Miracle-dz/UniFAR-FTUs huggingface dataset:
Author`s Reply

We thank the authors for their great interest in our work entitled “Effects of energy drinks on blood pressure, heart rate, and electrocardiographic parameters: an experimental study on healthy young adults” published in Anatol J Cardiol 2016; 16: 94-9 (1). In addition to our discussion, they also notified the incoherent results of different studies on the heart rate (HR) response after energy drink consumption. Authors of the letter, however, stated that an HR increase is an essential effect of catecholamine release and then considered the combination of “HR decline” and “catecholamine release” as conflicting. Although we agree that an HR increase is an effect of situations with pure catecholamine release, it must be emphasized that a combination of “HR decline and catecholamine release” is also possible in some conditions, of which the most well-known is the Cushing reflex. As we supposed in the article, the HR decrease after energy drink consumption is possibly due to direct central stimulation of the vagus nerve by caffeine (2). A similar mechanism has been previously described for the Cushing reflex where concurrent hypertension (owing to sympathetic activation) and bradycardia (owing to the vagus nerve stimulation) are seen (3). Given the known effects of smoking on sympathetic activation (4), as noted by the authors of the letter, we excluded all smokers from our study to avoid its possible confounding role on results. This was mentioned in the paper by excluding those with a history of “substance abuse. ” According to the valid definitions, including Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition (DSM-5) (5), tobacco consumption is an example of substance abuse. Finally, as we discussed in the abovementioned article (1), factors such as different types of energy drinks and durations of BP monitoring after energy drink consumption are among the possible reasons underlying the conflicting results of different studies on hemodynamic effects of energy drinks. Thus, we agree with the authors of the letter that considering follow-up duration and amount of energy drinks are of great importance in comparing the results of different investigations on energy drinks.
Regulation of glycogen synthase activity and phosphorylation by exercise

Glycogen synthase (GS) catalyses the rate-limiting step of UDP-glucose incorporation into glycogen. Exercise is a potent regulator of GS activity, leading to activation of GS immediately after exercise promoting glycogen repletion by mechanisms independent of insulin. The incorporation of UDP-glucose is energy demanding, and during intense exercise GS is deactivated, diminishing energy utilization but also increasing the potential for glycogen breakdown. An apparent activation of GS is observed during moderate exercise, which could be considered as a potential waste of energy, although the cellular capacity for glycogen breakdown is considerably higher than that for glycogen synthesis. The understanding of this complex regulation of GS activity in response to exercise is just at its beginning. In the present review potential mechanisms by which exercise regulates GS activity are described, factors that may promote GS activation and factors that may deactivate GS are discussed, pointing to the view that GS activity during exercise is the result of the relative strength of these opposing factors.
Nursing Management Lower Respiratory Problems 28

Reviewed by Christine L. Willis, RN, MSN, ANP, CS, Adult Nurse Practitioner, Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, N.C. acute bronchitis, p. ••• atelectasis, p. ••• chylothorax, p. community-acquired pneumonia, p. ••• cor pulmonale, p. ••• empyema, p. ••• fl ail chest, p. ••• hemothorax, p. ••• hospital-acquired pneumonia, p. ••• lung abscess, p. ••• pleural effusion, p. ••• pleurisy (pleuritis), p. ••• pneumoconiosis, p. ••• pneumonia, p. ••• pneumothorax, p. ••• pulmonary edema, p. ••• pulmonary embolism, p. ••• pulmonary hypertension, p. ••• tension pneumothorax, p. ••• thoracentesis, p. ••• thoracotomy, p. ••• tuberculosis, p. ••• KEY TERMS
Clinical Applications of Noninvasive Electrical Stimulation

Both transcranial direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS) can produce lasting aftereffects on cortical function that are thought to be due to the initial stages of synaptic potentiation/depression. They can also interact with processes of normal learning, to increase or decrease the rate of learning and retention. These features have spurred a number of investigators to test whether there is any clinical therapeutic potential for the methods to improve recovery of function after damage to the brain by injury or disease. The only condition where there is sufficient evidence is in certain forms of depression where excitatory rTMS is a recommended treatment protocol; there is insufficient evidence for any other condition. The problem facing investigators is the variety of possible paradigms that can be applied. Particularly for tDCS, only a small range of possible parameters has been tested, even in healthy volunteers; in addition, it is unclear whether stimulation should be applied at the same time as a behavioral therapy or whether stimulation should be applied at rest. Present trials give some evidence that can be used to address these questions, but until they are answered more securely it will be difficult to reach a consensus about “standard” protocols that can then be tested widely in multicenter trials.
Shared medical appointments based on the chronic care model: a quality improvement project to address the challenges of patients with diabetes with high cardiovascular risk

Objective: The epidemic proportions and management complexity of diabetes have prompted efforts to improve clinic throughput and efficiency. One method of system redesign based on the chronic care model is the Shared Medical Appointment (SMA) in which groups of patients (8–20) are seen by a multi-disciplinary team in a 1–2 h appointment. Evaluation of the impact of SMAs on quality of care has been limited. The purpose of this quality improvement project was to improve intermediate outcome measures for diabetes (A1c, SBP, LDL-cholesterol) focusing on those patients at highest cardiovascular risk. Setting: Primary care clinic at a tertiary care academic medical center. Subjects: Patients with diabetes with one or more of the following: A1c >9%, SBP blood pressure >160 mm Hg and LDL-c >130 mg/dl were targeted for potential participation; other patients were referred by their primary care providers. Patients participated in at least one SMA from 4/05 to 9/05. Study design: Quasi-experimental with concurrent, but non-randomised controls (patients who participated in SMAs from 5/06 through 8/06; a retrospective period of observation prior to their SMA participation was used). Intervention: SMA system redesign Analytical methods: Paired and independent t tests, χ2 tests and Fisher Exact tests. Results: Each group had up to 8 patients. Patients participated in 1–7 visits. At the initial visit, 83.3% had A1c levels >9%, 30.6% had LDL-cholesterol levels >130 mg/dl, and 34.1% had SBP ⩾160 mm Hg. Levels of A1c, LDL-c and SBP all fell significantly postintervention with a mean (95% CI) decrease of A1c 1.4 (0.8, 2.1) (p<0.001), LDL-c 14.8 (2.3, 27.4) (p = 0.022) and SBP 16.0 (9.7, 22.3) (p<0.001). There were no significant differences at baseline between control and intervention groups in terms of age, baseline intermediate outcomes, or medication use. The reductions in A1c in % and SBP were greater in the intervention group relative to the control group: 1.44 vs –0.30 (p = 0.002) for A1c and 14.83 vs 2.54 mm Hg (p = 0.04) for SBP. LDL-c reduction was also greater in the intervention group, 16.0 vs 5.37 mg/dl, but the difference was not statistically significant (p = 0.29). Conclusions: We were able to initiate a programme of group visits in which participants achieved benefits in terms of cardiovascular risk reduction. Some barriers needed to be addressed, and the operations of SMAs evolved over time. Shared medical appointments for diabetes constitute a practical system redesign that may help to improve quality of care.
Interleukin-13 gene transfer protects rat livers from antigen-independent injury induced by ischemia and reperfusion1

Background. Ischemia-reperfusion (I/R) injury is a prime inflammatory factor in the dysfunction of orthotopic liver transplants. Interleukin (IL)-13 suppresses macrophage production of proinflammatory mediators. This study explores the effects of adenovirus (Ad)-based IL-13 gene transfer in rat models of hepatic I/R injury. Methods. The authors used a model of warm in situ ischemia followed by reperfusion, and ex vivo cold ischemia followed by transplantation. Results. In a model of warm in situ ischemia followed by reperfusion, Ad-based IL-13 significantly diminished hepatocellular injury, assessed by serum glutamic oxaloacetic transaminase (SGOT) levels, as compared with Ad-based &bgr;-galactosidase (gal)-treated livers. In a model of ex vivo cold ischemia followed by transplantation, the survival of liver grafts increased from 50% in Ad-&bgr;-gal untreated controls to 100% after Ad-IL-13 gene therapy. This beneficial effect correlated with improved liver function (SGOT levels), preservation of hepatic histologic integrity and architecture (Suzuki criteria), and depression of neutrophil infiltration (myeloperoxidase assay). Ad-IL-13 diminished activation of macrophage-neutrophil–associated tumor necrosis factor-&agr;, macrophage inflammatory protein-2, and endothelial-dependent E-selectin, but increased type 2 IL-4 and IL-13 expression. Conclusions. This study documents striking cytoprotective effects of virally induced IL-13 against hepatic I/R injury in two clinically relevant rat models of hepatic I/R injury. These data provide the rationale for novel therapeutic approaches to maximize the organ donor pool through the safer use of liver transplants despite prolonged periods of warm or cold ischemia, or both.
The induction of thioredoxin-1 by epinephrine withdraws stress via interaction with β-arrestin-1

Stress regulates a panel of important physiological functions and disease states. Epinephrine is produced under stresses threaten to homeostasis. Thioredoxin-1(Trx-1) is a redox regulating protein which is induced to resist stresses and related with various diseases. Thus, it is important to examine whether Trx-1 is induced by epinephrine and to understand the underlying molecular mechanisms that Trx-1 modulates epinephrine stress. Here, we show that the expression of Trx-1 was induced by epinephrine via β-adrenergic receptor/Cyclic AMP/protein kinase A (PKA) signaling pathway in PC12 cells. The down-regulation of Trx-1 by siRNA aggravated accumulation of γ-H2AX and further decreased expression of p53 by epinephrine. Accordingly, Trx-1 overexpression alleviated accumulation of γ-H2AX and restored the expressions of p53 and C/EBP homologous protein (CHOP) in the cortex, hippocampus and thymus of mice. Moreover, Trx-1 overexpression reduced the malondialdehyde concentration by epinephrine. We further explored the mechanism on p53 and γ-H2AX regulated by Trx-1. We found that overexpression of Trx-1 suppressed β-arrestin-1 expression through interaction with β-arrestin-1. Consequently, the downregulation of β-arrestin-1 suppressed the cell viability and the expressions of γ-H2AX and cyclin D1, and increased p53 expression. Taken together, our data suggest that Trx-1/β-arrestin-1 interaction may represent a novel endogenous mechanism on protecting against stress.
Whole‐exome sequencing identifies compound heterozygous mutations in WDR62 in siblings with recurrent polymicrogyria

Polymicrogyria is a disorder of neuronal development resulting in structurally abnormal cerebral hemispheres characterized by over‐folding and abnormal lamination of the cerebral cortex. Polymicrogyria is frequently associated with severe neurologic deficits including intellectual disability, motor problems, and epilepsy. There are acquired and genetic causes of polymicrogyria, but most patients with a presumed genetic etiology lack a specific diagnosis. Here we report using whole‐exome sequencing to identify compound heterozygous mutations in the WD repeat domain 62 (WDR62) gene as the cause of recurrent polymicrogyria in a sibling pair. Sanger sequencing confirmed that the siblings both inherited 1‐bp (maternal allele) and 2‐bp (paternal allele) frameshift deletions, which predict premature truncation of WDR62, a protein that has a role in early cortical development. The probands are from a non‐consanguineous family of Northern European descent, suggesting that autosomal recessive PMG due to compound heterozygous mutation of WDR62 might be a relatively common cause of PMG in the population. Further studies to identify mutation frequency in the population are needed. © 2011 Wiley‐Liss, Inc.
Law, norms, piracy and online anonymity: Practices of de‐identification in the global file sharing community

Purpose – The purpose of this study is to understand more of online anonymity in the global file sharing community in the context of social norms and copyright law. The study describes the respondents in terms of use of VPN or similar service related to age, gender, geographical location, as well as analysing the correlation with file sharing frequencies.Design/methodology/approach – This study is to a large extent descriptively collecting data through a web‐based survey. This was carried out in collaboration with the BitTorrent tracker The Pirate Bay (TPB), allowing the authors to link the survey from the main logo of their site. In 72 hours the authors received over 75,000 responses, which gives the opportunity to compare use of anonymity services with factors of age, geographical region, file sharing frequency, etc.Findings – Overall, 17.8 per cent of the respondents use a VPN or similar service (free or paid). A core of high frequency uploaders is more inclined to use VPN or similar services than the .
A Case of Pancreatic Undifferentiated Carcinoma Mimicking Proximal-Type Epithelioid Sarcoma

We herein report a case of pancreatic undifferentiated/anaplastic carcinoma pathologically mimicking proximal-type epithelioid sarcoma. The patient was a 35-year-old female who complained of epigastralgia and back pain and presented with tarry stools and weight loss. A growing, hemorrhagic pancreatic mass more than 6 cm in diameter and multiple liver masses were revealed on abdomen images. A liver biopsy showed malignant cells and chemotherapy using TS-1 was performed, however, the patient accumulated a large amount of ascites by diffuse peritoneal dissemination and died after seven months. An autopsy demonstrated the manifestation of a large whitish, expansive-infiltrative mass with severe hemorrhage, measuring 18 x 13 cm, seated primarily in the head of the pancreas. Microscopically, the tumor showed a medullary growth consisted of pleomorphic spindle to epithelioid cells, which were loosely cohesive and included rhabdoid morphology. The glandular component, suggestive of ductal adenocarcinoma, could not be found even with extensive sampling. Immunohistochemical studies showed a diffuse positivity of cytokeratin (AE1/AE3), epithelial membrane antigen, vimentin, and CD34 and a negativity of specific differentiation markers. In addition, a loss of SMARCB1/INI-1 protein expression was observed, although its alterations were not confirmed at the deoxyribonucleic acid level. No KRAS mutations were detected. The tumor was considered as pancreatic undifferentiated/anaplastic carcinoma from the similarity to "monomorphic anaplastic subtype of pancreatic undifferentiated rhabdoid carcinoma" recently proposed by Agaimy A et al. However, its histological, immunohistological and molecular characters were completely identical to those of PES, thus the clinical treatment and care for proximal-type epithelioid sarcoma may be recommended rather than those for undifferentiated/anaplastic carcinoma as a subtype of ductal adenocarcnoma.
Joint Spectrum Allocation and Structure Optimization in Green Powered Heterogeneous Cognitive Radio Networks

We aim at maximizing the sum rate of secondary users (SUs) in OFDM-based Heterogeneous Cognitive Radio (CR) Networks using RF energy harvesting. Assuming SUs operate in a time switching fashion, each time slot is partitioned into three non-overlapping parts devoted for energy harvesting, spectrum sensing and data transmission. The general problem of joint resource allocation and structure optimization is formulated as a Mixed Integer Nonlinear Programming task which is NP-hard and intractable. Thus, we propose to tackle it by decomposing it into two subproblems. We first propose a sub-channel allocation scheme to approximately satisfy SUs' rate requirements and remove the integer constraints. For the second step, we prove that the general optimization problem is reduced to a convex optimization task. Considering the trade-off among fractions of each time slot, we focus on optimizing the time slot structures of SUs that maximize the total throughput while guaranteeing the rate requirements of both real-time and non-real-time SUs. Since the reduced optimization problem does not have a simple closed-form solution, we thus propose a near optimal closed-form solution by utilizing Lambert-W function. We also exploit iterative gradient method based on Lagrangian dual decomposition to achieve near optimal solutions. Simulation results are presented to validate the optimality of the proposed schemes.
Expression and regulation of the RepA protein of the RepFIB replicon from plasmid P307

The control of RepFIB replication appears to rely on the interaction between an initiator protein (RepA) and two sets of DNA repeat elements located on either side of the repA gene. Limited N-terminal sequence information obtained from a RepA:beta-galactosidase fusion protein indicates that although the first residue of RepA is methionine, the initiation of translation of RepA occurs from a CTG codon rather than from the predicted GTG codon located further downstream. Overexpressed RepA in trans is capable of repressing a repA:lacZ fusion plasmid in which the expression of the fusion protein is under the control of the repA promoter. The repA promoter has been located functionally by testing a series of repA:lacZ fusion plasmids. Both in vivo genetic tests and in vitro DNA-binding studies indicate that repA autoregulation can be achieved by RepA binding to one or more repeat elements which overlap the repA promoter sequence.
Surface Charges near the Guanidinium Neurotoxin Binding Site a

The guanidinium neurotoxins saxitoxin (STX) and tetrodotoxin (TTX) have been used to identify, classify, and purify voltage-dependent sodium channels in excitable membranes, as discussed in many papers in this volume. STX and TTX can also be used to probe the surface characteristics of sodium channels, e.g., whether there are fixed surface charges in the vicinity of the toxin binding site. '32 Addition of alkali metal cation salts to the extracellular solution bathing sodium channels decreases the binding of STX and TTX to the channels. This effect of the alkali metal cations on toxin binding can formally be described as a one-to-one competitive inhibition.Other studies have shown that increases in extracellular Ca2+ concentration inhibit the binding of the divalent STX more than the binding of the monovalent TTX. '*2 The results of the latter studies suggest that there are fixed negative surface charges near the toxin binding site. If this were the case, the interaction between alkali metal cations and the neurotoxins could result from a combination of a competitive displacement and a reduction in the local toxin concentration due to screening of surface charges and the associated reduction in surface potential. We report here the results of experiments designed to test whether sodium channels possess a net surface charge density near the neurotoxin binding site. This question can be studied using sodium channels that have been incorporated into planar lipid bilayers,' because one has control over the lipid composition of the host bilayer.
Traction Dynamics of Filopodia on Compliant Substrates

Cells sense the environment's mechanical stiffness to control their own shape, migration, and fate. To better understand stiffness sensing, we constructed a stochastic model of the “motor-clutch” force transmission system, where molecular clutches link F-actin to the substrate and mechanically resist myosin-driven F-actin retrograde flow. The model predicts two distinct regimes: (i) “frictional slippage,” with fast retrograde flow and low traction forces on stiff substrates and (ii) oscillatory “load-and-fail” dynamics, with slower retrograde flow and higher traction forces on soft substrates. We experimentally confirmed these model predictions in embryonic chick forebrain neurons by measuring the nanoscale dynamics of single–growth-cone filopodia. Furthermore, we experimentally observed a model-predicted switch in F-actin dynamics around an elastic modulus of 1 kilopascal. Thus, a motor-clutch system inherently senses and responds to the mechanical stiffness of the local environment.
Advances and challenges towards a vaccine against Chagas disease

Chagas disease is major public health problem, affecting nearly 10 million people, characterized by cardiac alterations leading to congestive heart failure and death of 20-40% of the patients infected with Trypanosoma cruzi, the protozoan parasite responsible for the disease. A vaccine would be key to improve disease control and we review here the recent advances and challenges of a T. cruzi vaccine. There is a growing consensus that a protective immune response requires the activation of a Th1 immune profile, with the stimulation of CD8+ T cells. Several vacines types, including recombinant proteins, DNA and viral vectors, as well as heterologous prime-boost combinations, have been found immunogenic and protective in mouse models, providing proof-of-concept data on the feasibility of a preventive or therapeutic vaccine to control a T. cruzi infection. However, several challenges such as better end-points, safety issues and trial design need to be addressed for further vaccine development to proceed.
White Mythologies: Writing History and the West

We are still living under the Empire of the Selfsame. The same masters domimate history from the beginning . history, as a story of phallocentrism hasn't moved except to repeat itself. ' Helene Cixous's indictment of history' as a story of phallocentrism' provides the starting point for Robert Young's exploration of the operations of history' in Western theory. History', Young argues, has always been a problematical concept. In the wake of Postmodernism, with its celebration of dislocation and disunity, the status of history has become ever less certain. White Mythologies traces various attempts to produce a coherent theory of history, from Hegel and Marx to Lukacs and Sartre, and to the more recent work of Althusser and Foucault who tried without success to produce a non-historicist history. Young suggests that all efforts to subsume history into a single narrative are doomed to failure: there remains always an unassimilable surplus. In Marxist accounts, in which history' is the struggle between the working class and the bourgeoisie, the Third World appears as this excess, surplus to the narrative of the West. Young goes on to consider strategies for a hon-historicist history which avoids the trap of Eurocentricism. While Edward Said's influential critique of Orientalism ends by repeating the very structures it attacks, Homi Bhabha and Gayatri Chakravorty Spivak have successfully exploited the ambivalence of history to deconstruct its totalising authority. At the same time, they suggest a way forward by means of a shift in the locational specifity of historical argument.