Miracle-dz/UniFAR-FTUs huggingface dataset:
Web page segmentation with structured prediction and its application in web page classification

We propose a framework which can perform Web page segmentation with a structured prediction approach. It formulates the segmentation task as a structured labeling problem on a transformed Web page segmentation graph (WPS-graph). WPS-graph models the candidate segmentation boundaries of a page and the dependency relation among the adjacent segmentation boundaries. Each labeling scheme on the WPS-graph corresponds to a possible segmentation of the page. The task of finding the optimal labeling of the WPS-graph is transformed into a binary Integer Linear Programming problem, which considers the entire WPS-graph as a whole to conduct structured prediction. A learning algorithm based on the structured output Support Vector Machine framework is developed to determine the feature weights, which is capable to consider the inter-dependency among candidate segmentation boundaries. Furthermore, we investigate its efficacy in supporting the development of automatic Web page classification.
Clinical and pathological response to primary chemotherapy in patients with locally advanced breast cancer grouped according to hormonal receptors, Her2 status, grading and Ki-67 proliferation index.

OBJECTIVES Biological markers that reliably predict clinical and pathological response to primary systemic therapy may have considerable clinical potential; this study evaluated response compared to expression of ER, PgR and Her2, grading and Ki-67 proliferation index before and after neoadjuvant chemotherapy in patients with locally advanced breast cancer (LABC). PATIENTS AND METHODS Fifty-five patients received neoadjuvant chemotherapy for LABC. The incidence of clinical and pathological responses was assessed with respect to basal clinical stage, absent/low vs. high ER and PgR status, low vs. high proliferation index, grading and Her2 overexpression. RESULTS Overall, 30 patients (54%) underwent downstaging of their primary tumor; pathological complete remission was observed in only one patient with Her2 positive breast tumor. Patients with pre-treatment Ki-67 >20%, Her2 overexpression, T2b/T3 vs. T4 clinical stage achieved higher response rate. CONCLUSION The future of neoadjuvant therapy lies in tailoring treatment to individual patients by identifying response predictors; although the number of patients reported is small, this study confirms that clinical stage at diagnosis, Ki-67 reduction and Her2 overexpression are predictive of tumor response to neoadjuvant regimens.
Relationships between measures of adiposity with subclinical atherosclerosis in patients with type 2 diabetes

Assess cross‐sectional relationships between body mass index (BMI), waist circumference (WC), pericardial (PAT), visceral (VAT), and subcutaneous adipose tissue (SAT) volumes with calcified plaque (CP) in African Americans (AAs) and European Americans (EAs) with type 2 diabetes.
Self-disclosure : theory, research, and therapy

Themes in the Study of Self-Disclosure. - A Neuropsychological Perspective of Interpersonal Communication. - Why Am I Telling You This? - Private Self-Consciousness and Self-Disclosure. - Gender and Self-Disclosure. - Responsiveness and Self-Disclosure. - Marriage and Verbal Intimacy. - Self-Disclosure and Relationship Disengagement. - The Relation of Loneliness and Self-Disclosure. - The Relationship between Psychopathology and Self-Disclosure. - The Dilemma of Distress Disclosure. - "I Have to Talk to Somebody". - Self-Disclosure in Cognitive Marital Therapy. - Counseling and Self-Disclosure. - Commentary.
Identification of the Kappa-Opioid Receptor as a Therapeutic Target for Oligodendrocyte Remyelination

Remyelinating therapies seek to promote restoration of function and normal cellular architecture following demyelination in diseases, such as multiple sclerosis (MS). Functional screening for small molecules or novel targets for remyelination is a major hurdle to the identification and development of rational therapeutics for MS. Recent findings and technical advances provide us with a unique opportunity to provide insight into the cell autonomous mechanisms for remyelination and address this unmet need. Upon screening a G-protein-coupled receptor small-molecule library, we report the identification of a cluster of κ-opioid receptor (KOR) agonists that significantly promotes oligodendrocyte differentiation and myelination. KOR agonists were validated in purified rat oligodendroglial cultures, and the (±)U-50488 compound proved to be most effective for differentiation. (±)U-50488 treatment significantly enhances differentiation and myelination in purified oligodendroglial cocultures and greatly accelerates the kinetics of remyelination in vivo after focal demyelination with lysolecithin. The effect of (±)U-50488 is attenuated by KOR antagonists and completely abolished in KOR-null oligodendroglia. Conditional deletion of KOR in murine oligodendrocyte precursor cells (OPCs) greatly inhibits remyelination after focal demyelination lacking any response to (±)U-50488 treatment. To determine whether agonism of KOR represents a feasible therapeutic approach, human induced pluripotent stem cell-derived OPCs were treated with (±)U-50488. Consistent with findings, differentiation of human OPCs into mature oligodendrocytes was significantly enhanced. Together, KOR is a therapeutic target to consider for future remyelination therapy. SIGNIFICANCE STATEMENT Remyelination represents a promising strategy to achieve functional recovery in demyelinating diseases, like MS. Thus, identification of potent compounds and targets that promote remyelination represents a critically unmet need. This study reports a cluster of compounds that are highly effective in enhancing remyelination and identifies κ-opioid receptor (KOR) as a positive regulator for oligodendroglial differentiation, implicating KOR agonism as a potential strategy to accelerate remyelination.
Dorsolateral Prefrontal Cortex Drives Mesolimbic Dopaminergic Regions to Initiate Motivated Behavior

How does the brain translate information signaling potential rewards into motivation to get them? Motivation to obtain reward is thought to depend on the midbrain [particularly the ventral tegmental area (VTA)], the nucleus accumbens (NAcc), and the dorsolateral prefrontal cortex (dlPFC), but it is not clear how the interactions among these regions relate to reward-motivated behavior. To study the influence of motivation on these reward-responsive regions and on their interactions, we used dynamic causal modeling to analyze functional magnetic resonance imaging (fMRI) data from humans performing a simple task designed to isolate reward anticipation. The use of fMRI permitted the simultaneous measurement of multiple brain regions while human participants anticipated and prepared for opportunities to obtain reward, thus allowing characterization of how information about reward changes physiology underlying motivational drive. Furthermore, we modeled the impact of external reward cues on causal relationships within this network, thus elaborating a link between physiology, connectivity, and motivation. Specifically, our results indicated that dlPFC was the exclusive entry point of information about reward in this network, and that anticipated reward availability caused VTA activation only via its effect on the dlPFC. Anticipated reward thus increased dlPFC activation directly, whereas it influenced VTA and NAcc only indirectly, by enhancing intrinsically weak or inactive pathways from the dlPFC. Our findings of a directional prefrontal influence on dopaminergic regions during reward anticipation suggest a model in which the dlPFC integrates and transmits representations of reward to the mesolimbic and mesocortical dopamine systems, thereby initiating motivated behavior.
A Matroid Framework for Noncoherent Random Network Communications

Models for noncoherent error control in random linear network coding (RLNC) and store and forward (SAF) have been recently proposed. In this paper, we model different types of random network communications as the transmission of flats of matroids. This novel framework encompasses RLNC and SAF and allows us to introduce a novel protocol, referred to as random affine network coding (RANC), based on affine combinations of packets. Although the models previously proposed for RLNC and SAF only consider error control, using our framework, we first evaluate and compare the performance of different network protocols in the error-free case. We define and determine the rate, average delay, and throughput of such protocols, and we also investigate the possibilities of partial decoding before the entire message is received. We thus show that RANC outperforms RLNC in terms of data rate and throughput thanks to a more efficient encoding of messages into packets. Second, we model the possible alterations of a message by the network as an operator channel, which generalizes the channels proposed for RLNC and SAF. Error control is thus reduced to a coding-theoretic problem on flats of a matroid, where two distinct metrics can be used for error correction. We study the maximum cardinality of codes on flats in general, and codes for error correction in RANC in particular. We finally design a class of nearly optimal codes for RANC based on rank metric codes for which we propose a low-complexity decoding algorithm. The gain of RANC over RLNC is thus preserved with no additional cost in terms of complexity.
3D Object Recognition in Cluttered Scenes with Local Surface Features: A Survey

3D object recognition in cluttered scenes is a rapidly growing research area. Based on the used types of features, 3D object recognition methods can broadly be divided into two categories-global or local feature based methods. Intensive research has been done on local surface feature based methods as they are more robust to occlusion and clutter which are frequently present in a real-world scene. This paper presents a comprehensive survey of existing local surface feature based 3D object recognition methods. These methods generally comprise three phases: 3D keypoint detection, local surface feature description, and surface matching. This paper covers an extensive literature survey of each phase of the process. It also enlists a number of popular and contemporary databases together with their relevant attributes.
Frequency of BRCA1 dysfunction in ovarian cancer.

BACKGROUND Ovarian cancer is one of the most common hereditary cancers in women. Mutations in the BRCA1 gene increase a woman's risk of ovarian cancer. Testing for BRCA1 mutations is cumbersome and impractical for large populations. Therefore, we developed an efficient strategy to detect various types of BRCA1 dysfunction and also determined the relative frequency of BRCA1 dysfunction in ovarian cancer. METHODS Tumors from 221 patients with epithelial ovarian cancer were screened for loss of heterozygosity (LOH) at the BRCA1 locus. BRCA1 complementary DNA (cDNA) and genomic DNA from all cancers with BRCA1 LOH (106 tumors) or noninformative status (15 tumors) were polymerase chain reaction (PCR) amplified and analyzed for protein truncation in a coupled transcription/translation test. When truncated BRCA1 protein was detected, the BRCA1 gene from both the tumor and a paired blood sample was sequenced. When BRCA1 expression in tumor cDNA was not detected with a protein truncation test, a methylation-specific PCR was used to determine whether the promoter region of BRCA1 was methylated and thus inactivated. All statistical tests were two-sided. RESULTS Fifty-one (23.1%) of 221 tumors had BRCA1 dysfunction, including 18 with germline mutations, 15 with somatic mutations, and 18 with monoallelic or biallelic hypermethylated promoters. By the consideration of only tumors with LOH or that were noninformative, the efficiency for detecting BRCA1 dysfunction improved to 45 (37.2%) of 121 tumors. Therefore, LOH/noninformative was a strong predictor of mutation status (Fisher's exact test, P<.001). However, this subset of tumors did not include those with BRCA1 missense mutations (estimated at six [2.7%] of 221 not detected by our method) or biallelic promoter methylation (estimated at six [2.7%] of 221). CONCLUSIONS BRCA1 dysfunction in ovarian cancer is common and occurs via multiple mechanisms. The use of LOH, rather than a family history of ovarian cancer, as a first step in a screening strategy, followed by protein truncation testing, appears to increase the chance of identifying tumors with BRCA1 dysfunction.
Stabilization of Hypoxia-inducible Factor-1α by Prostacyclin under Prolonged Hypoxia via Reducing Reactive Oxygen Species Level in Endothelial Cells*

Hypoxia-inducible factor-1 (HIF-1) takes part in the transcriptional activation of hypoxia-responsive genes. HIF-1α, a subunit of HIF-1, is rapidly degraded under normoxic conditions by the ubiquitin-proteosome system. Hypoxia up-regulates HIF-1α by inhibiting its degradation, thereby allowing it to accumulate to high levels with 3–6 h of hypoxia treatment and decreasing thereafter. In vascular tissues, prostacyclin (prostaglandin I2 (PGI2)) is a potent vasodilator and inhibitor of platelet aggregation and is known as a vasoprotective molecule. However, the role of PGI2 in HIF-1 activation has not been studied. In the present study, we investigated the effect of PGI2 on HIF-1 regulation in human umbilical vein endothelial cells under prolonged hypoxia (12 h). Augmentation of PGI2 via adenovirus-mediated gene transfer of both cyclooxygenase-1 and PGI2 synthase activated HIF-1 by stabilizing HIF-1α in cells under prolonged hypoxia or the hypoxia-normoxia transition but not under normoxia. Exogenous H2O2 abolished PGI2- and catalase-induced HIF-1α up-regulation, which suggests that degradation of HIF-1α under prolonged hypoxia is through a reactive oxygen species-dependent pathway. Moreover, PGI2 attenuated NADPH oxidase activity by suppressing Rac1 and p47phox expression under hypoxia. These data demonstrate a novel function of PGI2 in down-regulating reactive oxygen species production by attenuating NADPH oxidase activity, which stabilizes HIF-1α in human umbilical vein endothelial cells exposed to prolonged hypoxia.
Stanniocalcin 2 Is a Negative Modulator of Store-Operated Calcium Entry

ABSTRACT The regulation of cellular Ca2+ homeostasis is essential for innumerable physiological and pathological processes. Stanniocalcin 1, a secreted glycoprotein hormone originally described in fish, is a well-established endocrine regulator of gill Ca2+ uptake during hypercalcemia. While there are two mammalian Stanniocalcin homologs (STC1 and STC2), their precise molecular functions remain unknown. Notably, STC2 is a prosurvival component of the unfolded protein response. Here, we demonstrate a cell-intrinsic role for STC2 in the regulation of store-operated Ca2+ entry (SOCE). Fibroblasts cultured from Stc2 knockout mice accumulate higher levels of cytosolic Ca2+ following endoplasmic reticulum (ER) Ca2+ store depletion, specifically due to an increase in extracellular Ca2+ influx through store-operated Ca2+ channels (SOC). The knockdown of STC2 expression in a hippocampal cell line also potentiates SOCE, and the overexpression of STC2 attenuates SOCE. Moreover, STC2 interacts with the ER Ca2+ sensor STIM1, which activates SOCs following ER store depletion. These results define a novel molecular function for STC2 as a negative modulator of SOCE and provide the first direct evidence for the regulation of Ca2+ homeostasis by mammalian STC2. Furthermore, our findings implicate the modulation of SOCE through STC2 expression as one of the prosurvival measures of the unfolded protein response.
Engineering the cell wall by reducing de-methyl-esterified homogalacturonan improves saccharification of plant tissues for bioconversion

Plant cell walls represent an abundant, renewable source of biofuel and other useful products. The major bottleneck for the industrial scale-up of their conversion to simple sugars (saccharification), to be subsequently converted by microorganisms into ethanol or other products, is their recalcitrance to enzymatic saccharification. We investigated whether the structure of pectin that embeds the cellulose-hemicellulose network affects the exposure of cellulose to enzymes and consequently the process of saccharification. Reduction of de-methyl-esterified homogalacturonan (HGA) in Arabidopsis plants through the expression of a fungal polygalacturonase (PG) or an inhibitor of pectin methylesterase (PMEI) increased the efficiency of enzymatic saccharification. The improved enzymatic saccharification efficiency observed in transformed plants could also reduce the need for acid pretreatment. Similar results were obtained in PG-expressing tobacco plants and in PMEI-expressing wheat plants, indicating that reduction of de-methyl-esterified HGA may be used in crop species to facilitate the process of biomass saccharification.
Sleep and Biomarkers of Atherosclerosis in Elderly Alzheimer Caregivers and Controls

Background: Perturbed sleep might contribute to cardiovascular disease by accelerating atherosclerosis. Sleep is poor in Alzheimer caregivers who are also a group at increased cardiovascular risk. Objective: To test the hypothesis that impaired sleep relates to elevated levels of biomarkers of atherosclerosis in community-dwelling elderly and that this association would possibly be stronger in caregivers than in non-caregiving controls. Methods: We studied 97 Alzheimer caregivers and 48 non-caregiving controls (mean age 71 ± 8 years, 72% women) who underwent wrist actigraphy at their homes. Measures of objective sleep were averaged across 3 consecutive nights. The Pittsburgh Sleep Quality Index was administered by an interviewer to rate subjective sleep quality. Morning fasting blood samples were collected to determine measures of inflammation, coagulation and endothelial dysfunction. Results: There were independent associations between decreased subjective sleep quality and increased levels of fibrin D-dimer (p = 0.022, ΔR2 = 0.029) and von Willebrand factor antigen (p = 0.029, ΔR2 = 0.034) in all participants. Percent sleep (p = 0.025) and subjective sleep quality (p = 0.017) were lower in caregivers than in controls. In caregivers, the correlation between decreased percent sleep and elevated levels of interleukin-6 (p = 0.042, ΔR2 = 0.039) and C-reactive protein (p < 0.10, ΔR2 = 0.027) was significantly stronger than in controls. Conclusion: Perceived impairment in sleep related to increased coagulation activity and endothelial dysfunction in all participants, whereas objectively impaired sleep related to inflammation activity in caregivers. The findings provide one explanation for the increased cardiovascular risk in elderly poor sleepers and dementia caregivers in particular.
Phonological mediation in visual masked priming: evidence from phonotactic repair.

In a series of 4 experiments, the authors show that phonological repair mechanisms, known to operate in the auditory modality, are directly translated in the visual modality. This holds with the provision that printed stimuli are presented for a very brief duration and that the effect of phonological repair is tested after a delay of some 100 ms has elapsed after that presentation. The case of phonological repair chosen to exemplify the parallelism between print and speech is the prosthesis of /e/ in utterances beginning with /s/ followed by a consonant in Spanish. Native speakers of Spanish hear a prothetic /e/ in auditorily presented pseudowords such as special (/speojal/, derived from "especial") as well as stuto (/stuto/, derived from "astuto"). It is shown here that they also hear that same vowel /e/ when presented with the printed pseudowords "special" and "stuto. " This finding of a phonological repair effect in print has implications for the issue of phonological activation from print, as well as for the prelexical locus and mandatory nature of phonological repair mechanisms in general.
The Disability Rights Movement: From Deinstitutionalization to Self-Determination

Chapter 1 Preface Chapter 2 Acknowledgments Chapter 3 Defining and Counting Disability in a Changing World Chapter 4 A Brief History of the Disability Rights Movement Chapter 5 The Disabled as a Minority Group Chapter 6 Wave I of Deinstitutionalization- Persons with Mental Illness Chapter 7 Wave II of Deinstitutionalization- Persons with Mental Retardation Chapter 8 Early and Multiple Waves of Change for Persons with Physical Disabilities Chapter 9 The Growing Wave of Self-Determination Chapter 10 References Chapter 11 Index
Emotional modulation of the synapse

Abstract Acute stress and emotional arousal can enhance the consolidation of long-term memories in a manner that is dependent on β-adrenoceptor activation in the basolateral complex of the amygdala (BLA). The BLA interacts with multiple memory systems in the brain to modulate a variety of classes of memory. However, the synaptic mechanisms of this interaction remain unresolved. This review describes the evidence of modulation of memory and synaptic plasticity produced by emotional arousal, stress hormones, and pharmacological or electrophysiological stimulation of the amygdala. The amygdala modulation of local translation and/or degradation of the synaptic plasticity-related proteins, activity-regulated cytoskeletal-associated protein and calcium/calmodulin-dependent protein kinase IIα, is offered as a potential mechanism for the rapid memory consolidation that is associated with emotionally arousing events. This model shares features with synaptic tagging and the emotional tagging hypotheses.
Networked Flow: Towards an Understanding of Creative Networks

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Family Day Care Rating Scale

FDCRS consists of 32 items, organized under six major headings: Space and Furnishings for Care and Learning -- Basic Care -- Language and Reasoning -- Learning Activities -- Social Development -- Adult Needs. Eight additional items are included for rating a day care home's provisions for special-needs children. Each book contains one score sheet. Packages of 30 score sheets can be ordered separately.