Miracle-dz/UniFAR-FTUs huggingface dataset:
Use of Prescription Opioid Medication among Community‐Dwelling Older Adults with Noncancer Chronic Pain

&NA; Research exploring the use of prescription opioid medications among community‐dwelling older adults is lacking within the current body of health related literature. Previous studies on prescription opioid use have focused on misuse among young and middle‐aged adults. The purpose of this pilot study was to: (1) describe older adults' patterns of adherence to their prescription opioid medication regimens and their reasons for these medication use patterns; and (2) examine the associations between adherence of prescription opioids, pain intensity, and pain interference on daily activity. This study utilized a cross‐sectional design. Twenty‐one participants aged 65 years and older with non‐cancer chronic pain were recruited for this study. Findings revealed that almost half of the study participants reported taking less prescription opioids than prescribed, with 2 participants taking more than the recommended dose. There was no significant association between prescription opioid medication adherence and pain intensity. Participants with lower medication adherence reported greater pain interference with sleep (r = −.595; P < .05). It is imperative that clinicians initiate discussion with older adult clients who are prescribed opioid medications in order to evaluate their patients' adherence and the effectiveness of the medication.
Subrupture tendon fatigue damage

The mechanical and microstructural bases of tendon fatigue, by which damage accumulates and contributes to degradation, are poorly understood. To investigate the tendon fatigue process, rat flexor digitorum longus tendons were cyclically loaded (1–16 N) until reaching one of three levels of fatigue damage, defined as peak clamp‐to‐clamp strain magnitudes representing key intervals in the fatigue life: i) Low (6.0%–7.0%); ii) Moderate (8.5%–9.5%); and iii) High (11.0%–12.0%). Stiffness, hysteresis, and clamp‐to‐clamp strain were assessed diagnostically (by cyclic loading at 1–8 N) before and after fatigue loading and following an unloaded recovery period to identify mechanical parameters as measures of damage. Results showed that tendon clamp‐to‐clamp strain increased from pre‐ to post‐fatigue loading significantly and progressively with the fatigue damage level (p ≤ 0.010). In contrast, changes in both stiffness and hysteresis were significant only at the High fatigue level (p ≤ 0.043). Correlative microstructural analyses showed that Low level of fatigue was characterized by isolated, transverse patterns of kinked fiber deformations. At higher fatigue levels, tendons exhibited fiber dissociation and localized ruptures of the fibers. Histomorphometric analysis showed that damage area fraction increased significantly with fatigue level (p ≤ 0.048). The current findings characterized the sequential, microstructural events that underlie the tendon fatigue process and indicate that tendon deformation can be used to accurately assess the progression of damage accumulation in tendons. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:264–273, 2009
Assessment of possible immunotoxicity of the antipsychotic drug clozapine

The immunomodulatory effects of clozapine (CLZ), antipsychotic drug, were investigated in vivo using female Balb/c mice. The main aim of this study was to evaluate the immunomodulatory effects of CLZ, antipsychotic drug, following daily intraperitoneal injection to female Balb/c mice over a period of 21 days.
Activated platelets increase fibrinolysis of mesenchymal progenitor cells

Bone regeneration is initiated by the formation of a blood clot. Activated platelets within this fibrin‐rich matrix release signaling molecules that can attract mesenchymal progenitor cells. To gain insight into the cellular mechanism by which activated platelets can support the immigration of mesenchymal progenitors, we have tested the hypothesis that platelet‐released signaling molecules increase the capacity of bone marrow stromal cells (BMSC) to activate plasminogen. We report herein that platelet‐released supernatants (PRS) elevate total urokinase‐type plasminogen activator (uPA) and total plasminogen activator inhibitor‐1 (PAI‐1) levels in BMSC, as assessed by immunoassay. Quantitative polymerase chain reaction showed an upregulation of uPA, uPA receptor, and PAI‐1. Zymography and kinetic analysis based on casein hydrolysis revealed enhanced activity of cell‐associated uPA upon exposure of BMSC to PRS. Inhibiting c‐Jun N‐terminal kinase (JNK) and phosphatidylinositol 3‐kinase (PI3K) signaling reduced uPA production and decreased plasminogen activation. Corresponding Western blot analysis showed increased phosphorylation of JNK and AKT in BMSC treated with PRS. These results suggest that activated platelets can enhance the plasminogen activation capacity of mesenchymal progenitors through the stimulation of uPA production, requiring JNK and PI3K/AKT signaling. By this mechanism platelets may contribute to the organization of the blood clot during bone regeneration. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27: 972–980, 2009
Minimal Residual Disease in Acute Myelogenous Leukemia with PML/RARα or AML1/ETO mRNA and Phenotypic Analysis of Possible T and Natural Killer Cells in Bone Marrow

Here we studied minimal residual disease (MRD) of patients with acute myeloid leukemia (AML) who have PML/RARα or AML1/ETO as well as the phenotypic analysis of lymphocyte subsets involved in antitumor immunity. Eight patients in long-term (LT; 3 to 15 years) and 15 patients in short-term (ST; up to 3 years) remission were studied. Using the reverse transcription-polymerase chain reaction (RT) assay, the limit of detection was 10-5 to 10-6 for PML/RARα transcript and 10-4 to 10-5 for the AML1/ETO transcript. Simultaneously, T lymphocyte subsets and NK cells from the peripheral blood (PB) and bone marrow (BM) were investigated by flow cytometric analysis. Four of the eight patients in LT and 7 of the 15 patients in ST remission were MRD-positive. Although all MRD-positive patients in LT remission are still until now event-free, 3 of the 7 MRD-positive (MRD+) patients in ST remission soon relapsed. The total populations of CD4+, CD8+ and CD56+ [possible T-cell and natural killer (T/NK) populations] in the B.
Diagnostic accuracy of neutrophil‐derived circulating free DNA (cf‐DNA/NETs) for septic arthritis

The release of “neutrophil extracellular traps” (NETs) has been identified as a novel immune response in innate immunity. NETs are composed of neutrophil‐derived circulating free DNA (cf‐DNA) and neutrophil cytoplasm‐derived proteins such as proteases. In this study, we analyzed the putative diagnostic value of synovial cf‐DNA/NETs for identification of septic arthritis. Forty‐two patients with a joint effusion who had undergone arthrocentesis were included. From synovial fluid, cf‐DNA/NETs (j‐cf‐DNA) levels were directly quantified. Diagnostic value of j‐cf‐DNA was compared with white blood cells (WBC), synovial white blood cells (j‐WBC), C‐reactive protein (CRP), j‐IL‐6, j‐TNF alpha, j‐IL‐1 beta, and myeloperoxidase (j‐MPO). Sensitivity, specificity, positive and negative predictive value, as well as ROC‐curves for each parameter were calculated. Synovial fluid cf‐DNA/NETs values from patients with septic arthritis (3,286 ± 386 ng/ml, n = 9) were significantly increased compared to patients with noninfectious joint inflammation (1,040 ± 208 ng/ml, n = 17) or osteoarthritis (278 ± 34 ng/ml, n = 16, p < 0.01). In conjunction with j‐cf‐DNA, j‐IL‐6 and j‐IL‐1 beta were significantly elevated (p < 0.01), but WBC, CRP, and j‐WBC were not. At a cut‐off of 300 ng/ml, j‐cf‐DNA had a sensitivity of 0.89, a specificity of 1.0, a positive predictive value of 1.0, and a negative predictive value of 0.97. Receiver operation curves revealed largest areas under the curve for cf‐DNA/NETs (0.933) and j‐IL‐6 (0.951). cf‐DNA/NETs seem to be a valuable additional marker for the diagnosis of septic arthritis or periprosthetic infections. However, this result should be confirmed in a large clinical trial. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:1401–1407, 2009
Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease

Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of &bgr;-amyloid precursor protein (&bgr;APP), A&bgr;42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of &bgr;APP, A&bgr;40 and A&bgr;42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD. Aged, symptomatic 5xFAD mice showed the highest retinal abundance of A&bgr;42 peptides and the highest deficits in complement factor H. This may be a useful model to study the mechanisms of amyloid-mediated inflammatory degeneration. The superior colliculus and retina obtained from late-stage Alzheimer's disease revealed upregulated amyloidogenic and inflammatory signaling along the anteroposterior axis of the retinal-primary visual cortex pathway.
Lansoprazole enhances the antidiabetic effect of sitagliptin in mice with diet‐induced obesity and healthy human subjects

Proton pump inhibitors as adjunctive therapy would improve diabetes control and could enhance the hypoglycaemic activity of DPP‐4 inhibitors. The aim of the study was to investigate the short‐term effects of lansoprazole (LPZ), sitagliptin (SITA) and their combination therapy on glucose regulation and gut peptide secretion.
Effect of transfection strategy on growth factor overexpression by articular chondrocytes

Articular cartilage damage remains an unsolved problem in orthopaedics. Insulin‐like growth factor I (IGF‐I) and fibroblast growth factor‐2 (FGF‐2) are anabolic and mitogenic for articular chondrocytes, and are candidates for the application of gene therapy to articular cartilage repair. We tested the hypothesis that the production of IGF‐I and FGF‐2 can be augmented by modulating vector designs and delivery methods used for gene transfer to articular chondrocytes. We developed a novel adeno‐associated virus (AAV)‐based plasmid (pAAV) to overexpress IGF‐I and FGF‐2 cDNAs in adult bovine articular chondrocytes. We found that the pAAV‐based vectors generated significantly more growth factor than pcDNA vectors carrying the same cDNAs. Chondrocytes cotransfected with both IGF‐I and FGF‐2 cDNAs in two separate pAAV plasmids produced significantly more IGF‐I and FGF‐2 than cells transfected by a single pAAV plasmid carrying both cDNAs in a dicistronic cassette. These data indicate that pAAV vectors are more effective than pcDNA vectors for transfer of IGF‐I and FGF‐2 genes to articular chondrocytes. They further suggest that cotransfection may be an effective strategy for multiple gene transfer to these cells. These findings may be important in applying growth factor gene transfer to cell‐based articular cartilage gene therapy. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:103–109, 2010
Patellofemoral joint kinematics: The circular path of the patella around the trochlear axis

Differing descriptions of patellar motion relative to the femur have resulted from previous studies. We hypothesized that patellar kinematics would correlate to the trochlear geometry and that differing descriptions could be reconciled by accounting for differing alignments of measurement axes. Seven normal fresh‐frozen knees were CT scanned, and their kinematics with quadriceps loading was measured by an optical tracker system. Kinematics was calculated in relation to the femoral epicondylar, anatomic, and mechanical axes. A novel trochlear axis was defined, between the centers of spheres best fitted to the medial and lateral trochlear articular surfaces. The path of the center of the patella was circular and uniplanar (root‐mean‐square error 0.3 mm) above 16 ± 3° (mean ± SD) knee flexion. In the coronal plane, this circle was aligned 6 ± 2° from the femoral anatomical axis, close to the mechanical axis alignment. It was 91 ± 3° from the epicondylar axis, and 88 ± 3° from the trochlear axis. In the transverse plane it was 91 ± 3° and 88 ± 3° from the epicondylar and trochlear axes, respectively. Manipulation of the data to different axis alignments showed that differing previously published data could be reconciled. The circular path of patellar motion around the trochlea, aligned with the mechanical axis of the leg, is easily visualized and understood. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:589–594, 2010
Chondrogenic differentiation of human subchondral progenitor cells is impaired by rheumatoid arthritis synovial fluid

In microfracture, subchondral progenitors enter the cartilage defect and form cartilage repair tissue. We hypothesize that synovial fluid (SF) from rheumatoid arthritis (RA) donors affects chondrogenesis of human subchondral progenitors stimulated with transforming growth factor‐β3 (TGFB3), whereas SF from normal and osteoarthritis (OA) donors do not. Human progenitors from subchondral cortico‐spongious bone (pool of n = 4) were cultured in micromasses under serum‐free conditions and were stimulated with 10 ng/mL TGFB3 and with 5% SF from normal, OA, and RA donors (pool of n = 7, each). Histological staining of proteoglycan and immunostaining of type II collagen showed that progenitors stimulated with SF from RA donors show significantly reduced cartilage matrix formation compared to progenitors treated with TGFB3 or with SF from normal and OA donors (n = 3, each). Gene expression analysis of typical chondrocyte marker genes and genes encoding matrix modifying enzymes showed that SF from OA and RA donors influence the onset of TGFB3‐mediated chondrogenesis (pool of 20 micromasses), but had no effect on the gene expression profile after prolonged culture in micromasses. These results suggest that SF from RA patients may impair the chondrogenic development of mesenchymal progenitors in microfracture, whereas osteoarthritic SF may has no negative effect on the cartilage matrix formation. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:819–827, 2010
Penetration depth method—novel real‐time strategy for evaluating femoroacetabular impingement

We introduce a new method for computerized real‐time evaluation of femoroacetabular impingement (FAI). In contrast to previously presented stress analyses, this method is based on two types of predictions of penetration depths for two rotating bodies: curvilinear and radial penetration depth. This intuitive method allows the analysis of both bony and soft tissue structures (such as cartilage and acetabular labrum) in real time. Characteristic penetration depth patterns were found for different subtypes of FAI, such as cam and pincer pathologies. In addition, correlation between the penetration depths (estimated by applying this method) and the existing contact stresses (estimated by applying the finite element method) of various hip morphologies were found. A strong correlation with predicted stress values existed, with a mean correlation coefficient of 0.91 for the curvilinear and 0.80 for the radial penetration method. The results show that the penetration depth method is a promising, fast, and accurate method for quantification and diagnosis of FAI. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:880–886, 2010
Safety and pharmacokinetics of an intramuscular humanized monoclonal antibody to respiratory syncytial virus in premature infants and infants with bronchopulmonary dysplasia

Background.Respiratory syncytial virus (RSV) is the leading cause of lower respiratory disease in infants and children. MEDI-493 (palivizumab, Synagis®) is a humanized monoclonal IgG1 antibody to the fusion protein of RSV, and it is highly active in vitro against RSV A and B strains.Objective. To des
Do transport planning tools reflect the needs of the older traveller

This article describes a series of small‐scale investigations conducted with older people to understand the importance of independent transport to their daily lives and the key barriers that they face which constrain their travel patterns. The investigations used a blend of methods including literature review, focus groups, accompanied walks, geographical information system (GIS) mapping and interviews with older people and experts working in the field of transport planning. The findings were tested through a series of practitioner and user workshops.While other studies have also provided valuable evidence on the importance of transport to well‐being the article presents evidence as to important cultural aspects of the predominant approach to transport planning which lead to older people's needs not receiving the attention that they need or deserve. There is a lack of training of professionals in the specific needs of this group compounded by a lack of time devoted to understanding these. Efforts to automate the identification of problem areas using GIS mapping do not match well to the problems expressed by older people. This leads us to conclude that a more community‐based, user‐led approach is most likely to deliver the inclusive transport system that transport planners say they wish to develop and that older people would like to travel on.
Toxoplasma gondii: taux de portage chez les ovins de la région de Marrakech (Mnabha)

Toxoplasma gondii ist ein ubiquitar vorkommender Parasit mit einer unterschiedlichen Pravalenz von Land zu Land. In Marokko existieren nur wenige Studien, die sich diesem Thema widmen. Um diese Lucke zu schliessen, waren wir an einer epidemiologischen Studie uber diesen Parasiten interessiert, die auch das Vorkommen verschiedener Vektoren als mogliche Quelle menschlicher Infektionen abklaren sollte. Die Untersuchungen erfolgten durch direkten Nachweis von Zysten im Hirngewebe von 50 Schafen, die fur den menschlichen Konsum geschlachtet wurden. Die Ergebnisse dieser vorlaufigen Studie zeigen, dass bei 30% aller Tiere Zysten von T. gondii gefunden wurden. Um diesen Befund zu bestatigen und die Virulenz des Parasiten abzuklaren, wurden mit den infizierten Gewebsproben Mause inokuliert. Diese Ergebnisse sind vielversprechend und geben Anlass, auch serologische Methoden einzubeziehen und die Untersuchungen auf Kuhe und Ziegen in dieser Regio auszuweiten.
Expression of chondro‐osteogenic BMPs in ossified failed tendon healing model of tendinopathy

Chondrocytes phenotype/markers were expressed in clinical samples of tendinopathy and calcifying tendinopathy. This study examined the spatial‐temporal expression of chondro‐osteogenic Bone Morphogenetic Proteins (BMPs), which might contribute to ectopic chondro‐osteogenesis and failed healing process in tendinopathy. Collagenase was injected into patellar tendon of rats to induce ossified failed tendon healing. At week 2, 4, 8, 12, and 16, the patella tendon was harvested for immunohistochemical staining and analysis of BMP‐2/4/7. BMP‐4/7 showed similar expression patterns, which was different from BMP‐2. The expression of BMP‐2 in the tendon matrix increased at week 2 and was reduced to nearly undetectable level afterwards except at the chondro‐ossification sites. However, the expression of BMP‐4/7 in the healing tendon fibroblast‐like cells and matrix increased at week 2, reduced at week 4 and 8 and increased again at week 12 and 16, consistent with transient healing at week 8 in this animal model. There was increasing strong expression of BMP‐4/7 in the chondrocyte‐like cells in the un‐ossified and ossified areas from week 8–16. BMP‐4/7, besides BMP‐2, might also contribute to ectopic chondro‐osteogenesis and failed healing in tendon injuries. BMP‐4/7, but not BMP‐2, might be involved in regulating late events in ossified failed tendon healing. © 2010 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29:816–821
Primary tumor dependent inhibition of tumor growth, angiogenesis, and perfusion of secondary breast cancer in bone

The systemic balance of angiogenic and anti‐angiogenic factors has been proposed to play a key‐role in primary tumor growth dependent growth suppression of secondary tumors. Despite the importance of the organ microenvironment to angiogenesis and microcirculation, the influence of a primary tumor on secondary bone tumors has not been investigated so far. Since breast cancer has a high propensity to spread to bone, we used an in vivo xenograft model to determine the impact of growing breast cancer cells (MCF‐7) in the mammary fat pad on the microvascular properties of subsequently inoculated secondary breast cancer tumors in bone. Mice were either treated with a resection of the primary tumor (n = 10) or no surgery (n = 9) and intravital microscopy was performed over 25 days in bone tumors. Tumor growth in bone was temporarily suppressed by the primary tumor on days 10 and 14. While microvascular permeability and vascular diameter decreased in both groups over time, the presence of the primary tumor was accompanied by a decreased tumor perfusion on days 8 and 10 through a reduction in vessels with diameters between 5 and 20 µm. The results imply a potential benefit of a therapeutic regime in which the resection of the primary tumor is combined with an anti‐angiogenic therapy in the perioperative or direct postoperative period. This might result in reduced progression of bone metastasis subsequent to excision of the primary tumor. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29: 1251–1258, 2011
Are polymorphisms of molecules involved in bone healing correlated to aseptic femoral and tibial shaft non‐unions?

Fracture healing is a well‐organized process between several molecules and mediators. As known from other diseases, genetic polymorphisms may exhibit different expression patterns in these mediators. Concerning fracture healing, this may lead to an extended healing process or non‐union. We investigated the incidence of polymorphisms in patients with aseptic non‐unions after femoral and tibial shaft fractures as compared to patients with uneventful healing. Exclusion criteria were smoking, diabetes, bilateral fractures, systemic corticoid therapy, and septic non‐unions. Analysis of allele frequencies and genotype distribution of various mediators were carried out following PCR. Clinical parameters such as injury severity and in‐hospital were analyzed. Fifty patients following non‐union (group NU) were enrolled, the control group consisted of 44 patients (group H). A significant association of a PDGF haplotype and non‐unions following fracture could be observed. There was a significantly increased in‐hospital time and amount of surgical procedures in group NU. Polymorphisms within the PDGF gene seem to be a genetic risk factor for the development of non‐unions of the lower extremity following fracture. The early identification of high risk patients could result in an adapted therapeutical strategy and might contribute to a significant decrease of posttraumatic non‐unions. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29:1724–1731, 2011
The VCU Pressure Ulcer Summit: Collaboration to Operationalize Hospital-Acquired Pressure Ulcer Prevention Best Practice Recommendations

This executive summary reports outcomes of an interprofessional collaboration between experts in pressure ulcer prevention, bedside clinicians, regulatory agencies, quality improvement, informatics experts, and professional nursing organizations. The goal of the collaboration was to develop a framework to assist facilities to operationalize best practice recommendations to sustain organizational culture change in hospital-acquired pressure ulcer prevention, to develop a hospital-acquired pressure ulcer severity score, and to address topics related to the unavoidable pressure ulcer.