Miracle-dz/UniFAR-FTUs huggingface dataset:
Mobility of wheelchair users: a proposed performance assessment framework

Purpose : Few standardized outcome measures used in the clinical assessment of wheelchair user performance assess or document all the factors that influence mobility. This article presents a conceptual framework that suggests a more all-encompassing view of wheelchair mobility performance assessment. Method : After determining, through a survey of the literature, which factors influence wheelchair mobility, a conceptual framework was proposed. Outcome measures of wheelchair mobility were then surveyed. An analysis of these assessment tools allowed factors to be determined that were considered in the clinical assessment of wheelchair mobility performance. A comparison of these led to observations being drawn, which could allow the development of a valid and reliable standardized outcome measure to be used in clinics. Results and Conclusion : Future improvements to the clinical assessment of wheelchair mobility performance should focus on developing an assessment tool considering all categories of factors influencing wheelchair mobility. These categories are the user's profile, the wheelchair, the environment, the daily activities and social roles and the assessment and training received. A controlled-environment outcome measure using a standardized obstacle course with fundamental situations would allow rehabilitation therapists to evaluate clients for the selection of a wheelchair and to document their progress during training. This tool should make it possible to extrapolate the results and thereby apply them to daily activities and social roles.
The rise of regulation in the NHS

The current British government has created five national agencies to regulate the NHS. These new arrivals are simply additions to an already crowded regulatory landscape. But, if politicians can be persuaded to let go, the new regulators of the NHS could provide a genuinely new approach to improving performance and management During the past four years the British government has created five new national agencies to regulate the NHS in England (box). 1 2 3 4 The government has moved away from using markets, competition, and contracting to manage performance in the NHS. But it has been unwilling to rely on traditional bureaucratic structures to exert control, and has turned increasingly to regulation. In this article, I describe how and why organisational regulation in the NHS in England has grown in recent years. I examine how regulation was used in the NHS in the past and describe the characteristics of the new regulatory agencies. Finally, I use information from the wider literature on regulation to examine the regulatory model adopted by these new agencies and to explore what they might learn from regulation in other settings. #### Summary points Over the past 20 years, regulation has increased in Britain's private and public sectors In the past four years the British government has created five new national agencies to regulate the NHS The new agencies could be the start of a new approach to improving performance and management in the NHS The new agencies could learn from regulators in other sectors and adopt a responsive approach to regulation #### New national agencies to regulate the NHS National Institute for Clinical Excellence Commission for Health Improvement Modernisation Agency National Patient Safety Agency National Clinical Assessment Authority Regulation is “sustained and focused control exercised by a public agency over activities which are valued by a community. ”5 The key features of regulation are that …
Uniquely human evolution of sialic acid genetics and biology

Darwinian evolution of humans from our common ancestors with nonhuman primates involved many gene–environment interactions at the population level, and the resulting human-specific genetic changes must contribute to the “Human Condition. ” Recent data indicate that the biology of sialic acids (which directly involves less than 60 genes) shows more than 10 uniquely human genetic changes in comparison with our closest evolutionary relatives. Known outcomes are tissue-specific changes in abundant cell-surface glycans, changes in specificity and/or expression of multiple proteins that recognize these glycans, and novel pathogen regimes. Specific events include Alu-mediated inactivation of the CMAH gene, resulting in loss of synthesis of the Sia N-glycolylneuraminic acid (Neu5Gc) and increase in expression of the precursor N-acetylneuraminic acid (Neu5Ac); increased expression of α2–6-linked Sias (likely because of changed expression of ST6GALI); and multiple changes in SIGLEC genes encoding Sia-recognizing Ig-like lectins (Siglecs). The last includes binding specificity changes (in Siglecs -5, -7, -9, -11, and -12); expression pattern changes (in Siglecs -1, -5, -6, and -11); gene conversion (SIGLEC11); and deletion or pseudogenization (SIGLEC13, SIGLEC14, and SIGLEC16). A nongenetic outcome of the CMAH mutation is human metabolic incorporation of foreign dietary Neu5Gc, in the face of circulating anti-Neu5Gc antibodies, generating a novel “xeno-auto-antigen” situation. Taken together, these data suggest that both the genes associated with Sia biology and the related impacts of the environment comprise a relative “hot spot” of genetic and physiological changes in human evolution, with implications for uniquely human features both in health and disease.
Mucin‐like glycoproteins in the equine embryonic capsule

The equine embryonic capsule replaces the zona pellucida and envelops the conceptus during the second and third weeks of pregnancy. Although this capsule was described more than 100 years ago, its molecular structure has not been characterized. Here we present evidence that the glycoprotein(s) of the equine capsule resembles those of the mucin glycoprotein family. The resistance of the capsule to chemical and enzymatic solubilization was confirmed, and, as in mucins, protein constituted only 35–40% of its total dry mass. Determination of the sugar composition of the capsule using colorimetric assays and high‐performance anion‐exchange chromatography also showed it to have mucin‐like characteristics. Gal, GalNAc, sulfated sugars, and sialic acid make up a high proportion of the capsular carbohydrate, while GlcNAc, Glc, and Man are minor components. These findings were verified using lectin histochemical staining of frozen sections of conceptuses. The results of amino acid analysis were also consistent with the proposal that the capsular glycoproteins belong to the mucin family. Removal of the covalently bound carbohydrate by b̃‐elimination under reducing conditions demonstrated that the capsule is O‐glycosylated mainly on threonine residues. Affinity chromatography on jacalin‐agarose confirmed that, like mucins, the capsular glycoproteins are heavily O‐glycosylated. SDS‐PAGE analysis revealed a prominent 21‐kDa band, specific to the capsule, in preparations solubilized by trypsin but not by other proteases. Characterization of its constituent glycoprotein(s) should be helpful in elucidating the role of the capsule (and analogous blastocyst coverings in other species) during early pregnancy. © 1993 Wiley‐Liss, Inc.
Side effects of radiation therapy.

It has been described as a feeling of exhaustion, feeling completely worn out, feeling that the body is "heavy" and difficult to move, or an inability to concentrate. Fatigue can cause physical, emotional, and mental exhaustion. This fatigue is not caused by overactivity and is not usually relieved by rest, yet many people will suggest rest as a way to decrease the fatigue. Fatigue is the most common acute side effect of radiation therapy. It is believed to be caused by the tremendous amount of energy that is used by the body to heal itself in response to radiation therapy. Most people begin to feel fatigued about 2 weeks after radiation treatments begin. The tired feeling goes away gradually after the treatment is finished. Normal levels of energy generally return a few weeks after completing treatment, but can take as long as a year, particularly if you received chemotherapy as well. For more information on fatigue, go to Side Effect: Fatigue.
Complex zeros of two incomplete Riemann zeta functions

The computation of the complex zeros of an incomplete Riemann zeta function defined in an earlier paper is extended and new zero trajectories are given. A second in- complete Riemann zeta function is denned and its zero trajectories are investigated numer- ically as functions of the upper limit X of the definition integral. It becomes apparent that there exist three different classes of zero trajectories for this function, distinguished by their behaviour for X —► . were presented, X > 0 being a real parameter. These results were obtained by a systematic numerical investigation. It became apparent that not all, but only some, of the zero trajectories s(X), defined in the s-plane by A(s(\), X) = 0, reach a zero of the Riemann zeta function on the line °°. The remaining curves j(X) approach the zero trajectories s(X) of the incomplete gamma function P(s, X), which are denned by r°(s(X), X) = 0. It is the aim of this paper to present further solutions s(X) which again have been obtained by numerical calculation. Because of the fact that there exists the relation
Hepatitis C virus escape from the interferon regulatory factor 3 pathway by a passive and active evasion strategy

Hepatitis C virus (HCV) has been known to replicate with extremely varying efficiencies in different host cells, even within different populations of a single human hepatoma cell line, termed Huh‐7. Several reports have implicated the retinoic‐acid inducible gene I (RIG‐I)/ interferon regulatory factor 3 (IRF‐3) pathway of the innate antiviral response with differences in host cell permissiveness to HCV. To investigate the general impact of the IRF‐3 response onto HCV replication in cell culture, we generated an ample array of stable Huh‐7 cell lines with altered IRF‐3 responsiveness. Neither blocking IRF‐3 activation in various host cells by expression of dominant negative RIG‐I or HCV NS3/4A protease nor reconstitution of RIG‐I signaling in Huh7.5, a cell clone known to be defective in this pathway, had any impact on HCV replication. Only by overexpressing constitutively active RIG‐I or the signaling adaptor Cardif (also known as interferon‐beta promoter stimulator 1, mitochondrial anti‐viral signaling protein, or virus‐induced signaling adaptor), both leading to a stimulation of the IRF‐3 pathway in the absence of inducers, was HCV replication significantly inhibited. We therefore assessed the extent of RIG‐I– dependent IRF‐3 activation by different species of RNA, including full‐length HCV genomes and HCV RNA duplexes, and observed strong induction only in response to double‐stranded RNAs. Conclusion: Based on these findings, we propose a refined model of innate immune escape by HCV involving limited initial induction and stringent subsequent control of the IRF‐3 response. (HEPATOLOGY 2007.)
Executive functioning in childhood epilepsy: parent‐report and cognitive assessment

There is considerable interest in the assessment of executive function (EF) in pediatric clinical populations but only a few well‐standardized measures exist. We examined EF in 53 children aged 8 to 18 years with recent onset epilepsy (31 males, 22 females) and 50 control children (23 males, 27 females) using the Behavior Rating Inventory of Executive Function (BRIEF) and the Delis‐Kaplan Executive Function System (D‐KEFS). Thirty children had localization‐related epilepsy and 23 had idiopathic generalized epilepsy; average duration of 10 months (SD 4y 1mo) and onset age of 11 years 6 months (SD 3y 6mo). The study sample was characterized by good seizure control, with 40 participants taking one antiepileptic drug (AED), one taking two AEDs, and 12 not treated pharmacologically. Children with epilepsy showed greater executive difficulties on both measures than children in the control group. The BRIEF and D‐KEFS were significantly correlated, and an ‘at‐risk’ group identified from the BRIEF was more significantly impaired on the D‐KEFS than a ‘low risk’ group. The BRIEF was also a better predictor of performance on the D‐KEFS than the Child Behavior Checklist. These findings indicate that children with recent onset epilepsy show significant difficulties in E F, and demonstrate the utility of parent ratings (BRIEF) in the assessment of EF.
Reticular dystrophy of the retinal pigment epithelium. A clinical and electrophysiologic study of three generations.

Reticular dystrophy of the retinal pigment epithelium is characterized by a posterior pattern of pigment clumping like a "fishnet with knots. " Four patients in three successive generations were seen with typical reticular dystrophy. A fifth patient had abnormal dark adaptation. In this family reticular dystrophy was characterized by the typical reticular pigmentary pattern, good visual acuity, normal electroretinographic findings, abnormal electro-oculographic findings, and abnormal dark adaptation. The pedigree indicates autosomal dominance as the inheritance pattern.
WETTABILITY OF STEAM-WATER-ROCK SYSTEMS

A method has been developed to infer the wettability of steam-water-rock systems based on the relationship between permeability and capillary pressure by Purcell. The Purcell model was extended to two-phase flow to verify whether the wettability is a function of water saturation. The results calculated using the experimental data showed that the wettability index in drainage was greater than that in imbibition. The corresponding contact angle in drainage was smaller than that in imbibition, which is realistic and consistent with the existing experimental results. Both the receding (drainage) and advancing (imbibition) contact angles in steam-water-rock systems were reasonably independent of water saturation ranging from about 25 to 85%. It was also found that the wettability model could be reduced to the model reported by Slobod and Blum (1952) in specific cases. The method developed in this study to estimate wettability of steam-water-rock systems could be applied directly to other gas-liquid-rock and liquid-liquidrock systems.
Effects of Neoadjuvant Chemotherapy on Hepatoblastoma: A Morphologic and Immunohistochemical Study

Neoadjuvant chemotherapy followed by resection has become the mainstay in the treatment of hepatoblastoma (HB). The changes after chemotherapy typically result in tumor necrosis and a fibrohistiocytic response. We have observed that treated HBs undergo additional morphologic changes that have not been described. Herein, we report a 15-year retrospective study of HBs in 22 children who received neoadjuvant chemotherapy according to the Children's Oncology Group protocols. The medical records, diagnostic imaging, and histopathology were reviewed. Besides treated HBs having characteristic necrosis and fibrohistiocytic response, two-thirds had areas of cytoarchitectural differentiation (“maturation”) mimicking non-neoplastic liver, and a quarter had alterations mimicking hepatocellular carcinoma. Nuclear expression of β-catenin and keratin profiles were useful in distinguishing residual tumor with “maturation” from non-neoplastic liver and therefore in the assessment of surgical margins. Statistical analysis revealed that larger pretreatment and posttreatment imaged tumor size, larger tumor size at pathologic examination, and vascular invasion were significant univariate predictors of metastatic disease, whereas pretreatment imaged tumor size and vascular invasion were also significant independent predictors (multivariate logistic regression analysis). Multifocality, greater posttreatment necrosis and hepatocellular carcinoma-like morphology were more often associated with metastatic disease, but did not reach statistical significance.
The dermal microenvironment induces the expression of the alternative activation marker CD301/mMGL in mononuclear phagocytes, independent of IL‐4/IL‐13 signaling

Recently, we have shown that mononuclear phagocytes comprise the majority of interstitial cells in the mouse dermis, as indicated by their phenotypic and functional characteristics. In particular, these cells express the mouse macrophage galactose‐/N‐acetylgalactosamine‐specificlectin (mMGL)/CD301, identified by the monoclonal antibody ER‐MP23, as well as other macrophage markers. As expression of mMGL is induced by IL‐4 or IL‐13 and is therefore a marker of alternatively activated macrophages, we asked whether dermal mononuclear phagocytes are genuinely alternatively activated. We observed that these cells expressed, next to mMGL, two other alternative activation markers, namely, the mannose receptor/CD206 and Dectin‐1. Yet, as this expression profile was similar in IL‐4 receptor α knockout mice, neither IL‐4 nor IL‐13 signaling appeared to be required for this phenotype. We also found that Langerhans cells (LC), which showed only a low level of mMGL in the epidermis, up‐regulated mMGL expression upon migration through the dermis, allowing these cells to internalize limited amounts of mMGL ligands. LC isolated from epidermal preparations did not show this up‐regulation when cultured in standard medium, but whole skin‐conditioned medium did stimulate mMGL expression by LC. The vast majority of mMGL molecules was present in the cytoplasm, however. LC, which arrived in skin‐draining lymph nodes, quickly down‐regulated mMGL expression, and dermally derived cells retained significant mMGL levels. Taken together, these data suggest that the dermal microenvironment induces mononuclear phagocyte subpopulations to express mMGL and possibly other markers of alternatively activated macrophages, independent of IL‐4/IL‐13 signaling.
CcpA-Dependent Carbohydrate Catabolite Repression Regulates Galactose Metabolism in Streptococcus oligofermentans

ABSTRACT Streptococcus oligofermentans is an oral commensal that inhibits the growth of the caries pathogen Streptococcus mutans by producing copious amounts of H2O2 and that grows faster than S. mutans on galactose. In this study, we identified a novel eight-gene galactose (gal) operon in S. oligofermentans that was comprised of lacABCD, lacX, and three genes encoding a galactose-specific transporter. Disruption of lacA caused more growth reduction on galactose than mutation of galK, a gene in the Leloir pathway, indicating that the principal role of this operon is in galactose metabolism. Diauxic growth was observed in cultures containing glucose and galactose, and a luciferase reporter fusion to the putative gal promoter demonstrated 12-fold repression of the operon expression by glucose but was induced by galactose, suggesting a carbon catabolite repression (CCR) control in galactose utilization. Interestingly, none of the single-gene mutations in the well-known CCR regulators ccpA and manL affected diauxic growth, although the operon expression was upregulated in these mutants in glucose. A double mutation of ccpA and manL eliminated glucose repression of galactose utilization, suggesting that these genes have parallel functions in regulating gal operon expression and mediating CCR. Electrophoretic mobility shift assays demonstrated binding of CcpA to the putative catabolite response element motif in the promoter regions of the gal operon and manL, suggesting that CcpA regulates CCR through direct regulation of the transcription of the gal operon and manL. This provides the first example of oral streptococci using two parallel CcpA-dependent CCR pathways in controlling carbohydrate metabolism.
Quercetin-3-rutinoside Inhibits Protein Disulfide Isomerase by Binding to Its b′x Domain*

Background: Quercetin-3-rutinoside is an inhibitor of protein disulfide isomerase, a potential target for antithrombotic therapy. Results: Quercetin-3-rutinoside induces a compact conformation in PDI and binds to PDI with an IC50 of about 10 μm. Conclusion: Quercetin-3-rutinoside interacts with the b′x domain of protein disulfide isomerase with a 1:1 stoichiometry. Significance: The b′x domain reverses the antithrombotic properties of quercetin-3-rutinoside in a thrombosis model in a live mouse. Quercetin-3-rutinoside inhibits thrombus formation in a mouse model by inhibiting extracellular protein disulfide isomerase (PDI), an enzyme required for platelet thrombus formation and fibrin generation. Prior studies have identified PDI as a potential target for novel antithrombotic agents. Using a fluorescence enhancement-based assay and isothermal calorimetry, we show that quercetin-3-rutinoside directly binds to the b′ domain of PDI with a 1:1 stoichiometry. The binding of quercetin-3-rutinoside to PDI induces a more compact conformation and restricts the conformational flexibility of PDI, as revealed by small angle x-ray scattering. The binding sites of quercetin-3-rutinoside to PDI were determined by studying its interaction with isolated fragments of PDI. Quercetin-3-rutinoside binds to the b′x domain of PDI. The infusion of the b′x fragment of PDI rescued thrombus formation that was inhibited by quercetin-3-rutinoside in a mouse thrombosis model. This b′x fragment does not possess reductase activity and, in the absence of quercetin-3-rutinoside, does not affect thrombus formation in vivo. The isolated b′ domain of PDI has potential as an antidote to reverse the antithrombotic effect of quercetin-3-rutinoside by binding and neutralizing quercetin-3-rutinoside.
Variation in the tumor necrosis factor-alpha gene promoter region may be associated with death from meningococcal disease.

Tumor necrosis factor-alpha (TNF-alpha) plays a central role in the pathophysiology of sepsis. Levels of TNF-alpha are directly correlated with severity in meningococcal disease (MD). A polymorphism in the promoter region of the TNF-alpha gene is associated with differences in the secretion of TNF-alpha. The TNF2 allele is associated with higher constitutive and inducible levels of TNF-alpha secretion than is the TNF1 allele. To investigate whether possession of the TNF2 allele is associated with severity in MD, the frequency of TNF1 and TNF2 alleles in 98 children with MD was compared. There were more deaths among children who had the TNF2 allele (P = .03; relative risk [RR], 2.5; 95% confidence interval [CI], 1.1-5.7) than in those who did not. There was also an increased risk of severe disease in children with the TNF2 allele (P = .02; RR, 1.6; 95% CI, 1.1-2.3). Possession of the TNF2 allele predisposes to a worse outcome in children with meningococcal infection.
The Benefits of Consumer-Directed Services for Caregivers of Persons with Alzheimer's Disease

Because a substantial portion of care provided to persons with Alzheimer's disease comes from families, it is beneficial to understand what services are most useful to caregivers in supporting a family member in the community. This article summarizes a project designed to explore the benefits of consumer-directed services, in which 112 caregivers were randomly assigned to a treatment or control group at intake. Results suggest that caregivers who take a consumer-directed (self-determined) path have a greater likelihood of extending their caregiving role than those who have access to traditional aging services only. Encouraging consumer-directed behavior is discussed as an avenue for social service providers to pursue when supporting caregivers and care receivers in remaining in the community.