Miracle-dz/UniFAR-FTUs huggingface dataset:
The Political Model of Strikes: A New Twist

The political model of strikes in which work stoppages are viewed as the result of worker intransigence has occupied an influential position in the strikes literature since its empirical specification by Ashenfelter and Johnson [1]. There are two basic reasons for the popularity of the model. First, it is an eminently accessible treatment in a literature of highly abstract bargaining models, most of which do not have a direct bearing on strikes. Second, until the Ashenfelter-Johnson study, little progress had been made in applying models of union behavior. Drawing on Ross's [6] insight that the union was essentially a political institution operating in an economic environment, Ashenfelter and Johnson sought to examine the implications for strikes of the divergent goals of the union leadership and the rank-and-file membership. The basic idea is that strikes are "caused" by the unrealistically high wage aspirations of the latter, which are nonetheless processed by the better informed union leadership so as to deflect any incipient challenge to its authority and continued tenure in office. The function of a strike is an equilibrating mechanism to square up the membership's wage expectations with what the firm may be prepared to pay. Strikes are attributed exclusively to the "union" side. The difficulty with the model lies precisely in its assumption that it is the union side which "bargains" badly and hence precipitates strikes. For example, one can construct a model employing the opposite assumption after Eaton [2] and Rabinovitch and Swary [4]. Indeed, the assumption that it is the employer side which "bargains" badly forms the basis of our revisionist model. Conceptual issues apart, the twist is that our model is applied to the very same data set used by Farber [3] in his re-estimation of the Ashenfelter-Johnson model using data on eighty contract negotiations for ten large manufacturing firms (on which more below). ' We show that the two very differently assumptioned models both yield reasonable results using the same data set. The implications of this finding are then discussed.
Effective Small Social Community Aware D2D Resource Allocation Underlaying Cellular Networks

Social-aware device-to-device (D2D) resource allocation utilizes social ties in human-formed social networks to allocate spectrum resources between D2D users and cellular users. In this letter, we consider the small size social communities formed by people with similar interests and exploit them to optimize the resource allocation of the communities. This results in an optimal graph matching problem among communities to solve the D2D resource allocation problem. Solutions are derived via bipartite graph matching and an effective small social community resource allocation algorithm corresponding to the cases of small and high D2D user loads.
Dynamic pricing model for EV charging-discharging service based on cloud computing scheduling

Electric Vehicle (EV) and smart grids have gained much popularity in recent years. This has been enabled by the high increase of EVs on roads; however, this may lead to a significant impact on the power grids. In order to keep EVs far from causing peaks in power demand during the day, it is important to perform an intelligent scheduling for EVs charging and discharging by including metrics, such as price and demand-supply curve. In this paper, we propose a dynamic pricing model for EV charging (i.e., grid-to-vehicle, G2V) and discharging (i.e., vehicle-to-grid, V2G) services, in order to reduce the peak load. Our proposed model uses cloud computing architecture to schedule EV requests. We formulate our problem as a linear optimization problem and solve it using new algorithms for charging and discharging. To the best of our knowledge, this is the first paper that proposes a model that tries to solve all the aforementioned issues. The extensive simulations proved that our proposed pricing model, based on cloud computing and EVs interactions, optimizes the energy load during peak hours and satisfies EVs users and micro grid constraints.
Epidemiologists, Our Patient is Society

The common approach utilized in many epidemiologic studies is to measure and compare characteristics and exposures of afflicted and non-afflicted individuals from the same population. The subject of most contemporary chronic disease epidemiology, therefore, is not epidemics per se, nor their causes, but rather epidemics' victims. While these approaches and methods are entirely appropriate for investigating many vitally important health-related questions, it is argued here that epidemics themselves, including those that produce chronic illnesses, should also be the subject of epidemiologic investigations. Epidemics are viewed as phenomena that afflict social entities and should be approached as such.
Children's Sleep: An Interplay Between Culture and Biology

Pediatricians provide a major source of knowledge for parents about children's behavior and development, although their advice is largely based on their own cultural values and beliefs in interaction with their personal and clinical experience. This review presents cross-cultural aspects of children's sleep behavior in industrialized and complex modern societies and provides a basis for understanding dimensions and mechanisms of cultural differences. We submit that it is the interaction between culture and biology that establishes behavioral and developmental norms and expectations regarding normal and problematic children's sleep. Pediatricians need to recognize the cultural environment in which children live and be knowledgeable about how cultural beliefs and values of both families and physicians interact with the needs and biological characteristics of individual children.
Bronchopulmonary neuroendocrine tumors

Bronchopulmonary neuroendocrine tumors (BP‐NETs) comprise ≈20% of all lung cancers and represent a spectrum of tumors arising from neuroendocrine cells of the BP‐epithelium. Although they share structural, morphological, immunohistochemical, and ultrastructural features, they are separated into 4 subgroups: typical carcinoid tumor (TC), atypical carcinoid tumor (AC), large‐cell neuroendocrine carcinoma (LCNEC), and small‐cell lung carcinoma (SCLC), which exhibit considerably different biological characteristics. The clinical presentation includes cough, hemoptysis, and obstructive pneumonia but varies depending on site, size, and growth pattern. Less than 5% of BP‐NETs exhibit hormonally related symptoms such as carcinoid syndrome, Cushing, acromegaly, and SIADH. SCLC is the most common BP‐NET, while LCNEC is rare, ≈10% and ≤1%, respectively, of all lung cancers. Both SCLC and LCNEC progress rapidly, are aggressively metastatic, and exhibit a poor prognosis. The incidence of BP‐carcinoids (TC and AC) in the US was 1.57 of 100,000 in 2003 (an unexplained and substantial increase over the last 30 years, ≈6% per year). No curative treatment except for radical surgery (almost never feasible) exists. The slow‐growing TC exhibit a fairly good prognosis (≈88%, 5‐year survival), whereas AC demonstrate a 5‐year survival of ≈50%, and the highly malignant LCNEC and SCLC5‐year survival of 15% to 57% and <5%, respectively. This review provides a broad overview on BP‐NETs and focuses on the evolution of the disease, general features, and current diagnostic and therapeutic options. Cancer 2008. © 2008 American Cancer Society.
Coronavirus Protein Processing and RNA Synthesis Is Inhibited by the Cysteine Proteinase Inhibitor E64d

Abstract Mouse hepatitis virus strain A59 (MHV-A59) encodes within the 22-kb gene 1 a large polypretain containing three proteinase domains with proven or predicted cysteine catalytic residues. E64d, a specific, irreversible inhibitor of cysteine (thiol) proteinases, inhibits the processing of the gene 1 polyprotein. Specifically, E64d blocks the carboxy-terminal cleavage of p65, E64d also inhibits replication of MHV-A59 in murine DBT cells in a dose-dependent manner, resulting in reduced virus titers and viral syncytia formation. This inhibition of replication is associated with a rapid shutoff of new viral RNA synthesis, in a manner similar to that seen in the presence of cycloheximide. The E64d-associated inhibition of RNA synthesis likely results from E64d-specific inhibition of processing of the gene 1 polyprotein, resulting in inactive proteinase or replicase proteins. These results indicate that processing of the MHV-A59 gene 1-encoded polyprotein is required throughout infection to sustain RNA synthesis and virus replication.
Determination of the Efficacy of Two Building Decontamination Strategies by Surface Sampling with Culture and Quantitative PCR Analysis

ABSTRACT The efficacy of currently available decontamination strategies for the treatment of indoor furnishings contaminated with bioterrorism agents is poorly understood. Efficacy testing of decontamination products in a controlled environment is needed to ensure that effective methods are used to decontaminate domestic and workplace settings. An experimental room supplied with materials used in office furnishings (i.e., wood laminate, painted metal, and vinyl tile) was used with controlled dry aerosol releases of endospores of Bacillus atrophaeus (“Bacillus subtilis subsp. niger,” also referred to as BG), a Bacillus anthracis surrogate. Studies were performed using two test products, a foam decontaminant and chlorine dioxide gas. Surface samples were collected pre- and posttreatment with three sampling methods and analyzed by culture and quantitative PCR (QPCR). Additional aerosol releases with environmental background present on the surface materials were also conducted to determine if there was any interference with decontamination or sample analysis. Culture results indicated that 105 to 106 CFU per sample were present on surfaces before decontamination. After decontamination with the foam, no culturable B. atrophaeus spores were detected. After decontamination with chlorine dioxide gas, no culturable B. atrophaeus was detected in 24 of 27 samples (89%). However, QPCR analysis showed that B. atrophaeus DNA was still present after decontamination with both methods. Environmental background material had no apparent effect on decontamination, but inhibition of the QPCR assay was observed. These results demonstrate the effectiveness of two decontamination methods and illustrate the utility of surface sampling and QPCR analysis for the evaluation of decontamination strategies.
Visualizing the dynamics of p21Waf1/Cip1 cyclin-dependent kinase inhibitor expression in living animals

Although the role of p21Waf1/Cip1 gene expression is well documented in various cell culture studies, its in vivo roles are poorly understood. To gain further insight into the role of p21Waf1/Cip1 gene expression in vivo, we attempted to visualize the dynamics of p21Waf1/Cip1 gene expression in living animals. In this study, we established a transgenic mice line (p21-p-luc) expressing the firefly luciferase under the control of the p21Waf1/Cip1 gene promoter. In conjunction with a noninvasive bioluminescent imaging technique, p21-p-luc mice enabled us to monitor the endogenous p21Waf1/Cip1 gene expression in vivo. By monitoring and quantifying the p21Waf1/Cip1 gene expression repeatedly in the same mouse throughout its entire lifespan, we were able to unveil the dynamics of p21Waf1/Cip1 gene expression in the aging process. We also applied this system to chemically induced skin carcinogenesis and found that the levels of p21Waf1/Cip1 gene expression rise dramatically in benign skin papillomas, suggesting that p21Waf1/Cip1 plays a preventative role(s) in skin tumor formation. Surprisingly, moreover, we found that the level of p21Waf1/Cip1 expression strikingly increased in the hair bulb and oscillated with a 3-week period correlating with hair follicle cycle progression. Notably, this was accompanied by the expression of p63 but not p53. This approach, together with the analysis of p21Waf1/Cip1 knockout mice, has uncovered a novel role for the p21Waf1/Cip1 gene in hair development. These data illustrate the unique utility of bioluminescence imaging in advancing our understanding of the timing and, hence, likely roles of specific gene expression in higher eukaryotes.
Validation of a TIA Recognition Tool in Primary and Secondary Care: Implications for Generalizability

Background In spite of public education campaigns, patients with transient ischemic attack still present to primary care where accurate recognition of transient ischemic attack is essential so that specialist referral can be expedited to reduce stroke risk. The complex task of diagnosing transient ischemic attack is challenging in time-limited settings in primary care yet the potential for a transient ischemic attack recognition tool to improve diagnosis has not been determined. Aims We set out to examine the potential utility in primary care of the only existing transient ischemic attack recognition tool. Methods All primary care referrals with suspected transient ischemic attack from a total population of 91 000 people were analyzed over a four-year period from 2002 to 2006. Clinical and research records from the transient ischemic attack clinic and consultation notes and referral letters from primary care physicians were used to populate the Dawson recognition score. Results Of 513 referrals, 209 (47%) had a clinic confirmed diagnosis of transient ischemic attack. Agreement between primary care assessments and specialist assessments was greater for speech disturbance (kappa 0·68) than for unilateral facial weakness (0·58) and unilateral limb weakness (0·51). The Dawson score had greater accuracy in diagnosing all transient ischemic attack in specialist assessments than in primary care assessments (c statistics 0·80 vs. 0·70, P < 0·0001) and performed particularly poorly in primary care for detecting posterior circulation territory transient ischemic attack with a c statistic (95% confidence interval) of 0·52 (0·43–0·61). Conclusion The Dawson transient ischemic attack recognition score is less accurate in primary care than in its derivation setting of specialist care. Improving the recognition of transient ischemic attack by providers of first contact health care requires derivation of rules in the clinical setting in which they are to be used.
Role of histone deacetylase 9 in regulating adipogenic differentiation and high fat diet-induced metabolic disease

Adipose tissue serves as both a storage site for excess calories and as an endocrine organ, secreting hormones such as adiponectin that promote metabolic homeostasis. In obesity, adipose tissue expands primarily by hypertrophy (enlargement of existing adipocytes) rather than hyperplasia (generation of new adipocytes via adipogenic differentiation of preadipocytes). Progressive adipocyte hypertrophy leads to inflammation, insulin resistance, dyslipidemia, and ectopic lipid deposition, the hallmark characteristics of metabolic disease. We demonstrate that during chronic high fat feeding in mice, adipogenic differentiation is impaired due to the actions of histone deacetylase 9 (HDAC9), a member of the class II family of HDACs. Mechanistically, upregulated HDAC9 expression blocks the adipogenic differentiation program during chronic high fat feeding, leading to accumulation of improperly differentiated adipocytes with diminished expression of adiponectin. These adipocytes are inefficient at storing lipid, resulting in ectopic lipid deposition in the liver. HDAC9 gene deletion prevents the detrimental effects of chronic high fat feeding on adipogenic differentiation, increases adiponectin expression, and enhances energy expenditure by promoting beige adipogenesis, thus leading to reduced body mass and improved metabolic homeostasis. HDAC9 is therefore emerging as a critical regulator of adipose tissue health and a novel therapeutic target for obesity-related disease.
The Relationship between Caregivers’ Post-traumatic Stress Disorder and Their Asthma Health Beliefs in an Ethnic Minority Inner-City Sample

Objective. Caregivers’ asthma health beliefs can impact healthcare decisions. This study aimed to determine whether caregivers with a diagnosis of post-traumatic stress disorder (PTSD) had asthma illness representations less aligned with the professional model of asthma management and whether their children had worse asthma control. Methods. Participants were 120 children with asthma (age M = 9.25 ± 1.37) and their caregivers recruited from the Bronx, NY, USA. Participants were Puerto Rican (n = 55), African-American (n = 30), Afro-Caribbean (n = 22), and Mexican (n = 13). Caregivers completed: a psychiatric interview to determine diagnosis of PTSD, anxiety and depressive disorders; the Asthma Illness Representation Scale (AIRS) to assess beliefs about their children’s asthma; and the childhood asthma control test (C-ACT). Results. One in five caregivers had PTSD, and these caregivers had lower total AIRS scores, lower scores on the AIRS Emotional Aspects of Medication Use subscale, and the AIRS Nature of Symptoms subscale, indicating illness beliefs less aligned with the professional model. Caregivers with PTSD were more likely to perceive asthma as an acute, difficult to control illness and focused on the emotional aspects of medication use. There was no relationship between PTSD in caregivers and self-report of their children’s asthma control, but children with poorly controlled asthma had caregivers with lower total AIRS scores. Conclusion. Caregivers’ traumatic experiences impact their beliefs about their children’s asthma. Future interventions targeting these beliefs could improve the manner in which they understand and treat their children’s asthma.
A Novel Approach for the Increased Delivery of Pharmaceutical Agents to Peritoneum and Associated Lymph Nodes

A novel method for prolonging the retention of liposomes in the peritoneum while increasing liposome deposition in lymph nodes that drain the peritoneum is described. An aliquot (1 ml) of technetium-99m (99mTc)-biotin-liposomes encapsulating blue dye was injected intraperitoneally in rats. Thirty minutes after administration of the 99mTc-blue-biotin-liposomes, five rats (experimental) were administered avidin (5 mg) intraperitoneally, whereas the remaining five rats served as controls. Scintigraphic images were acquired at baseline and 1 and 24 h after the liposome injection followed by a tissue biodistribution study. Images at 24 h clearly demonstrated very different distributions between the experimental and control animals. In experimental rats, most of the activity was visualized in the abdominal region, and in abdominal and mediastinal lymph nodes. The percentage of the injected dose (% ID) in the blood was significantly higher in the control group than in the experimental group (14.0 ± 1.7 versus 0.17 ± 0.03%;P < 0.001). The % ID in the spleen was also significantly greater for controls (23.3 ± 3.9%) compared with the experimental group (0.78 ± 0.8%; P = 0.001). Significant 99mTc activity was detected in blue-stained abdominal nodes (4.7%) and mediastinal nodes (2.3%) from the experimental animals, whereas no blue-stained nodes were detectable in the control animals. The intraperitoneal biotin-liposome/avidin delivery system described in this study could potentially be used for delivery of liposome-encapsulated drugs to disease processes that become disseminated in the peritoneum such as metastatic ovarian, gastric, and colorectal cancer, as well as infectious peritonitis.
Adenine nucleotides modulate phosphatidylcholine metabolism in aortic endothelial cells

ATP and ADP, in concentrations ranging from 1—100 μM, increased the release of [3H]choline and [3H]phosphorylcholine (P‐choline) from bovine aortic endothelial cells (BAEC) prelabelled with [3H]choline. This action was detectable within 5 minutes and was maintained for at least 40 minutes. ATP and ADP were equiactive, and their action was mimicked by their phosphorothioate analogs (ATP‐γS and ADPβS) and adenosine 5′‐(β,γ imido) triphosphate (APPNP), but not by AMP, adenosine, and adenosine 5‐(α,β methylene)triphosphate (APCPP): these results are consistent with the involvement of P2Y receptors. ATP also induced an intracellular accumulation of [3H]choline: the intracellular level of [3H]choline was increased 30 seconds after ATP addition and remained elevated for a least 20 minutes. The action of ATP on the release of choline metabolites was reproduced by bradykinin (1 μM), the tumor promoter phorbol 12‐myristate 13‐acetate (PMA, 50 nM), and the calcium ionophore A23187 (0.5 μM). Down‐regulation of protein kinase C, following a 24‐hour exposure of endothelial cells to PMA, abolished the effects of PMA and ATP on the release of choline and P‐choline, whereas the response to A23187 was maintained. These results suggest that in aortic endothelial cells, ATP produces a sustained activation of a phospholipase D hydrolyzing phosphatidylcholine. The resulting accumulation of phosphatidic acid might have an important role in the modulation of endothelial cell function by adenine nucleotides. Stimulation of phospholipase D appears to involve protein kinase C, activated following the release of diacylglycerol from phosphatidylinositol bisphosphate by a phospholipase C coupled to the P2Y receptors (Pirotton et al., 1987a).
Anticytomegaloviral Activity of Esterified Milk Proteins and L-Polylysines

MRC-5 fibroblasts infected with human cytomegalovirus (HCMV) reference strain AD 169 were treated with different concentrations of methylated α-lactalbumin (Met-ALA) or methylated β-lactoglobulin (Met-BLG), as well as with their peptic hydrolysates, and with the highly basic polypeptides such as are L-polylysines (4–15 kDa). The antiviral activity was calculated by comparing the number of infected cells in the presence and absence of the tested substances. Both Met-ALA and Met-BLG, as well as their peptic hydrolysates, decreased the infectious activity of cytomegalovirus in fibroblast cells. As expected, L-polylysines showed the highest antiviral activity. However, the tested basic proteins and polypeptides despite their lower antiviral activities might be potentially quite useful in fight of arising drug resistance activities and the persistence capacities of this virus.
Risk stratification in patients with Brugada syndrome without previous cardiac arrest – prognostic value of combined risk factors.

BACKGROUND Risk stratification in patients with Brugada syndrome for primary prevention of sudden cardiac death is still an unsettled issue. A recent consensus statement suggested the indication of implantable cardioverter defibrillator (ICD) depending on the clinical risk factors present (spontaneous type 1 Brugada electrocardiogram (ECG) [Sp1], history of syncope [syncope], and ventricular fibrillation during programmed electrical stimulation [PES+]). The indication of ICD for the majority of patients, however, remains unclear. METHODS AND RESULTS A total of 218 consecutive patients (211 male; aged 46 ± 13 years) with a type 1 Brugada ECG without a history of cardiac arrest who underwent evaluation for ICD including electrophysiological testing were examined retrospectively. During a mean follow-up period of 78 months, 26 patients (12%) developed arrhythmic events. On Kaplan-Meier analysis patients with each of Sp1, syncope, or PES+ suffered arrhythmic events more frequently (P=0.018, P<0.001, and P=0.003, respectively). On multivariate analysis Sp1 and syncope were independent predictors of arrhythmic events. When dividing patients according to the number of these 3 risk factors present, patients with 2 or 3 risk factors experienced arrhythmic events more frequently than those with 0 or 1 risk factor (23/93 vs. 3/125; P<0.001). CONCLUSIONS Syncope, Sp1, and PES+ are important risk factors and the combination of these risks well stratify the risk of later arrhythmic events.