38 resultados para paradox
em BORIS: Bern Open Repository and Information System - Berna - Suiça
Resumo:
A 59-year-old woman was examined because of weight gain, increasing fatigue and secondary amenorrhoea, which occurred after a complicated delivery at age 18. The finding of an increased TSH concentration was initially considered as primary hypothyroidism and substitution therapy was commenced. Because of the concomitant secondary amenorrhoea the patient was referred for additional endocrinological investigations.
Resumo:
Six full-term newborn infants are described who suffered from severe adult respiratory distress syndrome (ARDS). The triggering event was intrauterine/perinatal asphyxia in five, and group B streptococcal (GBS) septicemia in three. All had severe respiratory distress/failure and were ventilated mechanically with high concentrations of inspired oxygen and positive end-expiratory pressure. Radiography of the chest showed dense bilateral consolidation with air bronchograms and reduced lung volume. Persistent pulmonary hypertension (PPH) was documented in all cases. The coincidence of ARDS and PPH rendered respiratory management extremely difficult. For this reason high-frequency ventilation was instituted in all patients in order to improve CO2 elimination and induce respiratory alkalosis. Acute complications of respiratory therapy were encountered in five patients (pneumothorax, pulmonary interstitial emphysema, pneumopericardium). Three infants died (irreversible septic shock, progressive severe hypoxemia, and sudden cardiac arrest) after 17, 80, and 175 h of life. Histologic examination of the lungs was possible in all fatal cases and revealed typical changes of acute to subacute stages of ARDS. Three infants survived, the mean time of mechanical respiratory support being 703 h. Two patients were still dependent on oxygen after 1 month of life, and all survivors had increased interstitial markings and increased lung volumes on their chest roentgenograms at this time.
Resumo:
Seit der richtungweisenden wie einflußreichen Arbeit von Downs (1957) wird in der empirischen Wahlforschung das „Paradox der Wahlbeteiligung“ kontrovers diskutiert. Kritiker des ökonomischen Ansatzes führen gerade dieses Paradox an, um die Grenzen von Rational-Choice-Theorien aufzuzeigen (z.B. Green und Shapiro 1994). Ausgangspunkt dieser Debatte ist zunächst der Versuch von Downs, die Beteiligung von Individuen an politischen Wahlen mit der Theorie rationaler Entscheidung zu erklären: Demnach beteiligen sich Wahlberechtigte an Wahlen, wenn aus ihrer Sicht der erwartete Nutzen der Wahlbeteiligung (etwa persönliche Vorteile nach dem Wahlsieg der präferierten Partei) die anfallenden Kosten der Wahlbeteiligung (etwa zeitlicher Aufwand für Beschaffung, Auswertung und Analyse von Informationen über das Politikangebot) übersteigt. Wahlberechtigte diskontieren den zu maximierenden Nutzen aus ihrer Wahlbeteiligung mit der Wahrscheinlichkeit, daß ihre eigene Stimme der präferierten Partei zum Wahlsieg verhilft. Allerdings tendiert diese Wahrscheinlichkeit, den Wahlausgang alleine zu entscheiden, mit der anwachsenden Größe des Elektorats gegen Null. Da aber aus Sicht des einzelnen Wählers die eigene Stimme so gut wie keinen entscheidenden Einfluß auf den Wahlausgang hat, aber mit Sicherheit Informations-, Opportunitäts- und Teilnahmekosten anfallen, die dann immer größer als die mit der Erfolgswahrscheinlichkeit gewichteten Nutzeneinkommen sind, ist es höchst unwahrscheinlich, daß sich ein instrumentell rationaler Akteur an politischen Wahlen beteiligt (Downs 1957: 244–245). Jedoch sind in modernen Demokratien die Beteiligungen an politischen Wahlen mitunter beträchtlich, und diese empirische Beobachtung widerspricht der ökonomischen Theorie des Wählens von Downs (1957)1. Es stellt sich also die Frage, warum sich Wahlberechtigte an politischen Wahlen beteiligen und warum die Wahlbeteiligungen zumeist recht hoch sind (vgl. Palfrey und Rosenthal 1993).
Resumo:
BACKGROUND Transmitted HIV-1 drug-resistance mutations(TDR) are transmitted from treatment-failing or treatment-naïve patients. Although prevalence of drug-resistance in treatment-failing patients has declined in developed countries, TDR prevalence has not. Mechanisms causing this paradox are poorly explored. METHODS We included recently-infected, treatment-naïve patients with genotypic-resistance-tests performed ≤1year post-infection and <2013. Potential risk factors for TDR were analyzed using logistic regression. Association of TDR prevalences with population viral load(PVL) from treatment-patients during 1997-2011 was estimated with Poisson regression for all TDR and individually for most frequent resistance-mutations against each drug class(M184V/L90M/K103N). RESULTS We included 2421 recently-infected, treatment-naïve patients and 5399 treatment-failing patients. TDR prevalence fluctuated considerably over time. Two opposing developments could explain these fluctuations: generally continuous increases in TDR(Odds Ratio[OR]=1.13,p=0.010), punctuated by sharp decreases when new drug-classes were introduced. Overall, TDR prevalence increased with decreasing PVL(Rate Ratio[RR]=0.91/1000Log10-PVL,p=0.033). Additionally, we observed that the transmitted high-fitness-cost mutation M184V was positively associated with PVL of treatment-failing patients carrying M184V(RR=1.50/100Log10-PVL,p<0.001). Such association was absent and negative for K103N(RR-K103N=1.00/100Log10-PVL,p=0.99) and L90M(RR-L90M=0.75/100Log10-PVL,p=0.022), respectively. CONCLUSIONS Transmission of antiretroviral drug-resistance is temporarily reduced by the introduction of new drug classes and driven by treatment-failing and treatment-naïve patients. These findings suggest a continuous need for new drugs, early detection/treatment of HIV-1-infection.
Resumo:
It has long been surmised that income inequality within a society negatively affects public health. However, more recent studies suggest there is no association, especially when analyzing small areas. This study aimed to evaluate the effect of income inequality on mortality in Switzerland using the Gini index on municipality level. The study population included all individuals >30 years at the 2000 Swiss census (N = 4,689,545) living in 2,740 municipalities with 35.5 million person-years of follow-up and 456,211 deaths over follow-up. Cox proportional hazard regression models were adjusted for age, gender, marital status, nationality, urbanization, and language region. Results were reported as hazard ratios (HR) with 95 % confidence intervals. The mean Gini index across all municipalities was 0.377 (standard deviation 0.062, range 0.202-0.785). Larger cities, high-income municipalities and tourist areas had higher Gini indices. Higher income inequality was consistently associated with lower mortality risk, except for death from external causes. Adjusting for sex, marital status, nationality, urbanization and language region only slightly attenuated effects. In fully adjusted models, hazards of all-cause mortality by increasing Gini index quintile were HR = 0.99 (0.98-1.00), HR = 0.98 (0.97-0.99), HR = 0.95 (0.94-0.96), HR = 0.91 (0.90-0.92) compared to the lowest quintile. The relationship of income inequality with mortality in Switzerland is contradictory to what has been found in other developed high-income countries. Our results challenge current beliefs about the effect of income inequality on mortality on small area level. Further investigation is required to expose the underlying relationship between income inequality and population health.
Resumo:
A. N. Turing’s 1936 concept of computability, computing machines, and computable binary digital sequences, is subject to Turing’s Cardinality Paradox. The paradox conjoins two opposed but comparably powerful lines of argument, supporting the propositions that the cardinality of dedicated Turing machines outputting all and only the computable binary digital sequences can only be denumerable, and yet must also be nondenumerable. Turing’s objections to a similar kind of diagonalization are answered, and the implications of the paradox for the concept of a Turing machine, computability, computable sequences, and Turing’s effort to prove the unsolvability of the Entscheidungsproblem, are explained in light of the paradox. A solution to Turing’s Cardinality Paradox is proposed, positing a higher geometrical dimensionality of machine symbol-editing information processing and storage media than is available to canonical Turing machine tapes. The suggestion is to add volume to Turing’s discrete two-dimensional machine tape squares, considering them instead as similarly ideally connected massive three-dimensional machine information cells. Three-dimensional computing machine symbol-editing information processing cells, as opposed to Turing’s two-dimensional machine tape squares, can take advantage of a denumerably infinite potential for parallel digital sequence computing, by which to accommodate denumerably infinitely many computable diagonalizations. A three-dimensional model of machine information storage and processing cells is recommended on independent grounds as better representing the biological realities of digital information processing isomorphisms in the three-dimensional neural networks of living computers.