Miracle-dz/UniFAR-FTUs huggingface dataset:
The role of pain in pulmonary rehabilitation: a qualitative study

Introduction One third of individuals with chronic obstructive pulmonary disease (COPD) report pain. To help inform a COPD-specific pain intervention, we explored the views of health care providers (HCPs) and individuals with COPD on pain during pulmonary rehabilitation (PR). Methods This is a qualitative study using inductive thematic analysis. Eighteen HCPs familiar with PR and 19 patients enrolled in PR participated in semi-structured interviews. Demographic data were recorded, and the patients completed the Brief Pain Inventory (Short Form). Results 1) Interaction between pain and COPD: pain is a common experience in COPD, heightened by breathlessness and anxiety. 2) Pain interfering with PR: a) Communicating pain: HCPs rarely ask about pain and patients are reluctant to report it for fear of being removed from PR. b) PR is a short-term aggravator but long-term reliever: although pain limits exercise, concentration, and program adherence, PR may reduce pain by increasing muscle strength and improving coping. c) Advice and strategies for pain: some attention is given to pain management but this is often counterproductive, encouraging patients to cease exercise. 3) An intervention to manage pain: HCPs were enthusiastic about delivering a pain intervention within their knowledge and time constraints. Early group education was preferred. Conclusion A pain intervention seems warranted in PR and may improve adherence and therefore clinical benefit. A pain intervention could be provided as part of PR education with HCP training.
SDM: A Stripe-Based Data Migration Scheme to Improve the Scalability of RAID-6

In large scale data storage systems, RAID-6 has received more attention due to its capability to tolerate concurrent failures of any two disks, providing a higher level of reliability. However, a challenging issue is its scalability, or how to efficiently expand the disks. The main reason causing this problem is the typical fault tolerant scheme of most RAID-6 systems known as Maximum Distance Separable (MDS) codes, which offer data protection against disk failures with optimal storage efficiency but they are difficult to scale. To address this issue, we propose a novel Stripe-based Data Migration (SDM) scheme for large scale storage systems based on RAID-6 to achieve higher scalability. SDM is a stripe-level scheme, and the basic idea of SDM is optimizing data movements according to the future parity layout, which minimizes the overhead of data migration and parity modification. SDM scheme also provides uniform data distribution, fast data addressing and migration. We have conducted extensive mathematical analysis of applying SDM to various popular RAID-6 coding methods such as RDP, P-Code, H-Code, HDP, X-Code, and EVENODD. The results show that, compared to existing scaling approaches, SDM decreases more than 72.7% migration I/O operations and saves the migration time by up to 96.9%, which speeds up the scaling process by a factor of up to 32.
The Rous Sarcoma Virus Env Glycoprotein Contains a Highly Conserved Motif Homologous to Tyrosine-Based Endocytosis Signals and Displays an Unusual Internalization Phenotype

ABSTRACT The cytoplasmic domains of retroviral transmembrane (TM) glycoproteins contain conserved sequence motifs that resemble tyrosine-based (YXXØ-type) endocytosis signals. We have previously described a mutant Rous sarcoma virus (RSV) Env protein, Env-μ26, with an L165R mutation in the membrane-spanning domain (MSD) of TM, that exhibited dramatically decreased steady-state surface expression (G. L. Davis and E. Hunter, J. Cell Biol. 105:1191–1203, 1987; P. B. Johnston, J. Y. Dong, and E. Hunter, Virology 206:353–361, 1995). We now demonstrate that the tyrosine of the Y190RKM motif in the RSV TM cytoplasmic domain is crucial for the μ26 phenotype and is part of an efficient internalization signal in the context of a mutant MSD. In contrast, despite the presence of the Y190RKM motif, wild-type RSV Env is constitutively internalized at a slow rate (1.1%/min) more characteristic of bulk uptake during membrane turnover than of active clustering into endocytic vesicles. The μ26 mutation and two MSD mutations that abrogate palmitoylation of TM resulted in enhanced Env endocytosis indicative of active concentration into coated pits. Surprisingly, an Env-Y190A mutant was apparently excluded from coated pits since its uptake rate of 0.3%/min was significantly below that expected for the bulk rate. We suggest that in RSV Env an inherently functional endocytosis motif is silenced by a counteracting determinant in the MSD that acts to prevent clustering of Env into endocytic vesicles. Mutations in either the cytoplasmic tail or the MSD that inactivate one of the two counteracting signals would thus render the remaining determinant dominant.
On Vertex Attack Tolerance in Regular Graphs

We have previously introduced vertex attack tolerance (VAT), denoted mathematically as $\tau(G) = \min_{S \subset V} \frac{|S|}{|V-S-C_{max}(V-S)|+1}$ where $C_{max}(V-S)$ is the largest connected component in $V-S$, as an appropriate mathematical measure of resilience in the face of targeted node attacks for arbitrary degree networks. A part of the motivation for VAT was the observation that, whereas conductance, $\Phi(G)$, captures both edge based and node based resilience for regular graphs, conductance fails to capture node based resilience for heterogeneous degree distributions. We had previously demonstrated an upper bound on VAT via conductance for the case of $d$-regular graphs $G$ as follows: $\tau(G) \le d\Phi(G)$ if $\Phi(G) \le \frac{1}{d^2}$ and $\tau(G) \le d^2\Phi(G)$ otherwise. In this work, we provide a new matching lower bound: $\tau(G) \ge \frac{1}{d}\Phi(G)$. The lower and upper bound combined show that $\tau(G) = \Theta(\Phi(G))$ for regular constant degree $d$ and yield spectral bounds as corollaries.
FLOWRATE MEASUREMENT ON METAL PIPES BY AIR-COUPLED ULTRASOUND

The characteristics of the measurement capacity of air-coupled ultrasonic sensor influenced by the incident angle were investigated analytically and experimentally. The optimized incident angle between ultrasound and test pipe was determined. The air-coupled ultrasonic sensor with this determined incident angle was applied to the flowrate measurement in the aluminium pipe. The measurement results were compared to those obtained by using the electromagnetic flowmeter. Since the measurement results show good linearity, the capacity of the air-coupled ultrasonic flowmeter is revealed.
Bicarbonate and Ca2+ Sensing Modulators Activate Photoreceptor ROS-GC1 Synergistically

Photoreceptor ROS-GC1, a prototype subfamily member of the membrane guanylate cyclase family, is a central component of phototransduction. It is a single transmembrane-spanning protein, composed of modular blocks. In rods, guanylate cyclase activating proteins (GCAPs) 1 and 2 bind to its juxtamembrane domain (JMD) and the C-terminal extension, respectively, to accelerate cyclic GMP synthesis when Ca2+ levels are low. In cones, the additional expression of the Ca2+-dependent guanylate cyclase activating protein (CD-GCAP) S100B which binds to its C-terminal extension, supports acceleration of cyclic GMP synthesis at high Ca2+ levels. Independent of Ca2+, ROS-GC1 activity is also stimulated directly by bicarbonate binding to the core catalytic domain (CCD). Several enticing molecular features of this transduction system are revealed in the present study. In combination, bicarbonate and Ca2+-dependent modulators raised maximal ROS-GC activity to levels that exceeded the sum of their individual effects. The F514S mutation in ROS-GC1 that causes blindness in type 1 Leber’s congenital amaurosis (LCA) severely reduced basal ROS-GC1 activity. GCAP2 and S100B Ca2+ signaling modes remained functional, while the GCAP1-modulated mode was diminished. Bicarbonate nearly restored basal activity as well as GCAP2- and S100B-stimulated activities of the F514S mutant to normal levels but could not resurrect GCAP1 stimulation. We conclude that GCAP1 and GCAP2 forge distinct pathways through domain-specific modules of ROS-GC1 whereas the S100B and GCAP2 pathways may overlap. The synergistic interlinking of bicarbonate to GCAPs- and S100B-modulated pathways intensifies and tunes the dependence of cyclic GMP synthesis on intracellular Ca2+. Our study challenges the recently proposed GCAP1 and GCAP2 “overlapping” phototransduction model (Peshenko et al., 2015b).
The Anatomy of Physician Payments: Contracting Subject to Complexity

Why do private insurers closely link their physician payment rates to the Medicare fee schedule despite its well-known limitations? We ask to what extent this relationship reflects the use of Medicare's relative price menu as a benchmark, in order to reduce transaction costs in a complex pricing environment. We analyze 91 million claims from a large private insurer, which represent $7.8 billion in spending over four years. We estimate that 75 percent of services, accounting for 55 percent of spending, are benchmarked to Medicare's relative prices. The Medicare-benchmarked share is higher for services provided by small physician groups. It is lower for capital-intensive treatment categories, for which Medicare's average-cost reimbursements deviate most from marginal cost. When the insurer deviates from Medicare's relative prices, it adjusts towards the marginal costs of treatment. Our results suggest that providers and private insurers coordinate around Medicare's menu of relative payments for simplicity, but innovate when the value of doing so is likely highest.
Influence of processing routes on the morphology and properties of polymer/nanofibrillated cellulose composites

The morphology of polymer/nanofibrillated cellulose (NFC) composite sheets produced using different techniques and its influence on low strain stiffness were assessed by optical and transmission electron microscopy. Solvent processing led to relatively homogeneous NFC dispersions and significant reinforcement of the in-plane Young's modulus. The continuous cellular networks obtained by wet-comingling of PLA powder or latex with NFC also provided efficient and essentially scale-independent reinforcement, in spite of the extensive agglomeration of the NFC. However, the irreversible nature of these networks is incompatible with low pressure thermoplastic processing routes such as physical foaming, and while they may be broken up by e.g. extrusion, this led to substantial loss in reinforcement, particularly above Tg, consistent with the observation of isolated low aspect ratio NFC aggregates in the extruded specimens.
Effect of Dietary Exogenous Enzyme Supplementation on Enteric Mucosal Morphological Development and Adherent Mucin Thickness in Turkeys

Anti-nutritional factors (ANFs) in feed ingredients can challenge gut health and reduce nutrient utilization. Birds typically activate their innate immune system as a protective response against the adverse effects of ANF, which often involves the secretion of mucin. Although dietary supplementation of exogenous enzymes are commonly used to alleviate the adverse effects of ANF on apparent nutrient digestibility, little is known about how they affect gut health, particularly in relation to the morphological development and mucin secretion of enteric mucosa. We carried out two trials to examine the effect of dietary supplementation of different types of exogenous enzymes on gut health of by accessing the effect of jejunum morphological development and ileal enteric adherent mucin thickness layer in turkeys. Dietary β-mannanase supplementation reduced ileal adherent mucin thickness layer (804 vs 823 μg/g; p < 0.05), while a commercial blend of xylanase, amylase, and protease (XAP) reduced ileal adherent mucin layer thickness (589 vs 740 μg/g; p < 0.05); thus reducing the apparent endogenous loss of nutrients. Both enzyme supplements also affected gut morphological characteristics. In comparison to the control treatment, dietary β-mannanase supplementation improved the jejunum tip width (219 vs 161; p < 0.05), base width (367 vs 300; p < 0.05), surface area (509,870 vs 380, 157; p < 0.05) and villi height/crypt depth ratio (7.49 vs 5.70; p < 0.05), and XAP improved the crypt depth (p < 0.05). In conclusion, dietary supplementation of exogenous enzymes may help alleviate the adverse effects of ANF on nutrient utilization by directly or indirectly removing the mucosal irritation that stimulates enteric mucin secretion.
Empirical analysis of generalization and learning in XCS with gradient descent

We analyze generalization and learning in XCS with gradient descent. At first, we show that the addition of gradient in XCS may slow down learning because it indirectly decreases the learning rate. However, in contrast to what was suggested elsewhere, gradient descent has no effect on the achieved generalization. We also show that when gradient descent is combined with roulette wheel selection, which is known to be sensitive to small values of the learning rate, the learning speed can slow down dramatically. Previous results reported no difference in the performance of XCS with gradient descent when roulette wheel selection or tournament selection were used. In contrast, we suggest that gradient descent should always be combined with tournament selection, which is not sensitive to the value of the learning rate. When gradient descent is used in combination with tournament selection, the results show that (i) the slowdown in learning is limited and (ii) the generalization capabilities of XCS are not affected.
Regulation of fucosyltransferase‐VII expression in peripheral lymph node high endothelial venules

Binding of L‐selectin to the highly glycosylated peripheral lymph node addressins (PNAd) plays a central role in the normal recirculation of lymphocytes between the bloodstream and the lymph node. This interaction requires correct fucosylation of the PNAd, mediated by the recently identified fucosyltransferase‐VII (Fuc‐TVII). Here we show that during ontogeny Fuc‐TVII is absent at the day of birth, barely detectable on day 1, and clearly present from day 2 onwards. PNAd expression as detected by the MECA‐79 antibody precedes the expression of Fuc‐TVII. Furthermore, we demonstrate that in adult mice antigenic stimulation of peripheral lymph nodes leads to a temporary disappearance of Fuc‐TVII at days 2 and 3 after stimulation, followed by a complete reappearance by day 4, while expression of MECA‐79 is never completely absent during this period. Finally, occlusion of afferent lymphatics to peripheral lymph nodes resulted in a decreased expression of Fuc‐TVII in the high endothelial venules by day 5, and complete disappearance within 8 days. We conclude that the activity of Fuc‐TVII in cells of high endothelial venules is directly affected by afferent lymph and activation processes that occur in the lymph node after antigenic stimulation. The expression of Fuc‐TVII is therefore yet another level at which the function of high endothelial venules, and thus lymphocyte trafficking, can be regulated.
Loss of Both ABCA 1 and ABCG 1 Results in Increased Disturbances in Islet Sterol Homeostasis , In fl ammation , and Impaired b-Cell Function

Cellular cholesterol homeostasis is important for normal b-cell function. Disruption of cholesterol transport by decreased function of the ATP-binding cassette (ABC) transporter ABCA1 results in impaired insulin secretion. Mice lacking b-cell ABCA1 have increased islet expression of ABCG1, another cholesterol transporter implicated in b-cell function. To determine whether ABCA1 and ABCG1 have complementary roles in b-cells, mice lacking ABCG1 and b-cell ABCA1 were generated and glucose tolerance, islet sterol levels, and b-cell function were assessed. Lack of both ABCG1 and b-cell ABCA1 resulted in increased fasting glucose levels and a greater impairment in glucose tolerance compared with either ABCG1 deletion or loss of ABCA1 in b-cells alone. In addition, glucose-stimulated insulin secretion was decreased and sterol accumulation increased in islets lacking both transporters compared with those isolated from knockout mice with each gene alone. Combined deficiency of ABCA1 and ABCG1 also resulted in significant islet inflammation as indicated by increased expression of interleukin-1b and macrophage infiltration. Thus, lack of both ABCA1 and ABCG1 induces greater defects in b-cell function than deficiency of either transporter individually. These data suggest that ABCA1 and ABCG1 each make complimentary and important contributions to b-cell function by maintaining islet cholesterol homeostasis in vivo.
Variability in human sensitivity to 1,3-butadiene: influence of polymorphisms in the 5'-flanking region of the microsomal epoxide hydrolase gene (EPHX1).

The carcinogenic effects of 1,3-butadiene (BD), a mutagenic chemical widely used in the manufacture of synthetic rubber, are likely initiated through its epoxide metabolites. In humans, these epoxides are detoxified predominantly by hydrolysis, a reaction mediated by the microsomal epoxide hydrolase (mEH; EPHX1) enzyme. It appears reasonable to hypothesize that BD-exposed individuals possessing lower mEH detoxification capacity may have elevated risk of adverse health effects. The interindividual levels of mEH enzymatic activity vary considerably, and polymorphisms in the mEH gene may contribute to this variability. In addition to the well-studied coding region polymorphisms encoding Tyr113His and His139Arg substitutions, seven other polymorphic sites in the 5'-flanking region of the mEH gene have been reported. These polymorphisms appear to differentially affect mEH gene transcriptional activities. The 5'-flanking region polymorphisms exist in two linkages, the -200 linkage (-200C/T, -259C/T, -290T/G) and the -600 linkage (-362A/G, -613T/C, -699T/C), whereas the -399T/C polymorphism exists as an independent site. Because these polymorphisms may affect total mEH enzymatic activity, we hypothesized that they influence the mutagenic response associated with occupational exposure to BD. We genotyped the 5'-region of the mEH gene in 49 non-smoking workers from two styrene-butadiene rubber facilities in southeast Texas and evaluated the linkage patterns against results obtained from an autoradiographic HPRT mutant lymphocyte assay, used as a biomarker of genotoxic effect. In the study population, 67% were exposed to low BD levels, <150 parts per billion, and 33% were exposed to >150 ppb. We used the observed HPRT mutant (variant) frequency (VF) in the studied population and a 4-way first-order interaction statistical model to estimate parameters that describe the influence of exposure, genotypes and the interaction between the two on the HPRT VF in the target population. The background (baseline) VF, defined as the VF (x 10(-6)) +/- S.E. M. at low levels of BD exposure (<150 ppb) where all the genotypes under study are homozygous wild-type, was estimated to be 4.02 +/- 1.32. Exposure to >150 ppb of BD alone resulted in an estimated increase in VF of 3.42 +/- 2.47 above the baseline level. Inheritance of the variant ATT allele in the -600 linkages resulted in an estimated increase in VF of 3.39 +/- 1.67 above the baseline level. When the interaction between BD exposure and the ATT allele in the -600 linkage group was considered, a statistically significant positive interaction was observed, with an estimated increase in the VF of 10.89 +/- 2.16 (95% CI = 6.56-15.20; p = 0.0027) above baseline. These new data confirm and extend our previous findings that sensitivity to the genotoxic effects of BD is inversely correlated with predicted mEH activity.
The influence of prematurity and low birthweight on transplacental antibody transfer in Sri Lanka.

The influence of gestational age, the neonate's birthweight, and maternal age, weight, height and parity on transplacental antibody transfer was assessed in 141 mothers from Sri Lanka and their neonates. Paired blood samples were collected from the mothers and the umbilical cords of the newborns. The sera separated from these samples were categorized as: preterm but adequate birthweight (< 37 weeks' gestation and birthweight > or = 2500 g); term but low birthweight (> or = 37 weeks' gestation and birthweight < 2500 g); or term and adequate birthweight (> or = 37 weeks' gestation and birthweight > or = 2500 g). Neonatal and maternal sera were assessed, in ELISA, for specific IgG antibodies against measles virus (MeV), herpes simplex virus type-1 (HSV1), respiratory syncytial virus (RSV), varicella-zoster virus (VZV), tetanus toxoid (TT), diphtheria toxoid (DT), and Streptococcus pneumoniae (Pn) and Haemophilus influenzae type-b (Hib) capsular antigens. Placental antibody transfer to certain antibody specificities was significantly lower in preterm neonates than term neonates. Thus the ratios between geometric mean cord antibody levels and geometric mean maternal antibody levels (the antibody-transfer ratios) were lower in preterm sera than term sera, for MeV (1.51 v. 2.03; P = 0.03), HSV1 (1.29 v. 1.76; P = 0.04), VZV (0.96 v. 2.50; P = 0.01), TT (1.13 v. 1.33; P = 0.04), DT (1.03 v. 2.39; P = 0.02), Pn (0.68 v. 0.98; P = 0.01) and Hib (0.58 v. 0.98; P = 0.00). Geometric mean levels of antibody to MeV, VZV, TT, DT and Pn were also significantly lower in preterm neonates than term. Compared with the values for 'adequate-birthweight' sera, low birthweight was independently associated with significantly lower levels of antibody transfer, for MeV (with antibody-transfer ratios of 1.51 v. 2.03; P = 0.02), VZV (0.99 v. 2.50; P = 0.03), TT (1.01 v. 1.33; P = 0.04) and DT (1.16 v. 2.39; P = 0.04) and significantly lower levels of antibodies to MeV, HSV1, VZV, TT, DT and Pn in the neonates. Maternal age, weight, height and parity had no independent influence on placental IgG transfer for antibodies to any of the pathogens investigated. These results demonstrate that prematurity and low birthweight may influence the level of maternally acquired immunity in Sri Lankan neonates.
Antithrombotic pretreatment increases very-early mortality in primary intracerebral hemorrhage

Objective: To analyze the effect of previous antiplatelet (AP) and vitamin K antagonist (VKA) treatments on outcome in patients with primary intracerebral hemorrhage (ICH). Methods: In this prospective observational study, we analyzed 529 patients according to antithrombotic pretreatment: none, AP, or VKA. Very-early (24-hour) death, 3-month mortality, and functional independence were analyzed. Results: Of 236 (44.6%) pretreated patients, 147 (27.8%) patients were taking AP and 89 (16.8%) VKA. Very-early death was observed in 13.4% and was increased in pretreated patients: 19.0% for AP and 27.0% for VKA treatment, compared to 6.5% in non-pretreated patients, p < 0.0001. Three-month mortality was 40.8% overall (49.7% for AP pretreated, 58.4% for VKA pretreated, and 31.1% for non-pretreated patients, p < 0.0001). The adjusted odds of very-early and 3-month mortality were 2.55 (p = 0.004) and 1.56 (p = 0.046) for AP-pretreated patients and 4.24 (p < 0.0001) and 2.34 (p = 0.01) for VKA-pretreated patients, respectively, compared with non-pretreated patients. The effect of antithrombotic pretreatment on mortality from 24 hours to 3 months was nonsignificant. At 3-month follow-up, 28.5% of patients remained functionally independent: 22.4% of AP-pretreated, 15.7% of VKA-pretreated, and 35.5% of non-pretreated patients (p < 0.0001). Conclusions: A high percentage of patients with ICH preventively treated with VKA or AP died during the first 24 hours after admission. Both treatments were predictors of very-early mortality. The final effect of antithrombotics on 3-month mortality remains significant through its strong effect on very-early mortality. Safety concerns about starting chronic antithrombotic treatment should be considered not only when VKA treatment is planned but also for AP treatment.