Miracle-dz/UniFAR-FTUs huggingface dataset:
Discriminative latent variable models for visual recognition

Visual Recognition is a central problem in computer vision, and it has numerous potential applications in many different fields, such as robotics, human computer interaction, and entertainment. In this dissertation, we propose two discriminative latent variable models for handling challenging visual recognition problems. In particular, we use latent variables to capture and model various prior knowledge in the training data. In the first model, we address the problem of recognizing human actions from still images. We jointly consider both poses and actions in a unified framework, and treat human poses as latent variables. The learning of this model follows the framework of latent SVM. Secondly, we propose another latent variable model to address the problem of automated tag learning on YouTube videos. In particular, we address the semantic variations (sub-tags) of the videos which have the same tag. In the model, each video is assumed to be associated with a sub-tag label, and we treat this sub-tag label as latent information. This model is trained using a latent learning framework based on LogitBoost, which jointly considers both the latent sub-tag label and the tag label. Moreover, we propose a novel discriminative latent learning framework, kernel latent SVM, which combines the benefit of latent SVM and kernel methods. The framework of kernel latent SVM is general enough to be applied in many applications of visual recognition. It is also able to handle complex latent variables with interdependent structures using composite kernels.
BJRD16174 1..11

Objective: To compare electrocardiographic (ECG)triggered high-pitch (HP) dual-source CT angiography (CTA) with non-ECG-triggered HP CTA of the aorta, particularly the ascending aorta, with regard to image quality, motion artefacts, contrast-to-noise ratio (CNR), signal-to-noise ratio (SNR) and radiation dose. Methods: 59 consecutive patients who had been referred for CTA for known or suspected aortic disease, previous aortic intervention or planned transapical or transfemoral aortic valve implantation were prospectively included. Patients underwent CTAs with HP, using a dual-source CTA system, with [control group (Group A); n530] or without (Group B; n529) ECG triggering after randomization. For evaluation, image quality and a motion artefact score (MAS) were assessed in a blinded fashion at different predefined anatomic regions. CNR and SNR were measured at the same levels. Radiation dose estimates and contrast enhancement were compared between the two groups. Results: There were no significant differences for image quality and MAS. The intra-arterial contrast resolution was significantly higher at the level of the aortic arch and descending aorta in the non-triggered group (CNR values, p50.002–0.018). No significant differences in the radiation dose were found. Conclusion: Non-triggered HP dual-source CTA provided comparable results with regard to image quality, MAS, CNR, SNR and radiation doses compared with ECG-triggered HP CTA. Therefore, ECG triggering of the ascending aorta might be obviated when HP scanning is available. Advances in knowledge: HP dual-source CTA might obviate ECG triggering in the ascending aorta. Nontriggered HP CTA of the ascending aorta provides an excellent image quality.
Trajectories of Ethnic-Racial Identity and Autonomy among Mexican-origin Adolescent Mothers in the U.S

This study examined trajectories of ethnic-racial identity (ERI) and autonomy development among Mexican-origin adolescent females in the U.S. (N = 181; Mage at Wave 1 = 16.80 years, SD = 1.00) as they transitioned through the first five years of parenthood. Trajectories of ERI and autonomy also were examined in relation to psychosocial functioning. Unconditional latent growth models indicated significant growth in autonomy, ERI resolution, and ERI affirmation from middle to late adolescence. Conditional latent growth models indicated that autonomy and ERI exploration growth trajectories were positively associated with psychosocial adjustment. Although adolescent mothers are experiencing transitions that are not normative during adolescence, they also engage in normative developmental processes, and their engagement in such processes is linked with better adjustment.
Deficiency of LKB1 in heart prevents ischemia-mediated activation of AMPK 2 but not AMPK 1

Kei Sakamoto, Elham Zarrinpashneh, Grant R. Budas, Anne-Catherine Pouleur, Anindya Dutta, Alan R. Prescott, Jean-Louis Vanoverschelde, Alan Ashworth, Aleksandar Jovanović, Dario R. Alessi, and Luc Bertrand Medical Research Council Protein Phosphorylation Unit, School of Life Sciences, University of Dundee, Dundee, United Kingdom; Division of Cardiology, School of Medicine, Université catholique de Louvain, Brussels, Belgium; Maternal and Child Health Sciences, Tayside Institute of Child Health, Ninewells Hospital and Medical School, University of Dundee, Dundee, United Kingdom; The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London, United Kingdom; and Division of Cell Biology and Immunology, School of Life Sciences, University of Dundee, Dundee, United Kingdom
Pulmonary Perspective Systemic Sclerosis-associated Pulmonary Arterial Hypertension

Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; Université Paris-Sud 11, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine Béclère, Assistance Publique Hôpitaux de Paris, Clamart, France; and the Université Paris-Descartes, Department of Internal Medicine, Hôpital Cochin, Assistance Publique Hôpitaux de Paris, Paris, France
WOUND CARE PRODUCTS Dermagraft: Use in the Treatment of Chronic Wounds

Problem: Lower limb ulceration is a common problem in clinical practice. A variety of metabolic and physical causes can lead to a diversity of chronic ulcer types, including diabetic foot ulcers (DFUs) and venous leg ulcers (VLUs). Solution: A wide variety of technologies have been developed to treat chronic wounds, with varying levels of success. Depending upon the type and severity of the wound being treated, treatments may include systemic or local antibiotic therapy, application of fillers such as collagen sponges, use of negative wound pressure, hyperbaric oxygen therapy, application of select growth factors, advanced wound dressings, and more recently, the use of cell-based tissueengineered products. New Technology: Dermagraft is a sterile, cryopreserved, human fibroblast– derived dermal substitute generated by the culture of neonatal dermal fibroblasts onto a bioabsorbable polyglactin mesh scaffold. During the product-manufacturing process, the human fibroblasts proliferate to fill the interstices of this scaffold and secrete collagen, other extracellular matrix proteins, growth factors, and cytokines, creating a three-dimensional human tissue containing metabolically active living cells. Indications for Use: Dermagraft has been approved for marketing in the United States for the treatment of DFUs. In addition, the product is in active development for the treatment of VLUs and has been clinically used in a variety of other indications to stimulate wound healing. Caution: When treating DFUs, Dermagraft should be used in conjunction with standard wound care regimens and in patients who have adequate blood supply to the involved foot.
Intravenous ethanol infusion decreases human cortical GABA and NAA as measured with 1H-MRS at 4T

Background—Ethanol modulates glutamate and GABA function. However, little is known about the acute pharmacologic effects of ethanol on levels of GABA, glutamate, and other metabolites measurable in the human cortex in vivo using 1H magnetic resonance spectroscopy (MRS). Methods—Eleven healthy social drinkers received two intravenous ethanol infusions that raised breath alcohol levels to a clamped plateau of 60 mg/dL over 60–70 minutes. The first infusion established tolerability of the procedure, and the second procedure, conducted 15±12 days later, was performed during 1H MRS of occipital GABA, glutamate, and other metabolites. Results—The time course of brain ethanol approximated that of breath ethanol, but venous ethanol lagged by about 7 minutes. GABA fell 13±8% after 5 minutes of the ethanol infusion and remained reduced (p=0.003) throughout the measurement. The combination of N-acetylaspartate and N-acetylaspartyl glutamate (summed as NAA) fell steadily during the infusion by 8±3% (p=0.0036). Conclusions—Ethanol reduced cortical GABA and NAA levels in humans. Reductions in GABA levels are consistent with facilitation of GABAA receptor function by ethanol. The gradual decline in NAA levels suggests inhibition of neural or metabolic activity in the brain.
KINETICS OF O6-Me-dG REPAIR BY O6-ALKYLGUANINE DNA ALKYLTRANSFERASE WITHIN K-RAS GENE DERIVED DNA SEQUENCES

O6-methyl-2'-deoxyguanosine (O6-Me-dG) is a potent mutagenic DNA adduct that can be induced by a variety of methylating agents, including tobacco-specific nitrosamine, 4(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). O6-Me-dG is directly repaired by the specialized DNA repair protein, O6-alkylguanine-DNA-alkyltransferase (AGT), which transfers the O6-alkyl group from the modified guanine to a cysteine thiol within the active site of the protein. Previous investigations suggested that AGT repair of O6-alkylguanines may be sequencedependent as a result of flanking nucleobase effects on DNA conformation and energetics. In the present work, a novel high performance/pressure liquid chromatography-electrospray ionization tandem mass spectrometry (HPLC-ESI+-MS/MS) based approach was developed to analyze the kinetics of AGT-mediated repair of O6-Me-dG adducts placed at different sites within the double stranded DNA sequence representing codons 8–17 of the K-ras protooncogene, 5'-G1TA G2TT G3G4A G5CT G6G7T G8G9C G10TA G11G12C AAG13 AG14T-3', where G5, G6, G7, G8, G9, G10, or G11 was replaced with O6-Me-dG. The second guanine of K-ras codon 12 (G7 in our numbering system) is a major mutational hotspot for G A transitions observed in lung tumors of smokers and in neoplasms induced in laboratory animals by exposure to methylating agents. O6Me-dG-containing duplexes were incubated with human recombinant AGT protein, and the reactions were quenched at specific times. Following acid hydrolysis to release purines, isotope dilution HPLC-ESI-MS/MS was used to determine the amounts of O6-Me-G remaining in DNA. The relative extent of demethylation for O6-Me-dG adducts located at G5, G6, G7, G8, G9, G10, or G11 following 10 second incubation with AGT showed little variation as a function of sequence position. Furthermore, the second order rate constants for the repair of O6-Me-dG adducts located at the first and second positions of the K-ras codon 12 (5'-G6G7T-3') were similar (1.4 × 107 M−1s−1 vs. 7.4 × 106 M−1s−1 respectively), suggesting that O6-Me-dG repair by AGT is not the determining factor for K-ras codon 12 mutagenesis following exposure to methylating agents. The new HPLC-ESI-MS/MS assay developed in this work is a valuable tool which will be used to further explore the role of local sequence environment and endogenous DNA modifications in shaping mutational spectra of NNK and other methylating agents. *To whom correspondence should be addressed: The Cancer Center, University of Minnesota, Mayo Mail Code 806, 420 Delaware St SE, Minneapolis, MN 55455, USA. ph: 612-626-3432 fax: 612-626-5135, trety001@umn.edu. NIH Public Access
Evidence for Proteolytic Processing and Stimulated Organelle Redistribution of iPLA2β

Over the past decade, important roles for the 84–88 kDa Group VIA Ca2+-independent phospholipase A2 (iPLA2β) in various organs have been described. We demonstrated that iPLA2β participates in insulin secretion, insulinoma cells and native pancreatic islets express full-length and truncated isoforms of iPLA2β, and certain stimuli promote perinuclear localization of iPLA2β. To gain a better understanding of its mobilization, iPLA2β was expressed in INS-1 cells as a fusion protein with EGFP, enabling detection of subcellular localization of iPLA2β by monitoring EGFP fluorescence. Cells stably-transfected with fusion protein expressed nearly 5-fold higher catalytic iPLA2β activity than control cells transfected with EGFP cDNA alone, indicating that co-expression of EGFP does not interfere with manifestation of iPLA2β activity. Dual fluorescence monitoring of EGFP and organelle Trackers combined with immunoblotting analyses revealed expression of truncated iPLA2β isoforms in separate subcellular organelles. Exposure to secretagogues and induction of ER stress are known to activate iPLA2β in β-cells and we find here that these stimuli promote differential localization of iPLA2β in subcellular organelles. Further, mass spectrometric analyses identified iPLA2β variants from which N-terminal residues were removed. Collectively, these findings provide evidence for endogenous proteolytic processing of iPLA2β and redistribution of iPLA2β variants in subcellular compartments. It might be proposed that in vivo processing of iPLA2β facilitates its participation in multiple biological processes.
Genetic Linkage Analysis in Familial Breast and Ovarian Cancer: Results from 214 Families

Breast cancer is known to have an inherited component, consistent in some families with autosomal dominant inheritance; in such families the disease often occurs in association with ovarian cancer. Previous genetic linkage studies have established that in some such families disease occurrence is linked to markers on chromosome 17q. This paper reports the results of a collaborative linkage study involving 214 breast cancer families, including 57 breast-ovarian cancer families; this represents almost all the known families with 17q linkage data. Six markers on 17q, spanning approximately 30 cM, were typed in the families. The aims of the study were to define more precisely the localization of the disease gene, the extent of genetic heterogeneity and the characteristics of linked families and to estimate the penetrance of the 17q gene. Under the assumption of no genetic heterogeneity, the strongest linkage evidence was obtained with D17S588 (maximum LOD score [Zm.] = 21.68 at female recombination fraction [Of] = .13) and D17S579 (Zmax = 13.02 at Of = .16). Multipoint linkage analysis allowing for genetic heterogeneity provided evidence that the predisposing gene lies between the markers D17S588 and D17S250, an interval whose genetic length is estimated to be 8.3 cM in males and 18.0 cM in females. This position was supported over other intervals by odds of 66:1. The location of the gene with respect to D17S579 could not be determined unequivocally. Under the genetic model used in the analysis, the best estimate of the proportion of linked breast-ovarian cancer families was 1.0 (lower LOD 1 limit 0.79). In contrast, there was significant evidence of genetic heterogeneity among the families without ovarian cancer, with an estimated 45% being linked. These results suggest that a gene(s) on chromosome 17q accounts for the majority of families in which both early-onset breast cancer and ovarian cancer occur but that other genes predisposing to breast cancer exist. By examining the fit of the linkage data to different penetrance functions, the cumulative risk associated with the 17q gene was estimated to be 59% by age 50 years and 82% by age 70 years. The corresponding estimates for the breast-ovary families were 67% and 76%, and those for the families without ovarian cancer were 49% and 90%; these penetrance functions did not differ significantly from one another.
Ultrasound-Guided Creation of a Small Animal Model of Aortic Injury

Purpose—To develop a small animal model of controlled aortic intimal injury with ultrasound imaging guidance. Materials and Methods—Via carotid artery cut down, we advanced a custom-made microcatheter/angled-metal-device system to damage the intima of the ascending aortas of 20 Sprague Dawley (SD) rats and 10 JCR atherosclerotic rats. This minimally invasive endovascular procedure was monitored by a clinical ultrasound imaging system. Injured aortas were harvested for histologic confirmations using a grading system: Grade I with intima injury, Grade II with injury to media, and Grade III with injury through the entire aortic wall. Neointimal reactions at the injury site were compared by calculating the ratio of intimal to medial thickness among different animal groups at various survival times (week 1, weeks 2–3 and weeks 4–7). Results—Clear visualization of the architectures of the heart, great vessels and the exact location of the angled-metal-device by ultrasound imaging ensured consistent intimal damage of the aorta. Histopathology confirmed that most of the aortic injures were classified as Grade I. There was no significant difference between the two rat groups. Analysis on pathophysiological reactions at the injury sites revealed increased thickening of neointimal hyperplasia as animal survival times extended from week 1 to weeks 4–7 after the aortic interventions. Conclusions—This study demonstrates the feasibility of using clinical ultrasound imaging to precisely guide the creation of controlled aortic intimal injury in rats, which may become a useful tool to facilitate research involving the prevention and treatment of atherosclerotic cardiovascular disease.
OF THE EXPERIMENTAL ANALYSIS OF BEHAVIOR DIFFERENTIAL REINFORCEMENT AND SIGNAL DETECTION '

Reinforcement was introduced for responses normally treated as errors in signal-detection procedures. The first experiment used a standard two-response discrete-trial procedure with no reinforcement for errors. Results showed that rats altered their response biases but maintained constant sensitivity to visual signals when reinforcement probabilities varied, and that their sensitivity depended on the physical difference between signals, in accordance with the predictions of signal-detection theory. Experiment II, with rats, and Experiment III, with pigeons, demonstrated that sensitivity decreased in this procedure when reinforcement was scheduled for errors with the signals held constant, despite independence of overall number of reinforcers and sensitivity. Experiment IV, with rats, replicated the decrease in sensitivity in a continuous proceduire employing only one response. The decrements in sensitivity were similar across Experiments II, III, and IV, and accorded well with earlier research. Thus, contrary to a fundamental assumption of signal-detection theory, estimates of sensitivity are not always invariant with respect to the outcomes of responding, but depend on relative reinforcement of correct responses.
THE EFFECT OF DIETARY PROTEIN ON THE UREA CLEARANCE OF CHILDREN WITH NEPHROSIS1

In so-called " pure lipoid nephrosis " in children the urea clearance is frequently elevated markedly above the normal level. There also may be elevated urea clearances in some children with hemorrhagic Bright's disease with a decided nephrotic component. The nature of this paradox of renal hyperfunction in the presence of renal involvement is not entirely clear, and the present work was undertaken in an attempt to elucidate the r6le of the diet in this phenomenon. The influence of the protein intake on the urea clearance has been studied in adults, but not in children. Cope (1) observed that in adult patients with nephritis, who had a normal or nearly normal clearance, there was a depression of the clearance when the protein intake was lowered from the moderate level of 75 grams per day to 40 grams. He found, however, that there was no increase in the clearance when the protein intake was raised from 75 to 125 grams. In adult patients with chronic renal disease sufficiently advanced to depress the urea clearance consistently below 50 per cent of normal, the effect of lowering the dietary protein was relatively slight. In such patients the urea clearance on 40 grams of protein per day remained about 90 per cent of the clearance on 75 grams. In 1934, Goldring, Razinsky, Greenblatt and Cohen (2) extended Cope's observations to normal men, and came to the same conclusions regarding normal men that Cope arrived at in regard to the patients with unimpaired ability to excrete urea. In Goldring's observations the diet was varied within somewhat greater limits. On the low diet there was observed an average reduction of the clearance of 23 per cent. High protein intakes caused no elevation above the usual normal clearance, even when the protein intake was pushed up to 280 grams per day. In the present study we have extended to ne-
Benefical Role of the GPR30 agonist G-1 in an Animal Model of Multiple Sclerosis

The beneficial effects of estrogens in multiple sclerosis are thought to be mediated exclusively by the classical nuclear estrogen receptors ERα and ERβ. However, recently many reports revealed that estrogens are able to mediate rapid signals through a G protein-coupled receptor (GPCR), known as GPR30. In the present study, we set out to explore whether effects mediated through this receptor were anti-inflammatory and could account for some of the beneficial effects of estrogen. We demonstrate that GPR30 is expressed in both human and mouse immune cells. Furthermore a GPR30selective agonist, G-1, previously described by us, inhibits the production of lipopolysaccharide (LPS)-induced cytokines such as TNF-α and IL-6 in a dose-dependent manner in human primary macrophages and in a murine macrophage cell line. These effects are likely mediated solely through the estrogen-specific receptor GPR30 since the agonist G-1 displayed an IC50 far greater than 10 μM on the classical nuclear estrogen receptors as well as a panel of 25 other GPCRs. Finally, we show that the agonist G-1 is able to reduce the severity of disease in both active and passive EAE models of multiple sclerosis in SJL mice and that this effect is concomitant with a G-1-mediated decrease in proinflammatory cytokines, including IFN-γ and IL-17, in immune cells harvested from these mice. The effect of G-1 appears indirect, as the GPR30 agonist did not directly influence IFNγ or IL-17 production by purified T cells. These data indicate that G-1 may represent a novel therapeutic agent for the treatment of chronic autoimmune, inflammatory diseases.
AN IL-6 HAPLOTYPE ON HUMAN CHROMOSOME 7P21 CONFERS RISK FOR IMPAIRED RENAL FUNCTION IN TYPE 2 DIABETES

Human chromosome 7p21 potentially harbors a major gene for end-stage renal disease (ESRD) and variation in glomerular filtration rate. The pro-inflammatory IL-6 is a prime positional candidate gene since chronic inflammation has been implicated in diabetic nephropathy. To test this hypothesis, single SNP and haplotype analyses were performed using a case-control study design with 295 cases and 174 normoalbuminuric controls. Cases were subcategorized into those with proteinuria (n=138) or chronic renal failure (CRF)/ESRD (n=157). Tagging SNPs (rs2069827, rs1800795 (-174G>CSNP), rs2069837, rs2069840, rs2069861) were chosen based on linkage disequilibrium patterns and genotyped along with rs1800796 (-634G>C SNP). Single SNP analyses suggested that the rs1800795 may be associated with risk of CRF/ESRD (P=0.028) but this was not significant after Bonferroni correction. While haplotype analyses revealed no association with the presence of proteinuria, there was significant evidence for such an association with CRF/ESRD. Strikingly, there was an excess of the G-G-G-A-G-C haplotype among cases with CRF/ESRD (25.5%) compared to controls (15.4%) (P=0.0016). This association remained statistically significant even after correction for multiple testing (Bonferroni corrected P-value = 0.0224). In conclusion, our study has yielded first evidence for an IL-6 haplotype that confers risk for impaired renal function in type 2 diabetes.