Miracle-dz/UniFAR-FTUs huggingface dataset:
Hypermethods for EEG hyperscanning

Until now, in EEG studies the activity of the brain during simple or complex tasks have been recorded in a single subject. Often, during such EEG recordings, subjects interacts with the external devices or the researchers in order to reproduce conditions similar to the those usually occurring in the real-life. However, in order to study the concurrent activity in subjects interacting in cooperation or competition activities, the issue of the simultaneous recording of their brain activity became mandatory. The simultaneous recording of hemodynamic or neuroelectric activity of the brain is called "hyperscanning". We would like present results obtained by EEG hyperscannings performed on a group of subjects engaged in cooperative games. The EEG hyperscannings have been performed with the simultaneous use of high resolution EEG devices on groups of three and four subjects while they were playing cooperative games. The analysis of such data have been conducted with analysis method that taken into account the particular nature of the data simultaneously gathered from different subjects. We called these methods hypermethods. In particular, we estimate the concurrent activity in multiple brains of the group and we depicted the causal connections between regions of different brains (hyperconnectivity). The resulting causality patterns will link certain areas of the brain of a subject to the waveforms obtained from the other brain areas of another subject of the same group. Results obtained in a study of several groups recorded by the hyperscanning reveals causal links between prefrontal areas of the different subjects when they are performing cooperative games in different frequency bands. Hypermethods for hyperscanning will open a different area for the study of neuroscience, in which the activity of multiple brains during social cooperation could be investigated. In such area the importance of EEG will be relevant due to its temporal and spatial resolution now obtainable with the high resolution EEG techniques
I-Metaiodobenzylguanidine Scintigraphy in Parkinson’s Disease and Related Disorders

Autonomic dysfunction is common in Lewy body disorders (Parkinson’s disease, Dementia with Lewy Bodies, Pure Autonomic Failure, and REM sleep disorder). The loss of post-ganglionic myocardial sympathetic nerve fibers is a prominent feature of autonomic dysfunction in such disorders. Imetaiodobenzylguanidine (MIBG) scintigraphy that visualizes catecholaminergic terminals in vivo is a biomarker used to detect cardiac sympathetic degeneration. Abnormal MIBG uptake has been consistently reported in Lewy body disorders. Some studies agree in the notion that increasing bradykinesia is related with an incremental cardiac sympathetic denervation, whereas tremor is not closely linked to cardiac denervation. ‘‘Atypical’’ parkinsonian syndromes, including Multiple System Atrophy, Progressive Supranuclear Palsy, and others, show modest reductions of cardial MIBG uptake. MIBG scintigraphy is moderately sensitive and specific in differentiating Parkinson’s disease from such syndromes. Conversely, its sensitivity and specificity might be better in cognitively impaired patients, helping differential diagnosis between Dementia with Lewy Bodies, and Alzheimer disease. Confounding factors (comorbidities, comedications) should be carefully controlled before analyzing MIBG scintigraphy. 2009 Movement Disorder Society
Tyrosine D oxidation at cryogenic temperature in photosystem II.

Photosystem II (PSII) contains two redox-active tyrosines (TyrZ and TyrD) possessing very different properties. TyrD is stable in its oxidized form, while TyrZ is kinetically competent in the water oxidizing reaction. The temperature dependence of the formation of light-induced tyrosyl radical was studied as a function of pH in Mn-depleted PS II from cyanobacteria and plants. Tyrosyl radical formation was observed in the majority of the centers at pH 8.5 and 15 K. The use of two Synechocystis mutants where either TyrZ or TyrD was replaced by a phenylalanine residue allowed a clear demonstration that only TyrD and not TyrZ was oxidized under these conditions. By lowering the pH, the fraction of centers undergoing TyrD oxidation greatly diminished. This pH dependence could be fitted by assuming a single protonable group with a pK(a) of approximately 7.6. This pH dependence correlates with the unexpectedly rapid oxidation of TyrD at room temperature [Faller, P., Debus, R. J., Brettel, K. , Sugiura, M. , Rutherford, A. W. , and Boussac, A. (2001) Proc. Nat. Acad. Sci. U.S.A. 98, 14368]. The equally unexpectedly ability to undergo oxidation at cryogenic temperatures reported here, puts limitations on the nature of the protonation reactions associated with electron transfer in this system, raising the possibility of proton tunneling along the hydrogen bond or alternatively the presence of deprotonated TyrD (tyrosinate) prior to oxidation.
Social-Aware Incentivized Caching for D2D Communications

The device-to-device (D2D) channels allow content sharing when two devices are in close proximity, which can help improve resource utilization and network capacity. The data caching is introduced in D2D networks to enable the quick data access in mobile networks. Due to the selfish nature of users, they wish to get as much replication as possible in the opportunistic connections, seeking to maximize their own profits. However, caching data for other nodes may result in additional cost to the node serving as cache, where the cost is invoked by the cache placement of cache nodes and accessing cost of other nodes. In this paper, we propose a social-aware caching game to incentivize nodes to cache data for others. In the game, we consider the social ties and physical distance as the factors to formulate the caching cost. We obtain the Nash equilibrium of the game and propose a social-aware algorithm to minimize the total cost of getting object data in the network. The extensive simulation results show that our algorithm gains significant cache benefit.
Changes in astroglial scar formation in rat optic nerve as a function of development

Although astroglial scar formation is a common response to almost any type of injury to the adult central nervous system, lesions in fetal and neonatal rats have been reported to induce little or no scar formation. To examine this developmental difference further, rats ranging in age from 1 to 65 days postnatal were unilaterally enucleated, a surgical procedure that causes the axons in the optic nerve to degenerate. The optic nerves were processed for light and electron microscopy at times ranging from 7 to 365 days postenucleation. Pronounced and permanent glial scars were formed in every age group examined, including the neonates. However, the time course for removal of the degenerating axonal debris and formation of a compact, debris‐free glial scar varied as a function of developmental age. In neonatal rats, a compact glial scar formed in 1–2 weeks whereas 3–5 months were required for compact glial scar formation in juveniles and adults. Changes in cross‐sectional area were also associated with optic nerve degeneration and glial scar formation. Whereas lesioned neonatal optic nerves underwent little change in area, there was a substantial decrease in area in the juvenile and adult. Morphometric analysis showed that irrespective of the age of the animal at the time of enucleation, the final area of the compact glial scar was 10–20% of the unlesioned adult control. These results suggest that conflict in the literature over the ability of neonatal astrocytes to form a glial scar may be due to the nature of the lesion or the method of detection since astrocytes in the neonatal rat optic nerve clearly have the capacity to become reactive and form a glial scar.
Thoracoscopy talc poudrage : a 15-year experience.

OBJECTIVES To review our experience with thoracoscopy and talc poudrage during the previous 15 years with regards to efficacy, side effects, morbidity, and mortality. METHODS Six hundred fourteen consecutive patients (58.6% female; mean age, 54.5 years) underwent thoracoscopy with talc poudrage from August 1983 to May 1999. Of these, 457 patients had malignant pleural effusions, 108 patients had benign pleural effusions, and 49 patients had spontaneous pneumothorax. RESULTS Sixty-four patients were excluded from evaluation for efficacy: 30 patients (4.9%) because the lung did not expand at the time of the procedure and 34 patients (5.5%) because they died within 30 days of the thoracoscopy. All exclusions were in the malignant group. The overall success rate of the 393 patients with malignant pleural effusions was 93.4%, while the overall success for the 108 patients with benign effusions was 97%, although 7 patients (7%) with benign effusions required a second thoracoscopy. The success rate with pneumothorax was 100%. Major morbidity included empyema in 4%, reexpansion pulmonary edema in 2.2%, and respiratory failure 1.3%. CONCLUSION Thoracoscopy with talc poudrage is effective in producing a pleurodesis in malignant and benign pleural effusion and in spontaneous pneumothorax. However, it should be noted that the insufflation of talc has a systemic distribution associated with a low rate of morbidity and perhaps does induce ARDS, which is sometimes fatal in a small percentage of patients. Because of these side effects, the search for a better agent should be continued.
Architecture-Driven Level Set Optimization: From Clustering to Subpixel Image Segmentation

Thanks to their effectiveness, active contour models (ACMs) are of great interest for computer vision scientists. The level set methods (LSMs) refer to the class of geometric active contours. Comparing with the other ACMs, in addition to subpixel accuracy, it has the intrinsic ability to automatically handle topological changes. Nevertheless, the LSMs are computationally expensive. A solution for their time consumption problem can be hardware acceleration using some massively parallel devices such as graphics processing units (GPUs). But the question is: which accuracy can we reach while still maintaining an adequate algorithm to massively parallel architecture? In this paper, we attempt to push back the compromise between, speed and accuracy, efficiency and effectiveness, to a higher level, comparing with state-of-the-art methods. To this end, we designed a novel architecture-aware hybrid central processing unit (CPU)-GPU LSM for image segmentation. The initialization step, using the well-known k-means algorithm, is fast although executed on a CPU, while the evolution equation of the active contour is inherently local and therefore suitable for GPU-based acceleration. The incorporation of local statistics in the level set evolution allowed our model to detect new boundaries which are not extracted by the used clustering algorithm. Comparing with some cutting-edge LSMs, the introduced model is faster, more accurate, less subject to giving local minima, and therefore suitable for automatic systems. Furthermore, it allows two-phase clustering algorithms to benefit from the numerous LSM advantages such as the ability to achieve robust and subpixel accurate segmentation results with smooth and closed contours. Intensive experiments demonstrate, objectively and subjectively, the good performance of the introduced framework both in terms of speed and accuracy.
Megakaryocytopoiesis and apoptosis in patients with myelodysplastic syndromes

In order to investigate simultaneously the megakaryocytopoiesis and apoptotic characteristics in bone marrow in patients with myelodysplastic syndromes (MDS), we used CD41 immunoenzyme (alkaline phosphatase anti-alkaline phosphatase) and DNA in situ end-labeling techniques on plastic embedded bone marrow biopsy sections of 29 MDS patients. Fourteen patients with iron deficiency anemia served as controls. The results showed that CD41-positive cells in MDS marrow numbered 26.2 ± 18.2/mm2 (mean ± standard deviation) compared with 15.6 ± 7.1/mm2 in controls (P < 0.05). Numbers of cells with the morphology of micro-megakaryocytes in MDS marrow were significantly higher than in controls (P < 0.01). Furthermore, megakaryocytes in MDS marrow were frequently distributed along trabeculae (in 27 cases) and formed clusters (in 25 cases). Apoptotic megakaryocytes in MDS marrow accounted for just 4.4 and 9.3% of all CD41-positive cells and all apoptotic cells, respectively (P > 0.05 compared with controls), but apoptosis occurred only in micro-megakaryocytes. Based on these observations, we conclude that megakaryocytosis and dysmegakaryocytosis are the features of dyshematopoiesis in MDS marrow. Decreased thrombocyte production and thrombocyte release coming from increased dys(micro)megakaryocytes and abnormally located megakaryocytes perhaps play a more important role in peripheral thrombocytopenia than megakaryocytic apoptosis itself. Apoptosis of micro-megakaryocytes may be a protective biological mechanism to remove useless megakaryocytes.
Review: The role of insulin resistance in nonalcoholic fatty liver disease.

CONTEXT Insulin resistance is an almost universal finding in nonalcoholic fatty liver disease (NAFLD). This review outlines the evidence linking insulin resistance and NAFLD, explores whether liver fat is a cause or consequence of insulin resistance, and reviews the current evidence for treatment of NAFLD. EVIDENCE ACQUISITION Evidence from epidemiological, experimental, and clinical research studies investigating NAFLD and insulin resistance was reviewed. EVIDENCE SYNTHESIS Insulin resistance in NAFLD is characterized by reductions in whole-body, hepatic, and adipose tissue insulin sensitivity. The mechanisms underlying the accumulation of fat in the liver may include excess dietary fat, increased delivery of free fatty acids to the liver, inadequate fatty acid oxidation, and increased de novo lipogenesis. Insulin resistance may enhance hepatic fat accumulation by increasing free fatty acid delivery and by the effect of hyperinsulinemia to stimulate anabolic processes. The impact of weight loss, metformin, and thiazolidinediones, all treatments aimed at improving insulin sensitivity, as well as other agents such as vitamin E, have been evaluated in patients with NAFLD and have shown some benefit. However, most intervention studies have been small and uncontrolled. CONCLUSION Insulin resistance is a major feature of NAFLD that, in some patients, can progress to steatohepatitis. Treatments aimed at reducing insulin resistance have had some success, but larger placebo-controlled studies are needed to fully establish the efficacy of these interventions and possibly others in reducing the deleterious effects of fat accumulation in the liver.
Risk of Venous Thromboembolism Recurrence: High Negative Predictive Value of D-dimer Performed after Oral Anticoagulation Is Stopped

Summary In some patients with previous venous thromboembolism (VTE) D-dimer levels (D-Dimer) tend to increase after oral anticoagulant therapy (OAT) is stopped. The aim of our study was to evaluate the predictive value of D-Dimer for the risk of VTE recurrence after OAT withdrawal. After a first episode of deep vein thrombosis (DVT) of the lower limbs and/or pulmonary embolism (PE), 396 patients (median age 67 years, 198 males) were followed from the day of OAT discontinuation for 21 months. D-dimer was measured on the day of OAT withdrawal (T1), 3-4 weeks (T2) and 3 months (+/− 10 days, T3) thereafter. The main outcome events of the study were: objectively documented recurrent DVT and/or PE. D-dimer was found to be increased in 15.5%, 40.3% and 46.2% of the patients at T1, T2 and T3, respectively. In 199 (50.2%) patients, D-dimer levels were elevated in at least one measurement. During a follow-up of 628.4 years, 40 recurrences were recorded (10.1% of patients; 6.4% patient-years of follow-up). D-dimer was increased in at least one measurement in 28 of these cases, but remained normal in 11 subjects (three of whom had recurrent events triggered by circumstantial factors, three with malignancyassociated factors) (in one subject D-dimer was not measured). The negative predictive value (NPV) of D-dimer was 95.6% (95% CI 91.6-98.1) at T3 and was even higher (96.7%; 95% CI 92.9-98.8) after exclusion of the six recurrences due to circumstantial factors. Only five idiopathic recurrences occurred in the 186 patients with consistently normal D-dimer. In conclusion, D-dimer has a high NPV for VTE recurrence when performed after OAT discontinuation.
Association of coronary heart disease mortality with risk factors according to length of follow-up and serum cholesterol level in men: the Oslo Study cohort

Aim: We aimed to clarify the strength of the association between conventional and metabolic risk factors to coronary heart disease (CHD) mortality across short, intermediate, and long periods of follow-up and whether the effects of risk factors are heterogeneous across serum cholesterol levels. Methods: The Oslo Study prospective cohort of 14,846 men aged 40–49 years was followed from screening in 1972–73 until 2006, during which time 1655 subjects died of CHD. Multivariate-adjusted Cox proportional models compared hazard ratios (HRs) and 95% confidence intervals (CIs) for CHD mortality across 0–12, 12–24, and 24–33 years of follow-up. Interactions between risk factors and quartile level of total serum cholesterol were assessed. Results: Total cholesterol, blood pressure, and cigarette smoking were associated with CHD mortality in multivariate analyses across all follow-up periods. Nonfasting triglyceride levels were associated with CHD in multivariate analyses (0–12 years, HR 1.12, 95% CI 1.00–1.25; 12–24 years, HR 1.13, 95% CI 1.04–1.23; 24–33 years, HR 1.09, 95% CI 1.00–1.19; 0–33 years, HR 1.10, 95% CI 1.05–1.16). A metabolic risk factor score (based on blood pressure, triglycerides, body mass index, and glucose) retained predictivity across all periods. The relations between systolic blood pressure, triglycerides, and metabolic risk factor score to CHD were stronger in the lower than the upper quartiles of serum cholesterol (p < 0.001). Conclusions: Conventional risk factors and nonfasting triglycerides increased CHD mortality across all periods of follow-up. The association with metabolic variables was strongest in men with low total cholesterol levels supporting the idea that lowering cholesterol should be the primary target of primary prevention.
TL1, a Novel Tumor Necrosis Factor-like Cytokine, Induces Apoptosis in Endothelial Cells

TL1 is a recently discovered novel member of the tumor necrosis factor (TNF) cytokine family. TL1 is abundantly expressed in endothelial cells, but its function is not known. The present study was undertaken to explore whether TL1 induces apoptosis in endothelial cells and, if so, to explore its mechanism of action. Cultured bovine pulmonary artery endothelial cells (BPAEC) exposed to TL1 showed morphological (including ultrastructural) and biochemical features characteristic of apoptosis. TL1-induced apoptosis in BPAEC was a time- and concentration-dependent process (EC50 = 72 ng/ml). The effect of TL1 was not inhibited by soluble TNF receptors 1 or 2. TL1 up-regulated Fas expression in BPAEC at 8 and 24 h after treatment, and significantly activated stress-activated protein kinase (SAPK) and p38 mitogen-activated protein kinase (p38 MAPK). The peak activities of SAPK and p38 MAPK in TL1-treated BPAEC were increased by 9- and 4-fold, respectively. TL1-induced apoptosis in the BPAEC was reduced by expression of a dominant-interfering mutant of c-Jun (62.8%,p < 0.05) or by a specific p38 inhibitor, SB203580 (1–10 μm) dose-dependently. TL1 also activated caspases in BPAEC, and TL1-induced apoptosis in BPAEC was significantly attenuated by the caspase inhibitor, ZVAD-fluromethyl-ketone. The major component activated by TL1 in BPAEC was caspase-3, which was based on substrate specificity and immunocytochemical analysis. These findings suggest that TL1 may act as an autocrine factor to induce apoptosis in endothelial cells via activation of multiple signaling pathways, including stress protein kinases as well as certain caspases.
Oxidation of pharmaceuticals during ozonation and advanced oxidation processes.

This study investigates the oxidation of pharmaceuticals during conventional ozonation and advanced oxidation processes (AOPs) applied in drinking water treatment. In a first step, second-order rate constants for the reactions of selected pharmaceuticals with ozone (k(O3)) and OH radicals (k(OH)) were determined in bench-scale experiments (in brackets apparent k(O3) at pH 7 and T = 20 degrees C): bezafibrate (590 +/- 50 M(-1) s(-1)), carbamazepine (approximately 3 x 10(5) M(-1) s(-1)), diazepam (0.75 +/- 0.15 M(-1) s(-1)), diclofenac (approximately 1 x 10(6) M(-1) s(-1)), 17alpha-ethinylestradiol (approximately 3 x 10(6) M(-1) s(-1)), ibuprofen (9.6 +/- 1.0 M(-1) s(-1)), iopromide (<0.8 M(-1) s(-1)), sulfamethoxazole (approximately 2.5 x 10(6) M(-1) s(-1)), and roxithromycin (approximately 7 x 10(4) M(-1) s(-1)). For five of the pharmaceuticals the apparent k(O3) at pH 7 was >5 x 10(4) M(-1) s(-1), indicating that these compounds are completely transformed during ozonation processes. Values for k(OH) ranged from 3.3 to 9.8 x 10(9) M(-1) s(-1). Compared to other important micropollutants such as MTBE and atrazine, the selected pharmaceuticals reacted about two to three times faster with OH radicals. In the second part of the study, oxidation kinetics of the selected pharmaceuticals were investigated in ozonation experiments performed in different natural waters. It could be shown that the second-order rate constants determined in pure aqueous solution could be applied to predict the behavior of pharmaceuticals dissolved in natural waters. Overall it can be concluded that ozonation and AOPs are promising processes for an efficient removal of pharmaceuticals in drinking waters.
Protective effect of selenium in cardiac ischemia and reperfusion.

The purpose of the present investigation was to establish whether pretreatment with selenium enhances the stores of selenium-dependent glutathione peroxidase in the tissues and to verify if and to what extent alterations of mechanical and biochemical cardiac properties induced by ischemia in the myocardium may be thus prevented. Ten rats had sodium selenite (6 micrograms/day) added to their drinking water for 4 weeks, while 10 control rats received no treatment. At the end of 4 weeks, the hearts were perfused by the Langendorff technique with oxygenated Krebs-Henseleit solution at a rate of 10 ml/min for 30 minutes at 37 degrees C. Ischemia was then induced by reducing the perfusion to 1 ml/min for 60 minutes; reperfusion followed at the control rate for a further 30 minutes. Isometrically developed pressure and its maximum first derivative at different ventricular volumes was measured before and after the ischemic period. Lactate and creatine kinase activity were measured in the effluent throughout. Tissue concentrations of adenine nucleotides and creatine phosphate and lutathione peroxidase activity were estimated after reperfusion. The rats treated with selenium showed a wide-spread increase in the activity of Se-dependent glutathione peroxidase in all tissues. There was an improved recovery of ventricular contraction during reperfusion and an increased myocardial content of adenine nucleotides and creatine phosphate. During reperfusion, the loss of creatine kinase into the perfusate was less in the treated animals, and there was a similar trend for the production of lactate. (ABSTRACT TRUNCATED AT 250 WORDS)