tbuckley/cabot-search huggingface dataset:
Clinical use of objective measures of physical activity
Authors: Stewart G Trost, Margaret O'Neil
Journal: British Journal of Sports Medicine (2013)

With measurement of physical activity becoming more common in clinical practice, it is imperative that healthcare professionals become more knowledgeable about the different methods available to objectively measure physical activity behaviour. Objective measures do not rely on information provided by the patient, but instead measure and record the biomechanical or physiological consequences of performing physical activity, often in real time. As such, objective measures are not subject to the reporting bias or recall problems associated with self-report methods. The purpose of this article was to provide an overview of the different methods used to objectively measure physical activity in clinical practice. The review was delimited to heart rate monitoring, accelerometers and pedometers since their small size, low participant burden and relatively low cost make these objective measures appropriate for use in clinical practice settings. For each measure, strengths and weakness were discussed; and whenever possible, literature-based examples of implementation were provided.
The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim
Authors: Sabine Jurado, Kimberly Gleeson, Kristy O’Donnell, David J. Izon, Carl R. Walkley, Andreas Strasser, David M. Tarlinton, Jörg Heierhorst
Journal: The Journal of Experimental Medicine (2012)

Developing B lymphocytes expressing defective or autoreactive pre-B or B cell receptors (BCRs) are eliminated by programmed cell death, but how the balance between death and survival signals is regulated to prevent immunodeficiency and autoimmunity remains incompletely understood. In this study, we show that absence of the essential ATM (ataxia telangiectasia mutated) substrate Chk2-interacting Zn2+-finger protein (ASCIZ; also known as ATMIN/ZNF822), a protein with dual functions in the DNA damage response and as a transcription factor, leads to progressive cell loss from the pre-B stage onwards and severely diminished splenic B cell numbers in mice. This lymphopenia cannot be suppressed by deletion of p53 or complementation with a prearranged BCR, indicating that it is not caused by impaired DNA damage responses or defective V(D)J recombination. Instead, ASCIZ-deficient B cell precursors contain highly reduced levels of DYNLL1 (dynein light chain 1; LC8), a recently identified transcriptional target of ASCIZ, and normal B cell development can be restored by ectopic Dynll1 expression. Remarkably, the B cell lymphopenia in the absence of ASCIZ can also be fully suppressed by deletion of the proapoptotic DYNLL1 target Bim. Our findings demonstrate a key role for ASCIZ in regulating the survival of developing B cells by activating DYNLL1 expression, which may then modulate Bim-dependent apoptosis.
The Clinically Inapparent Adrenal Mass: Update in Diagnosis and Management
Authors: Georg Mansmann, Joseph Lau, Ethan Balk, Michael Rothberg, Yukitaka Miyachi, Stefan R. Bornstein
Journal: Endocrine Reviews (2004)

Clinically inapparent adrenal masses are incidentally detected after imaging studies conducted for reasons other than the evaluation of the adrenal glands. They have frequently been referred to as adrenal incidentalomas. In preparation for a National Institutes of Health State-of-the-Science Conference on this topic, extensive literature research, including Medline, BIOSIS, and Embase between 1966 and July 2002, as well as references of published metaanalyses and selected review articles identified more than 5400 citations. Based on 699 articles that were retrieved for further examination, we provide a comprehensive update of the diagnostic and therapeutic approaches focusing on endocrine and radiological features as well as surgical options. In addition, we present recent developments in the discovery of tumor markers, endocrine testing for subclinical disease including autonomous glucocorticoid hypersecretion and silent pheochromocytoma, novel imaging techniques, and minimally invasive surgery. Based on the statements of the conference, the available literature, and ongoing studies, our aim is to provide practical recommendations for the management of this common entity and to highlight areas for future studies and research.
Tissue inhibitor of metalloproteinases-1 attenuates spontaneous liver fibrosis resolution in the transgenic mouse
Authors: Hitoshi Yoshiji, Shigeki Kuriyama, Junichi Yoshii, Yasuhide Ikenaka, Ryuichi Noguchi, Toshiya Nakatani, Hirohisa Tsujinoue, Koji Yanase, Tadashi Namisaki, Hiroo Imazu, Hiroshi Fukui
Journal: Hepatology (2002)

It has been suggested that the tissue inhibitor of metalloproteinases-1 (TIMP-1) is involved in spontaneous resolution of liver fibrosis. The aim of this study was to investigate whether TIMP-1 altered spontaneous resolution of liver fibrosis in conjunction with matrix metalloproteinases (MMP) inhibition and hepatic stellate cell (HSC) activation. The livers of liver-targeted TIMP-1 transgenic (TIMP-Tg) and control hybrid (Cont) mice were harvested at 0, 3, 7, and 28 days following spontaneous recovery from CCl 4 -induced liver fibrosis. The extent of fibrosis resolution, MMP expression, α-smooth-muscle actin (α-SMA) positive cells, and procollagen-(I) messenger RNA (mRNA) in the liver were assessed at the respective periods in both groups. We also examined the effect of TIMP-1 on HSC apoptosis. The TIMP-Tg mice showed significantly attenuated resolution of spontaneous liver fibrosis compared with the Cont mice. The hydroxyproline content, number of α-SMA positive cells, and procollagen-(I) mRNA rapidly decreased with time in the Cont mice, whereas these markers were little changed in TIMP-Tg mice. The level of the active form of metalloproteinases-2 (MMP-2) in the TIMP-Tg mice was less than that in the Cont mice. TIMP-1 markedly decreased the nonparenchyma apoptotic cells in the liver fibrosis resolution model, and it also inhibited HSC apoptosis associated with suppression of caspase-3 activity in vitro . In conclusion, TIMP-1 significantly attenuated spontaneous resolution of liver fibrosis by the combination of a net reduction of the MMP activity and suppression of apoptosis in HSC.
Measurement of activity return after injury
Authors: J Agel, E Harvey
Journal: British Journal of Sports Medicine (2011)

Background Injury results in a limitation of activity participation. Treatment of injury is designed to return the patient to as a high level of activity as desired. Objective To design an activity measure that allows clinicians to: Determine patients' pre-injury preferred activities, level of participation, intensity, and frequency of participation. Determine patients' recovery level of participation, intensity, and frequency of participation in the pre-injury preferred activities. Determine if the patients' lack of full return to activity is due to the injury or to other reasons external to the injury. Setting Orthopaedic community based clinics. Participants Patients with musculoskeletal complaints. Intervention Treatment of injury. Main outcome measure The composite of the patients' current activity participation, level of limitation, and reason for limitation. Results Favourite/Most Important Activity Q1 What is this activity? Prior to Your Injury Q2 Prior to your injury: A How long would you normally participate in this activity? |__|__| Hours per Time B On average how many days a week would you participate in this activity? |__| Days per Week Current Time Q3 Do you still engage in this sport or activity? 1 □ Yes 2 □ No Q4 How much is your ability to participate in this activity limited by your injury? 0 1 2 3 4 5 6 7 8 9 10 None Completely If None (0) (Go to Q6 – top of next column) If Limited (1–10) continue with Q5 Q5 What is the primary reason you are limited in this sport or activity anymore? 1 □ Your Injury 2 □ Other Reason – Describe: Conclusion This measure allows clinicians to track return to activity over time and understand if the decision to return to pre-injury activity is due to the injury or life events.
Downregulation of Intestinal Cytochrome P450 in Chronic Renal Failure
Authors: Francois A. Leblond, Martin Petrucci, Pierre Dubé, Gilbert Bernier, Alain Bonnardeaux, Vincent Pichette
Journal: Journal of the American Society of Nephrology (2002)

ABSTRACT. Chronic renal failure (CRF) is associated with a decrease in intestinal drug metabolism. The mechanisms remain poorly understood, but one hypothesis involves a reduction in cytochrome P450 levels. This study aimed to investigate the effects of CRF on intestinal cytochrome P450. Two groups of rats were defined, i.e., rats with CRF (induced by 5/6 nephrectomy) and control pair-fed rats. Total cytochrome P450 levels and protein and mRNA expression of cytochrome P450 isoforms, as well as in vitroN-demethylation of erythromycin (a probe for CYP3A activity) and 7-ethoxyresorufin o-deethylase activity (a probe for CYP1A), were assessed in intestinal microsomes. Body weights were similar in the two groups. Creatinine clearance was reduced by 77% (P < 0.001) in CRF rats, compared with control pair-fed animals. Total intestinal cytochrome P450 activity was reduced by 32% (P < 0.001) in CRF rats. CYP1A1 and CYP3A2 protein expression was considerably reduced (>40%, P < 0.001) in rats with CRF. CYP2B1, CYP2C6, and CYP2C11 levels were the same in the two groups. RT-PCR assays revealed marked downregulation of CYP1A1 and CYP3A2 gene expression in CRF rats (P < 0.001). Although intestinal cytochrome P450 levels were reduced in CRF, induction by dexamethasone was present. N-Demethylation of erythromycin and 7-ethoxyresorufin o-deethylase activity were decreased by 25% (P < 0.05) in CRF rats, compared with control rats. In conclusion, CRF in rats is associated with decreases in intestinal cytochrome P450 activity (mainly CYP1A1 and CYP3A2) secondary to reduced gene expression.
Matrix metalloproteinase-2 and -9 are induced differently by doxorubicin in H9c2 cells: The role of MAP kinases and NAD(P)H oxidase
Authors: P SPALLAROSSA, P ALTIERI, S GARIBALDI, G GHIGLIOTTI, C BARISIONE, V MANCA, P FABBI, A BALLESTRERO, C BRUNELLI, A BARSOTTI
Journal: Cardiovascular Research (2005)

Dysregulation of myocardial metalloproteinases (MMPs) is now regarded as an early contributory mechanism for the initiation and progression of heart failure. Doxorubicin is a strongly cardiotoxic anticancer drug. This study investigates the effects of doxorubicin on myocardial MMP-2 and MMP-9 activation.After pre-treatment with or without carvedilol or dexrazoxane, we exposed H9c2 cardiomyocytes to doxorubicin to evaluate reactive oxygen species (ROS) formation and MMP-2 and MMP-9 expression and activation. To investigate the signaling pathways leading to doxorubicin-induced MMP activation, we also examined the phosphorylation of three members of the MAPK family (ERK1/2, p38, and JNK), the effects of selective inhibitors of ERK1/2, p38, and JNK on MMP transcription and activity, the transcription of the NAD(P)H oxidase subunit Nox1, and the effects of the NAD(P)H oxidase inhibitor DPI on MMP activation.Doxorubicin induces a significant increase in ROS formation and a rapid increase of MMP expression and activation. Pre-treatment with carvedilol or dexrazoxane prevented these effects. We also found that p38 is the MAPK that is mainly responsible for MMP-9 activation through an NAD(P)H-independent mechanism. ERK and JNK modulate the transcription of the NAD(P)H oxidase subunit Nox1, while the JNK/ERK NAD(P)H oxidase cascade is an important pathway that mediates doxorubicin signaling to MMP-2. Inhibition of NAD(P)H oxidase attenuates the increase in MMP-2, but augments the doxorubicin-induced increase in MMP-9.Enhancement of MMP-2 and MMP-9 in cardiac myocytes in response to doxorubicin is mediated by the cooperation of ERK, JNK, and p38 kinase pathways, most of which are redox dependent.
Selective Reporting Biases in Cancer Prognostic Factor Studies
Authors: Panayiotis A. Kyzas, Konstantinos T. Loizou, John P. A. Ioannidis
Journal: JNCI Journal of the National Cancer Institute (2005)

Nonreported and selectively reported information and the use of different definitions may introduce biases in the literature of prognostic factors. We probed these biases in a meta-analysis of a prognostic factor for head and neck squamous cell cancer (HNSCC) mortality that has drawn wide attention--the status of the tumor suppressor protein TP53.We compared results of meta-analyses that included published data plus unpublished data retrieved from investigators; published data; and only published data indexed with "survival" or "mortality" in MEDLINE/EMBASE, with or without standardized definitions. We also evaluated whether previously published meta-analyses on mortality predictors for various malignancies addressed issues of retrieval and standardized information. All statistical tests were two-sided.For the 18 studies with 1364 patients that included published and indexed data, we obtained a highly statistically significant association between TP53 status and mortality. When we used the definitions preferred by each publication, the association was stronger (risk ratio [RR] = 1.38, 95% confidence interval [CI] = 1.13 to 1.67; P = .001) than when we standardized definitions (RR = 1.27, 95% CI = 1.06 to 1.53; P = .011). The addition of 13 studies with 1028 subjects that included published but not indexed data reduced the observed association (RR = 1.23, 95% CI = 1.03 to 1.47; P = .02). Finally, when we obtained data from investigators (11 studies with 996 patients) and analyzed it with all other data, statistical significance was lost (RR = 1.16, 95% CI = 0.99 to 1.35; P = .06). Among 18 published meta-analyses of 37 cancer prognostic factors, 13 (72%) did not use standardized definitions and 16 (89%) did not retrieve additional information.Selective reporting may spuriously inflate the importance of postulated prognostic factors for various malignancies. We recommend that meta-analyses thereof should maximize retrieval of information and standardize definitions.
Targeting Amino Acid Transport in Metastatic Castration-Resistant Prostate Cancer: Effects on Cell Cycle, Cell Growth, and Tumor Development
Authors: Qian Wang, Jessamy Tiffen, Charles G Bailey, Melanie L Lehman, William Ritchie, Ladan Fazli, Cynthia Metierre, Yue Julie Feng, Estelle Li, Martin Gleave, Grant Buchanan, Colleen C Nelson, John E J Rasko, Jeff Holst
Journal: JNCI Journal of the National Cancer Institute (2013)

L-type amino acid transporters (LATs) uptake neutral amino acids including L-leucine into cells, stimulating mammalian target of rapamycin complex 1 signaling and protein synthesis. LAT1 and LAT3 are overexpressed at different stages of prostate cancer, and they are responsible for increasing nutrients and stimulating cell growth.We examined LAT3 protein expression in human prostate cancer tissue microarrays. LAT function was inhibited using a leucine analog (BCH) in androgen-dependent and -independent environments, with gene expression analyzed by microarray. A PC-3 xenograft mouse model was used to study the effects of inhibiting LAT1 and LAT3 expression. Results were analyzed with the Mann-Whitney U or Fisher exact tests. All statistical tests were two-sided.LAT3 protein was expressed at all stages of prostate cancer, with a statistically significant decrease in expression after 4-7 months of neoadjuvant hormone therapy (4-7 month mean = 1.571; 95% confidence interval = 1.155 to 1.987 vs 0 month = 2.098; 95% confidence interval = 1.962 to 2.235; P = .0187). Inhibition of LAT function led to activating transcription factor 4-mediated upregulation of amino acid transporters including ASCT1, ASCT2, and 4F2hc, all of which were also regulated via the androgen receptor. LAT inhibition suppressed M-phase cell cycle genes regulated by E2F family transcription factors including critical castration-resistant prostate cancer regulatory genes UBE2C, CDC20, and CDK1. In silico analysis of BCH-downregulated genes showed that 90.9% are statistically significantly upregulated in metastatic castration-resistant prostate cancer. Finally, LAT1 or LAT3 knockdown in xenografts inhibited tumor growth, cell cycle progression, and spontaneous metastasis in vivo.Inhibition of LAT transporters may provide a novel therapeutic target in metastatic castration-resistant prostate cancer, via suppression of mammalian target of rapamycin complex 1 activity and M-phase cell cycle genes.
A double-blind, placebo-controlled trial of topical 1,25-dihydroxycholecalciferol in psoriasis
Authors: C.A. HENDERSON, J. PAPWORTH-SMITH, W.J. CUNLIFFE, A.S. HIGHET, H.K. SHAMY, B.M. CZARNETZKI
Journal: British Journal of Dermatology (1989)

In a double-blind trial of topical I,25-dihydroxycholecalciferol in 47 patients with psoriasis no benefit was shown compared with placebo.
Failure of Trasylol to reduce intestinal content of trypsin and chymotrypsin in man
Authors: D. M. Goldberg, R. Campbell, A. D. Roy
Journal: Gut (1970)

The daily output of trypsin and chymotrypsin was measured in the stools of four patients with an established ileostomy under controlled dietary and metabolic conditions for a control period of four days. Trasylol, given intravenously in a dose of 500,000 units over eight hours, failed to affect the output of enzymes over the next two days, or to alter the distribution of bound and soluble enzymes.
The place of perceived exertion ratings in exercise prescription for cardiac transplant patients before and after training.
Authors: R J Shephard, T Kavanagh, D J Mertens, M Yacoub
Journal: British Journal of Sports Medicine (1996)

OBJECTIVE: Heart rate provides a poor guide to exercise prescription after cardiac transplantation. This study explores whether the rating of perceived exertion (RPE) provides useful alternative information. METHODS: Borg's original categoric scale was applied to 36 male patients [T, age 47(SD 9 years] as they performed a progressive cycle ergometer test an average of seven months (range two to 23 months) after cardiac transplantation. The test was repeated after 16(7) months of progressive exercise centred rehabilitation. Sedentary but healthy controls [C, n = 45, age 45(7) years] performed a similar progressive cycle test. RESULTS: Initially, 13 RPE units corresponded to 66(12)% of peak VO2 in T and 50(11)% in C. Rehabilitation augmented peak VO2 (by 19%) and estimated lean body mass (by 3.5%) in the cardiac transplant patients. The increase of heart rate (HR) at 13 RPE units [delta HR = 10(17) beats.min-1] showed moderate correlations with gains of lean mass (r = 0.72) and gains of peak VO2 (r = 0.58). The relative oxygen intake at 13 RPE units remained unchanged at 68(12)% of peak VO2. CONCLUSIONS: Large inter-individual variations of RPE at a given VO2 limit the value of perceived exertion in exercise prescription. Ratings seem best restricted to fine tuning fixed distance/fixed speed exercise prescriptions in patients undergoing rehabilitation after cardiac transplantation.
Zoledronic Acid Has Differential Antitumor Activity in the Pre- and Postmenopausal Bone Microenvironment<i>In Vivo</i>
Authors: Penelope D. Ottewell, Ning Wang, Hannah K. Brown, Kimberly J. Reeves, C. Anne Fowles, Peter I. Croucher, Colby L. Eaton, Ingunn Holen
Journal: Clinical Cancer Research (2014)

Clinical trials in early breast cancer have suggested that benefits of adjuvant bone-targeted treatments are restricted to women with established menopause. We developed models that mimic pre- and postmenopausal status to investigate effects of altered bone turnover on growth of disseminated breast tumor cells. Here, we report a differential antitumor effect of zoledronic acid (ZOL) in these two settings.Twleve-week-old female Balb/c-nude mice with disseminated MDA-MB-231 breast tumor cells in bone underwent sham operation or ovariectomy (OVX), mimicking the pre- and postmenopausal bone microenvironment, respectively. To determine the effects of bone-targeted therapy, sham/OVX animals received saline or 100 μg/kg ZOL weekly. Tumor growth was assessed by in vivo imaging and effects on bone by real-time PCR, micro-CT, histomorphometry, and measurements of bone markers. Disseminated tumor cells were detected by two-photon microscopy.OVX increased bone resorption and induced growth of disseminated tumor cells in bone. Tumors were detected in 83% of animals following OVX (postmenopausal model) compared with 17% following sham operation (premenopausal model). OVX had no effect on tumors outside of bone. OVX-induced tumor growth was completely prevented by ZOL, despite the presence of disseminated tumor cells. ZOL did not affect tumor growth in bone in the sham-operated animals. ZOL increased bone volume in both groups.This is the first demonstration that tumor growth is driven by osteoclast-mediated mechanisms in models that mimic post- but not premenopausal bone, providing a biologic rationale for the differential antitumor effects of ZOL reported in these settings. Clin Cancer Res; 20(11); 2922-32. ©2014 AACR.
Prevalence and prognostic implications of CEBPA mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group
Authors: Phoenix A. Ho, Todd A. Alonzo, Robert B. Gerbing, Jessica Pollard, Derek L. Stirewalt, Craig Hurwitz, Nyla A. Heerema, Betsy Hirsch, Susana C. Raimondi, Beverly Lange, Janet L. Franklin, Jerald P. Radich, Soheil Meshinchi
Journal: Blood (2009)
The significance of the Trp 64 Arg mutation of the β3-adrenergic receptor gene in impaired glucose tolerance, non—insulin-dependent diabetes mellitus, and insulin resistance in Japanese subjects
Authors: Nobuyuki Azuma, Yasunao Yoshimasa, Haruo Nishimura, Yuji Yamamoto, Hiroaki Masuzaki, Junko Suga, Michika Shigemoto, Naoki Matsuoka, Tokuji Tanaka, Noriko Satoh, Toshio Igaki, Yoshihiro Miyamoto, Hiroshi Itoh, Takaaki Yoshimasa, Kiminori Hosoda, Shigeo Nishi, Kazuwa Nakao
Journal: Metabolism (1998)
Challenges in Athletics injury and illness prevention: implementing prospective studies by standardised surveillance
Authors: Pascal Edouard, Pedro Branco, Juan-Manuel Alonso
Journal: British Journal of Sports Medicine (2014)

Athletes’ health protection through prevention research is an important goal of the International Olympic Committee (IOC)1 and is a task taken seriously by several major international sports federations including the International Association of Athletics Federations (IAAF)2–5 and the European Athletics (EAA).6 ,7 To this end, surveillance studies have been conducted at 13 international Athletics championships in recent years,2–7 using standardised methods developed by the IOC1 and IAAF.2 ,3 Thus, important data on injury and illness incidences and characteristics in elite athletes during international Athletics competition have been reported and, as demonstrated in the paper by Feddermann et al ,5 successfully monitored over time.

However, the nature of Athletics requires that a vast majority of athletes’ time is spent preparing to compete rather than actually competing. Consequently, injury and illness risk is expected to be higher during training periods than during competition periods only. Our knowledge on their risk of injury and illness during out-of-competition periods …
DERMATO-STOMATITIS (BAADER): COMPLICATIXCT A CASE OF MANIC-DEPRESSIVE INSANITY
Authors: E. BRUCE LOW, J. H. TWISTON DAVIES
Journal: British Journal of Dermatology (1938)

Journal Article DERMATO‐STOMATITIS (BAADER): COMPLICATIXCT A CASE OF MANIC‐DEPRESSIVE INSANITY Get access E. BRUCE LOW, E. BRUCE LOW Medical Superintendent, Southlands Hospital, Shoreham‐by‐Sea Search for other works by this author on: Oxford Academic Google Scholar J. H. TWISTON DAVIES J. H. TWISTON DAVIES Hon. Dermatologist, Royal Sussex County Hospital, Brighton Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 50, Issue 3, 1 March 1938, Pages 141–150, https://doi.org/10.1111/j.1365-2133.1938.tb10514.x Published: 01 March 1938