic analyses for all outcomes at all observed levels of 25(OH)D concentrations. Interpretation Stratified Mendelian randomisation analyses suggest a lack of causal relationship for 25(OH)D concentrations with both cardiovascular and mortality outcomes for individuals at all levels of 25(OH)D. Our findings suggest that substantial reductions in mortality and cardiovascular morbidity due to long-term low-dose vitamin D supplementation are unlikely even if targeted at individuals with low vitamin D status

    Using the DNA Profile as the Unique Patient Identifier in the Community Health Information Network: Legal Implications, 15 J. Marshall J. Computer & Info. L. 227 (1997)

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    One of the greatest obstacles to electronic medical record keeping is the absence of a unique patient identifier. With the sharing of patient\u27s information, an increased risk of error exists. Among these risks are the transmission of the wrong patient\u27s records and security of confidential patient information. Implementation of a uniform patient identifier will eliminate the obstacle to cooperation and information-sharing of health data. This article proposes the application of a unique protocol, which utilizes DNA fingerprints as a patient\u27s personal identifier. Since each individual\u27s DNA profile is distinctly different, the fingerprint would act as the patient\u27s personal bar code, which is distinguishable from other patients. Use of DNA profiles significantly safeguard the confidentiality of patient records by reducing the risks of alternative databases that gain access to personal information about patients. Adoption of the author\u27s proposal will facilitate a more effective and unified manner of sharing information within the healthcare industry

    Restatement (Second) of Torts Section 324A: An Innovative Theory of Recovery for Patients Injured Through Use or Misuse of Health Care Information Services, 14 J. Marshall J. Computer & Info. L. 73 (1995)

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    The author in this comment discusses how developments in information technology and widespread utilization of technology and software in the patient care context raise the issue of clinical liability for health care information systems vendors. The comment discusses a theory of recovery of tort damages for the negligence of health care information systems vendors under section 324A of the Restatement (Second) of Torts. Section 324A provides in essence that one who undertakes ... for consideration, to render services to another which he should recognize as necessary for the protection of a third person ... is subject to liability to the third person for physical harm. The comment discusses the terminology specific to the computer industry and the types of disclaimers health care information systems vendors use in their contracts. The comment also analyzes the public policies for and against the use of section 324A as a theory of recovery for damages as a result of negligence by a health care information system vendors. The author opposes establishing any bright-line rule defining when a patient can obtain tort damages against a health information systems vendor. The author argues that the use strict liability against health information systems vendor for negligent acts could cause a chilling effect in advances in information technology. However, the author proposes that a patient should only recover damages against a health information systems vendor where the vendor purposely disregards the general health and well-being of the public
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