Miracle-dz/UniFAR-FTUs huggingface dataset:
Selective Spanning with Fast Enumeration: A Near Maximum-Likelihood MIMO Detector Designed for Parallel Programmable Baseband Architectures

ML and near-ML MIMO detectors have attracted a lot of interest in recent years. However, almost all of the reported implementations are delivered in ASIC or FPGA. Our contribution is to co-optimize the near-ML MIMO detector algorithm and implementation for parallel programmable base-band architectures, such as DSPs with VLIW, SIMD or vector processing features. Although for hardware the architecture can be tuned to fit algorithms, for programmable platforms the algorithm must be elaborately designed to fit the given architecture, so that efficient resource-utilizations can be achieved. By thoroughly analyzing and exploiting the interaction between algorithms and architectures, we propose the SSFE (selective spanning with fast enumeration) as an architecture-friendly near-ML MIMO detector. The SSFE has a distributed and greedy algorithmic structure that brings a completely deterministic and regular dataflow. The SSFE has been evaluated for coded OFDM transmissions over 802.11n channels and 3GPP channels. Under the same performance constraints, the complexity of the SSFE is significantly lower than the K-Best, the most popular detector implemented in hardware. More importantly, SSFE can be easily parallelized and efficiently mapped on programmable baseband architectures. With TI TMS320C6416, the SSFE delivers 37.4 - 125.3 Mbps throughput for 4x4 64 QAM transmissions. To the best of our knowledge, this is the first reported near-ML MIMO detector explicitly designed for parallel programmable architectures and demonstrated on a real-life platform.
Photoperiodic effects on body mass, energy balance and hypothalamic gene expression in the bank vole

SUMMARY We examined the effect of increasing photoperiod, at a constant low temperature, on the body mass and energy budget of the bank vole Clethrionomys glareolus. Simultaneously, we determined the hypothalamic gene expression of neuropeptides and receptors known to be involved in short-term energy balance. Despite an increase in body mass (approximately 10% of initial mass), we found no significant changes in any energetic parameters (food intake, energy assimilation rate, resting metabolic rate and total daily energy expenditure by doubly-labelled water). Apparent energy assimilation efficiency was higher in voles exposed to long-days (LD) compared to short-days (SD). Surprisingly, gene expression of corticotrophin releasing factor (CRF; in the paraventricular nucleus), and the melanocortin-3 receptor (in the arcuate nucleus), both known to be involved in appetite suppression and elevation of energy expenditure in short-term energy balance, were higher in voles kept in LD compared to SD. CRF expression was also elevated in females compared to males. These paradoxical data suggest an alternative mechanism for the control of seasonal body mass changes compared to short-term body mass changes, and between male and female voles. Furthermore, they highlight the need for studies to perform simultaneous measurements at both the molecular and whole animal levels.
Antiphosphatidylserine/prothrombin antibodies in primary antiphospholipid syndrome

Antiprothrombin (aPT) antibodies may be detected by an enzyme-linked immunosorbent assay (ELISA) using a purified antigen or a phosphatidylserine/prothrombin complex (aPS/PT). IgG/IgM antibodies directed against aPS/PT were assessed in 158 patients with primary antiphospholipid syndrome (PAPS). They were detected in 80/158 (50.6%) PAPS patients; IgG alone was positive in 12 (7.6%), IgM alone in 36 (22.8%), and both IgG and IgM isotypes in 32 (20.2%) PAPS patients. IgG and IgM aPS/PT were significantly associated with both vascular thrombosis and pregnancy morbidity. IgG aPS/PT was significantly associated with venous thrombosis (p = 0.023), whilst IgG and IgM aPS/PT were associated with arterial thrombosis (p < 0.001 and p < 0.001, respectively). Logistic regression analysis showed that IgM and IgG aPS/PT were independent risk factors for thrombosis (odds ratio (OR) 3.5 [95% confidence interval (CI) 1.6–7.9] and OR 4.1 [95% CI 1.4–11.7], respectively) and IgM aPS/PT was an independent risk factor for arterial thrombosis (OR 2.7 [95% CI 1.1–6.7]). In conclusion, these findings indicate that aPS/PT are clinically relevant in PAPS.
Interleukin-6 Plasmatic Levels in Patients with Head Trauma and Intracerebral Hemorrhage

The exact role of inflammatory response in hemorrhagic contusions is not fully characterized. The present study quantified IL-6 plasmatic levels in patients with closed head trauma and hemorrhagic contusions during the first 6 to 12 hours postrauma. The association between the plasmatic IL-6 levels, severity of trauma according to the Glasgow Coma Scale, volume of intracerebral hemorrhage and patient's clinical evolution were investigated. Although inflammation is a multifactorial process, a strong correlation between IL-6 levels, volume of traumatic hemorrhage and in-hospital evolution could be observed. A correlation between the IL-6 levels quantified 6 hours postrauma and progression of lesion volume between admission and 12 hours postrauma is suggested. The present study reinforces the importance of IL-6 in influencing the clinical conditions of a patient with cerebral injuries, particularly hemorrhagic contusions.
Prevalence in the Usa of Rilpivirine Resistance-Associated Mutations in Clinical Samples and Effects on Phenotypic Susceptibility to Rilpivirine and Etravirine

Background The prevalence of rilpivirine resistance-associated mutations (RAMs) in the USA, and their effect on phenotypic susceptibility to rilpivirine and etravirine, was evaluated in clinical samples from HIV-1-infected patients. Methods In total, 15,991 samples submitted to Monogram Biosciences (South San Francisco, CA, USA) for routine resistance testing between January 2010 and June 2011 were assessed for the presence of known rilpivirine RAMs K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L; non-nucleoside reverse transcriptase inhibitor (NNRTI) RAMs K103N, L100I and L100I+K103N; and the nucleoside reverse transcriptase inhibitor (NRTI) RAMs M184I/V and their combinations with rilpivirine RAMs. Phenotypic susceptibility (PhenoSenseGT® assay; Monogram Biosciences) was evaluated, with reduced susceptibility defined as fold change (FC) in 50% inhibitory concentration (IC50)>2.0 for rilpivirine and FC>2.9 for etravirine. Results Of the 15,991 samples, 17% harboured ≥1 rilpivirine RAMs. The prevalence of most rilpivirine RAMs and combinations of NNRTI RAMs of interest was low (≤3%), except for Y181C (7%). Rilpivirine RAMs were often associated with reduced rilpivirine phenotypic susceptibility. Median FC values >2.0 were observed for clinical isolates with rilpivirine RAMs K101P, E138Q/R, Y181C/I/V, Y188L or M230L, and for the combination of E138K with M184I/V, and K101E with M184I. Most rilpivirine FC values >2.0 were associated with etravirine FC values >2.9 for individual rilpivirine RAMs and those combined with M184I/V. There was no relationship between the presence of K103N and rilpivirine FC. However, the L100I+K103N combination (without rilpivirine RAMs), at <2% prevalence, was associated with a rilpivirine FC>2.0. Conclusions Based on 15,991 US clinical samples from HIV-1-infected patients, the frequency of most known rilpivirine RAMs apart from Y181C was low.
The Reverse Ludloff Osteotomy for Bunionette Deformity

Background. The typical bunionette deformity often presents as pain over the lateral margin of the fifth metatarsal head. There have been numerous operative treatments described for this pathology. The purpose of this study was to evaluate the results after a reverse Ludloff osteotomy in cases of severe bunionette deformities. Methods. Between 2008 and 2012, 16 patients received a reverse Ludloff osteotomy of the fifth metatarsal due to a symptomatic type II or III bunionette that failed nonoperative treatment. We retrospectively reviewed charts, radiographic images, postoperative AOFAS (American Orthopaedic Foot and Ankle Society) lesser toe scores, and the EQ-5D at a mean of 41.9 months (range, 31-74 months) of follow-up. Additionally, limitation in activities of daily living, pain, and patient satisfaction were assessed. Results. At latest follow-up, the mean AOFAS lesser toe score was 86.6 points and the mean EQ-5D score was 14.1. Fifteen patients had no or only little limitations. Fifteen out of 16 patients were satisfied or predominantly satisfied. Radiographic analysis showed for type II deformities a correction of the lateral bowing from 8.1° down to 0.67° (P < .001). The fourth-fifth intermetatarsal angle (4-5 IMA) improved from a mean of 13.2° to a mean of 5.2° (P < .001). The length of the fifth metatarsal was unchanged (P > .05). There were no observed complications, and no revision was necessary. Conclusion. In the present study, the reverse Ludloff osteotomy had a high satisfaction rate and no complications. It provided radiographic correction of the deformity and may be considered in the surgical treatment of severe bunionette deformities. Levels of evidence: Therapeutic, Level IV: Case series
Hyporheic Source and Sink of Nitrous Oxide

Nitrous oxide (N2O) is a potent greenhouse gas with an estimated 10% of anthropogenic N2O coming from the hyporheic zone of streams and rivers. However, difficulty in making accurate fine‐scale field measurements has prevented detailed understanding of the processes of N2O production and emission at the bedform and flowline scales. Using large‐scale, replicated flume experiments that employed high‐density chemical concentration measurements, we have been able to refine the current conceptualization of N2O production, consumption, and emission from the hyporheic zone. We present a predictive model based on a Damköhler‐type transformation (τ̃) in which the hyporheic residence times (τ) along the flowlines are multiplied by the dissolved oxygen consumption rate constants for those flowlines. This model can identify which bedforms have the potential to produce and emit N2O, as well as the portion and location from which those emissions may occur. Our results indicate that flowlines with τ̃up (τ̃ as the flowline returns to the surface flow) values between 0.54 and 4.4 are likely to produce and emit N2O. Flowlines with τ̃up values of less than 0.54 will have the same N2O as the surface water and those with values greater than 4.4 will likely sink N2O (reference conditions: 17C, surface dissolved oxygen 8.5 mg/L). N2O production peaks approximately at τ̃ = 1.8. A cumulative density function of τ̃up values for all flowlines in a bedform (or multiple bedforms) can be used to estimate the portion of flowlines, and in turn the portion of the streambed, with the potential to emit N2O.
Unique and combinatorial functions of Fgf3 and Fgf8 during zebrafish forebrain development

Complex spatiotemporal expression patterns of fgf3 and fgf8 within the developing zebrafish forebrain suggest their involvement in its regionalisation and early development. These factors have unique and combinatorial roles during development of more posterior brain regions, and here we report similar findings for the developing forebrain. We show that Fgf8 and Fgf3 regulate different aspects of telencephalic development, and that Fgf3 alone is required for the expression of several telencephalic markers. Within the diencephalon, Fgf3 and Fgf8 act synergistically to pattern the ventral thalamus, and are implicated in the regulation of optic stalk formation, whereas loss of Fgf3 alone results in defects in ZLI development. Forebrain commissure formation was abnormal in the absence of either Fgf3 or Fgf8; however, most severe defects were observed in the absence of both. Defects were observed in patterning of both the midline territory, within which the commissures normally form, and neuronal populations, whose axons comprise the commissures. Analysis of embryos treated with an FGFR inhibitor suggests that continuous FGF signalling is required from gastrulation stages for normal forebrain patterning, and identifies additional requirements for FGFR activity.
A Comparison of Two Methods for Recording Entheseal Change on a Post-Medieval Urban Skeletal Collection from Aalst (Belgium)

This research compares two current methods for recording bony changes at muscle attachment sites, called entheseal changes (EC); the Mariotti method and the Coimbra method, to evaluate the concordance and comparability of results in a post‐medieval skeletal collection from Aalst, Belgium (n = 116). For both methods, the EC scores produce broadly similar patterns, are symmetrical and differ between age groups. Statistical differences between the upper and lower limb and the lower limb of males and females only occur in the Mariotti method. With careful consideration of the influence of different EC score ranges, the results from the two methods can generally be compared.
Computer‐aided diagnosis of urodynamic stress incontinence with vector‐based perineal ultrasound using neural networks

Adequately defining the anatomical and functional defects in women with stress urinary incontinence prior to surgical repair is essential. Differences in dynamic changes of the bladder neck on perineal ultrasound have been shown to be effective in differentiating between women with and those without urodynamic stress incontinence (USI). This study evaluated a system to diagnose USI with computer‐aided vector‐based perineal ultrasound.
Second messenger/signal transduction pathways in major mood disorders: moving from membrane to mechanism of action, part II: bipolar disorder

In this second of two articles on second messenger/signal transduction cascades in major mood disorders, we will review the evidence in support of intracellular dysfunction and its rectification in the etiopathogenesis and treatment of bipolar disorder (BD). The importance of these cascades is highlighted by lithium's (the gold standard in BD psychopharmacology) ability to inhibit multiple critical loci in second messenger/signal transduction cascades including protein kinase C (involved in the IP3/PIP2 pathway) and GSK-3β (canonically identified in the Wnt/Fz/Dvl/GSK-3β cascade). As a result, and like major depressive disorder (MDD), more recent pathophysiological studies and rational therapeutic targets have been directed at these and other intracellular mediators. Even in the past decade, intracellular dysfunction in numerous neuroprotective/apoptotic cascades appears important in the pathophysiology and may be a future target for pharmacological interventions of BD.
A Unified Framework for Automated 3-D Segmentation of Surface-Stained Living Cells and a Comprehensive Segmentation Evaluation

This work presents a unified framework for whole cell segmentation of surface stained living cells from 3-D data sets of fluorescent images. Every step of the process is described, image acquisition, prefiltering, ridge enhancement, cell segmentation, and a segmentation evaluation. The segmentation results from two different automated approaches for segmentation are compared to manual segmentation of the same data using a rigorous evaluation scheme. This revealed that combination of the respective cell types with the most suitable microscopy method resulted in high success rates up to 97%. The described approach permits to automatically perform a statistical analysis of various parameters from living cells.
Renal Hemodynamic Effects of Serelaxin in Patients With Chronic Heart Failure: A Randomized, Placebo-Controlled Study

Background—Serelaxin is a promising therapy for acute heart failure. The renal hemodynamic effects of serelaxin in patients with chronic heart failure are unknown. Methods and Results—In this double-blind, randomized, placebo-controlled, multicenter study, patients with New York Heart Association Class II to III chronic heart failure, left ventricular ejection fraction ⩽45%, and estimated glomerular filtration rate (GFR) 30 to 89 mL/min per 1.73 m2 received intravenous serelaxin 30 &mgr;g/kg per day or placebo for 24 hours. Primarily, we assessed the difference between serelaxin and placebo on renal plasma flow (para-aminohippuric acid clearance) and GFR (iothalamate clearance) over 8 to 24 hours. All 22 patients from 1 clinical site were excluded from primary analyses before unblinding because of implausible measurements. The primary analysis comprised 65 patients, mean age was 68 (±10) years, 89% were male, mean estimated GFR was 64 (±19) mL/min per 1.73 m2, and 34% had New York Heart Association Class III symptoms. Renal plasma flow increased by 29% with serelaxin and 14% with placebo (13% relative increase with serelaxin; P=0.0386), whereas GFR changes did not differ significantly during 8 to 24 hours. Filtration fraction increased by 36% with serelaxin and 62% with placebo (16% relative decrease with serelaxin; P=0.0019) during 8 to 24 hours. Changes in systolic blood pressure were largely similar, and creatinine clearance did not differ between groups. Adverse event rates were similar with serelaxin (20.5%) and placebo (25.0%). Conclusions—In patients with chronic heart failure, serelaxin increased renal plasma flow and reduced the increase in filtration fraction compared with placebo, but did not affect GFR. These results suggest beneficial renal hemodynamic effects in patients with chronic heart failure. Clinical Trial Registration—URL: http://www.clinicaltrials. gov. Unique identifier: NCT01546532.
The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes

Myocardial infarction (MI) elicits massive inflammatory leukocyte recruitment to the heart. Here, we hypothesized that excessive leukocyte invasion leads to heart failure and death during acute myocardial ischemia. We found that shortly and transiently after onset of ischemia, human and mouse cardiac fibroblasts produce granulocyte/macrophage colony-stimulating factor (GM-CSF) that acts locally and distally to generate and recruit inflammatory and proteolytic cells. In the heart, fibroblast-derived GM-CSF alerts its neighboring myeloid cells to attract neutrophils and monocytes. The growth factor also reaches the bone marrow, where it stimulates a distinct myeloid-biased progenitor subset. Consequently, hearts of mice deficient in either GM-CSF or its receptor recruit fewer leukocytes and function relatively well, whereas mice producing GM-CSF can succumb from left ventricular rupture, a complication mitigated by anti–GM-CSF therapy. These results identify GM-CSF as both a key contributor to the pathogenesis of MI and a potential therapeutic target, bolstering the idea that GM-CSF is a major orchestrator of the leukocyte supply chain during inflammation.
Genetic variation in APOB, PCSK9, and ANGPTL3 in carriers of pathogenic autosomal dominant hypercholesterolemic mutations with unexpected low LDL‐Cl Levels

Autosomal Dominant Hypercholesterolemia (ADH) is caused by LDLR and APOB mutations. However, genetically diagnosed ADH patients do not always exhibit the expected hypercholesterolemic phenotype. Of 4,669 genetically diagnosed ADH patients, identified through the national identification screening program for ADH, 75 patients (1.6%) had LDL‐cholesterol (LDL‐C) levels below the 50th percentile for age and gender prior to lipid‐lowering therapy. The genes encoding APOB, PCSK9, and ANGPTL3 were sequenced in these subjects to address whether monogenic dominant loss‐of‐function mutations underlie this paradoxical phenotype. APOB mutations, resulting in truncated APOB, were found in five (6.7%) probands, reducing LDL‐C by 56%. Rare variants in PCSK9, and ANGPTL3 completely correcting the hypercholesterolemic phenotype were not found. The common variants p.N902N, c.3842+82T>A, p.D2312D, and p.E4181K in APOB, and c.1863+94A>G in PCSK9 were significantly more prevalent in our cohort compared to the general European population. Interestingly, 40% of our probands carried at least one minor allele for all four common APOB variants compared to 1.5% in the general European population. While we found a low prevalence of rare variants in our cohort, our data suggest that regions in proximity of the analyzed loci, and linked to specific common haplotypes, might harbor additional variants that correct an ADH phenotype. Hum Mutat 33:448–455, 2012. © 2011 Wiley Periodicals, Inc.
A Three-Level Model for Plan Exploration

In modeling the structure of task-related discourse using plans, it is important to distinguish between plans that the agent has adopted and is pursuing and those that are only being considered and explored, since the kinds of utterances arising from a particular domain plan and the patterns of reference to domain plans and movement within the plan tree are quite different in the two cases. This paper presents a three-level discourse model that uses separate domain and exploration layers, in addition to a layer of discourse metaplans, allowing these distinct behavior patterns and the plan adoption and reconsideration moves they imply to be recognized and modeled.
Local VE-cadherin mechanotransduction triggers long-ranged remodeling of endothelial monolayers

ABSTRACT In this study, we present results demonstrating that mechanotransduction by vascular endothelial cadherin (VE-cadherin, also known as CDH5) complexes in endothelial cells triggers local cytoskeletal remodeling, and also activates global signals that alter peripheral intercellular junctions and disrupt cell–cell contacts far from the site of force application. Prior studies have documented the impact of actomyosin contractile forces on adherens junction remodeling, but the role of VE-cadherin in force sensation and its ability to influence endothelial cell and tissue mechanics globally have not been demonstrated. Using mechanical manipulation of VE-cadherin bonds and confocal imaging, we demonstrate VE-cadherin-based mechanotransduction. We then demonstrate that it requires homophilic VE-cadherin ligation, an intact actomyosin cytoskeleton, Rho-associated protein kinase 1 (ROCK1) and phosphoinositide 3-kinase. VE-cadherin-mediated mechanotransduction triggered local actin and vinculin recruitment, as well as global signals that altered focal adhesions and disrupted peripheral intercellular junctions. Confocal imaging revealed that VE-cadherin-specific changes appear to propagate across cell junctions to disrupt distant inter-endothelial junctions. These results demonstrate the central role of VE-cadherin adhesions and the actomyosin cytoskeleton within an integrated, mechanosensitive network that both induces local cytoskeletal remodeling at the site of force application and regulates the global integrity of endothelial tissues.