tbuckley/cabot-search huggingface dataset:
Sit to stand transfer: performance in rising power, transfer time and sway by age and sex in senior athletes
Authors: J B Feland, R Hager, R M Merrill
Journal: British Journal of Sports Medicine (2005)

To observe the differences in performance variables of the sit to stand transfer (as measured on the NeuroCom Balance Master) in a population of senior athletes.A convenience sample of 173 subjects aged 50 years and older. Data were obtained from voluntary participation in a health fair offered at the annual Huntsman World Senior Games in St George, Utah, USA. All sit to stand tests were performed on the NeuroCom Balance Master. The measured parameters were weight transfer time (WTT), rising power (force exerted to rise), and centre of gravity sway (COG sway) during the rising phase.A significant difference was found between stratified age groups (50-64 and 65+ years) on rising power. There was also a sex difference in rising power. No significant differences were found in weight transfer time or COG sway.While rising power decreases with increasing age in senior athletes, WTT and COG sway remain similar regardless of age or sex. The maintenance of these other two variables (WTT and COG sway) may be attributable to physical activity and/or participation in sport.
The Bcl-2 Protein: a Prognostic Indicator Strongly Related to p53 Protein in Lymph Node-Negative Breast Cancer Patients
Authors: Rosella Silvestrini, Silvia Veneroni, Maria Grazia Daidone, Elvira Benini, Patrizia Boracchi, Maura Mezzetti, Giovanni Di Fronzo, Franco Rilke, Umberto Veronesi
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article The Bcl-2 Protein: a Prognostic Indicator Strongly Related to p53 Protein in Lymph Node-Negative Breast Cancer Patients Get access Rosella Silvestrini, Rosella Silvestrini Search for other works by this author on: Oxford Academic PubMed Google Scholar Silvia Veneroni, Silvia Veneroni Search for other works by this author on: Oxford Academic PubMed Google Scholar Maria Grazia Daidone, Maria Grazia Daidone Search for other works by this author on: Oxford Academic PubMed Google Scholar Elvira Benini, Elvira Benini Search for other works by this author on: Oxford Academic PubMed Google Scholar Patrizia Boracchi, Patrizia Boracchi Search for other works by this author on: Oxford Academic PubMed Google Scholar Maura Mezzetti, Maura Mezzetti Search for other works by this author on: Oxford Academic PubMed Google Scholar Giovanni Di Fronzo, Giovanni Di Fronzo Search for other works by this author on: Oxford Academic PubMed Google Scholar Franco Rilke, Franco Rilke Search for other works by this author on: Oxford Academic PubMed Google Scholar Umberto Veronesi Umberto Veronesi Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 7, 6 April 1994, Pages 499–504, https://doi.org/10.1093/jnci/86.7.499 Published: 06 April 1994 Article history Received: 28 June 1993 Revision received: 30 December 1993 Accepted: 10 January 1994 Published: 06 April 1994
Management of latent tuberculosis infection
Authors: James Brown
Journal: Thorax (2012)

Management of latent tuberculosis infectionTreatment for latent tuberculosis has the potential to significantly reduce the incidence of active tuberculosis infection, but patient adherence to treatment regimens is often limited by the lengthy duration of treatment required.This study evaluated the efficacy of a 3-month regimen of rifapentine plus isoniazid administered as directly observed once-weekly therapy compared with 9 months daily self-administered isoniazid.The investigators carried out an open-label non-inferiority trial in which 3986 subjects were randomised to combination therapy and 3745 randomised to isoniazid monotherapy.Subjects were enrolled if they had a positive tuberculin skin test or were a close contact of a patient with tuberculosis.Contacts of patients with drug-resistant tuberculosis were excluded.Subjects were followed-up for 33 months from enrolment and the primary end point evaluated was the development of active tuberculosis in the study subjects.The study demonstrated that 3 months directly observed weekly combination therapy is non-inferior to 9 months daily self-administered isoniazid.Seven patients developed tuberculosis in the combination group (0.19%) compared with 15 in the monotherapy group (0.43%).There was a trend to improved efficacy in the combination therapy group.Rates of hepatotoxicity were greater in the isoniazid only group, and hypersensitivity reactions were greater with combination therapy, but serious adverse events did not differ significantly between the groups.Rifapentine plus isoniazid could be an alternative to standard preventive therapy.
Metastatic Growth Progression Caused by PSGL-1–Mediated Recruitment of Monocytes to Metastatic Sites
Authors: Alexandra Hoos, Darya Protsyuk, Lubor Borsig
Journal: Cancer Research (2013)

Abstract Tumor cell–derived selectin ligands mediate contact to the endothelium, platelets, and leukocytes through binding to selectins that facilitates metastasis. Here, we describe the mechanism of how endogenous (non–tumor derived) selectin ligands contribute to metastasis using α(1,3)fucosyltransferase 7 (Fuc-TVII−/−)–deficient mice. Experimental metastasis of MC-38GFP and Lewis lung (3LL) carcinoma cells was attenuated in Fuc-TVII−/− mice, which express minimal amount of selectin ligands. We show that metastasis is dependent on selectin ligands carried on hematopoietic cells. P-selectin glycoprotein ligand-1 (PSGL-1) was identified as the major ligand facilitating monocyte accumulation at metastatic sites. Reduced recruitment of monocytes to metastasizing tumor cells in Fuc-TVII−/− mice correlated with attenuated metastasis. Adoptive transfer of Fuc-T7+ monocytes rescued metastasis in Fuc-TVII−/− mice, indicating that selectin ligand–dependent recruitment of monocytes is required for cancer progression. Cytokine analysis in metastatic lungs revealed high expression of CCL2 in C57BL/6 mice that was significantly lower in Fuc-TVII−/− mice. The absence of monocyte recruitment in Fuc-TVII−/− mice correlated with increased apoptosis of tumor cells. Thus, the recruitment of monocytes to metastasizing tumor cells is facilitated by endogenous selectin ligands on monocytes that enable efficient tumor cell survival, extravasation, and metastasis. Cancer Res; 74(3); 695–704. ©2013 AACR.
Colorectal cancer pulmonary oligometastases: pooled analysis and construction of a clinical lung metastasectomy prognostic model
Authors: S. Salah, K. Watanabe, S. Welter, J.S. Park, J.W. Park, J. Zabaleta, F. Ardissone, J. Kim, M. Riquet, K. Nojiri, M. Gisabella, S.Y. Kim, K. Tanaka, B. Al-Haj Ali
Journal: Annals of Oncology (2012)
Malaria held captive
Authors: Heather L. Van Epps
Journal: The Journal of Experimental Medicine (2005)

Malaria sporozoites that lack a certain protease get trapped in their cyst-like breeding ground (the oocyst), as shown by Aly and Matuschewski (page 225). Unable to break free, these captive parasites turn in helpless circles inside the oocyst and their life cycle halts.






Figure 

Malaria sporozoites that lack egress cysteine protease 1 get trapped inside the oocyst (shown) in the mosquito midgut.




Malaria-causing parasites (Plasmodium species) have a complex life cycle that includes several distinct stages of intracellular growth in vertebrate and mosquito hosts. Movement from one stage to the next requires exit from one host cell and entry into another. Invasion of target cells has been shown to require parasite-encoded proteases that, by poorly defined mechanisms, allow the bug to penetrate cell membranes. Parasite exit from target cells has been even less well-studied.Aly and Matuschewski now identify a cysteine protease that is selectively expressed at the late sporozoite stage, just before sporozoite release and entry into the mosquito salivary glands. Elimination of this protease from the parasite caused mature sporozoites to become trapped inside the oocyst, a protective compartment forged from the basal lamina of the mosquito midgut where the sporozoites divide and grow. There they commenced an unusual circular motion, the significance of which is not yet understood.

These data suggest that Plasmodium egress is an active process that requires the protease—dubbed egress cysteine protease 1—to actively break down the oocyst wall, rather than a passive one in which the oocyst simply ruptures once it is filled to capacity.
Antibodies to basement membrane collagen and to laminin are present in sera from patients with poststreptococcal glomerulonephritis.
Authors: N A Kefalides, M T Pegg, N Ohno, T Poon-King, J Zabriskie, H Fillit
Journal: The Journal of Experimental Medicine (1986)

Sera from patients with poststreptococcal glomerulonephritis (PSGN) known to have antibodies to proteoglycans were studied for the presence of antibodies against other basement membrane (BM) components. BM collagen (type IV) was isolated in the native state by extracting bovine anterior lens capsule (ALC) with 0.5 M acetic acid. The 7-S (collagenous) domain and the NC-1 (noncollagenous) domain of type IV collagen were obtained after bacterial collagenase digestion of ALC followed by gel filtration. Laminin was isolated from the mouse EHS tumor and fibronectin from human plasma. Immunologic studies, using an ELISA and electroimmunoblot, revealed the presence of antibodies that reacted with intact, native type IV collagen and the 7-S collagenous domain of this molecule. Reaction with the NC-1 (noncollagenous) domain was minimal, and not higher than that obtained with control sera. Laminin reaction strongly with the patients' sera, but fibronectin did not. Unlike sera from patients with Goodpasture syndrome, which contain antibodies primarily against the NC-1 (noncollagenous) domain of type IV collagen, sera from patients with acute PSGN contain antibodies against all the major macromolecular components of BM. This difference in immunologic reactivity may account for the observed differences in the pathologic picture at the glomerular level.
Phosphorylcholine-specific helper T cells in mice with an X-linked defect of antibody production to the same hapten.
Authors: R B Kaplan, J Quintáns
Journal: The Journal of Experimental Medicine (1979)

F1 male mice with the CBA/N X-linked defect that are unable to produce plaque-forming cell responses to phosphorylcholine (PC) provide normal PC-specific helper T-cell activity when compared to F1 female littermates. Inhibition of helper activity with anti-idiotypic antiserum indicates that PC-specific T cells from both NBF1 female and male mice possess predominantly BALB/c myeloma protein HOPC-8 idiotypic determinants. Therefore, the CBA/N defect cannot be explained as a deletion of genes coding for V-region anti-PC specificities. The demonstration of helper activity in NBF1 male mice, which occurs in the absence of anti-PC antibody synthesis, also demonstrates the endogenous origin of the T-cell receptor.
Heart failure and mortality outcomes in patients with type 2 diabetes taking alogliptin versus placebo in EXAMINE: a multicentre, randomised, double-blind trial
Authors: Faiez Zannad, Christopher P Cannon, William C Cushman, George L Bakris, Venu Menon, Alfonso T Perez, Penny R Fleck, Cyrus R Mehta, Stuart Kupfer, Craig Wilson, Hung Lam, William B White
Journal: The Lancet (2015)
Influence of Oct1/Oct2-Deficiency on Cisplatin-Induced Changes in Urinary <i>N</i>-Acetyl-β-D-Glucosaminidase
Authors: Ryan M. Franke, Ashley M. Kosloske, Cynthia S. Lancaster, Kelly K. Filipski, Chaoxin Hu, Oliver Zolk, Ron H. Mathijssen, Alex Sparreboom
Journal: Clinical Cancer Research (2010)

This study aimed to test the influence of functional renal organic cation transporters (OCT2 in humans, Oct1 and Oct2 in mice) on biomarkers of cisplatin nephrotoxicity, such as urinary activity of N-acetyl-beta-D-glucosaminidase (NAG).Temporal cisplatin-induced nephrotoxicity was assessed by histopathology and biomarkers. Cisplatin-mediated NAG changes and survival were determined in wild-type and Oct1/2(-/-) mice. Identification of OCT2 inhibitors was done in transfected 293Flp-In cells, and the NCI(60) cell line panel was used to assess contribution of OCT2 to cisplatin uptake in cancer cells.Classical biomarkers such as blood urea nitrogen and serum creatinine were not elevated until 72 hours after cisplatin administration and substantial kidney damage had occurred. Oct1/2(-/-) mice had 2.9-fold lower NAG by 4 hours (P < 0.0001) and 2.3-fold increased survival (P = 0.0097). Among 16 agents, cimetidine strongly inhibited uptake of tetraethylammonium bromide (P = 0.0006) and cisplatin (P < 0.0001), but did not have an influence on cisplatin uptake in SK-OV-3 cells, the cancer line with the highest OCT2 mRNA levels. In wild-type mice, cimetidine inhibited cisplatin-induced NAG changes (P = 0.016 versus cisplatin alone) to a degree similar to that seen in Oct1/2(-/-) mice receiving cisplatin (P = 0.91). Cumulative NAG activity of >0.4 absorbance units (AU) was associated with 21-fold increased odds for severe nephrotoxicity (P = 0.0017), which was linked with overall survival (hazard ratio, 8.1; 95% confidence interval, 2.1-31; P = 0.0078).Cimetidine is able to inhibit OCT2-mediated uptake of cisplatin in the kidney, and subsequently ameliorate nephrotoxicity likely with minimal effect on uptake in tumor cells.
Perioperative FOLFOX4 chemotherapy and surgery versus surgery alone for resectable liver metastases from colorectal cancer (EORTC 40983): long-term results of a randomised, controlled, phase 3 trial
Authors: Bernard Nordlinger, Halfdan Sorbye, Bengt Glimelius, Graeme J Poston, Peter M Schlag, Philippe Rougier, Wolf O Bechstein, John N Primrose, Euan T Walpole, Meg Finch-Jones, Daniel Jaeck, Darius Mirza, Rowan W Parks, Murielle Mauer, Erik Tanis, Eric Van Cutsem, Werner Scheithauer, Thomas Gruenberger
Journal: The Lancet Oncology (2013)
Comparative Profiling of the Novel Epothilone, Sagopilone, in Xenografts Derived from Primary Non–Small Cell Lung Cancer
Authors: Stefanie Hammer, Anette Sommer, Iduna Fichtner, Michael Becker, Jana Rolff, Johannes Merk, Ulrich Klar, Jens Hoffmann
Journal: Clinical Cancer Research (2010)

Characterization of new anticancer drugs in a few xenograft models derived from established human cancer cell lines frequently results in the discrepancy between preclinical and clinical results. To take the heterogeneity of tumors into consideration more thoroughly, we describe here a preclinical approach that may allow a more rational clinical development of new anticancer drugs.We tested Sagopilone, an optimized fully synthetic epothilone, in 22 well-characterized patient-derived non-small cell lung cancer models and correlated results with mutational and genome-wide gene expression analysis.Response analysis according to clinical trial criteria revealed that Sagopilone induced overall responses in 64% of the xenograft models (14 of 22), with 3 models showing stable disease and 11 models showing partial response. A comparison with response rates for established drugs showed the strong efficacy of Sagopilone in non-small cell lung cancer. In gene expression analyses, Sagopilone induced tubulin isoforms in all tumor samples, but genes related to mitotic arrest only in responder models. Moreover, tumors with high expression of genes involved in cell adhesion/angiogenesis as well as of wild-type TP53 were more likely to be resistant to Sagopilone therapy. As suggested by these findings, Sagopilone was combined with Bevacizumab and Sorafenib, drugs targeting vascular endothelial growth factor signaling, in Sagopilone-resistant models and, indeed, antitumor activity could be restored.Analyses provided here show how preclinical studies can provide hypotheses for the identification of patients who more likely will benefit from new drugs as well as a rationale for combination therapies to be tested in clinical trials.
Intracoronary cardiosphere-derived cells for heart regeneration after myocardial infarction (CADUCEUS): a prospective, randomised phase 1 trial
Authors: Raj R Makkar, Rachel R Smith, Ke Cheng, Konstantinos Malliaras, Louise EJ Thomson, Daniel Berman, Lawrence SC Czer, Linda Marbán, Adam Mendizabal, Peter V Johnston, Stuart D Russell, Karl H Schuleri, Albert C Lardo, Gary Gerstenblith, Eduardo Marbán
Journal: The Lancet (2012)
Amine Precursors, Amines, and False Neurotransmitters in Depressed Patients
Authors: DENNIS L. MURPHY
Journal: American Journal of Psychiatry (1972)

Some inconsistencies in the biogenic amine hypothesis of depression have arisen from clinical studies with L-dopa and L-tryptophan, the metabolic precursors of the amines. The evidence obtained from the studies of changes in cellular amine levels in depressed patients reported here suggests that the interactions between catecholamines and indoleamines, and possibly other "false transmitter" amines, need to be considered in reevaluating the role of biogenic amines in the affective disorders.
Precursors to theories of mind in nonhuman brains
Authors: Stephen F. Walker
Journal: Behavioral and Brain Sciences (1998)

Heyes is right that behavioural tests able to distinguish mentalistic from nonmentalistic alternatives should be sought, but the theoretical issue is less about the passing of behavioural tests than it is about the internal mechanisms which allow the passing of the tests. It may be helpful to try to assess the internal mechanisms directly by measuring brain activities.
Treatment of Experimental Viral Myocarditis With Interleukin-10
Authors: Ryosuke Nishio, Akira Matsumori, Tetsuo Shioi, Hiroshi Ishida, Shigetake Sasayama
Journal: Circulation (1999)

Background —The T helper cell type 2–associated cytokine interleukin (IL)-10 has a variety of immunomodulatory properties. However, the effects of the cytokine on viral myocarditis remain unclear. Methods and Results —We studied the effects of recombinant human IL-10 (rhIL-10) fully active on mouse cells in a murine experimental model of acute viral myocarditis caused by the encephalomyocarditis virus (EMCV). Four-week-old DBA/2 mice were inoculated with EMCV (day 0). rhIL-10 (10 μg/mouse) was administered once daily, starting on day 0, and control mice received vehicle only. Survival rates were determined on day 14. Myocardial histopathology, cytokine levels in the heart by ELISA assay, and myocardial virus concentration were examined on day 6, and the expression levels of myocardial inducible nitric oxide synthase (iNOS) mRNA were measured by competitive polymerase chain reaction. The 14-day survival in mice treated with rhIL-10 was significantly higher (80%) than in the control group (30%, n=10 in each, P &lt;0.05). rhIL-10 treatment significantly attenuated myocardial lesions and suppressed tumor necrosis factor-α and IL-2 in the heart. rhIL-10 treatment had little effect on myocardial virus concentration. The expression levels of myocardial iNOS mRNA were significantly decreased in the group treated with rhIL-10 (8.6±4.7 amol/mg total RNA in treated versus 26.5±7.1 amol/mg total RNA in control mice, P &lt;0.05). Conclusions —These findings provide new insights into the in vivo effects of IL-10 on viral infection and suggest a therapeutic effect of IL-10 on viral myocarditis.
Anemia and Iron Deficiency — New Therapeutic Targets in Heart Failure?
Authors: G. William Dec
Journal: New England Journal of Medicine (2009)

Anemia ranges in prevalence from below 10% among patients with mild heart failure symptoms to over 40% for patients with advanced disease.1 Its prevalence is similar among patients who have systolic dysfunction and among patients who have heart failure with preserved systolic function.2,3 Anemia has been associated with older age, diabetes mellitus, chronic renal dysfunction, more advanced heart failure symptoms, lower peak exercise capacity, and worse health-related quality-of-life metrics.3 Anemia has also been shown to be a powerful predictor of rehospitalization rates and survival in chronic heart failure.A complex interaction between impaired cardiac performance, activation of neurohormonal and . . .
Combined 1p/19q Loss in Oligodendroglial Tumors: Predictive or Prognostic Biomarker?
Authors: Michael Weller, Hilmar Berger, Christian Hartmann, Johannes Schramm, Manfred Westphal, Matthias Simon, Roland Goldbrunner, Dietmar Krex, Joachim P. Steinbach, Christoph B. Ostertag, Markus Loeffler, Torsten Pietsch, Andreas von Deimling
Journal: Clinical Cancer Research (2007)

Abstract Purpose: The combined loss of genetic material on chromosomes 1p and 19q is strongly associated with favorable outcome in patients with WHO grade 3 anaplastic oligodendroglial tumors. The prognostic value of 1p/19q loss in WHO grade 2 oligodendroglial tumors is less well defined. Importantly, the possible effect of combined 1p/19q loss has not been studied in patients who were not treated with radiotherapy or chemotherapy. Experimental Design: Seventy-six patients with oligodendroglioma (n = 33), oligoastrocytoma (n = 30), anaplastic oligodendroglioma (n = 6), or anaplastic oligoastrocytoma (n = 7) were identified who had not received radiotherapy or chemotherapy after their first operation until the end of follow-up or until the first progression and had tissue for 1p/19q status available. 1p/19q status was assessed by multiplex ligation–dependent probe amplification. Results: After a median follow-up of 3.8 years, progressive disease was documented in 34 patients. The estimated median progression-free survival was 4.6 years. Fifty-eight of the 76 patients had a combined loss of 1p and 19q. The absence or presence of combined 1p/19q loss was not prognostic for progression-free survival using multivariate adjustment for histology, extent of resection, and gender. Conclusions: Combined 1p/19q loss is not a sensitive prognostic biomarker in patients with oligodendroglial tumors who do not receive radiotherapy or chemotherapy. The gene products lost as a consequence of this codeletion may include mediators of resistance to genotoxic therapies. Alternatively, 1p/19q loss might be an early oncogenic lesion promoting the formation of glial neoplasms, which retain high sensitivity to genotoxic stress.
Thymocyte Maturation Is Regulated by the Activity of the Helix-Loop-Helix Protein, E47
Authors: Gretchen Bain, Melanie W. Quong, Rachel S. Soloff, Stephen M. Hedrick, Cornelis Murre
Journal: The Journal of Experimental Medicine (1999)

The E2A proteins, E12 and E47, are required for progression through multiple developmental pathways, including early B and T lymphopoiesis. Here, we provide in vitro and in vivo evidence demonstrating that E47 activity regulates double-positive thymocyte maturation. In the absence of E47 activity, positive selection of both major histocompatibility complex (MHC) class I– and class II–restricted T cell receptors (TCRs) is perturbed. Additionally, development of CD8 lineage T cells in an MHC class I–restricted TCR transgenic background is sensitive to the dosage of E47. Mice deficient for E47 display an increase in production of mature CD4 and CD8 lineage T cells. Furthermore, ectopic expression of an E2A inhibitor helix-loop-helix protein, Id3, promotes the in vitro differentiation of an immature T cell line. These results demonstrate that E2A functions as a regulator of thymocyte positive selection.