Nurses should pay attention to their Internet activity and whether it adds to their fatigue levels. Addictive behaviour should promptly be dealt with to ensure that the best care is provided to patients.

Introduction. Helicobacter pylori (H. pylori) infection could lead to chronic local and systemic immune response. The resulting increase in proinflammatory cytokines could affect bone resorption and might increase the risk of osteoporosis. This study aimed to investigate the association between H. pylori infection and osteoporosis in elderly female patients with upper gastrointestinal diseases. Methods. A retrospective patient record review study was conducted in a regional teaching hospital in south Taiwan. Relevant information on female patients aged 65 and over who were diagnosed with diseases of esophagus, gastric ulcer, or duodenal ulcer during January 2008 to December 2010 were abstracted. Association between H. pylori infection and osteoporosis was evaluated using multivariate logistic regression analysis. Results. Of the 365 patients with a mean age of 77.3 years, 77 (21.1%) had H. pylori infection and 101 (27.7%) had been diagnosed with osteoporosis. Multivariate logistic regression analysis revealed that osteoporosis was significantly associated with H. pylori infection (adjusted odds ratio = 2.03, 95% confidence interval = 1.14–3.62) after adjusting for age group, body mass index group, and use of proton pump inhibitor. Conclusion. Osteoporosis was found to be associated with H. pylori infection in Taiwanese female patients with upper gastrointestinal diseases. Further studies with information on potential confounders are needed to confirm the association.

Functional imaging in patients with movement disorders has suggested abnormalities of regional cerebral blood flow (rCBF). We describe a patient with thoracic cord lesion with subsequent severe neuropathic pain. Right hemichorea developed and was related to adjunctive therapy with gabapentin. The patient's hemichorea decreased gradually after cessation of gabapentin. The study of rCBF revealed hypoperfusion in the contralateral basal ganglia compared with the previous study of rCBF. Our patient is the first patient with neuropathic pain, treated with gabapentin who developed hemichorea, in the absence of brain lesions. Imaging studies of rCBF showed a perfusion defect in the contralateral basal ganglion.

BackgroundPrevious studies have shown that depressive symptoms in middle-aged women were associated with a number of factors such as climacteric symptoms. Nevertheless, studies based on population-based data with a wide range of potential correlates are still scarce. Therefore, the aim of this study was to investigate the correlates of depressive symptoms in late middle-aged Taiwanese women using data from a nationally-representative, population-based survey.MethodsWomen aged 50.0–65.0 years were identified from the dataset of the 2009 Taiwan National Health Interview Survey. The outcome measure was depressive symptoms in the past week, evaluated using the Center for Epidemiologic Studies Short Depression Scale (CES-D 10) with a cut-off score of 10 or greater. Univariate and multiple logistic regression analyses were used to evaluate the correlates of depressive symptoms.ResultsThe mean age of the 533 respondents was 56.7 years. Depressive symptoms were present in 53 respondents (9.9%). Multiple logistic regression analysis revealed that an education level of elementary school or below (adjusted odds ratio [AOR] = 3.19, P = 0.003), nulliparity (AOR = 8.10, P = 0.001), living alone (AOR = 5.47, P = 0.003), never having worked (AOR = 4.14, P = 0.008), lack of regular exercise (AOR = 3.01, P = 0.003), a perceived health status of fair or bad (AOR = 4.34, P < 0.001), and somatic climacteric symptoms (AOR = 2.32, P = 0.012) were independent and significant factors of depressive symptoms in late middle-aged Taiwanese women.ConclusionsFindings from this secondary analysis of a population-based survey suggested independent associations of somatic climacteric symptoms, and a number of socio-demographic and health-related factors with depressive symptoms in late middle-aged Taiwanese women.

Molecular biologists have long recognized carcinogenesis as an evolutionary process that involves natural selection. Cancer is driven by the somatic evolution of cell lineages. In this study, the evolution of somatic cancer cell lineages during carcinogenesis was modeled as an equilibrium point (ie, phenotype of attractor) shifting, the process of a nonlinear stochastic evolutionary biological network. This process is subject to intrinsic random fluctuations because of somatic genetic and epigenetic variations, as well as extrinsic disturbances because of carcinogens and stressors. In order to maintain the normal function (ie, phenotype) of an evolutionary biological network subjected to random intrinsic fluctuations and extrinsic disturbances, a network robustness scheme that incorporates natural selection needs to be developed. This can be accomplished by selecting certain genetic and epigenetic variations to modify the network structure to attenuate intrinsic fluctuations efficiently and to resist extrinsic disturbances in order to maintain the phenotype of the evolutionary biological network at an equilibrium point (attractor). However, during carcinogenesis, the remaining (or neutral) genetic and epigenetic variations accumulate, and the extrinsic disturbances become too large to maintain the normal phenotype at the desired equilibrium point for the nonlinear evolutionary biological network. Thus, the network is shifted to a cancer phenotype at a new equilibrium point that begins a new evolutionary process. In this study, the natural selection scheme of an evolutionary biological network of carcinogenesis was derived from a robust negative feedback scheme based on the nonlinear stochastic Nash game strategy. The evolvability and phenotypic robustness criteria of the evolutionary cancer network were also estimated by solving a Hamilton–Jacobi inequality – constrained optimization problem. The simulation revealed that the phenotypic shift of the lung cancer-associated cell network takes 54.5 years from a normal state to stage I cancer, 1.5 years from stage I to stage II cancer, and 2.5 years from stage II to stage III cancer, with a reasonable match for the statistical result of the average age of lung cancer. These results suggest that a robust negative feedback scheme, based on a stochastic evolutionary game strategy, plays a critical role in an evolutionary biological network of carcinogenesis under a natural selection scheme.