Miracle-dz/UniFAR-FTUs huggingface dataset:
The Frequency of Third-Party Involvement in Incidents of Barroom Aggression

This paper examines the frequency and nature of third-party involvement in aggressive incidents occurring in young people's bars and the effects of third parties on incident outcomes. Observational data were collected in 12 bars frequented by young people, and telephone interviews were conducted with 31 young people who responded to advertisements posted at the university campus. In total, 154 incidents of barroom aggression were analyzed. Overall, 49% (76) of incidents included third-party involvement by other patrons. About 40% (n=31) of third-party incidents involved nonaggressive third parties, 22% (n=17) involved aggressive third parties, and 38% (n=29) involved both aggressive and nonaggressive third-party participants. Nonaggressive interventions were more likely to decrease aggression, while aggressive interventions were more likely to increase aggression (χ2=65.5, p<.0001). Females appeared to be somewhat more likely than males to intervene nonaggressively (χ2=11.3, p<.1). The intoxication levels of participants were highest in incidents involving both nonaggressive and aggressive third parties (F-ratio=4.6, p<.01). These findings suggest that third parties play a significant role in the outcome of barroom aggression among young people, and that further research is needed on the role and impact of third parties.
Peripheral Arterial Disease Is Prevalent But Underdiagnosed and Undertreated in the Primary Care Setting in Central Greece

We investigated the prevalence of peripheral arterial disease (PAD). Primary Care Health Centers (n = 14) in Thessaly (central Greece) recruited 436 participants, mean age 71 (50-79) years. Peripheral arterial disease was considered present if the ankle–brachial index (ABI) was <0.9 or >1.4 in at least 1 leg. Asymptomatic PAD was defined as an abnormal ABI and no symptoms or history of limb revascularization. The prevalence of PAD was 13% (mostly asymptomatic, 11.7%). Only 5 (8.77%) of 57 patients with PAD were aware of their disease and only in these patients were the physicians aware of the presence of PAD. The risk factors associated with PAD were age, smoking, and the combination of diabetes mellitus and coronary artery disease. All symptomatic patients were on antiplatelet therapy but 33% did not take statins. For asymptomatic patients, 74.5% were not on antiplatelet therapy and 57% did not receive statins. In the primary health care setting, PAD is underdiagnosed and undertreated.
The Emerging Role of Immunoregulation of Fibrinogen‐Related Procoagulant Fgl2 in the Success or Spontaneous Abortion of Early Pregnancy in Mice and Humans

PROBLEM: Abortion of chromosomally normal embryos in the CBA X DBA/2 mating combination is triggered by release of Th1 cytokines (tumor necrosis factor [TNF]‐α, interferon [IFN]‐γ, and interleukin [IL]‐1), which cause abortion via a novel prothrombinase, fgl2, and polymorphonuclear leukocytes. The site of activation may be maternal vascular endothelium on arteries and veins nourishing the placenta. Activation of coagulation is also prominent in spontaneous abortion of chromosomally normal human embryos. We asked where is fgl2 up‐regulated in the uterus in murine abortions, and if similar fgl2 expression occurs in human pregnancy failure.
Myocardial depressant effects of interleukin 6 in meningococcal sepsis are regulated by p38 mitogen-activated protein kinase*

Objectives:Myocardial failure, leading to inotrope-unresponsive shock, is the predominant cause of death in meningococcal and other forms of septic shock. Proinflammatory cytokines released in septic shock are known to have myocardial depressant effects. We previously showed that interleukin 6 is a major myocardial depressant factor in children with meningococcal septicemia. In the current study, we aimed to investigate the mechanisms by which interleukin 6 induces myocardial failure in meningococcal sepsis and to identify potential novel therapeutic targets. Design:Laboratory-based study. Setting:University hospital and laboratories. Patients:Children with a clinical diagnosis of meningococcal septic shock. Methods:We studied interleukin 6-induced signaling events, both in vitro using isolated rat ventricular cardiac myocytes as a model of myocardial contractility and in whole blood from children with meningococcal sepsis. Interventions:None. Measurements and Main Results:We demonstrated involvement of Janus kinase 2, phosphatidylinositol 3-kinase, Akt, and p38 mitogen-activated protein kinase in interleukin 6-induced negative inotropy in isolated cardiac myocytes. Inhibition of p38 mitogen-activated protein kinase not only reversed interleukin 6-induced myocardial depression in both rat and human myocytes, but restored inotrope responsiveness. Cardiomyocytes transduced with dominant-negative p38 mitogen-activated protein kinase showed no interleukin 6-induced myocardial depression. To investigate p38 mitogen-activated protein kinase in vivo, we profiled global RNA expression patterns in peripheral blood of children with meningococcal septicemia. Transcripts for genes mapping to the p38 mitogen-activated protein kinase pathway showed significantly altered levels of abundance with a high proportion of genes of this pathway affected. Conclusions:Our findings demonstrate an integral role of the p38 mitogen-activated protein kinase pathway in interleukin 6-mediated cardiac contractile dysfunction and inotrope insensitivity. Dysregulation of the p38 mitogen-activated protein kinase pathway in meningococcal septicemia suggests that this pathway may be an important target for novel therapies to reverse myocardial dysfunction in patients with meningococcal septic shock who are not responsive to inotropic support.
Transgenic expression of mammalian heparanase uncovers physiological functions of heparan sulfate in tissue morphogenesis, vascularization, and feeding behavior

We have generated homozygous trans¬genic mice (hpa‐tg) overexpressing human hepara¬nase (endo‐β‐D‐glucuronidase) in all tissues and char¬acterized the involvement of the enzyme in tissue morphogenesis, vascularization, and energy metabo¬lism. Biochemical analysis of heparan sulfate (HS) isolated from newborn mice and adult tissues re¬vealed a profound decrease in the size of HS chains derived from hpa‐tg vs. control mice. Despite this, the mice appeared normal, were fertile, and exhib¬ited a normal life span. A significant increase in the number of implanted embryos was noted in the hpa‐tg vs. control mice. Overexpression of heparanase resulted in increased levels of urinary protein and creatinine, suggesting an effect on kidney func¬tion, reflected also by electron microscopy examina¬tion of the kidney tissue. The hpa‐tg mice exhibited a reduced food consumption and body weight com¬pared with control mice. The effect of heparanase on tissue remodeling and morphogenesis was best dem¬onstrated by the phenotype of the hpa‐tg mammary glands, showing excess branching and widening of ducts associated with enhanced neovascularization and disruption of the epithelial basement membrane. The hpa‐tg mice exhibited an accelerated rate of hair growth, correlated with high expression of heparanase in hair follicle keratinocytes and increased vascularization. Altogether, characterization of the hpa‐tg mice emphasizes the involvement of heparanase and HS in processes such as embryonic implan¬tation, food consumption, tissue remodeling, and vascularization. —Zcharia, E. , Metzger, S. , ChajekShaul, T. , Aingorn, H. , Elkin, M. , Friedmann, Y. , Weinstein, T. , Li, J.‐P., Lindahl, U. , Vlodavsky, I. Transgenic expression of mammalian heparanase uncovers physiological functions of heparan sulfate in tissue morphogenesis, vascularization, and feeding behavior. FASEB J. 18, 252–263 (2004)
Ubiquitination of Keap1, a BTB-Kelch Substrate Adaptor Protein for Cul3, Targets Keap1 for Degradation by a Proteasome-independent Pathway*

Keap1 is a BTB-Kelch protein that functions as a substrate adaptor protein for a Cul3-dependent E3 ubiquitin ligase complex. Keap1 targets its substrate, the Nrf2 transcription factor, for ubiquitination and subsequent degradation by the 26 S proteasome. Inhibition of Keap1-dependent ubiquitination of Nrf2 increases steady-state levels of Nrf2 and enables activation of cytoprotective Nrf2-dependent genes. In this report, we demonstrate that Keap1 and three other BTB-Kelch proteins, including GAN1, ENC1, and Sarcosin, are ubiquitinated by a Cul3-dependent complex. Ubiquitination of Keap1 is markedly increased in cells exposed to quinone-induced oxidative stress, occurs in parallel with inhibition of Keap1-dependent ubiquitination of Nrf2, and results in decreased steady-state levels of Keap1, particularly in cells that are unable to synthesize glutathione. Degradation of Keap1 is independent of the 26 S proteasome, because inhibitors of the 26 S proteasome do not prevent loss of Keap1 following exposure of cells to quinone-induced oxidative stress. Our results suggest that a switch from substrate to substrate adaptor ubiquitination is a critical regulatory step that controls steady-state levels of both BTB-Kelch substrate adaptor proteins and their cognate substrates.
When Machine Learning Meets AI and Game Theory

We study the problem of development of intelligent machine learning applications to exploit the problems of adaptation that arise in multi-agent systems, for expected-long-termprofit maximization. We present two results. First, we propose a learning algorithm for the Iterated Prisoners Dilemma (IPD) problem. Using numerical analysis we show that it performs strictly better than the tit-for-tat algorithm and many other adaptive and non-adaptive strategies. Second, we study the same problem from the aspect of zero-sum games. We discuss how AI and Machine Learning techniques work closely to give our agent a ’mind-reading’ capability.
Pilot Study of Impact of Medical-Legal Partnership Services on Patients’ Perceived Stress and Wellbeing

Medical-legal partnerships (MLPs) bring legal services into health care settings to address patients’ unmet legal needs. This pilot project examined whether MLP services impact patients’ perceptions of stress and wellbeing. Methods. Providers referred patients with legal concerns to the Tucson Family Advocacy Program (TFAP), an MLP within a family medicine clinic. Stress levels and wellbeing were assessed before and after legal services using self-administered 10-item Perceived Stress Scale (PSS-10) and Measure Yourself Concerns and Wellbeing (MYCaW) instruments. Results. Sixty-seven participants completed pre- and post-service questionnaires. Within this group, the mean PSS-10 score decreased 8.1 points. Wellbeing scores improved by 1.8 points. Individual changes in perceived stress were strongly related to participants’ level of concern regarding the particular legal issues addressed. Conclusions. Services in patient-centered medical homes to address unmet legal needs have the potential to reduce perceived stress and improve overall wellbeing. Additional studies concerning MLPs and patient outcomes are needed.
Ryanodine receptors in human bladder smooth muscle

The role of intracellular Ca2+ release in the activation of human bladder smooth muscle is controversial. We have measured the expression of mRNA encoding for the ryanodine receptor (RyR) isoforms (RyR1, RyR2 and RyR3) in isolated human detrusor smooth muscle. mRNA for RyR2 was detected in all samples but no mRNA for RyR1 or RyR3 could be found. Human bladder smooth muscle cells in culture are unresponsive to caffeine, suggesting the absence of a functional RyR system. However, mRNA encoding for RyR2 was detected in these cells. Using saponin‐permeabilized cells, a Ruthenium Red‐sensitive Ca2+‐dependent 45Ca2+ release could be demonstrated from the sarcoplasmic reticulum (SR). These data confirm the functional presence of Ca2+‐induced Ca2+ release (CICR) in cells and suggest that the properties of the RyR2 isoform in human detrusor may change when the cells are maintained in culture. The implications of these observations to detrusor smooth muscle function are discussed.
The correlation between anterior‐posterior translation and cross‐sectional area of anterior cruciate ligament reconstructions

Total anterior‐posterior translation is commonly used to assess the integrity of the cruciate ligaments and the success of reconstructive surgery. The purpose of this study was to determine, after surgical reconstruction of the anterior cruciate ligament with a biological graft, if total anterior‐posterior translation correlated with graft length, cross‐sectional area, or mechanical properties. These factors were investigated by analyzing data from three previous studies. These studies involved replacement of the anterior cruciate ligament in cynomolgus monkeys and goats, with free and vascularized patellar tendon autografts and both patellar tendon and anterior cruciate ligament allografts. Data were available at time periods of 6 and 12 months after surgery. We found statistically significant inverse correlations between the amount of anterior‐posterior translation and cross‐sectional area of a graft at the time of sacrifice. The Pearson correlation coefficients ranged from −0.966 (p < 0.002) to −0.830 (p < 0.05). We hypothesize that these correlations result from the following mechanism: the increased anterior translation reflects a slack graft; a slack graft is stress shielded by other structures about the knee; the reduced in vivo stresses on the graft modulate cellular metabolism in a way that over time produces a small cross‐sectional area.
A Capacitor-Free CMOS Low-Dropout Regulator

A 2.5V capacitor-free CMOS low dropout regulator for powering analog circuits is presented. Stable operation is achieved with or without a large load capacitor by replacing the bulky external output capacitor with an operational amplifier-based active circuit. The regulator provides a 100mA output current and consumes 80muA regardless of the load current.
Pedagogies of the Global: Knowledge in the Human Interest. Cultural Politics & The Promise of Democracy.

Part I. Perspectives on Pedagogy Chapter 1. Arif Dirlik, "Introduction: Our Ways of Knowing-and What to Do About Them? " Chapter 2. Peter McLaren and Ramin Farahmandpur, "Who Will Educate the Educators? Critical Pedagogy in the Age of Globalization" Chapter 3. Henry A. Giroux, "Radical Pedagogy and the Terror of Neoliberalism: Rethinking the Significance of Cultural Politics" Chapter 4. Alexander Woodside, "Transnationalism, Technology, Identity: How New Is the World of the Internet? " Part II. Our Ways of Knowing Chapter 5. Arthur Ray, "Anthropology, History, and Aboriginal Rights: Politics and the Rise of Ethnohistory in North America" Chapter 6. Dylan Rodriguez and Viet Mike Ngo, "Ethnic Studies in the Age of the Prison-Industrial Complex: Reflections on 'Freedom' and Capture, Praxis and Immobilization" Chapter 7. Susan Searls Giroux, "The Drug War Is the New Jim Crow: Legislating Black Educational Exclusion in the Post-Civil Rights Era" Chapter 8. Robert Chang, "Who Are You Rooting For? Transnationalism, the World Cup, and War Part III. Counter-Knowledges Chapter 9. John Brown Childs, "Boundaries and Community in a Borderless World: Suggestions for Cooperation and Rootedness with a Focus on Black History Month" Chapter 10. Lily Mendoza, "Strategic Parochialism" Chapter 11. Dorothee Schreiber and Dianne Newell, "Why Spend a Lot of Time Dwelling on the Past? Understanding Resistance to Contemporary Salmon Farming in Kwakwaka'wakw Territory" Chapter 12. Jason Younker, "Challenging Infallible Histories: A Miraculous Revival of Dead Indians".
Animal Models of Cancer-Associated Hypercalcemia

Cancer-associated hypercalcemia (CAH) is a frequently-occurring paraneoplastic syndrome that contributes to substantial patient morbidity and occurs in both humans and animals. Patients with CAH are often characterized by markedly elevated serum calcium concentrations that result in a range of clinical symptoms involving the nervous, gastrointestinal and urinary systems. CAH is caused by two principle mechanisms; humorally-mediated and/or through local osteolytic bone metastasis resulting in excessive calcium release from resorbed bone. Humoral hypercalcemia of malignancy (HHM) is the most common mechanism and is due to the production and release of tumor-associated cytokines and humoral factors, such as parathyroid hormone-related protein (PTHrP), that act at distant sites to increase serum calcium concentrations. Local osteolytic hypercalcemia (LOH) occurs when primary or metastatic bone tumors act locally by releasing factors that stimulate osteoclast activity and bone resorption. LOH is a less frequent cause of CAH and in some cases can induce hypercalcemia in concert with HHM. Rarely, ectopic production of parathyroid hormone has been described. PTHrP-mediated hypercalcemia is the most common mechanism of CAH in human and canine malignancies and is recognized in other domestic species. Spontaneous and experimentally-induced animal models have been developed to study the mechanisms of CAH. These models have been essential for the evaluation of novel approaches and adjuvant therapies to manage CAH. This review will highlight the comparative aspects of CAH in humans and animals with a discussion of the available animal models used to study the pathogenesis of this important clinical syndrome.
Increased analgesia and alterations in distribution and metabolism of methadone by desipramine in the rat.

Treatment of rats with desipramine (DMI) 1 hour before the subcutaneous administration of methadone increased the intensity and prolonged the duration of methadone analgesia, as determined by the hot plate method. DMI significantly reduced the analgesic ED50 of methadone from a control value of 3.4 to 1.6 or 0.5 mg/kg in rats treated with 20 or 30 mg/kg of DMI, respectively. DMI treatment also significantly reduced the LD50 of methadone. DMI (20 mg/kg i.p.) was given 1 hour prior to administration of 14C-methadone (5 mg/kg s.c.) and the distribution of total 14C, unchanged methadone and methadone metabolites in various tissues was studied. DMI treatment greatly increased the brain uptake of 14C and the methadone brain/plasma concentration ratios for up to 3 hours. The concentrations of 14C and unchanged methadone were higher in kidneys and lower in lungs of DMI-treated rats as compared to controls. However, the ratios of unchanged methadone to its metabolites in kidneys and lungs were not changed significantly by DMI treatment. The level of unchanged methadone in liver was markedly elevated by DMI treatment at 45 and 90 minutes (190 and 183% of controls, respectively). The level of a water-soluble glucuronide metabolite of methadone was significantly decreased at 45-, 90- and 180-minute intervals (37, 36 and 54% of controls, respectively.) However, the total 14C in liver and the concentrations of two N-demethylated metabolites of methadone were not changed significantly. In vitro addition of DMI to liver microsomal incubations resulted in inhibition of the N-demethylation of methadone. It is suggested that DMI potentiated and prolonged methadone analgesia by increasing the brain concentration of methadone and by inhibiting metabolism of methadone in the liver.
Prognostic value of bronchiectasis in patients with moderate-to-severe chronic obstructive pulmonary disease.

RATIONALE The prevalence of bronchiectasis is high in patients with moderate-to-severe chronic obstructive pulmonary disease (COPD) and it has been associated with exacerbations and bacterial colonization. These have demonstrated some degree of prognostic value in patients with COPD but no information about the relationship between bronchiectasis and mortality in patients with COPD is currently available. OBJECTIVES To assess the prognostic value of bronchiectasis in patients with moderate-to-severe COPD. METHODS Multicenter prospective observational study in consecutive patients with moderate-to-severe COPD. Bronchiectasis was diagnosed by high-resolution computed tomography scan. A complete standardized protocol was used in all patients covering general, anthrophometric, functional, clinical, and microbiologic data. After follow-up, the vital status was recorded in all patients. Multivariate Cox analysis was used to determine the independent adjusted prognostic value of bronchiectasis. MEASUREMENTS AND MAIN RESULTS Ninety-nine patients in Global Initiative for Chronic Obstructive Lung Disease (GOLD) II, 85 in GOLD III, and 17 in GOLD IV stages were included. Bronchiectasis was present in 115 (57.2%) patients. During the follow-up (median, 48 mo [interquartile range, 35-53]) there were 51 deaths (43 deaths in the bronchiectasic group). Bronchiectasis was associated with an increased risk of fully adjusted mortality (hazard ratio, 2.54; 95% confidence interval, 1.16-5.56; P = 0.02). CONCLUSIONS Bronchiectasis was associated with an independent increased risk of all-cause mortality in patients with moderate-to-severe COPD.
Inefficient TLR4/MD-2 Heterotetramerization by Monophosphoryl Lipid A

Synthetic forms of E. coli monophosphoryl lipid A (sMLA) weakly activate the MyD88 (myeloid differentiation primary response protein) branch of the bifurcated TLR4 (Toll-like receptor 4) signaling pathway, in contrast to diphosphoryl lipid A (sDLA), which is a strong activator of both branches of TLR4. sMLA’s weak MyD88 signaling activity is apparent downstream of TLR4/MyD88 signaling as we show that sMLA, unlike sDLA, is unable to efficiently recruit the TNF receptor-associated factor 6 (TRAF6) to the Interleukin-1 receptor-associated kinase 1 (IRAK1). This reduced recruitment of TRAF6 explains MLA’s lower MAPK (Mitogen Activated Protein Kinase) and NF-κB activity. As further tests of sMLA’s ability to activate TLR4/Myeloid differentiation factor 2 (MD-2), we used the antibody MTS510 as an indicator for TLR4/MD-2 heterotetramer formation. Staining patterns with this antibody indicated that sMLA does not effectively drive heterotetramerization of TLR4/MD-2 when compared to sDLA. However, a F126A mutant of MD-2, which allows lipid A binding but interferes with TLR4/MD-2 heterotetramerization, revealed that while sMLA is unable to efficiently form TLR4/MD-2 heterotetramers, it still needs heterotetramer formation for the full extent of signaling it is able to achieve. Monophosphoryl lipid A’s weak ability to form TLR4/MD-2 heterotetramers was not restricted to synthetic E. coli type because cells exposed to a biological preparation of S. minnesota monophosphoryl lipid A (MPLA) also showed reduced TLR4/MD-2 heterotetramer formation. The low potency with which sMLA and MPLA drive heterotetramerization of TLR4/MD-2 contributes to their weak MyD88 signaling activities.
Automatic Essay Grading with Probabilistic Latent Semantic Analysis

Probabilistic Latent Semantic Analysis (PLSA) is an information retrieval technique proposed to improve the problems found in Latent Semantic Analysis (LSA). We have applied both LSA and PLSA in our system for grading essays written in Finnish, called Automatic Essay Assessor (AEA). We report the results comparing PLSA and LSA with three essay sets from various subjects. The methods were found to be almost equal in the accuracy measured by Spearman correlation between the grades given by the system and a human. Furthermore, we propose methods for improving the usage of PLSA in essay grading.