tbuckley/cabot-search huggingface dataset:
SELF-REPORTED 12-MONTH OVERUSE INJURY HISTORY IN YOUTH BASKETBALL AND FLOORBALL
Authors: M Leppänen, K Pasanen, UM Kujala, J Parkkari
Journal: British Journal of Sports Medicine (2014)

Background The popularity of organized sports, especially team sports is growing among youth. High training volume and intensity at early age may predispose young athletes to overuse injuries. Objective To examine the occurrence, nature and severity of overuse injuries in youth basketball and floorball. Design A descriptive retrospective study. Setting Finnish youth basketball and floorball. Participants: 406 athletes (mean age 15.9, SD 2.0) from six basketball and floorball clubs (210 basketball and 196 floorball players). Main outcome measurements Self-reported history of overuse injuries over the preceding 12-month period. Data was obtained from a questionnaire. The severity of injuries was defined according to time-loss from full-time game or training. Results 172 overuse injuries (sustained by 139 players) were reported. Basketball players sustained 97 and floorball players 75 overuse injuries. Injury incidence in basketball was 1.1 and in floorball 0.8 injuries/1000h of exposure. Most of the overuse injuries involved the lower extremities (72% of all injuries). Most commonly injured site was the knee (45%). Another common site of the injury was the area of lower back/pelvis (26%), followed by the calf/shin (11%). No differences between the genders or the two sports were observed. Most of the injuries were slight (time-loss 1–3 days) injuries (33%). 23% of injuries were mild (time-loss 4–7 days), 20% were moderate (time-loss 8–28 days) and 25% of injuries were severe (time-loss ≥29 days) injuries. Overuse injuries caused an average time-loss of 24 days (SD 52). Conclusions Over a one third of the players participating in the study reported having sustained an overuse injury in the preceding 12 months. Remarkable proportion of overuse injuries were severe injuries. Overuse injuries often cause long absence from full-time game and training. Prospective studies to assess the risk factors and mechanisms of overuse injuries among youth team sports are needed.
Injuries among elite snowboarders (FIS Snowboard World Cup)
Authors: J Torjussen, R Bahr
Journal: British Journal of Sports Medicine (2006)

Although snowboarding is already established as an Olympic sport, it is still a developing sport, with new disciplines, more demanding snow installations, and spectacular tricks. A recent study on subjects at Norwegian national elite level showed that injury risk is high and that injuries among competitive snowboarders differ from those seen in recreational snowboarders, with fewer wrist injuries and more knee and back injuries.To describe the incidence and type of injuries among female and male snowboarders at international elite level.At the last race of the Fédération Internationale de Ski Snowboard World Cup, acute injuries resulting in missed participation and overuse injuries influencing performance, were recorded during a retrospective interview (91% response rate). The registration period was from April 2002 (end of season) until March 2003. Exposure was recorded as the number of runs in all disciplines, and the incidence was calculated as number of injuries per 1000 runs.The 258 athletes interviewed reported 3193 competition days (n = 46 879 runs) in all disciplines. In total, 135 acute injuries were recorded; 62 (46%) during competition in the official disciplines. Of the 135 acute injuries, the most common injury locations were knee (n = 24; 18%), shoulder (n = 18; 13%), back (n = 17; 13%), and wrist (n = 11; 8%). The overall incidence during competition was 1.3 (95% confidence interval 1.0 to 1.7) injuries per 1000 runs; 2.3 (0.9 to 3.8) for big air (n = 10), 1.9 (1.1 to 2.8) for halfpipe (n = 21), 2.1 (1.2 to 3.0) for snowboard cross (n = 20), 0.6 (0.2 to 1.0) for parallel giant slalom (n = 8), and 0.3 (0.0 to 0.7) for parallel slalom (n = 3). The severity of injuries was graded based on time loss (27% lost >21 days) and score on the Abbreviated Injury Scale (AIS) (38% AIS 1, 61% AIS 2 and 1% AIS 3). There were 122 overuse injuries, 38 (31%) of these to the knee.The injury risk for big air, snowboard cross, and halfpipe disciplines is high, while that for the snowboard slalom disciplines is lower. The injury pattern is different from recreational athletes, with a greater share of knee injuries and fewer wrist injuries. Compared with national level, the injury risk appears to be lower at World Cup level.
Abstract 2502: p53 is critical for the Aurora B kinase inhibitor-mediated apoptosis in acute myelogenous leukemia cells
Authors: Takayuki Ikezoe, Jing Yang, Chie Nishioka, Akihito Yokoyama
Journal: Cancer Research (2010)

Abstract We previously showed that AZD1152-HQPA, the inhibitor of Aurora B kinase potently induced growth arrest and apoptosis of various types of human leukemia cells including MV4-11 acute myelogenous leukemia (AML) cells, although the molecular mechanisms by which this class of kinase inhibitors induces apoptosis remain to be fully elucidated. We have recently established the MV4-11 subline, designated as MV4-11 TP53 R248W, which possesses transcriptionally inactive R248W mutation in the TP53 gene. MV4-11 TP53 R248W cells were relatively resistant to AZD1152-HQPA-mediated growth arrest, as measured by MTT and clonogenic assays. AZD1152-HQPA (10-100 nM, 48 hrs) strikingly induced apoptosis of MV4-11 cells, as assessed by Annexin V binding, loss of mitochondrial outer membrane potential, and activation of caspase cascade, in parallel with up-regulation of p53 and its target molecules Bax and Noxa. Notably, AZD1152-HQPA (10-100 nM, 48 hrs) induced polyploidy rather than apoptosis in MV4-11 TP53 R248W cells. The polyploid cells were eventually eliminated via apoptosis at later time period (72-120 hrs) in association with up-regulation of p73. Taken together, p53 plays an important role in AZD1152-HQPA induced growth arrest and early-onset of apoptosis in AML cells. P73 may mediate the late-onset of apoptosis to eliminate the polyploid cells caused by the inhibitor of Aurora B kinase. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2502.
Aldehyde dehydrogenase-2 regulates nociception in rodent models of acute inflammatory pain
Authors: Vanessa O. Zambelli, Eric R. Gross, Che-Hong Chen, Vanessa P. Gutierrez, Yara Cury, Daria Mochly-Rosen
Journal: Science Translational Medicine (2014)

Pain sensitivity can be modulated by an enzyme that degrades aldehydes in rodents, pointing to a promising therapeutic target.
Endothelial leukocyte adhesion molecule-1 mediates antigen-induced acute airway inflammation and late-phase airway obstruction in monkeys.
Authors: R H Gundel, C D Wegner, C A Torcellini, C C Clarke, N Haynes, R Rothlein, C W Smith, L G Letts
Journal: Journal of Clinical Investigation (1991)

This study examines the role of endothelial leukocyte adhesion molecule-1 (ELAM-1) in the development of the acute airway inflammation (cell influx) and late-phase airway obstruction in a primate model of extrinsic asthma. In animals sensitive to antigen, a single inhalation exposure induced the rapid expression of ELAM-1 (6 h) exclusively on vascular endothelium that correlated with the influx of neutrophils into the lungs and the onset of late-phase airway obstruction. In contrast, basal levels of ICAM-1 was constitutively expressed on vascular endothelium and airway epithelium before antigen challenge. After the single antigen exposure, changes in ICAM-1 expression did not correlate with neutrophil influx or the change in airway caliber. This was confirmed by showing that pretreatment with a monoclonal antibody to ICAM-1 did not inhibit the acute influx of neutrophils associated with late-phase airway obstruction, whereas a monoclonal antibody to ELAM-1 blocked both the influx of neutrophils and the late-phase airway obstruction. This study demonstrates a functional role for ELAM-1 in the development of acute airway inflammation in vivo. We conclude that, in primates, the late-phase response is the result of an ELAM-1 dependent influx of neutrophils. Therefore, the regulation of ELAM-1 expression may provide a novel approach to controlling the acute inflammatory response, and thereby, affecting airway function associated with inflammatory disorders, including asthma.
Are Transition Zone Biopsies Still Necessary to Improve Prostate Cancer Detection?
Authors: Alexandre E. Pelzer, Jasmin Bektic, Andreas P. Berger, Ethan J. Halpern, Florian Koppelstätter, Andrea Klauser, Peter Rehder, Wolfgang Horninger, Georg Bartsch, Ferdinand Frauscher
Journal: European Urology (2005)
Does history of concussion affect current cognitive status?
Authors: A Collie, P McCrory, M Makdissi
Journal: British Journal of Sports Medicine (2006)

The association between self reported history of concussion and current neurocognitive status is controversial. Some football studies suggest that athletes with a history of concussion display cognitive impairment relative to athletes with no history of concussion, but other studies have not been able to reproduce such findings. This study shows that there is no relation between the number of previous self reported episodes of concussion and current cognitive state, directly contradicting the findings of previous research.
Clinical Implications of the Colorectal Cancer Risk Associated With <i>MUTYH</i> Mutation
Authors: Steven J. Lubbe, Maria Chiara Di Bernardo, Ian P. Chandler, Richard S. Houlston
Journal: Journal of Clinical Oncology (2009)

Purpose Biallelic mutations in the base excision DNA repair gene MUTYH predispose to colorectal cancer (CRC). Evidence that monoallelic mutations also confer an elevated CRC risk is controversial. Precise quantification of the CRC risk and the phenotype associated with MUTYH mutations is relevant to the counseling, surveillance, and clinical management of at-risk individuals. Methods We analyzed a population-based series of 9,268 patients with CRC and 5,064 controls for the Y179C and G396D MUTYH mutations. We related genotypes to phenotype and calculated genotype-specific CRC risks. Results Overall, biallelic mutation status conferred a 28-fold increase in CRC risk (95% CI,17.66 to 44.06); this accounted for 0.3% of CRCs in the cohort. Genotype relative risks of CRC were strongly age dependent, but penetrance was incomplete at age 60 years. CRC that developed in the context of biallelic mutations were microsatellite stable. Biallelic mutation carriers were more likely to have proximal CRC (P = 4.0 × 10 −4 ) and synchronous polyps (P = 5.7 × 10 −9 ) than noncarriers. The performance characteristics of clinicopathologic criteria for the identification of biallelic mutations are poor. Monoallelic mutation was not associated with an increased CRC risk (odds ratio, 1.07; 95% CI, 0.87 to 1.31). Conclusion The high risk and the propensity for proximal disease associated with biallielic MUTYH mutation justify colonoscopic surveillance. Although mutation screening should be directed to patients with APC-negative polyposis and early-onset proximal MSS CRC in whom detection rates will be highest, the expanded phenotype associated with MUTYH mutation needs to be recognized. There is no evidence than monoallelic mutation status per se is clinically important.
A New Role of Protein Phosphatase 2A in Adenoviral E1A Protein-Mediated Sensitization to Anticancer Drug-Induced Apoptosis in Human Breast Cancer Cells
Authors: Yong Liao, Mien-Chie Hung
Journal: Cancer Research (2004)

Abstract The adenoviral type 5 E1A protein has been shown to induce sensitization to different categories of anticancer drug-induced apoptosis, partly by down-regulation of the activity of a critical oncogenic kinase Akt in both normal fibroblasts and epithelial breast cancer cells. Currently, the adenoviral E1A gene is being tested as an antitumor gene in multiple clinical trials. However, molecular mechanisms underlying E1A-mediated chemosensitization and down-regulation of Akt activity are still not completely defined. Here, we show that E1A by up-regulation of the catalytic subunit of protein phosphatase 2A [PP2A (PP2A/C)] enhanced the activity of PP2A, which results in repression of Akt activation in E1A-expressing cells. In addition, activation of PP2A/C is required for E1A-mediated sensitization to drug-induced apoptosis, because blocking PP2A/C expression using a specific small interfering RNA against PP2A/C reduced drug sensitivity in E1A-expressing cells. Deletion mutation of the conserved domain of E1A, which is required for E1A-mediated sensitization to drug-induced apoptosis, also abolished the ability of E1A to up-regulate PP2A/C. Thus, the up-regulation of PP2A may represent a novel mechanism for E1A-mediated sensitization to anticancer drug-induced apoptosis.
Airway dendritic cell phenotypes in inflammatory diseases of the human lung
Authors: M. Lommatzsch, K. Bratke, A. Bier, P. Julius, M. Kuepper, W. Luttmann, J. C. Virchow
Journal: European Respiratory Journal (2007)

Airway dendritic cells (DCs) are key regulators of pulmonary immune responses. However, information is limited regarding the characteristics of airway DCs in human lung diseases. Plasmacytoid DCs (pDCs) and myeloid DCs (mDCs) were analysed using four-colour flow cytometry in bronchoalveolar lavage fluid (BALF) from nonsmoking controls and patients with sarcoidosis, idiopathic pulmonary fibrosis (IPF) and pneumonia (in the presence or absence of immunosuppression). Compared with controls, immunocompetent patients with pneumonia displayed strongly enhanced pDC counts in BALF. In contrast, pDC counts in BALF from immunocompromised patients with pneumonia were even lower than in controls. This discrepancy was not explained by a different chemotactic milieu in the airways; all patients with pneumonia were characterised by strongly increased concentrations of the pDC-attracting chemokine, CXC chemokine ligand 10, in BALF. Patients with IPF were characterised by normal percentages of DC subtypes. However, the mDCs of patients with IPF were not as mature (CD83-positive) as those of controls. Patients with sarcoidosis displayed a unique increase in CD1a-negative mDCs in the airways. In addition, there was altered expression of costimulatory molecules (increased CD80 and decreased CD86 expression) on mDCs in patients with sarcoidosis. These data suggest that inflammatory diseases of the human lung are associated with a differential phenotype and recruitment of airway dendritic cells.
Amyloid fibril protein in familial amyloidotic polyneuropathy, Portuguese type. Definition of molecular abnormality in transthyretin (prealbumin).
Authors: M J Saraiva, S Birken, P P Costa, D S Goodman
Journal: Journal of Clinical Investigation (1984)

Amyloid fibril protein in patients with familial amyloidotic polyneuropathy is known to be chemically related to transthyretin (TTR), the plasma protein that is usually referred to as prealbumin. A genetically abnormal TTR may be involved in this disease. Studies were conducted on amyloid fibril protein (AFp) isolated from tissues of two Portuguese patients who died with familial amyloidosis, and on TTR isolated from sera of patients with this disease. AFp, purified by affinity chromatography on retinol-binding protein linked to Sepharose, resembled plasma TTR in forming a stable tetrameric structure, and in its binding affinities for both thyroxine and retinol-binding protein. The structural studies included: (a) comparative peptide mappings by reverse-phase high performance liquid chromatography (HPLC) after trypsin digestion; (b) cyanogen bromide cleavage studies; and (c) amino acid microsequence analysis of selected tryptic and CNBr peptides. On the basis of the known amino acid sequence of TTR, comparative tryptic peptide maps showed the presence of a single aberrant tryptic peptide (peptide 4, residues 22-34) in AFp as compared with TTR. This aberrant peptide contained a methionine residue, not present in normal tryptic peptide 4. CNBr cleavage of AFp produced two extra peptide fragments, which were demonstrated, respectively, by HPLC analysis and by sodium dodecyl sulfate-gel electrophoresis. Sequence analyses indicated the presence of a methionine-for-valine substitution at position 30 in AFp as compared with TTR. Thus, the purified amyloid fibril protein comprised a TTR variant with a methionine-forvaline substitution at position 30. A single nucleotide change in a possible codon for valine 30 could explain the substitution. The variant TTR was also present in the TTR isolated from the pooled sera of amyloidoses patients, together with larger (four- to six-fold) amounts of the normal TTR. Thus, in these patients, the variant TTR was circulating in plasma, along with larger amounts of normal TTR. We suggest that the variant TTR represents the specific biochemical cause of the disease, and that this abnormal form of TTR selectively deposits in tissues as the amyloid characteristic of the disease.
Post–Cardiac Surgery Mechanical Support
Authors: Daniel Marelli, Richard J. Shemin
Journal: Circulation (2007)

Circulation is timely and important.Compiled from the Society of Thoracic Surgeons voluntary database, it comprises an analysis of the largest series of patients treated with mechanical support to date.The authors have reviewed outcomes of 5735 patients who had a ventricular assist device (VAD) placed for low cardiac output after having undergone a cardiac surgical procedure.Remarkably, this represents Ͻ0.5% of all cardiac operations.The authors observed significant improvement in outcome for these patients over a recent 10-year study period.Survival improved from 38.5% to 59.2%.Similarly, during the same time period, there was a reduction in major assist-device morbidity of bleeding, stroke, and renal failure.These results are in keeping with those from smaller, single-institution reports.
Hepatic lipid accumulation, altered very low density lipoprotein formation and apolipoprotein E deposition in apolipoprotein E3-Leiden transgenic mice
Authors: Arjen R Mensenkamp, Marja J.A.van Luyn, Harry van Goor, Vincent Bloks, Frank Apostel, Jobst Greeve, Marten H Hofker, Miek C Jong, Bart J.M.van Vlijmen, Louis M Havekes, Folkert Kuipers
Journal: Journal of Hepatology (2000)
Impact of Blood Sampling on Circulating Tissue Inhibitors of Metalloproteinases
Authors: Klaus Jung
Journal: Clinical Cancer Research (2006)

To the Editor: I read with great interest the article by Ruokolainen et al. ([1][1]) reporting on the clinical validity of tissue inhibitor of matrix metalloproteinase (MMP)-1 (TIMP-1) in head and neck squamous cell carcinoma. Comparing the preoperative serum TIMP-1 concentrations and the
Clinical significance of respiratory bronchiolitis on open lung biopsy and its relationship to smoking related interstitial lung disease
Authors: J. Moon, R. M du Bois, T. V Colby, D. M Hansell, A. G Nicholson
Journal: Thorax (1999)

Respiratory bronchiolitis-associated interstitial lung disease (RBILD) is a rare form of interstitial lung disease which may present in similar fashion to other types of chronic interstitial pneumonia. The purpose of this study was to undertake a clinicopathological review of 10 patients with RBILD and to examine the clinical and imaging data related to its histopathological pattern, in particular the relationship of RBILD to smoking.Thirteen out of 168 retrospectively reviewed patients, from whom biopsy specimens were taken for suspected diffuse lung disease, were identified with a histopathological pattern of RBILD. Three cases were rejected as follow up data were unavailable. The 10 remaining cases constituted the study group and both clinical and imaging data were collected from patients' notes and referring physicians.Histopathologically, four cases of RBILD overlapped with the pattern of desquamative interstitial pneumonitis (DIP) and nine also had microscopic evidence of centrilobular emphysema. Nine patients were smokers, ranging from 3 to 80 pack years. The one non-smoker had an occupational exposure to the fumes of solder flux. The sex distribution was equal with an age range of 32-65 years. Two patients were clubbed. Lung function tests showed both restrictive and obstructive patterns together with severe reductions in carbon monoxide transfer factor in seven patients. Chest radiographs showed reticular or reticulonodular infiltrates in five patients and a ground glass pattern in two. CT scans were consistent with either DIP or RBILD in six of eight patients. Although seven patients remained stable or improved, either with or without treatment, three patients deteriorated.This study adds weight to the hypothesis that smoking can cause clinically significant interstitial lung disease, with deterioration in pulmonary function despite treatment. Given the overlapping histopathological patterns of RBILD and DIP and their strong association with smoking, the term "smoking related interstitial lung disease" is suggested for those patients who are smokers.
Labeling Human Mesenchymal Stem Cells with Gold Nanocages for <i>in vitro</i> and <i>in vivo</i> Tracking by Two-Photon Microscopy and Photoacoustic Microscopy
Authors: Yu Shrike Zhang, Yu Wang, Lidai Wang, Yucai Wang, Xin Cai, Chi Zhang, Lihong V. Wang, Younan Xia
Journal: Theranostics (2013)

Stem cell tracking is a highly important subject.Current techniques based on nanoparticle-labeling, such as magnetic resonance imaging, fluorescence microscopy, and micro-computed tomography, are plagued by limitations including relatively low sensitivity or penetration depth, involvement of ionizing irradiation, and potential cytotoxicity of the nanoparticles.Here we introduce a new class of contrast agents based on gold nanocages (AuNCs) with hollow interiors and porous walls to label human mesenchymal stem cells (hMSCs) for both in vitro and in vivo tracking using two-photon microscopy and photoacoustic microscopy.As demonstrated by the viability assay, the AuNCs showed negligible cytotoxicity under a reasonable dose, and did not alter the differentiation potential of the hMSCs into desired lineages.We were able to image the cells labeled with AuNCs in vitro for at least 28 days in culture, as well as to track the cells that homed to the tumor region in nude mice in vivo.