Miracle-dz/UniFAR-FTUs huggingface dataset:
Lower eccentric hamstring strength and single leg hop for distance predict hamstring injury in PETE students

Abstract Hamstring injuries have not been under research in physical education teacher education (PETE) students so far. Within the frame of the development of an injury prevention program, for this study we conducted an analysis of modifiable risk factors for hamstring injuries in PETE students. Hamstring injuries of 102 freshmen bachelor PETE students were registered prospectively during one academic year. Eighty-one students completed maximum muscle strength tests of hip extensors, hamstrings, quadriceps (isometric) and hamstrings (eccentric) at the start of the academic year. Sixty-nine of the latter completed a single leg hop for distance (SLHD). Risk factors for hamstring injuries were statistically detected using logistic regression. Sixteen hamstring injuries (0.16 injuries/student/academic year; 0.46 injuries/1000 h) occurred to 10 participants. Eight cases were included in the risk factor analysis. Lower eccentric hamstring strength (odds ratio (ODD) = 0.977; p = 0.043), higher isometric/eccentric hamstring strength ratio (ODD = 970.500; p = 0.019) and lower score on the SLHD (ODD = 0.884; p = 0.005) were significant risk factors for hamstring injury. A combination of eccentric hamstring strength test and SLHD could give a good risk analysis of hamstring injuries in PETE students. This might offer great perspectives for easily applicable screening in a clinical setting.
Current body composition measurement techniques

Purpose of review The current article reviews the most innovative and precise, available methods for quantification of in-vivo human body composition. Recent findings Body composition measurement methods are continuously being perfected. Ongoing efforts involve multisegmental and multifrequency bioelectrical impedance analysis, quantitative magnetic resonance for total body water, fat, and lean tissue measurements, imaging to further define ectopic fat depots. Available techniques allow for the measurement of fat, fat-free mass, bone mineral content, total body water, extracellular water, total adipose tissue and its subdepots (visceral, subcutaneous, and intermuscular), skeletal muscle, select organs, and ectopic fat depots. Summary There is an ongoing need for methods that yield information on metabolic and biological functions. Based on the wide range of measurable properties, analytical methods and known body composition models, clinicians, and scientists can quantify a number of body components and with longitudinal assessment, can track changes in health and disease with implications for understanding efficacy of nutritional and clinical interventions, diagnosis, prevention, and treatment in clinical settings. With the greater need to understand precursors of health risk beginning prior to conception, a gap exists in appropriate in-vivo measurement methods with application beginning during gestation, that is, fetal development.
Modeling of human Heart Rate response during walking, cycling and rowing

The aim of this paper is to study the human Heart Rate (HR) response during walking, cycling and rowing exercises using linear time varying (LTV) models. We used the frequency of exercise locomotion as the input to the model. This frequency characterizes the stride rate, cadence rate and strokes rate of the walking, cycling and rowing exercises respectively. The time varying parameters in the LTV models were estimated by the Kalman Filter (KF). The results in this study demonstrate that HR responses to these exercises exhibit some degree of time varying nature.
Beneficial Effect of Human Induced Pluripotent Stem Cell-Derived Neural Precursors in Spinal Cord Injury Repair

Despite advances in our understanding and research of induced pluripotent stem cells (iPSCs), their use in clinical practice is still limited due to lack of preclinical experiments. Neural precursors (NPs) derived from a clone of human iPSCs (IMR90) were used to treat a rat spinal cord lesion 1 week after induction. Functional recovery was evaluated using the BBB, beam walking, rotarod, and plantar tests. Lesion morphology, endogenous axonal sprouting, graft survival, and iPSC-NP differentiation were analyzed immunohistochemically. Quantitative polymerase chain reaction (qPCR) was used to evaluate the effect of transplanted iPSC-NPs on endogenous regenerative processes and also to monitor their behavior after transplantation. Human iPSC-NPs robustly survived in the lesion, migrated, and partially filled the lesion cavity during the entire period of observation. Transplanted animals displayed significant motor improvement already from the second week after the transplantation of iPSC-NPs. qPCR revealed the increased expression of human neurotrophins 8 weeks after transplantation. Simultaneously, the white and gray matter were spared in the host tissue. The grafted cells were immunohistochemically positive for doublecortin, MAP2, bIII-tubulin, GFAP, and CNPase 8 weeks after transplantation. Human iPSC-NPs further matured, and 17 weeks after transplantation differentiated toward interneurons, dopaminergic neurons, serotoninergic neurons, and ChAT-positive motoneurons. Human iPSC-NPs possess neurotrophic properties that are associated with significant early functional improvement and the sparing of spinal cord tissue. Their ability to differentiate into tissue-specific neurons leads to the long-term restoration of the lesioned tissue, making the cells a promising candidate for future cell-based therapy of SCI.
An Evolutionarily Conserved Mechanism Delimiting SHR Movement Defines a Single Layer of Endodermis in Plants

Intercellular protein movement plays a critical role in animal and plant development. SHORTROOT (SHR) is a moving transcription factor essential for endodermis specification in the Arabidopsis root. Unlike diffusible animal morphogens, which form a gradient across multiple cell layers, SHR movement is limited to essentially one cell layer. However, the molecular mechanism is unknown. We show that SCARECROW (SCR) blocks SHR movement by sequestering it into the nucleus through protein-protein interaction and a safeguard mechanism that relies on a SHR/SCR-dependent positive feedback loop for SCR transcription. Our studies with SHR and SCR homologs from rice suggest that this mechanism is evolutionarily conserved, providing a plausible explanation why nearly all plants have a single layer of endodermis.
Pharmacist-Physician Collaboration for Diabetes Care: The Diabetes Initiative Program

BACKGROUND: Multiple complications can arise secondary to poor control of glucose, blood pressure, and cholesterol in a patient with diabetes. OBJECTIVE: To evaluate the effect of a pharmacist-physician collaboration on attainment of diabetes-related measures of control. METHODS: This was a prospective, multicenter, cohort study. Patients were enrolled from 7 practice sites throughout Tennessee if they had been diagnosed with type 2 diabetes, were aged 18 years or older with a life expectancy greater than 1 year, and were English speaking. Pregnant women were excluded. Patients were followed for 12 months following enrollment by informed consent. The pharmacist-physician collaboration method was established prior to study initiation. Primary outcomes included hemoglobin A1c (A1C), number of patients with A1C less than 7%, and percentage of patients with A1C greater than 9%. RESULTS: Of the 206 patients enrolled, the mean age was 59.73 years, and most were male (59.71%) and white (66.02%). The A1C was reduced by an average of 1.16% (p < 0.0001). The proportion of patients with A1C less than 7% increased from 12.75% at baseline to 36.76% at study conclusion (p = 0.0002). The proportion of patients with A1C greater than 9% decreased from 34.15% to 16.50%, (p < 0.0001). CONCLUSIONS: Pharmacist-physician collaborative management at multiple practice locations and types of setting (eg, private, academic, Veterans Affairs medical center) has a positive impact on glycemic control and diabetes-related health maintenance. This was accomplished without increasing the total number of antihyperglycemic agents prescribed and without an increase in patient-reported episodes of hypoglycemia.
Differences in survival‐promoting effects and intracellular signaling properties of BDNF and IGF‐1 in cultured cerebral cortical neurons

Brain‐derived neurotrophic factor (BDNF) and insulin‐like growth factor‐1 (IGF‐1) act on various neurons of the CNS as neurotrophic factors promoting neuronal differentiation and survival. We examined the survival‐promoting effects of BDNF and IGF‐1 on serum deprivation‐induced death in cultured cerebral cortical neurons, and compared the intracellular signaling pathways stimulated by BDNF and IGF‐1 in the neurons. We found that the survival‐promoting effect of BDNF was much weaker than that of IGF‐1 in serum deprivation‐induced death of cultured cortical neurons. We found no differences in the levels of phosphatidylinositol 3‐kinase (PtdIns3‐K) activity or Akt (also called PKB) phosphorylation induced by BDNF and IGF‐1 in the cultured cortical neurons, although many reports suggest that PtdIns3‐K and Akt are involved in survival promotion. In addition, phosphorylation signals of mitogen‐activated protein kinase (MAPK) and cAMP responsive element‐binding protein (CREB), which have also been reported to be involved in survival promotion, were stimulated by BDNF much more potently than by IGF‐1. These results show that there may be, as yet unidentified, intracellular signaling pathways other than the PtdIns3‐K‐Akt, MAPK and CREB signaling, to regulate survival promotion. These unidentified signaling pathways may be responsible for the distinct strengths of the survival‐promoting effects of BDNF and IGF‐1.
A comparison of central venous pressure and common iliac venous pressure in critically ill mechanically ventilated patients.

OBJECTIVE To investigate the possibility of using common iliac venous pressure (CIVP) as an alternative to superior vena cava pressure (SVCP) in mechanically ventilated, critically ill, adult patients. DESIGN A randomized, blinded comparison. SETTING Multidisciplinary intensive care unit at a university teaching hospital. PATIENTS Twenty mechanically ventilated, critically ill, adult patients. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS All patients had a catheter in situ for measuring the SVCP. A new triple-lumen catheter, with a length ranging from 15 to 20 cm, was placed into the common iliac vein via the femoral route. The SVCP and CIVP were simultaneously measured at hourly intervals for 6 hrs. Positive end-expiratory pressure, mean airway pressure, and intra-abdominal pressure were measured at the same time intervals. For 140 paired measurements of CIVP and SVCP in 20 patients, the mean difference was 0.1 +/- 1.06 (SD) mm Hg (95% confidence interval -0.10 to 0.25); the limits of agreement were -2.04 to 2.20 mm Hg (95% confidence interval -2.34 to 2.50). Mean airway pressure, intra-abdominal pressure, and positive end-expiratory pressure had no measurable effect on the difference between SVCP and CIVP. Serious complications arising from insertion of the catheter through the femoral route were not observed. CONCLUSION For clinical purposes, CIVP measured by a catheter of 15 to 20 cm placed through the femoral route is interchangeable with SVCP in mechanically ventilated adult patients. This finding provides an alternative route for assessment of central venous pressure when other routes are not appropriate.
Macrophage Activation Downregulates the Degradative Capacity of the Phagosome

The phagosome is key to most macrophage functions. It is the site of degradation of particulate material, of bacterial killing and the generation of peptides for antigen presentation. Despite its role at the fulcrum of the innate and acquired immune systems, little is known about the physiology of this organelle in activated macrophages. In this study, we utilize fluorometric techniques to characterize functional alterations in the lumenal environment of the maturing phagosome following stimulation of macrophages with interferon‐γ and/or lipopolysaccharide. In addition to modulating the kinetics of phagosomal acidification, activation results in a phagosome with diminished hydrolytic activities that varies markedly with the activation status of the cell. Differential levels of proteolytic, lipolytic and β‐galactosidase activities were observed in the phagosome but not in the total lysosomal extract, indicating selective delivery of enzymes to the developing phagosome. Despite the suppression of hydrolytic activities observed in early phagosomes, late phagosomes exhibit an enhanced and protracted accumulation of lysosomal cargo. The data are consistent with limiting proteolysis in the early phagosome to maximize epitope generation and antigen presentation while sequestering the degradative capacity in the late phagolysosome.
Effectiveness of a working memory intervention program in children with language disorders

ABSTRACT The aim of this study was twofold: first, to obtain a neuropsychological characterization of children with language disorders, and second, to evaluate the effectiveness of an intervention program on working memory. We used a pretest-instruction–posttest design, carefully identifying a sample of 32 children with language disorders whom we then evaluated for short-term verbal and visuospatial memory, verbal and visuospatial working memory, attention, processing speed, and lexical-semantic skills. We then implemented an intervention program on working memory consisting of 72 sessions of 15 minutes each, after which we repeated the neuropsychological assessment of these functions. Children with language disorders performed worse than children in the control group in all memory tasks evaluated and in the lexical-semantic processing task. After the intervention, children with language disorders showed a significant increase over their own previous performance in all variables. Children with language disorders show significant cognitive deficits and not just linguistic impairment. We offer conclusive findings on the effectiveness of the intervention program used. Finally, we obtained partial support for the existence of a causal link between improved performance on memory tasks and performance in a lexical-semantic task.
Quantitative structure–activity relationship analysis of human neutrophil elastase inhibitors using shuffling classification and regression trees and adaptive neuro-fuzzy inference systems

The purpose of this study was to develop quantitative structure–activity relationship models for N-benzoylindazole derivatives as inhibitors of human neutrophil elastase. These models were developed with the aid of classification and regression trees (CART) and an adaptive neuro-fuzzy inference system (ANFIS) combined with a shuffling cross-validation technique using interpretable descriptors. More than one hundred meaningful descriptors, representing various structural characteristics for all 51 N-benzoylindazole derivatives in the data set, were calculated and used as the original variables for shuffling CART modelling. Five descriptors of average Wiener index, Kier benzene-likeliness index, subpolarity parameter, average shape profile index of order 2 and folding degree index selected by the shuffling CART technique have been used as inputs of the ANFIS for prediction of inhibition behaviour of N-benzoylindazole derivatives. The results of the developed shuffling CART-ANFIS model compared to other techniques, such as genetic algorithm (GA)-partial least square (PLS)-ANFIS and stepwise multiple linear regression (MLR)-ANFIS, are promising and descriptive. The satisfactory results ( = 0.845, = 0.861, = 0.829, RMSELOO = 0.305 and RMSEL25%O = 0.336) demonstrate that shuffling CART-ANFIS models present the relationship between human neutrophil elastase inhibitor activity and molecular descriptors, and they yield predictions in excellent agreement with the experimental values.
Dynamic or inert metabolism? Turnover of N‐acetyl aspartate and glutathione from d‐[1‐13C]glucose in the rat brain in vivo

The rate of 13C‐label incorporation into both aspartyl (NAA C3) and acetyl (NAA C6) groups of N‐acetyl aspartate (NAA) was simultaneously measured in the rat brain in vivo for up to 19 h of [1‐13C]glucose infusion (n = 8). Label incorporation was detected in NAA C6 approximately 1.5 h earlier than in NAA C3 because of the delayed labeling of the precursor of NAA C3, aspartate, compared to that of NAA C6, glucose. The time courses of NAA were fitted using a mathematical model assuming synthesis of NAA in one kinetic compartment with the respective precursor pools of aspartate and acetyl coenzyme A (acetyl‐CoA). The turnover rates of NAA C6 and C3 were 0.7 ± 0.1 and 0.6 ± 0.1 µmol/(g h) with the time constants 14 ± 2 and 13 ± 2 h, respectively, with an estimated pool size of 8 µmol/g. The results suggest that complete label turnover of NAA from glucose occurs in approximately 70 h. Several hours after starting the glucose infusion, label incorporation into glutathione (GSH) was also detected. The turnover rate of GSH was 0.06 ± 0.02 µmol/(g h) with a time constant of 13 ± 2 h. The estimated pool size of GSH was 0.8 µmol/g, comparable to the cortical glutathione concentration. We conclude that NAA and GSH are completely turned over and that the metabolism is extremely slow (< 0.05% of the glucose metabolic rate).
[miR-221 mediates epithelial-mesenchymal transition-related gene expressions via regulation of PTEN/Akt signaling in drug-resistant glioma cells].

OBJECTIVE To investigate the correlation between miR-221 and epithelial-mesenchymal transition (EMT) in drug-resistant glioma cells. METHODS The expression levels of miR-221, PTEN, p-Akt, E-cadherin, vimentin, and MRP1 were quantitatively analyzed in Z1 cells (primary drug-resistant cells), Z2 cells (drug-sensitive cells) and Z2-BCNU cells (drug-resistant cells) using fluorescent real-time PCR and Western blotting. RESULTS The expression levels of PTEN were significantly increased in Z2 cells compared with Z1 and Z2-BCNU cells which overexpressed miR-221 and vimentin. The expression levels of vimentin, p-Akt and MRP1 were significantly decreased in Z2 cells overexpressing E-cadherin. CONCLUSION MiR-221 regulates the expression of EMT-related genes through down-regulation of PTEN and activation of PI3-K/Akt signaling.
Mitochondrial glutathione transferases involving a new function for membrane permeability transition pore regulation

The mitochondria in mammalian cells are a predominant resource of reactive oxygen species (ROS), which are produced during respiration-coupled oxidative metabolism or various chemical stresses. End-products from membrane-lipid peroxidation caused by ROS are highly toxic, thereby their elimination/scavenging are protective of mitochondria and cells against oxidative damages. In mitochondria, soluble (kappa, alpha, mu, pi, zeta) and membrane-bound glutathione transferases (GSTs) (MGST1) are distributed. Mitochondrial GSTs display both glutathione transferase and peroxidase activities that detoxify such harmful products through glutathione (GSH) conjugation or GSH-mediated peroxide reduction. Some GST isoenzymes are induced by oxidative stress, an adaptation mechanism for the protection of cells from oxidative stress. Membrane-bound MGST1 is activated through the thiol modification in oxidative conditions. Protective action of MGST1 against oxidative stress has been confirmed using MCF7 cells highly expressed of MGST1. In recent years, mitochondria have been recognized as a regulator of cell death via both apoptosis and necrosis, where oxidative stress-induced alteration of the membrane permeability is an important step. Recent studies have shown that MGST1 in the inner mitochondrial membrane could interact with the mitochondrial permeability transition (MPT) regulator proteins, such as adenine nucleotide translocator (ANT) and/or cyclophilin D, and could contribute to oxidant-induced MPT pores. Interaction of GST alpha with ANT has also been shown. In this review, functions of the mitochondrial GSTs, including a new role for mitochondria-mediated cell death, are described.
Targeting focal adhesion kinase signaling in tumor growth and metastasis

Importance of the field: Focal adhesion kinase (FAK), a crucial mediator of integrin and growth factor signaling, is a novel and promising target in cancer therapy. FAK resides within focal adhesions which are contact points between extracellular matrix (ECM) and cytoskeleton, and increased expression of the kinase has been linked with cancer cell migration, proliferation and survival. The aim of this review is to summarize the current research in the area and to assess the potential of different FAK-targeting strategies for cancer therapy. Areas covered in this review: We briefly examine the evidence pointing towards FAK as potential anti-cancer target since its discovery in 1992. Then, we summarize different approaches developed to interfere with FAK signaling and important results reported from these experiments. Finally, we discuss the potential of these strategies to accomplish inhibition of tumor growth and distant spread as well as potentially meaningful combinations with other therapeutic modalities in the context of the currently available evidence. What the reader will gain: The review emphasizes the link between FAK biology and the consequences of interference with FAK signaling. Based on this foundation an opinion is formed with regard to the future of FAK as therapeutic target. Take home message: Inhibition of FAK harbours the potential to restrain malignant growth and progression with minimal side effects in normal tissues. Small molecule inhibitors of the kinase should be examined in further clinical studies and combinations with existing therapies need to be explored. More efforts are required to identify markers which predict response towards FAK inhibition.
Effect of anti‐CD4 monoclonal antibody administration on rat small bowel allograft survival and circulating leukocyte populations

Abstract This study assessed the effect of an anti‐rat CD4 monoclonal antibody (OX38) on heterotopic small bowel allograft rejection. Fully allogeneic small bowel transplants were performed in the PVG‐to‐DA‐rat strain combination. Animals received either i) short course (days ‐1, 0 and 1) of 1 mg/kg per day OX38, ii) short course of 5 mg/kg per day or iii) extended course (days ‐2, ‐1, 0, 1, 2 and twice weekly thereafter) of 1 mg/kg per day. Both the high dose (13 days) and extended low‐dose (12 days) courses prolonged graft survival compared to untreated control animals (7 days). The low‐dose, short‐course treatment had no effect. Similar regimens were given to animals that did not receive transplants and in which peripheral blood CD4+ cell counts fell to between 20 and 55% of pretreatment levels and 20–30% of binding sites were blocked. In summary, anti‐CD4 monoclonal antibody therapy delayed rejection of rat small bowel allografts; however, long‐term survival was not achieved.