Miracle-dz/UniFAR-FTUs huggingface dataset:
Een meetinstrument voor individuele verschillen in sociale dominantie oriëntatie

Het concept Sociale Dominantie Oriëntatie (SDO) wordt gedefinieerd als een algemene opvatting over intergroepsrelaties die aangeeft in welke mate iemand verkiest dat deze relaties egalitair dan wel hierarchisch gestructureerd zijn (Pratto, Sidanius, Stallworth & Malle, 1994). Dit concept reflecteert dus de mate waarin iemand ertoe neigt maatschappelijke groepen te klasseren op de dimensie superieur-inferieur, alsook de mate waarin iemand een beleid huldigt dat sociale ongelijkheid in stand houdt. Hoewel de motivatie om anderen te domineren aanvankelijk werd aanzien als een onderdeel van het autoritarismeconcept (Maslow, 1943), wees onderzoek uit dat beide concepten zo goed als ongerelateerd zijn (zie o.a. Altemeyer, 1998) en onafhankelijk van elkaar sterk gerelateerd zijn aan conservatieve opvattingen zoals nationalisme, patriotisme, een harde aanpak van de criminaliteit, steun voor militaire programma's en discriminatie (voor een overzicht, zie Pratto, 1999). Gezien het groeiend belang in de sociaal psychologische literatuur van SDO, wensen wij in dit artikel de Nederlandstalige versie van deze vragenlijst te introduceren. We zullen aantonen dat deze schaal, net zoals de originele schaal, slechts één dimensie meet die een hoge mate van interne consistentie vertoont. Naar analogie met eerder onderzoek, werd hierbij gekozen voor gelegenheidsteekproeven van studenten en volwassenen, maar aangezien dit concept ook belangrijk is voor de politieke psychologie, werd er eveneens een steekproef van politiek actieven bevraagd.
Structures of Arenaviral Nucleoproteins with Triphosphate dsRNA Reveal a Unique Mechanism of Immune Suppression*

Background: Arenaviral nucleoproteins play a critical role in innate immune suppression. Results: Structures of Lassa nucleoprotein in complex with triphosphate dsRNA and Tacaribe virus nucleoprotein have been determined. Conclusion: Both Lassa and Tacaribe nucleoproteins can strongly inhibit IFN-β production by degrading immune-stimulatory dsRNA. Significance: A unique immune suppression mode of arenaviral nucleoproteins has been revealed. A hallmark of severe Lassa fever is the generalized immune suppression, the mechanism of which is poorly understood. Lassa virus (LASV) nucleoprotein (NP) is the only known 3′-5′ exoribonuclease that can suppress type I interferon (IFN) production possibly by degrading immune-stimulatory RNAs. How this unique enzymatic activity of LASV NP recognizes and processes RNA substrates is unknown. We provide an atomic view of a catalytically active exoribonuclease domain of LASV NP (LASV NP-C) in the process of degrading a 5′ triphosphate double-stranded (ds) RNA substrate, a typical pathogen-associated molecular pattern molecule, to induce type I IFN production. Additionally, we provide for the first time a high-resolution crystal structure of an active exoribonuclease domain of Tacaribe arenavirus (TCRV) NP. Coupled with the in vitro enzymatic and cell-based interferon suppression assays, these structural analyses strongly support a unified model of an exoribonuclease-dependent IFN suppression mechanism shared by all known arenaviruses. New knowledge learned from these studies should aid the development of therapeutics against pathogenic arenaviruses that can infect hundreds of thousands of individuals and kill thousands annually.
A Role for Syndecan-1 and Claudin-2 in Microbial Translocation During HIV-1 Infection

Microbial translocation from the gastrointestinal tract has been implicated in chronic activation of the immune system during progressive HIV-1 infection by ill-defined mechanisms. We recently identified a gene encoding syndecan-1 (SYN1) in microarray studies of HIV-1 infection in lymphatic tissues and show here that increased expression of SYN1 in the gut of HIV-1-infected individuals is associated with increased microbial translocation. We further show that: (1) microbial access to SYN1 in the intestinal epithelium could be mediated by compromised barrier function through the upregulation of claudin-2; (2) increases in SYN1 and microbial translocation are associated with systemic immune activation; and (3) SYN1 expression and microbial translocation are inversely correlated with peripheral blood CD4+ T-cell counts. We thus propose a new mechanism in which claudin-2 and SYN1 work in concert to enhance microbial translocation across the intestinal epithelial barrier to contribute to chronic immune activation and CD4+ T-cell depletion.
Hemolytic uremic syndrome following taipan envenomation with response to plasmapheresis

Summary We report a case of hemolytic uremic syndrome (HUS) in a 33 year old male who was bitten by a taipan, with apparent massive envenomation. The microangiopathic hemolytic anemia (MAHA) and thrombocytopenic aspects of his HUS appeared to respond to plasmapheresis, but his anuric renal failure persisted. He also had prolonged severe muscular paralysis which gradually began to resolve over the course of two weeks. At this point he suffered a cardiac arrest sustaining severe and subsequently fatal hypoxic brain injury. This case raises the possibility that the taipan venom may have induced HUS by damaging the renal endothelium. His cardiac arrest was not apparently related to his HUS.Abbreviations: aPTT, activated partial thomboplastin time; DIC, disseminated intravascular coagulation; HUS, hemolytic uremic syndrome; MAHA, microangiopathic hemolytic anemia; PT, Prothrombic time; TTP, thrombotic thrombocytopenic purpura.
Seroprevalence of human granulocytic ehrlichiosis among permanent residents of northwestern Wisconsin.

Four-hundred seventy-five permanent residents of Wisconsin were tested for antibodies to the agent of human granulocytic ehrlichiosis (HGE) by indirect immunofluorescent antibody (IFA) testing with Ehrlichia equi as antigen marker. Each resident completed a standard survey questionnaire about outdoor activities, animal and tick exposure, and any febrile illness during the preceding 12 months. Seventy-one serum samples (14.9%) contained E. equi antibodies. The mean IFA titer for seropositive residents was 250 (range, 80-10,240). Seropositive residents were older than seronegative ones (62 vs. 56 years; P = .019). None of the seropositive residents had a history suggestive of ehrlichiosis. There was no association between the IFA test outcome and specific demographic variables or history of tick bites. HGE appears to be a common subclinical or mild infection among residents in northwestern Wisconsin.
The CRISPR RNA-guided surveillance complex in Escherichia coli accommodates extended RNA spacers

Bacteria and archaea acquire resistance to foreign genetic elements by integrating fragments of foreign DNA into CRISPR (clustered regularly interspaced short palindromic repeats) loci. In Escherichia coli, CRISPR-derived RNAs (crRNAs) assemble with Cas proteins into a multi-subunit surveillance complex called Cascade (CRISPR-associated complex for antiviral defense). Cascade recognizes DNA targets via protein-mediated recognition of a protospacer adjacent motif and complementary base pairing between the crRNA spacer and the DNA target. Previously determined structures of Cascade showed that the crRNA is stretched along an oligomeric protein assembly, leading us to ask how crRNA length impacts the assembly and function of this complex. We found that extending the spacer portion of the crRNA resulted in larger Cascade complexes with altered stoichiometry and preserved in vitro binding affinity for target DNA. Longer spacers also preserved the in vivo ability of Cascade to repress target gene expression and to recruit the Cas3 endonuclease for target degradation. Finally, longer spacers exhibited enhanced silencing at particular target locations and were sensitive to mismatches within the extended region. These findings demonstrate the flexibility of the Type I-E CRISPR machinery and suggest that spacer length can be modified to fine-tune Cascade activity.
Landfill externalities and property values dilemma – emerging insights from three Ghanaian cities

ABSTRACT Though debates about the negative impact landfill exerts on land and property values are by no means historically new, research into the case of developing countries has only recently begun. This article attempts to synthesise existing literature on the subject through the analysis of three case studies to enhance our understanding, especially the contextual conditions surrounding the relationship. Applying this theoretical framework to the disposal practices occurring in three cities in Ghana, this article offers insight into the culpability of landfills in negatively impacting property values. In an illuminating analysis, we argue that most engineered landfills in the country serve as a catalyst in correcting the ills of uncontrolled urbanisation (governance, attitudinal and financial constraints, etc.). We opine that landfills’ relationship with host communities must be understood in relation to our overall underdevelopment, coupled with the increasing economic and technical challenges shaping much of the country’s history.
Simvastatin exerts antiproliferative and differentiating effects on MG63 osteoblast‐like cells: Morphological and immunocytochemical study

BACKGROUND AND OBJECTIVE Current evidence suggests that statins exert an anabolic effect on bone and may therefore impact on osteogenic differentiation and proliferation. These effects can be useful for their use in guided bone regeneration. The objective of this study was to determine the in vitro effects of simvastatin on the differentiation and proliferation of MG63 human osteoblast tumor cells. MATERIAL AND METHODS MG63 human osteosarcoma cells were cultured in the presence of simvastatin or solvent alone for 72 hours, and their proliferation was assessed by MTT assay. Cells from the culture were prepared for light, transmission and scanning electron microscopy studies. immunocytochemical was used to analyze the differentiation and proliferation markers Musashi-1, Ki-67, CD56 and CD44. RESULTS Cultured MG63 control cells showed spheroid morphology with numerous secretion vesicles accumulated on the surface, observing no cytoplasmic projections with intercellular connections. However, cells cultured with simvastatin had a polygonal and spindle-shaped morphology, with cytoplasmic projections that interconnected cells. There were numerous microvilli-like filamentous projections on the surface with no defined pattern. At 72 hours of culture, CD56, Ki-67 and Musashi-1 expression was significantly reduced (P < .001) in simvastatin-treated cells. CD44 expression was intense in both groups and was not affected by simvastatin treatment. CONCLUSION MG63 cells cultured with simvastatin for 72 hours undergo morphological and surface changes. Simvastatin treatment exerts antiproliferative and differentiating effects on these cells as well as promoting recovery of cellular homeostasis.
Gentamicin, netilmicin, dibekacin, and amikacin nephrotoxicity and its relationship to tubular reabsorption in rabbits

The role of the tubular reabsorption of aminoglycosides in nephrotoxicity was considered. The tubular reabsorption rate, fractional reabsorption, and net balance, expressed as the excreted to infused aminoglycoside ratio, were concomitantly studied in male rabbits by continuous infusion of gentamicin, netilmicin, dibekacin, and amikacin. Aminoglycoside nephrotoxicity was evaluated by creatinine levels in serum and pathological renal damage after 14 days of a low- or high-dose regimen, comprising either eight, hourly intramuscular injections of gentamicin, netilmicin, or dibekacin (4 mg/kg) or amikacin (16 mg/kg); twelve, hourly intramuscular injections of gentamicin, netilmicin, or dibekacin (15 mg/kg) or amikacin (60 mg/kg); or injections of saline for the control group. Aminoglycosides exhibited three degrees of tubular reabsorption: gentamicin had the highest, netilmicin had the lowest, and dibekacin and amikacin had intermediate degrees of reabsorption. Nephrotoxicity associated with alteration in renal histology was observed with gentamicin and, to a lesser extent, with dibekacin in the high-dose regiment. No nephrotoxicity was noted with netilmicin or amikacin compared with the control group. Concentrations of the aminoglycosides in renal cortex and serum were not predictive of renal toxicity. Except for amikacin, which appeared to exhibit the lowest intrinsic renal toxicity, nephrotoxicity was correlated with the tubular reabsorption of each aminoglycoside. It was concluded that aminoglycoside renal toxicity can be determined by two major factors: importance of transport into tubular cells and intrinsic intracellular toxicity.
Self‐employment among women: Do children matter more than we previously thought?

This paper presents an estimation approach that addresses the problems of sample selection and endogeneity of fertility decisions when estimating the effect of young children on women's self-employment. Using data from the National Longitudinal Survey of Youth 1979, 1982-2006, we find that ignoring self-selection and endogeneity leads to underestimating the effect of young children. Once both sources of biases are accounted for, the estimated effect of young children more than doubles when compared to uncorrected results. This finding is robust to the several changes in specification and to the use of a different data set.
Giant melanocytic nevi with neurocutaneous melanosis masquerading as neurofibromas

Neurocutaneous melanosis is congenital melanocytic nevus with neurological manifestations. We report a 4-year-old female child presenting with hyperpigmented and nodular skin lesion associated with developmental delay and convulsions. The child had multiple brownish-black nevi on the face and chest and giant melanocytic nevi on thoraco-abdomen, back, and gluteal region. Computed tomography scan of the brain showed calcification in the pons, right cerebellar hemisphere, and left medial temporal lobe. Skin biopsy done from nodular hyperpigmented site was suggestive of melanocytic nevi. Electroencephalogram showed multifocal epileptiform discharges.
Tolerance, hospital stay, and recovery after uterine artery embolization for fibroids: the Ontario Uterine Fibroid Embolization Trial.

PURPOSE Uterine artery embolization (UAE) is gaining popularity as an alternative to hysterectomy for the treatment of fibroids. Although minimally invasive treatments such as UAE offer the potential of fewer complications, shorter hospital stay, and quicker recovery than surgery, there have been few published data on tolerance and recovery in patients undergoing UAE. MATERIALS AND METHODS This was a multicenter prospective single-arm clinical treatment trial involving the practices of 11 interventional radiologists in eight Ontario university-affiliated and community hospitals. Between November 1998 and November 2000, 555 women underwent UAE for symptomatic uterine fibroids. Follow-up included ultrasound examinations and telephone interviews. UAE was performed under conscious sedation. Polyvinyl alcohol particles (355-500 micro m) were the primary embolic agent, and the procedural endpoint involved stasis in the uterine arteries. Pain protocols included antiinflammatory medications and narcotics and a planned overnight hospital admission. Tolerance and recovery were measured by patient-reported pain intensity (10-point numeric rating and five-point descriptor scale), hospital length of stay (LOS), and time until return to work. RESULTS Intraprocedural pain was reported by 30% of patients and postprocedural pain was reported by 92% of patients (mean pain rating +/- SD, 7.0 +/- 2.47). The mean hospital LOS was 1.3 nights. Postprocedural pain was the most common indication for an LOS greater than 1 night (18%) or 2 nights (5%). Return visits to the hospital (10%) and readmissions (3%) were primarily for pain. The overall postprocedural complication rate was 8.0% (95% CI: 5.9%-10.6%). Of the 44 complications, 32 (73%) were pain-related. The mean recovery time after UAE was 13.1 days (median, 10.0 d). CONCLUSION The majority of patients had a 1-night LOS after UAE and recovered within 2 weeks. Postprocedural pain varied considerably and was the major indication for extended hospital stay and recovery.
Increased Interleukin‐6 Production in Mouse Osteoblastic MC3T3‐E1 Cells Expressing Activating Mutant of the Stimulatory G Protein

The McCune–Albright syndrome (MAS) is characterized by polyostotic fibrous dysplasia, café‐au‐lait spots, and multiple endocrine hyperfunction. An activating missense mutation of the α subunit of the Gs protein (Gsα) was found in several affected tissues, resulting in prolonged stimulation of adenylate cyclase. Our recent study has indicated that the cells derived from the fibrous bone dysplasia tissues in MAS patients produced increased levels of interleukin‐6 (IL‐6), which may be responsible for the increased bone resorption in this disease. In the present investigation, to analyze the molecular mechanism of the increased IL‐6 production by activating mutant Gsα in bone cells, we established mouse osteoblastic MC3T3‐E1 cells stably transfected with the activating mutant Gsα expression vector. These cells showed a significant increase of intracellular cAMP levels and produced a higher amount of IL‐6 than the cells transfected with control vector or wild‐type Gsα expression vector. Analysis of the IL‐6 promoter revealed that any of the AP‐1, nuclear factor (NF)‐IL6, and NF‐κB binding elements are important for the activating mutant Gsα‐induced gene expression. Electrophoretic mobility‐shift assays using nuclear extracts of the mutant Gsα‐expressing cells showed that phospho(Ser133)‐cAMP‐responsive element binding protein (CREB), AP‐1, NF‐IL6, and NF‐κB were increased, compared with the control cells or the wild‐type Gsα‐expressing cells. These results indicate that activating mutant Gsα increases the transcriptional factors binding to CRE, AP‐1, NF‐IL6, and NF‐κB elements to induce IL‐6 gene expression in the osteoblastic cells.
Clinical and radiologic characteristics of bone metastases in breast cancer

Metastatic bone disease was evaluated in 380 consecutive patients at the time of first metastasis of breast cancer. Studies included radiographic examination, radionuclide examination, and bone marrow biopsy. Radiographs of the skeleton demonstrated metastases in 120 patients (32%), and in 40 of these patients (13%) the bone was the only site of metastases. The diagnostic efficiency was 82% for bone scanning, 80% for pain evaluation, 59% for s‐calcium analyses, and 77% for s‐alkaline phosphatase analyses. Bone scanning is an effective method to exclude metastatic bone disease (sensitivity: 96%). A positive scan, however, requires radiologic confirmation (specificity: 66%). Bone scanning of the skeleton should be the initial staging procedure in all patients with recurrent breast cancer with no clinical or biochemical signs of bone metastases. Bilateral posterior iliac crest bone marrow aspirations and bone biopsies were positive in 82 out of the 320 patients who underwent biopsy. The frequency of positive bone marrow biopsy was significantly correlated with both the site of radiographic metastases and with the total number of involved bone regions. Routine bone marrow biopsies are indicated in patients with a positive bone scan, but a negative x‐ray examination. In these cases biopsies should be performed bilaterally.
A randomized prospective comparison of chemotherapy to total body irradiation as initial treatment for the indolent lymphoproliferative diseases.

One hundred eight consecutive patients with indolent lymphoproliferative diseases were stratified into chronic lymphocytic leukemia (CLL), stage III and IV well-differentiated lymphocytic lymphoma (WDLL), and stage III and IV follicular lymphoma (FL). Within each stratum, patients were prospectively and randomly assigned to receive chemotherapy with chlorambucil and prednisone (CP) or fractionated total body irradiation (TBI). Morbidity from both regimens was negligible. Complete response (CR) was defined as the resolution of organ enlargement and the return of blood count to normal. The CR rate for the entire CP group (n = 54) was 59% and that for the TBI group (n = 54), 52%; median survivals were 53 and 57 months respectively. In the 41 patients with CLL the CR rate for CP (n = 17) was 47% and that for TBI (n = 24), 50%; the median survival for CP was 48 months, and for TBI it was 51 months. In the 21 patients with WDLL the CR rate for CP (n = 15) was 53% and that for TBI (n = 6), 67%; the median survival for CP was 42 months and has not yet been reached for TBI. For the 46 patients with FL the CR rate for CP (n = 22) was 72% and that for TBI (n = 24), 50%; the median survival was 55 months, and for TBI it was 56 months. None of the differences in CR or survival are statistically significant (P greater than .05). In these indolent lymphoproliferative diseases, CP and TBI are equally effective forms of initial treatment irrespective of the end point being defined as CR or survival.
Spinal Cord Stimulation in Chronic Pain: Mode of Action

Study Design. Literature review. Objective. A review of the literature that presents a perspective on mechanisms of actions behind spinal cord stimulation (SCS) therapy for chronic pain. Summary of Background Data. SCS is an effective therapeutic alternative for the treatment of intractable chronic pain. Its application has been mostly based on the gate control theory of pain. Computational models have been fundamental on the understanding of clinical observations and the design of therapies that provide optimal neuromodulation. Research has provided insight into the involvement of specific neurotransmitters that support segmental and supraspinal mechanisms of action. Methods. A literature review was performed with emphasis on mechanisms of action for SCS including the effects of electrical fields on spinal cord structures based on computational models and preclinical and clinical explorations. Results. This review provides background on the development of SCS, which has been driven around a paresthesia-based paradigm as a result of the gate control theory. A review of computational models emphasizes their importance on our current understanding of the mechanism of action and clinical optimization of therapy. Electrophysiology and molecular biology have provided a closer, yet narrow, view of the effect of SCS on neurotransmitters and their receptors, which have led to the formulation of segmental and supraspinal mechanisms. Literature supporting the involvement of glial cells in chronic pain and their characteristic response to electrical fields should motivate further investigation of mechanisms involving neuroglia. Finally, a review of recent results paresthesia-free strategies should encourage research on mechanisms of action. Conclusion. The mechanisms of SCS have been extensively studied and several consistent phenomena have emerged. The activation of A-beta fibers to induce paresthesia also involve neurotransmitter release via segmental and supraspinal pathways. Despite advancements, much remains to be understood, particularly as new stimulation strategies are developed. Level of Evidence: N /A