Miracle-dz/UniFAR-FTUs huggingface dataset:
Anger Management Style and Hostility Among Patients With Chronic Pain: Effects on Symptom-Specific Physiological Reactivity During Anger- and Sadness- Recall Interviews

Objectives: We examined whether anger-in, anger-out, and hostility predicted symptom-specific muscle tension reactivity during anger induction (but not sadness induction) among patients with chronic low back pain (CLBP). For patients with CLBP, relevant muscles are the lower paraspinals (LPs). Anger-in × hostility and anger-out × hostility interactions were tested to determine whether particularly reactive groups of patients could be identified with a multivariable profile approach. Methods: Ninety-four patients with CLBP underwent anger recall (ARI) and sadness recall (SRI) interviews, whereas LP and trapezius electromyography and systolic blood pressure, diastolic blood pressure, and heart rate were recorded. They completed anger-in, anger-out, hostility, and trait anger measures. Results: Hierarchical regressions were used to test anger-in × hostility and anger-out ×hostility interactions for physiological changes during the ARI and SRI. A significant anger-in × hostility interaction was found for LP change during the ARI (but not SRI) such that high anger-in/high hostility patients evinced the greatest reactivity. Effects for trapezius reactivity were nonsignificant. Significant anger-in × hostility interactions were also found for systolic blood pressure and diastolic blood pressure changes during the ARI such that high anger-in/low hostility patients showed the smallest changes. The anger-out × hostility interaction for diastolic blood pressure change during ARI was also significant such that high anger-out/low hostility patients showed the smallest changes. All effects remained significant with trait anger controlled. Conclusions: A multivariable profile approach may help identify especially vulnerable patient groups. Patients with CLBP who tend to suppress anger and are cynically hostile may be more likely to experience high levels of muscle tension near the site of pain and injury during anger, but not during sadness, than other groups. CLBP = chronic low back pain; EMG = electromyography; AOS = anger-out scale; AIS = anger-in scale; Ho = Cook-Medley Hostility scale; TAS = Trait Anger scale; ARI = anger recall interview; SRI = sadness recall interview; LP = lower paraspinal muscles; SBP = systolic blood pressure; DBP = diastolic blood pressure; HR = heart rate.
First-Order Solutions for the Buckling Loads of Euler-Bernoulli Weakened Columns

In this work, closed-form expressions for the buckling loads of a weakened column with different boundary conditions are presented. The cracked-column model is based on the well-known method consisting of dividing the column into two segments connected by a rotational linear spring whose flexibility is related to the crack size and the geometry of the cross section. For the formulation of closed-form expressions, the perturbation method is used and the results are compared with those found by directly solving the eigenvalue problem.
Down regulation by p60v-src of genes specifically expressed and developmentally regulated in postmitotic quail neuroretina cells

The avian neuroretina (NR) is composed of photoreceptors and different neurons that are derived from proliferating precursor cells. Neuronal differentiation takes place after terminal mitosis. We have previously shown that differentiating NR cells can be induced to proliferate by infection with Rous sarcoma virus (RSV) and that cell multiplication requires expression of a functional v-src gene. We speculated that the quiescence of NR cells could be determined by specific genes. Cell proliferation could then result from the negative regulation of these genes by the v-src protein. By differential hybridization of a cDNA library, we isolated eight clones corresponding to genes expressed in postmitotic NR cells from 13-day-old quail embryos, transcriptional levels of which are significantly reduced in NR cells induced to proliferate by tsNY68, an RSV mutant with temperature-sensitive mitogenic activity. Partial sequencing analysis indicated that one RNA encoded the calmodulin gene, whereas the other seven showed no similarity to known sequences. By using v-src mutants that induce NR cell proliferation in the absence of transformation, we showed that transcription of six genes was negatively regulated by the v-src protein and that of four genes was correlated with NR cell quiescence. We also report that a subset of genes are specifically transcribed in neural cells and developmentally regulated in the NR. These results indicate that the v-src protein regulates expression of genes likely to play a role in the control of neural cell growth or differentiation.
Changes in Rat Serum Corticosterone After Treatment with Metabotropic Glutamate Receptor Agonists or Antagonists

From previous work, it appears that glutamate can activate the hypothalamic‐pituitary‐adrenocortical (HPA) axis by an interaction at either ionotopic or metabotropic (G‐protein coupled) receptors. For example, (1S,3R)‐1‐aminocyclopentane‐1,3‐dicarboxylate (ACPD), a metabotropic glutamate (mGlu) receptor agonist, has been shown to increase the levels of serum corticosterone in rats. The present study was undertaken to further characterize which of the mGlu receptors are substantially involved in control of the HPA axis. The group I mGlu receptor agonists, 3,5‐dihydroxyphenylglycine (DHPG), 1S,3R‐ACPD, and 2‐chloro‐5‐hydroxyphenylglycine (CHPG) but not the inactive isomer 1R,3S‐ACPD were found to dose‐dependently increase serum corticosterone 1 h after intracerebroventricular (i.c.v.) injection in male rats. The relative potency, DHPG (EC50 = 520 nmol) > 1S,3R‐ACPD (1.4 µmol) = CHPG (2.7 µmol) ≫ 1R,3S‐ACPD (≫ 3 µmol) is consistent with activation of group I (mGlu1/5) receptors. The effects of DHPG were long lasting with substantial elevations in corticosterone remaining for at least 3 h. In a similar manner, the group III mGlu receptor agonists, L‐AP4 (4‐phosphono‐2‐aminobutyric acid) and L‐SOP (serine‐O‐phosphate), were found to increase serum corticosterone levels at 1 h. In contrast, the mGlu group II selective agonists LY354740 (10 mg/kg, i.p.) and subtype‐selective doses of the group II antagonist LY341495 (1 mg/kg, i.p.) did not significantly elevate serum corticosterone. Given the group I agonists results, it was surprising to find that group I selective and mGlu1 selective antagonists given alone also increased serum corticosterone. As with the agonists, the rise in serum corticosterone with LY393675 (an mGlu1/5 antagonist, EC50 = 20 nmol, i.c.v.) and LY367385 (an mGlu1 antagonist, 325 nmol, i.c.v.) were dose‐dependent and consistent with their relative affinity for the group I mGlu receptors. The selective mGlu5 antagonist MPEP [2‐methyl‐6‐(phenylethylnyl)pyridine] increased serum cortocosterone but only at high doses (> 30 mg/kg, i.p.). A model involving the high glutamatergic tone on GABAergic interneurons in the paraventricular nucleus of the hypothalamus is discussed as a possible explanation for these results.
Enhanced Output Power of InGaN-Based Light-Emitting Diodes With AlGaN/GaN Two-Dimensional Electron Gas Structure

We demonstrate high-performance InGaN-based light-emitting diodes (LEDs) with tunneling-junction-induced 2-D electron gas (2DEG) at an AlGaN/GaN heterostructure, which is inserted in the middle of the P+-GaN contact layer of a conventional LED structure. The output power of a LED with a 2DEG insertion layer shows 17% enhancement compared to that of a conventional LED at 20 mA. This enhancement in output power for the LED with a 2DEG insertion layer could be attributed to both enhanced hole-injection efficiency and lateral current spreading by the presence of 2DEG at the AlGaN/GaN heterostructure.
Monogenic dyslipidemias: window on determinants of plasma lipoprotein metabolism.

Andrea Mok and Susan Near helped with manuscript preparation. The author sincerely thanks Dr. Murray Huff, Nica Borradaile, and Dr. Geoff Pickering for their constructive comments. The author is grateful for laboratory support by grants from the Canadian Institutes for Health Research, the Heart and Stroke Foundation of Ontario, the Canadian Genetic Diseases Network, the Canadian Diabetes Association, and the Blackburn Group. The author is a Career Investigator of the Heart and Stroke Foundation of Ontario and holds a Canada Research Chair in Human Genetics.
p53 protein accumulation and gene mutation in the progression of human prostate carcinoma.

BACKGROUND Nuclear accumulation of p53 protein has been shown to be strongly associated with missense p53 mutations. Studies of nuclear accumulation of p53 protein in prostate carcinoma cells have to date been confined to material from primary tumors. PURPOSE We studied the accumulation of p53 protein in specimens obtained from primary and metastatic sites of prostate carcinoma. By examining the accumulation of this protein as a function of stage, histologic grade, and androgen responsiveness of the tumor, we hoped to determine the role of p53 mutation in the progression of prostate carcinoma. METHODS The accumulation of the p53 protein in the cell nuclei was determined by immunohistochemical methods using polyclonal antibody to human p53 CM-1. The material studied consisted of formalin-fixed, paraffin-embedded tissue obtained from primary tumors and metastases of 92 patients with prostate carcinoma. Twelve samples from 11 patients were analyzed for the presence of mutations within exons 5-8 of the p53 gene (also known as TP53) by polymerase chain reaction-single-stranded conformation polymorphism (PCR-SSCP) analysis. Sequence analysis was subsequently performed on DNA obtained by polymerase chain reaction amplification of PCR-SSCP reactions produced from six different specimens. The chi-square test, Fisher's exact test, and the Freeman Halton test were used for statistical analyses of the results. RESULTS All tumors with p53 accumulation were metastatic (stage D), poorly differentiated, and androgen independent. Nuclear accumulation of p53 protein was strongly associated with stage (D2 versus D1 versus A-C, P < .0001), grade (Gleason score 8-10 versus 5-7, P < .003), and androgen sensitivity (androgen independent versus dependent, P < .0001). Logistic regression analysis demonstrated that androgen sensitivity predicted p53 outcome better than did stage (P < .0001) or grade alone (P < .006). There was a perfect concordance between the results obtained by PCR-SSCP analysis and the p53 protein accumulation determined by immunohistochemistry in the 12 samples studied. Mutation of the p53 gene was confirmed by sequencing DNA obtained from six specimens positive in the PCR-SSCP assay. CONCLUSIONS p53 gene mutation is a late event in the progression of prostate cancer and is associated with advanced (metastatic) stage, loss of differentiation, and the transition from androgen-dependent to androgen-independent growth. IMPLICATION Testing of prostate cancer biopsy specimens from metastatic sites for p53 protein accumulation and gene mutation may provide useful prognostic information and could influence the recommended course of treatment.
Acoustic Emission Precursors of M6.0 2004 Parkfield and M7.0 1989Loma Prieta Earthquakes

Two recent strike-slip earthquakes on the San Andreas Fault(SAF) in California, the M6.0 2004 Parkfield and M7.0 1989 Loma Prietaevents, revealed peaks in the acoustic emission (AE) activity in thesurrounding crust several months prior to the main events. Earthquakesdirectly within the SAF zone were intentionally excluded from theanalysis. The observed increase in AE is assumed to be a signature of theincreasing stress level in the surrounding crust, while the peak andsubsequent decrease in AE starting several months prior to the mainevents is attributed to damage-induced softening processes as discussedherein. Further, distinctive zones of low seismic activity surroundingthe epicentral regions in the pre-event time period are present for thetwo studied events. Both AE increases in the crust surrounding apotential future event and the development of a low-seismicity epicentralzone can be regarded as promising precursory information that could helpsignal the arrival of large earthquakes.
Numerical Simulation of High Drag Reduction in a Turbulent Channel Flow with Polymer Additives

Abstract : The addition of small amounts of long chain polymer molecules to wall-bounded flows can lead to dramatic drag reduction. Although this phenomenon has been known for about fifty years, the action of the polymers and its effect on turbulent structures are still unclear. Detailed experiments have characterized two distinct regimes (Warholic et at. 1999), which are referred to as low drag reduction (LDR) and high drag reduction (HDR). The first regime exhibits similar statistical trends as Newtonian flow: the log- law region of the mean velocity profile remains parallel to that of the Newtonian flow but its lower bound moves away from the wall and the upward shift of the log-region is a function of drag reduction, DR. Although streamwise fluctuations are increased and transverse ones are reduced, the shape of the rms velocity profiles is not qualitatively modified. At higher drag reductions, of the order of 40-50%, the flow enters the HDR regime for which the slope of the log-law is dramatically augmented and the Reynolds shear stress is small (Warholic et at. 1999; Ptasinski et at. 2001). The drag reduction is eventually bounded by a maximum drag reduction (MDR) (Virk & Mickley 1970) which is a function of the Reynolds number. while several experiments report mean velocity profiles very close to the empirical profile of Virk & Mickley (1970) for MDR conditions, the observations regarding the structure of turbulence can differ significantly. For instance, Warholic et at. (1999) measured a near-zero Reynolds shear stress, whereas a recent experiment (Ptasinski et at. 2001) shows evidence of non-negligible Reynolds stress in their MDR flow. To the knowledge of the authors, only the LDR regime has been documented in numerical simulations (Sureshkumar et at. 1997; Dimitropoulos et al. 1998; Min et at. 2001; Dubief & Lele 2001; Sibilla & Baron 2002).
Surface Expression of Notch1 on Thymocytes: Correlation with the Double-Negative to Double-Positive Transition 1

Notch1 plays a critical role in regulating T lineage commitment during the differentiation of lymphoid precursors. The physiological relevance of Notch1 signaling during subsequent stages of T cell differentiation has been more controversial. This is due in part to conflicting data from studies examining the overexpression or targeted deletion of Notch1 and to difficulties in distinguishing between the activities of multiple Notch family members and their ligands, which are expressed in the thymus. We employed a polyclonal antiserum against the extracellular domain of Notch1 to study surface expression during thymopoiesis. We found high levels of Notch1 on the cell surface only on double negative (DN) stage 2 through the immature single-positive stage of thymocyte development, before the double-positive (DP) stage. The Notch signaling pathway, as read out by Deltex1 expression levels, is highly active in DN thymocytes. When an active Notch1 transgene, Notch1IC, is exogenously introduced into thymocytes of recombinase-activating gene 2-deficient mice, it promotes proliferation and development to the DP stage following anti-CD3 treatment without apparently affecting the intensity of pre-TCR signaling. In addition, a stromal cell line expressing the Notch ligand, Delta-like-1, promotes the in vitro expansion of wild-type DN3 thymocytes in vitro. Consistent with other recent reports, these data suggest a role for Notch1 during the DN to DP stage of thymocyte maturation and suggest a cellular mechanism by which Notch1IC oncogenes could contribute to thymoma development and maintenance.
Pak2 Regulates Hematopoietic Progenitor Cell Proliferation, Survival, and Differentiation

p21‐Activated kinase 2 (Pak2), a serine/threonine kinase, has been previously shown to be essential for hematopoietic stem cell (HSC) engraftment. However, Pak2 modulation of long‐term hematopoiesis and lineage commitment remain unreported. Using a conditional Pak2 knockout mouse model, we found that disruption of Pak2 in HSCs induced profound leukopenia and a mild macrocytic anemia. Although loss of Pak2 in HSCs leads to less efficient short‐ and long‐term competitive hematopoiesis than wild‐type cells, it does not affect HSC self‐renewal per se. Pak2 disruption decreased the survival and proliferation of multicytokine stimulated immature progenitors. Loss of Pak2 skewed lineage differentiation toward granulocytopoiesis and monocytopoiesis in mice as evidenced by (a) a three‐ to sixfold increase in the percentage of peripheral blood granulocytes and a significant increase in the percentage of granulocyte‐monocyte progenitors in mice transplanted with Pak2‐disrupted bone marrow (BM); (b)Pak2‐disrupted BM and c‐kit+ cells yielded higher numbers of more mature subsets of granulocyte‐monocyte colonies and polymorphonuclear neutrophils, respectively, when cultured in the presence of granulocyte‐macrophage colony‐stimulating factor. Pak2 disruption resulted, respectively, in decreased and increased gene expression of transcription factors JunB and c‐Myc, which may suggest underlying mechanisms by which Pak2 regulates granulocyte‐monocyte lineage commitment. Furthermore, Pak2 disruption led to (a) higher percentage of CD4+CD8+ double positive T cells and lower percentages of CD4+CD8− or CD4−CD8+ single positive T cells in thymus and (b) decreased numbers of mature B cells and increased numbers of Pre‐Pro B cells in BM, suggesting defects in lymphopoiesis. Stem Cells 2015;33:1630–1641
Every thing old is new again.

In Advent 2011, the Englishspeaking Catholic Church will begin to pray a new translation of the Mass. At Notre Dame, there will be a variety of opportunities to learn the rationale underlying the translation as well as the “new” words of the Mass. However, consider what it takes to become an excellent speaker of a language. We really know French or Spanish or Mandarin when we begin to think like someone who speaks this language. We come to live the way of thinking characteristic of that linguistic community. If we want to learn to speak the words of the Mass in such a way that we think like someone who speaks the language of our faith, we will need to do more than learn or become used to the new texts. Rather, we will need to come to pray these texts so that the mysteries of that they present become a part of us. Of course, life-transforming prayer, whether within the Eucharist or outside of it, takes practice. Over the coming weeks, we will become acquainted with and “practice” the new texts of the Mass through reflection upon the words we pray. But we will also need to meditate more deeply on the virtues that our prayer seeks to cultivate. Remember this about
Development of neural network models for a crude oil distillation column

This paper discusses the development of artificial neural network (ANN) models for a crude oil distillation column. Since the model is developed for real time optimisation (RTO) applications they are steady state, multivariable models. Training and testing data used to develop the models were generated from a reconciled steady-state model simulated in a process simulator. The radial basis function networks (RBFN), a type of feedforward ANN model, were able to model the crude tower very well, with the root mean square error for the prediction of each variable less than 1%. Grouping related output variables in a network model was found to give better predictions than lumping all the variables in a single model; this also allowed the overall complex, multivariable model to be simplified into smaller models that are more manageable. In addition, the RBFN models were also able to satisfactorily perform range and dimensional extrapolation, which is necessary for models that are used in RTO.
Constrained reconstructions for 4D intervention guidance

Image-guided interventions are an increasingly important part of clinical minimally invasive procedures. However, up to now they cannot be performed under 4D (3D + time) guidance due to the exceedingly high x-ray dose. In this work we investigate the applicability of compressed sensing reconstructions for highly undersampled CT datasets combined with the incorporation of prior images in order to yield low dose 4D intervention guidance. We present a new reconstruction scheme prior image dynamic interventional CT (PrIDICT) that accounts for specific image features in intervention guidance and compare it to PICCS and ASD-POCS. The optimal parameters for the dose per projection and the numbers of projections per reconstruction are determined in phantom simulations and measurements. In vivo experiments in six pigs are performed in a cone-beam CT; measured doses are compared to current gold-standard intervention guidance represented by a clinical fluoroscopy system. Phantom studies show maximum image quality for identical overall doses in the range of 14 to 21 projections per reconstruction. In vivo studies reveal that interventional materials can be followed in 4D visualization and that PrIDICT, compared to PICCS and ASD-POCS, shows superior reconstruction results and fewer artifacts in the periphery with dose in the order of biplane fluoroscopy. These results suggest that 4D intervention guidance can be realized with today’s flat detector and gantry systems using the herein presented reconstruction scheme.
8 × 320-Gb/s transmission over 5600 km using all-ETDM 80-Gbaud polarization multiplexed QPSK transmitter and coherent receiver

WDM transmission over 5600 km of ultra-large-area fiber is achieved using an 80-Gbaud all-electronically multiplexed polarization-division multiplexed quadrature phase-shift-keyed (PDM-QPSK) transmitter and off-line intradyne detection with four synchronized 120-GSamples/s, 45-GHz inputs of an oscilloscope prototype.