Miracle-dz/UniFAR-FTUs huggingface dataset:
Induction of the cell survival kinase Sgk1: A possible novel mechanism for α-phenyl-N-tert-butyl nitrone in experimental stroke

Nitrones (e.g. α-phenyl-N-tert-butyl nitrone; PBN) are cerebroprotective in experimental stroke. Free radical trapping is their proposed mechanism. As PBN has low radical trapping potency, we tested Sgk1 induction as another possible mechanism. PBN was injected (100 mg/kg, i.p.) into adult male rats and mice. Sgk1 was quantified in cerebral tissue by microarray, quantitative RT-PCR and western analyses. Sgk1+/+ and Sgk1−/− mice were randomized to receive PBN or saline immediately following transient (60 min) occlusion of the middle cerebral artery. Neurological deficit was measured at 24 h and 48 h and infarct volume at 48 h post-occlusion. Following systemic PBN administration, rapid induction of Sgk1 was detected by microarray (at 4 h) and confirmed by RT-PCR and phosphorylation of the Sgk1-specific substrate NDRG1 (at 6 h). PBN-treated Sgk1+/+ mice had lower neurological deficit (p < 0.01) and infarct volume (p < 0.01) than saline-treated Sgk1+/+ mice. PBN-treated Sgk1−/− mice did not differ from saline-treated Sgk1−/− mice. Saline-treated Sgk1−/− and Sgk1+/+ mice did not differ. Brain Sgk3:Sgk1 mRNA ratio was 1.0:10.6 in Sgk1+/+ mice. Sgk3 was not augmented in Sgk1−/− mice. We conclude that acute systemic treatment with PBN induces Sgk1 in brain tissue. Sgk1 may play a part in PBN-dependent actions in acute brain ischemia.
Prices, Wages and the U.S. NAIRU in the 1990s

Using quarterly macro data and annual state panel data, we examine various explanations of the low rate of price inflation, strong real wage growth, and low rate of unemployment in the U.S. economy during the late 1990s. Many of these explanations imply shifts in the coefficients of price and wage Phillips curves. We find, however, that once one accounts for the univariate trends in the unemployment rate and in the rate of productivity growth, these coefficients are stable. This suggests that many explanations, such as persistent beneficial supply shocks, changes in firms' pricing power, changes in price expectations arising from shifts in Fed policy, and changes in wage setting behavior miss the mark. Rather, we suggest that explanations of movements of wages, prices and unemployment over the 1990s, and indeed over the past forty years, must focus on understanding the univariate trends in the unemployment rate and in productivity growth and, perhaps, the relation between the two.
A New Test of the Real Interest Rate Parity Hypothesis: Bounds Approach and Structural Breaks

We test the real interest rate parity hypothesis using data for the G7 countries over the period 1970-2008. Our contribution is two-fold. First, we utilize the ARDL bounds approach of Pesaran et al. (2001) which allows us to overcome uncertainty about the order of integration of real interest rates. Second, we test for structural breaks in the underlying relationship using the multiple structural breaks test of Bai and Perron (1998, 2003). Our results indicate significant parameter instability and suggest that, despite the advances in economic and financial integration, real interest rate parity has not fully recovered from a breakdown in the 1980s.
Vγ4+γδT Cells Aggravate Severe H1N1 Influenza Virus Infection-Induced Acute Pulmonary Immunopathological Injury via Secreting Interleukin-17A

The influenza A (H1N1) pdm09 virus remains a critical global health concern and causes high levels of morbidity and mortality. Severe acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the major outcomes among severely infected patients. Our previous study found that interleukin (IL)-17A production by humans or mice infected with influenza A (H1N1) pdm09 substantially contributes to ALI and subsequent morbidity and mortality. However, the cell types responsible for IL-17A production during the early stage of severe influenza A (H1N1) pdm09 infection remained unknown. In this study, a mouse model of severe influenza A (H1N1) pdm09 infection was established. Our results show that, in the lungs of infected mice, the percentage of γδT cells, but not the percentages of CD4+Th and CD8+Tc cells, gradually increased and peaked at 3 days post-infection (dpi). Further analysis revealed that the Vγ4+γδT subset, but not the Vγ1+γδT subset, was significantly increased among the γδT cells. At 3 dpi, the virus induced significant increases in IL-17A in the bronchoalveolar lavage fluid (BALF) and serum. IL-17A was predominantly secreted by γδT cells (especially the Vγ4+γδT subset), but not CD4+Th and CD8+Tc cells at the early stage of infection, and IL-1β and/or IL-23 were sufficient to induce IL-17A production by γδT cells. In addition to secreting IL-17A, γδT cells secreted interferon (IFN)-γ and expressed both an activation-associated molecule, natural killer group 2, member D (NKG2D), and an apoptosis-associated molecule, FasL. Depletion of γδT cells or the Vγ4+γδT subset significantly rescued the virus-induced weight loss and improved the survival rate by decreasing IL-17A secretion and reducing immunopathological injury. This study demonstrated that, by secreting IL-17A, lung Vγ4+γδT cells, at least, in part mediated influenza A (H1N1) pdm09-induced immunopathological injury. This mechanism might serve as a promising new target for the prevention and treatment of ALI induced by influenza A (H1N1) pdm09.
Labor Supply, Employment and Unemployment in the Egyptian Economy, 1988-2006

This paper analyzes data from the Egypt Labor Market Panel Survey of 2006 (ELMPS 06) and its predecessor surveys from 1988 and 1998 to reveal that the employment outlook in Egypt has broadly improved since 1998. Despite continued rapid growth of the working age population since 1998, overall participation rates have increased, unemployment rates have decreased, and employment growth has been robust. In many instances, the levels of these variables have returned to or exceeded their levels in 1988, prior to the initiation of the 1991 stabilization and structural adjustment programs. The performance of the labor market in Egypt in the past eight years has been helped by favorable demographic as well as economic developments. The generation at the peak of the youth bulge, which was putting severe pressures on the labor market in the 1990s, has now completed its labor market transition, for the most part, and demographic pressures are easing. These demographic developments have been accompanied by important changes in the structure of the economy. While employment in state-owned enterprises (SOEs) had begun to decline in the 1988-98 decade, employment in government was still growing rapidly during that period at about twice the rate of growth of overall employment. This has clearly changed in the 1998-06. Employment growth in the civil service has slowed dramatically and much of the burden of employment creation has shifted to the private sector. Concurrent with the decline of employment opportunities in the public sector, the trend toward informalization of the labor market, begun in the 1990s, is continuing unabated. By 2006, 61 percent of all employment was informal, up from 57 percent in 1998. Moreover, 75 percent of new entrants who entered the labor market in the first five years of this decade were entering into informal work.
Phytoestrogen calycosin‐7‐O‐β‐D‐glucopyranoside ameliorates advanced glycation end products‐induced HUVEC damage

Vasculopathy including endothelial cell (EC) apoptosis and inflammation contributes to the high incidence of stroke and myocardial infarction in diabetic patients. The aim of the present study was to investigate the effect of calycosin‐7‐O‐β‐D‐glucopyranoside (CG), a phytoestrogen, on advanced glycation end products (AGEs)‐induced HUVEC damage. We observed that CG can significantly ameliorate AGEs‐induced HUVEC oxidative stress and apoptosis. The ratio of SOD/MDA was significantly increased to the normal level by CG pretreatment. CG preincubation dramatically increased anti‐apoptotic Bcl‐2 while decreased pro‐apoptotic Bax and Bad expressions as detected by immunocytochemistry. Moreover, CG ameliorated macrophage migration and adhesion to HUVEC; the monocyte chemotactic protein‐1 and interleukin‐6 levels in the culture supernatant were dramatically reduced by CG as determined by ELISA; the expressions of inflammatory proteins including ICAM‐1, TGF‐β1, and RAGE in both protein and mRNA levels were significantly reduced to the normal level by CG pretreatment as determined by immunocytochemistry and real‐time RT‐PCR. The intracellular investigation suggests that CG can reverse AGEs‐activated ERK1/2 and NF‐κB phosphorylation, in which estrogen receptors were involved in. Our results strongly indicate that CG can modulate EC dysfunction by ameliorating AGEs‐induced cell apoptosis and inflammation. J. Cell. Biochem. 112: 2953–2965, 2011. © 2011 Wiley‐Liss, Inc.
FDSOI Floating Body Cell eDRAM Using Gate-Induced Drain-Leakage (GIDL) Write Current for High Speed and Low Power Applications

A Capacitorless IT-DRAM cell using gate-induced drain leakage (GIDL) current for write operation was demonstrated for the first time on FDSOI substrate, 9.5 nm silicon film and 19 nm BOX. 20 nm gate scaling improves 20% memory effect amplitude. GIDL mechanism allows low bias, low power, fast write time and does not affect intrinsic retention time. A similar value of 10 ms at 85degC is obtained like for impact ionization (II) optimised devices.
Lentivirus‐mediated overexpression of angiotensin‐(1–7) attenuated ischaemia‐induced cardiac pathophysiology

Myocardial infarction (MI) results in cell death, development of interstitial fibrosis, ventricular wall thinning and ultimately, heart failure. Angiotensin‐(1–7) [Ang‐(1–7)] has been shown to provide cardioprotective effects. We hypothesize that lentivirus‐mediated overexpression of Ang‐(1–7) would protect the myocardium from ischaemic injury. A single bolus of 3.5 × 108 transducing units of lenti‐Ang‐(1–7) was injected into the left ventricle of 5‐day‐old male Sprague–Dawley rats. At 6 weeks of age, MI was induced by ligation of the left anterior descending coronary artery. Four weeks after the MI, echocardiography and haemodynamic parameters were measured to assess cardiac function. Postmyocardial infarction, rats showed significant decreases in fractional shortening and dP/dt (rate of rise of left ventricular pressure), increases in left ventricular end‐diastolic pressure, and ventricular hypertrophy. Also, considerable upregulation of cardiac angiotensin‐converting enzyme (ACE) mRNA was observed in these rats. Lentivirus‐mediated cardiac overexpression of Ang‐(1–7) not only prevented all these MI‐induced impairments but also resulted in decreased myocardial wall thinning and an increased cardiac gene expression of ACE2 and bradykinin B2 receptor (BKR2). Furthermore, in vitro experiments using rat neonatal cardiac myocytes demonstrated protective effects of Ang‐(1–7) against hypoxia‐induced cell death. This beneficial effect was associated with decreased expression of inflammatory cytokines (tumour necrosis factor‐α and interleukin‐6) and increased gene expression of ACE2, BKR2 and interleukin‐10. Our findings indicate that overexpression of Ang‐(1–7) improves cardiac function and attenuates left ventricular remodelling post‐MI. The protective effects of Ang‐(1–7) appear to be mediated, at least in part, through modulation of the cardiac renin–angiotensin system and cytokine production.
Total Lesion Glycolysis in Positron Emission Tomography Can Predict Gefitinib Outcomes in Non–Small-Cell Lung Cancer with Activating EGFR Mutation

Introduction: The purpose of this study was to evaluate the predictive role of quantitative metabolic parameters using total lesion glycolysis (TLG) in 18F-2-fluoro-2-deoxyglucose-positron emission tomography/computed tomography for developing gefitinib resistance in epidermal growth factor receptor (EGFR)-mutant non–small-cell lung cancer (NSCLC) patients treated with first-line gefitinib. Methods: A total of 75 NSCLC patients harboring activating EGFR mutation and receiving first-line gefitinib were analyzed. Whole-body 18F-2-fluoro-2-deoxyglucose positron emission tomography/computed tomography scans were acquired before first-line gefitinib. The maximal standardized uptake value and TLG of all lesions were calculated. Maximal standardized uptake value and TLG were categorized using the tertile cutoff. Treatment outcomes were compared between groups. Results: Overall response rate of gefitinib was 69.4%, and median progression-free survival (PFS) of gefitinib was 11.5 months. Overall response rates were similar between low, intermediate, and high TLG groups (68.0% versus 76.0% versus 68.0%, p = 0.274). However, PFS significantly differed by TLG groups, and high TLG was associated with shorter PFS (7.2 months in high TLG; 11.9 months in intermediate TLG; and 24.2 months in low, p < 0.001). Multivariate models adjusted for disease status and response to gefitinib showed that TLG was an independent predictive factor for PFS. TLG was also significantly associated with overall survival (p = 0.005). Conclusion: TLG can predict PFS and development of gefitinib resistance in EGFR-mutant NSCLC patients treated with first-line gefitinib. Baseline metabolic tumor burdens measured with TLG before first-line gefitinib will be of great help in predicting time to acquired resistance.
Loss of Sphingosine Kinase Alters Life History Traits and Locomotor Function in Caenorhabditis elegans

Sphingolipid metabolism is important to balance the abundance of bioactive lipid molecules involved in cell signaling, neuronal function, and survival. Specifically, the sphingolipid sphingosine mediates cell death signaling, whereas its phosphorylated form, sphingosine-1-phosphate (S1P), mediates cell survival signaling. The enzyme sphingosine kinase produces S1P, and the activity of sphingosine kinase impacts the ability of cells to survive under stress and challenges. To examine the influence of sphingolipid metabolism, particularly enzymes regulating sphingosine and S1P, in mediating aging, neuronal function and stress response, we examined life history traits, locomotor capacities and heat stress responses of young and old animals using the model organism Caenorhabditis elegans. We found that C. elegans sphk-1 mutants, which lack sphingosine kinase, had shorter lifespans, reduced brood sizes, and smaller body sizes compared to wild type animals. By analyzing a panel of young and old animals with genetic mutations in the sphingolipid signaling pathway, we showed that aged sphk-1 mutants exhibited a greater decline in neuromuscular function and locomotor behavior. In addition, aged animals lacking sphk-1 were more susceptible to death induced by acute and prolonged heat exposure. On the other hand, older animals with loss of function mutations in ceramide synthase (hyl-1), which converts sphingosine to ceramide, showed improved neuromuscular function and stress response with age. This phenotype was dependent on sphk-1. Together, our data show that loss of sphingosine kinase contributes to poor animal health span, suggesting that sphingolipid signaling may be important for healthy neuronal function and animal stress response during aging.
The Contribution of Maternal Care and Control, and Community Type to Children’s Adjustment to Political Violence

Objectives: This study explored the behavioral and emotional adjustment of Israeli school-age children who are exposed to political violence. Based on Bronfenbrenner’s (1986) ecological model and ecological model of psychosocial trauma (Harvey, 2007), we examined the direct contribution of exposure, gender, maternal characteristics (mother’s posttraumatic stress symptoms [PTSS], maternal care and maternal control), and community type (development town vs. kibbutz), to school-age children’s adjustment. In addition, we examined whether maternal characteristics and community type moderated the association between exposure and adjustment. Method: There were 121 mother-child dyads from the development town of Sderot (n = 62) and from the surrounding kibbutzim (n = 58) participated. Results: Revealed that being a boy, living in Sderot, and mothers’ higher PTSS, contributed directly to children’s total difficulties (i.e., externalizing and internalizing problems), and that maternal control moderated the association between personal exposure and children’s total difficulties. Furthermore, being a girl and mother’s higher PTSS and higher maternal control contributed directly to children’s PTSS. Mother’s PTSS moderated the association between personal exposure and children’s PTSS. Maternal care was not associated with children’s adjustment. Conclusions: Both the child’s gender and the type of community in which he or she lives are associated with maternal distress and children’s adjustment to political violence.
Serum Amyloid A Facilitates the Binding of High-Density Lipoprotein From Mice Injected With Lipopolysaccharide to Vascular Proteoglycans

Objective—Levels of serum amyloid A (SAA), an acute-phase protein carried on high-density lipoprotein (HDL), increase in inflammatory states and are associated with increased risk of cardiovascular disease. HDL colocalizes with vascular proteoglycans in atherosclerotic lesions. However, its major apolipoprotein, apolipoprotein A-I, has no proteoglycan-binding domains. Therefore, we investigated whether SAA, which has proteoglycan-binding domains, plays a role in HDL retention by proteoglycans. Methods and Results—HDL from control mice and mice deficient in both SAA1.1 and SAA2.1 (SAA knockout mice) injected with bacterial lipopolysaccharide (LPS) was studied. SAA mRNA expression in the liver and plasma levels of SAA increased dramatically in C57BL/6 mice after LPS administration, although HDL cholesterol did not change. Fast protein liquid chromatography analysis showed most of the SAA to be in HDL. Mass spectrometric analysis indicated that HDL from LPS-injected control mice had high levels of SAA1.1/2.1 and reduced levels of apolipoprotein A-I. HDL from LPS-injected control mice demonstrated high-affinity binding to biglycan relative to normal mouse HDL. In contrast, HDL from LPS-injected SAA knockout mice showed very little binding to biglycan, consistent with SAA facilitating the binding of HDL to vascular proteoglycans. Conclusion—SAA enrichment of HDL under inflammatory conditions plays an important role in the binding of HDL to vascular proteoglycans.
Bubbles, Post-Crash Dynamics, and the Housing Market

This paper documents and explains previously unrecognized post-crash dynamics following the collapse of a housing bubble. A simple model predicts that speculative developers ensure stable pre-crash relative prices between small and large homes while their post-crash exit allows small-home relative values to fall. Evidence from Phoenix supports the model. Although home prices doubled 2004-2006, relative prices of small-to-large homes remained nearly constant but then plummeted post-crash. As speculative developers return relative prices must return to pre-boom levels, consistent with patterns since 2011. Anticipated mean reversion indicates that cities can reduce post-crash volatility and mispricing by publicizing size-stratified house price indexes.
SIGCSE by the numbers

At the 2011 SIGCSE Symposium business meeting, someone asked whether the SIGCSE Symposia or ITiCSE conferences have a bias towards papers from a geographical region. We analyzed the number of submissions and acceptances for SIGCSE 2011 and ITiCSE 2011, according to the continent(s) of the author(s).
Gamma-Ray Detectors

In order for a gamma ray to be detected, it must interact with matteu that interaction must be recorded. Fortunately, the electromagnetic nature of gamma-ray photons allows them to interact strongly with the charged electrons in the atoms of all matter. The key process by which a gamma ray is detected is ionization, where it gives up part or all of its energy to an electron. The ionized electrons collide with other atoms and liberate many more electrons. The liberated charge is collected, either directly (as with a proportional counter or a solid-state semiconductor detector) or indirectly (as with a scintillation detector), in order to register the presence of the gamma ray and measure its energy. The final result is an electrical pulse whose voltage is proportional to the energy deposited in the detecting medhtm. In this chapter, we will present some general information on types of’gamma-ray detectors that are used in nondestructive assay (NDA) of nuclear materials. The electronic instrumentation associated with gamma-ray detection is discussed in Chapter 4. More in-depth treatments of the design and operation of gamma-ray detectors can be found in Refs. 1 and 2.
SNAP-II and SNAPPE-II: Simplified newborn illness severity and mortality risk scores.

OBJECTIVES Illness severity scores for newborns are complex and restricted by birth weight and have dated validations and calibrations. We developed and validated simplified neonatal illness severity and mortality risk scores. The primary outcome was in-hospital mortality. STUDY DESIGN Thirty neonatal intensive care units in Canada, California, and New England collected data on all admissions during the mid 1990s; patients moribund at birth or discharged to normal newborn care in <24 hours were excluded. Starting with the 34 data elements of the Score for Neonatal Acute Physiology (SNAP), we derived the most parsimonious logistic model for in-hospital mortality using 10,819 randomly selected Canadian cases. SNAP-II includes 6 physiologic items; to this are added points for birth weight, low Apgar score, and small for gestational age to create a 9-item SNAP-Perinatal Extension-II (SNAPPE-II). We validated SNAPPE-II on the remaining 14,610 cases and optimized the calibration. RESULTS In all birth weights, SNAPPE-II had excellent discrimination and goodness of fit. Area under the receiver operator characteristic curve was . 91 +/- 0.01. Goodness of fit (Hosmer-Lemeshow) was 0.90. CONCLUSIONS SNAP-II and SNAPPE-II are empirically validated illness severity and mortality risk scores for newborn intensive care. They are simple, accurate, and robust across populations.
Risk Factors Associated With Pressure Ulcer Development in Critically Ill Traumatic Spinal Cord Injury Patients

Critically ill spinal cord injury (SCI) patients are at high risk for pressure ulcers. Research is needed to identify risk factors for pressure ulcers. The aim of this study was to investigate risk factors and outcomes of pressure ulcers in critically ill SCI patients. This is a retrospective cohort study. Data were gathered from medical records of adult patients with SCI admitted to surgical intensive care units. Ninety-four SCI patients participated in this study. Clinical variables associated with pressure ulcers were as follows: fecal management systems, incontinence, acidosis, support surfaces, steroids, and additional equipment. Hypotension was the strongest predictor of pressure ulcers. Nursing interventions may address risk factors and improve patient outcomes.