Discriminative Analysis of Brain Functional Connectivity Patterns for Mental Fatigue Classification

Mental fatigue is a commonly experienced state that can be induced by placing heavy demands on cognitive systems. This often leads to lowered productivity and increased safety risks. In this study, we developed a functional-connectivity based mental fatigue monitoring method. Twenty-six subjects underwent a 20-min mentally demanding test of sustained attention with high-resolution EEG monitoring. Functional connectivity patterns were obtained on the cortical surface via source localization of cortical activities in the first and last 5-min quartiles of the experiment. Multivariate pattern analysis was then adopted to extract the highly discriminative functional connectivity information. The algorithm used in the present study demonstrated an overall accuracy of 81.5% (p < 0.0001) for fatigue classification through leave-one-out cross validation. Moreover, we found that the most discriminative connectivity features were located in or across middle frontal gyrus and several motor areas, in agreement with the important role that these cortical regions play in the maintenance of sustained attention. This work therefore demonstrates the feasibility of a functional-connectivity-based mental fatigue assessment method, opening up a new avenue for modeling natural brain dynamics under different mental states. Our method has potential applications in several domains, including traffic and industrial safety.     

Complications in the clinical course of tako-tsubo cardiomyopathy

Objective

This study evaluated the frequency, severity and outcome of complications in the clinical course of tako-tsubo cardiomyopathy (TTC).

Background

TTC is regarded as a benign disease since left ventricular (LV) function returns to normal within a short time. However, severe complications have been reported in selected patients.

Methods

From 37 hospitals, 209 patients (189 female, age 69 ± 12 years) were prospectively included in a TTC registry.

Results

Complications developed in 108/209 patients (52%); 23 (11%) had > 2 complications. Complications occurred median 1 day after symptom onset, and 77% were seen within 3 days. Arrhythmias were documented in 45/209 patients (22%) including atrial fibrillation in 32 (15%) and ventricular tachycardia in 17 (8%). Of 8 patients resuscitated (4%), 6 survived. Additional complications were right ventricular involvement (24%), pulmonary edema (13%), cardiogenic shock (7%), transient intraventricular pressure gradients (5%), LV thrombi (3%) and stroke (1%). During hospitalization, 5/209 patients (2.5%) died. Patients with complications were older (70 ± 13 vs 67 ± 10 years, p = 0.012), had a higher heart rate (91 ± 26 vs 83 ± 19/min, p = 0.025), more frequently Q\ waves on the admission ECG (36% vs 21%, p = 0.019) and a lower LV ejection fraction (47 ± 15 vs 54 ± 14%, p = 0.002). Multivariate regression analysis identified Q-waves on admission (OR 2.49, 95% CI 1.23–5.05, p = 0.021) and ejection fraction ≤ 30% (OR 4.03, 95% CI 1.04–15.67, p = 0.022) as independent predictors for complications.

Conclusions

TTC may be associated with severe complications in half of the patients. Since the majority of complications occur up to day 3, monitoring is advisable for this time period.     

Dynamical evidence for causality between galactic cosmic rays and interannual variation in global temperature

As early as 1959, it was hypothesized that an indirect link between solar activity and climate could be mediated by mechanisms controlling the flux of galactic cosmic rays (CR) [Ney ER (1959) Nature 183:451–452]. Although the connection between CR and climate remains controversial, a significant body of laboratory evidence has emerged at the European Organization for Nuclear Research [Duplissy J, et al. (2010) Atmos Chem Phys 10:1635–1647; Kirkby J, et al. (2011) Nature 476(7361):429–433] and elsewhere [Svensmark H, Pedersen JOP, Marsh ND, Enghoff MB, Uggerhøj UI (2007) Proc R Soc A 463:385–396; Enghoff MB, Pedersen JOP, Uggerhoj UI, Paling SM, Svensmark H (2011) Geophys Res Lett 38:{"type":"entrez-nucleotide","attrs":{"text":"L09805","term_id":"177519"}}L09805], demonstrating the theoretical mechanism of this link. In this article, we present an analysis based on convergent cross mapping, which uses observational time series data to directly examine the causal link between CR and year-to-year changes in global temperature. Despite a gross correlation, we find no measurable evidence of a causal effect linking CR to the overall 20th-century warming trend. However, on short interannual timescales, we find a significant, although modest, causal effect between CR and short-term, year-to-year variability in global temperature that is consistent with the presence of nonlinearities internal to the system. Thus, although CR do not contribute measurably to the 20th-century global warming trend, they do appear as a nontraditional forcing in the climate system on short interannual timescales.The basic principles behind a possible connection between galactic cosmic rays (CR) and global temperature (GT) are as follows: It has been known since the invention of the cloud chamber in 1911 by Charles Thomson Rees Wilson that ionizing radiation leads to atmospheric cloud nucleation. Although the prime source of ionizing radiation in the global troposphere is CR, the flux of CR reaching the troposphere depends on the solar wind. The solar wind is a stream of ionized gases that blows outward from the Sun, and its intensity varies strongly with the level of surface activity on the Sun. The Earth''s magnetic field shields the planet from much of the solar wind, deflecting that wind like water around the bow of a ship. When solar activity is great, the solar wind is strong, swiping away CR arriving at the top of the atmosphere. These CR are hypothesized to affect cloud formation and cloudiness, and therefore GT. The net radiative effect of cloudiness depends on the difference between incoming solar radiation and outgoing long-wave radiation. Increased cloudiness in the upper troposphere reduces outgoing long-wave radiation, thereby resulting in warming of the planet. Increased cloudiness in the lower troposphere causes less incoming radiation, and therefore cooling of the planet. Data suggest (6) that the amount of CR is positively correlated with the amount of low-level clouds but has no effect on middle- or high-level clouds. Although this is still an open question (7, 8), the reduction in flux in CR in times of high solar activity is hypothesized to result in less cloud nucleation and fewer cloud condensation nuclei, and consequently, reduced low-level cloud amounts. This, in turn, leads to a higher solar radiation flux at the Earth’s surface, and warmer temperatures. Conversely, a weaker solar wind results in cooler temperatures. The actual chemical processes and reactions involved in this problem are complex, but a growing body of experimental and theoretical work has uncovered a chemical pathway by which CR ionization may increase nucleation rates to levels appropriate for cloud condensation nuclei (2–5, 9–11 and references therein). This suggests a superficially simple network linking the Sun, CR, and global climate, with the interaction between the Sun and CR having a potential influence on the climate system. However reasonable this may be, as described in a 2006 review (12), “The suggested mechanisms are, however, too complex to evaluate meaningfully at present.”     

Acute phase markers for the differentiation of infectious and malignant pleural effusions

Acute-phase markers, such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha), have been studied in inflammatory and malignant disorders. We examined the diagnostic value of these markers for the differentiation among parapneumonic, tuberculous and malignant effusions. We studied 124 patients with pleural effusions, classified as exudates [total (n=97), parapneumonic (n=15), tuberculous (n=25), malignant (n=57)] and transudates due to congestive heart failure (n=27). CRP, IL-6 and TNF-alpha were measured in pleural fluid and serum. Pleural fluid CRP was higher in parapneumonic compared to tuberculous and malignant effusions, providing 100% sensitivity for a cut-off point of 5.3mg/dL. IL-6 was higher in both parapneumonic and tuberculous compared to malignant effusions. TNF-alpha was higher in tuberculous compared to malignant effusions, providing 96.0% sensitivity, and 93.0% specificity for a cut-off point of 88.1 pg/mL. Pleural fluid CRP levels were lower than serum in all groups, probably reflecting systemic inflammation, whereas IL-6 and TNF-alpha were higher in pleural fluid indicating local production. Our data suggest that these markers may provide useful information for the differentiation of infectious and malignant effusions in clinical practice. However, further studies are needed for the validation of these findings in usual clinical circumstances.     

Tamoxifen induced hepatotoxicity in breast cancer patients with pre-existing liver steatosis: the role of glucose intolerance

OBJECTIVE: Tamoxifen induced hepatotoxicity has not been investigated in breast cancer patients with pre-existing liver steatosis. The aim of our study was to investigate the most common predisposing factors for non-alcoholic fatty liver disease in breast cancer patients with liver steatosis, treated with adjuvant tamoxifen therapy, in order to evaluate their role in the appearance of tamoxifen induced hepatotoxicity. METHODS: Clinical and laboratory evaluation, including an oral glucose tolerance test, was done in 60 women with breast cancer and liver steatosis before the beginning of adjuvant tamoxifen treatment and every 6 months during treatment. Tamoxifen induced hepatotoxicity was defined as abnormal liver function tests during tamoxifen treatment whereas these test results were below the normal range at baseline control. Statistical evaluation of data was performed using parametric methodology (the chi-squared test, and Student's t-test, P < 0.05). RESULTS: Twenty-six patients (43.3%) exhibited tamoxifen induced hepatotoxicity (group A) whereas 34 (56.7%) did not (group B). The mean overall follow-up period for the whole group was 37.5 months (SD 27.8, range 6-120 months) and did not differ between the two groups (P = 0.055). There was significant statistical difference in body mass index (BMI) and baseline fasting glucose, cholesterol and triglyceride levels between the two groups. Eighteen of 26 patients (69.2%) from group A had impaired glucose tolerance compared with only 8/34 patients (23.5%) from group B (P < 0.001), a finding observed even in BMI matched patients from the two groups (62.5% vs 12.5%, P = 0.002). CONCLUSIONS: Tamoxifen induced hepatotoxicity is observed in a great proportion of breast cancer patients with pre-existing liver steatosis, especially those with higher BMI and higher glucose and lipid levels at baseline control. Glucose intolerance before the beginning of tamoxifen treatment seems to be a predictor of the hepatotoxicity, unrelated to baseline BMI.     

Spontaneous bacterial peritonitis due to carbapenemase-producing Enterobacteriaceae: Etiology and antibiotic treatment

Carbapenem antibiotics were first introduced in the 1980s and have long been considered the most active agents for the treatment of multidrug-resistant gram-negative bacteria. Over the last decade, carbapenem-resistant Enterobacteriaceae (CRE) have emerged as organisms causing spontaneous bacterial peritonitis. Infections caused by CRE have shown a higher mortality rate than those caused by bacteria sensitive to carbapenem antibiotics. Current antibiotic guidelines for the treatment of spontaneous bacterial peritonitis are insufficient, and rapid de-escalation of empiric antibiotic treatment is not widely recognized. This review summarizes the molecular characteristics, epidemiology and possible treatment of spontaneous bacterial peritonitis caused by CRE.     

Modifiable factors affecting inpatient violence in an acute child and adolescent psychiatric unit: A 16‐year retrospective study

Violent incidents in acute inpatient units for children and adolescents are a major and persistent problem. The demographic, clinical, and modifiable (environmental–organizational) risk factors that affect inpatient violence in an Acute Child and Adolescent Psychiatric Unit were investigated via a retrospective study. Data were collected from nursing and medical reports and the unit's census and included 100 days per year for 16 years. Incidents of violence and assault types were recorded, and variables such as the diagnostic category of assailants, total number of patients, and staffing factors during the incident were examined. Of the 2390 violent incidents recorded, 50% were attributed to cases of physical violence towards another patient, 17% to physical violence towards nursing staff, 19% to physical violence towards self and 14% to destruction of property. According to the final multivariable model, for each additional patient in the unit, the risk of a violent event increased by 9.51%; for each additional offender patient, the risk increased by 14.06%; the number of assistant nurses was associated with a 25.03% increased risk; and, after 2006, the risk increased by 68.99%. The most significant factor associated with a 59.98% decreased risk was the total number of nursing staff. All variables significantly and independently contributed to the model. Acute inpatient psychiatric units with a small number of hospitalized patients, adequate, well‐trained and specialized nursing staff, and the hospitalization of different types of patients in separate wards or units are expected to facilitate a reduction in the frequency of violent incidents.