tbuckley/cabot-search huggingface dataset:
HLA-DR expression on keratinocytes is a common feature of diseased skin
Authors: J. AUBOCK, N. ROMANI, G. GRUBAUER, P. FRITSCH
Journal: British Journal of Dermatology (1986)

Journal Article HLA‐DR expression on keratinocytes is a common feature of diseased skin Get access J. AUBÖCK, J. AUBÖCK Department of Dermatology, University of Innsbruck, Austria Dr Josef Auböck, Department of Dermatology, University of Innsbruck, Anichstr. 35, A‐6020 Innsbruck, Austria. Search for other works by this author on: Oxford Academic Google Scholar N. ROMANI, N. ROMANI Department of Dermatology, University of Innsbruck, Austria Search for other works by this author on: Oxford Academic Google Scholar G. GRUBAUER, G. GRUBAUER Department of Dermatology, University of Innsbruck, Austria Search for other works by this author on: Oxford Academic Google Scholar P. FRITSCH P. FRITSCH Department of Dermatology, University of Innsbruck, Austria Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 114, Issue 4, 1 April 1986, Pages 465–472, https://doi.org/10.1111/j.1365-2133.1986.tb02851.x Published: 01 April 1986 Article history Accepted: 12 September 1985 Published: 01 April 1986
Myocyte cell loss and myocyte cellular hyperplasia in the hypertrophied aging rat heart.
Authors: P Anversa, T Palackal, E H Sonnenblick, G Olivetti, L G Meggs, J M Capasso
Journal: Circulation Research (1990)

To determine the effects of age on the myocardium, the functional and structural characteristics of the heart were studied in rats at 4, 12, 20, and 29 months of age. Mean arterial pressure, left ventricular pressure and its first derivative (dP/dt), and heart rate were comparable in rat groups up to 20 months. During the interval from 20 to 29 months, elevated left ventricular end-diastolic pressure and decreased dP/dt indicated that a significant impairment of ventricular function occurred with senescence. In the period between 4 and 12 months, a reduction of nearly 19% in the total number of myocytes was measured in both ventricles. In the subsequent ages, similar decreases in myocyte cell number were found in the left ventricle, whereas in the right ventricle, the initial loss was fully reversed by 20 months. Moreover, from 20 to 29 months, a 59% increase in the aggregate number of myocytes occurred in the right ventricular myocardium. In the left ventricle, a 3% increment was also seen, but this small change was not statistically significant. These estimations of myocyte cellular hyperplasia, however, were complicated by the fact that cell loss continued to take place with age. The volume fraction of collagen in the tissue, in fact, progressively increased from 8% and 7% at 4 months to 16% and 22% at 29 months in the left and right ventricles, respectively. In conclusion, myocyte cellular hyperplasia tends to regenerate the ventricular mass being lost with age in the adult mammalian rat heart.
Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease
Authors: D. Scheuner, C. Eckman, M. Jensen, X. Song, M. Citron, N. Suzuki, T.D. Bird, J. Hardy, M. Hutton, W. Kukull, E. Larson, L. Levy-Lahad, M. Viitanen, E. Peskind, P. Poorkaj, G. Schellenberg, R. Tanzi, W. Wasco, L. Lannfelt, D. Selkoe, S. Younkin
Journal: Nature Medicine (1996)
Physical Activity and Survival After Breast Cancer Diagnosis
Authors: Michelle D. Holmes, Wendy Y. Chen, Diane Feskanich, Candyce H. Kroenke, Graham A. Colditz
Journal: JAMA (2005)

ContextPhysical activity has been shown to decrease the incidence of breast cancer, but the effect on recurrence or survival after a breast cancer diagnosis is not known.ObjectiveTo determine whether physical activity among women with breast cancer decreases their risk of death from breast cancer compared with more sedentary women.Design, Setting, and ParticipantsProspective observational study based on responses from 2987 female registered nurses in the Nurses’ Health Study who were diagnosed with stage I, II, or III breast cancer between 1984 and 1998 and who were followed up until death or June 2002, whichever came first.Main Outcome MeasureBreast cancer mortality risk according to physical activity category (&lt;3, 3-8.9, 9-14.9, 15-23.9, or ≥24 metabolic equivalent task [MET] hours per week).ResultsCompared with women who engaged in less than 3 MET-hours per week of physical activity, the adjusted relative risk (RR) of death from breast cancer was 0.80 (95% confidence interval [CI], 0.60-1.06) for 3 to 8.9 MET-hours per week; 0.50 (95% CI, 0.31-0.82) for 9 to 14.9 MET-hours per week; 0.56 (95% CI, 0.38-0.84) for 15 to 23.9 MET-hours per week; and 0.60 (95% CI, 0.40-0.89) for 24 or more MET-hours per week (P for trend = .004). Three MET-hours is equivalent to walking at average pace of 2 to 2.9 mph for 1 hour. The benefit of physical activity was particularly apparent among women with hormone-responsive tumors. The RR of breast cancer death for women with hormone-responsive tumors who engaged in 9 or more MET-hours per week of activity compared with women with hormone-responsive tumors who engaged in less than 9 MET-hours per week was 0.50 (95% CI, 0.34-0.74). Compared with women who engaged in less than 3 MET-hours per week of activity, the absolute unadjusted mortality risk reduction was 6% at 10 years for women who engaged in 9 or more MET-hours per week.ConclusionsPhysical activity after a breast cancer diagnosis may reduce the risk of death from this disease. The greatest benefit occurred in women who performed the equivalent of walking 3 to 5 hours per week at an average pace, with little evidence of a correlation between increased benefit and greater energy expenditure. Women with breast cancer who follow US physical activity recommendations may improve their survival.
Mannose-binding lectin in pre-menopausal women with recurrent urinary tract infections
Authors: R. Colodner, O. Nitzan, B. Chazan, H. Edelstein, R. Raz
Journal: Clinical Microbiology and Infection (2010)

Mannose-binding lectin (MBL) comprises an oligomeric serum protein that is a member of the collectin class of the C-type lectin superfamily. Its deficiency is genetically determined and confers predisposition to recurrent infections as well as increased infection severity. This correlation has been demonstrated in recurrent furunculosis caused by Staphylococcus aureus, and in pneumococcal and Candida infections. The present study aimed to determine whether there is a correlation between MBL serum levels and recurrent urinary tact infections (UTI) in pre-menopausal women. The present aged-matched double-blind controlled study was conducted in 100 pre-menopausal adult women: 50 who suffered from recurrent UTI and 50 without UTI. The MBL concentration was measured in a single serum sample from each patient using an enzyme-linked immunosorbent assay. MBL serum levels [median (range)] were 2500 (4-12,000) ng/mL and 2105 (4-22,800) ng/mL for the research and control groups, respectively. The results from the two groups were compared and were not statistically different (p 0.4). According to these results, MBL serum levels are not associated with an increased risk for recurrent UTI in pre-menopausal women.
Sham procedures and the ethics of clinical trials
Authors: F. G Miller, T. J Kaptchuk
Journal: Journal of the Royal Society of Medicine (2004)

Placebo-controlled trials of pharmacological treatments are typically conducted double-blind—that is, neither the patients nor the investigators know whether the substance administered is the agent under investigation or placebo. The process of masking treatment assignment is generally considered ethically acceptable provided that the 'shared ignorance'1 has been made clear in the consent process. However, in circumstances where a surgical or medical procedure itself constitutes the treatment, a randomized placebo-controlled trial raises different issues. Here only the patient-subject is kept in ignorance, and the clinician, who can distinguish active from inactive treatment, may be required to engage in active deception. Examples are surgical operations, acupuncture and specific methods of psychotherapy. Recent papers on the ethics of such trials have focused on the risk–benefit assessment of invasive sham interventions.2–11 Little attention has been given to the psychological and ethical concerns generated by the need for deliberate deception.
Chronic Inhalation of Cigarette Smoke by F344 Rats23
Authors: Walden E. Dalbey, Paul Nettesheim, Richard Griesemer, John E. Caton, Michael R. Guerin
Journal: JNCI Journal of the National Cancer Institute (1980)

Journal Article Chronic Inhalation of Cigarette Smoke by F344 Rats Get access Walden E. Dalbey, Walden E. Dalbey 4Biology Division, Oak Ridge National Laboratory, P.O. Box Y, Oak Ridge, Tenn. 37830. Search for other works by this author on: Oxford Academic PubMed Google Scholar Paul Nettesheim, Paul Nettesheim 5National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, N.C. 27709. Search for other works by this author on: Oxford Academic PubMed Google Scholar Richard Griesemer, Richard Griesemer 6Division of Cancer Cause and Prevention, National Cancer Institute, National Institutes of Health, Public Health Service, U.S. Department of Health, Education, and Welfare, Bethesda, Md. 20205. Search for other works by this author on: Oxford Academic PubMed Google Scholar John E. Caton, John E. Caton 7Analytical Chemistry Division, Oak Ridge National Laboratory, P.O. Box X, Oak Ridge, Tenn. 37830. Search for other works by this author on: Oxford Academic PubMed Google Scholar Michael R. Guerin Michael R. Guerin 7Analytical Chemistry Division, Oak Ridge National Laboratory, P.O. Box X, Oak Ridge, Tenn. 37830. 8We thank Mr. Bob Gill, Mrs. Lavonne Phipps, Mr. Wayne Parsons, Mr. Jesse Webb, and Mr. Charles Knowles for their capable technical assistance, and we thank Dr. Dennis Wolf for statistical analysis. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 64, Issue 2, February 1980, Pages 383–390, https://doi.org/10.1093/jnci/64.2.383 Published: 01 February 1980 Article history Received: 02 May 1979 Accepted: 09 July 1979 Published: 01 February 1980
H-40, an antigen controlled by an Igh linked gene and recognized by cytotoxic T lymphocytes. I. Genetic analysis of H-40 and distribution of its product on B cell tumors.
Authors: J Forman, R Riblet, K Brooks, E S Vitetta, L A Henderson
Journal: The Journal of Experimental Medicine (1984)

C.B-20 ( Ighb ) mice challenged with BALB/c ( Igha ) spleen cells (or vice-versa) generate cytotoxic T lymphocytes (CTL) that recognize an antigen, H-40, controlled by an Igh-linked gene. The gene maps to the Igh-C region end of the Igh complex, telomeric to Tsu in the region of Pre-1. At least three alleles, a, b, and c, can be defined. Using a cold target competition assay, no polymorphism of the a allele was detected. Both surface Igh-5a positive and negative spleen cells from (C.B-20 X BALB/c)F1 animals express the a allele of the antigen, indicating that this gene is not allelically excluded. Recognition of the target antigen by CTL is restricted by the D-end of H-2d. The tissue distribution of H-40 was explored using both bulk-cultured and cloned CTL. The antigen is expressed on surface immunoglobulin positive (sIg+) cells and correlates with the expression of sIgM. This was determined by analysis of several B lymphomas as well as of other tumors that varied in their extent of expression of sIg. Four subclones of BCL1 were analyzed. Two of the subclones are sIg+ and express H-40, while two other subclones are sIg- and H-40-. Thus, these data define an Igh-linked gene, separate from immunoglobulin structural loci, that controls an antigen expressed on sIg+ cells. Possible mechanisms to account for this finding are discussed.
Expansion of Cyclin D and CDK1 Paralogs in Oikopleura dioica, a Chordate Employing Diverse Cell Cycle Variants
Authors: C. Campsteijn, J. I. Ovrebo, B. O. Karlsen, E. M. Thompson
Journal: Molecular Biology and Evolution (2011)

Proliferative and endoreduplicative cell cycles are used to variable extents during the ontogeny of individual organisms and in different evolutionary lineages. Chordate growth and development is typically dominated by proliferative cycles, but the urochordate, Oikopleura dioica, has systemically elaborated a number of endocycling modes to support rapid development and growth in an extraordinarily short chordate life cycle. Here, we identify the O. dioica cyclin and cyclin-dependent kinase (CDK) complements and assess their deployment with respect to mitotic, meiotic, and endoreduplicative life cycle phases. Oikopleura dioica's "transcriptional" cyclin and CDK complements are similar to other complex invertebrates, whereas both the "cell cycle" cyclin and CDK complements display astonishing amplifications centered on the cyclin D, cyclin B, and CDK1 families. Somatic endocycles in O. dioica involve downregulation of cyclins B and A, as in other endocycle model systems, but are also characterized by overlapping expression of an array of cyclin D isoforms. Amplification of the mitotic CDK1 family to five paralogs, which continue to be expressed in endocycling phases, is unexpected as suppression of CDK1 activity is central to endocycle transitions in Drosophila and mammals. This amplification is unique among metazoans, and substitutions in odCDK1 paralogs in the nearly invariant cyclin interaction PSTAIRE helix show striking parallels to those in the only other known eukaryotic CDK1 paralogs, plant CDKA and CDKB. As plant CDK1 paralogs exhibit an expanded repertoire of cyclin partners, including cyclin D, the evolutionary coexpansion of odCDK1 and odCyclin D families suggests that multiple CDK1–cyclin D complexes may modulate spatiotemporal control of kinase activity and substrate specificity in diverse cell cycle variants.
Feasibility, diagnostic accuracy, and effectiveness of decentralised use of the Xpert MTB/RIF test for diagnosis of tuberculosis and multidrug resistance: a multicentre implementation study
Authors: Catharina C Boehme, Mark P Nicol, Pamela Nabeta, Joy S Michael, Eduardo Gotuzzo, Rasim Tahirli, Ma Tarcela Gler, Robert Blakemore, William Worodria, Christen Gray, Laurence Huang, Tatiana Caceres, Rafail Mehdiyev, Lawrence Raymond, Andrew Whitelaw, Kalaiselvan Sagadevan, Heather Alexander, Heidi Albert, Frank Cobelens, Helen Cox, David Alland, Mark D Perkins
Journal: The Lancet (2011)
The Cost-Effectiveness of Screening Mammography beyond Age 65 Years
Authors: Jeanne Mandelblatt, Somnath Saha, Steven Teutsch, Tom Hoerger, Albert L. Siu, David Atkins, Jonathan Klein, Mark Helfand
Journal: Annals of Internal Medicine (2003)

There are few data on the effects of disease biology and competing mortality on the effectiveness of screening women for breast cancer after age 65 years. The authors performed a review to determine the costs and benefits of mammography screening after age 65 years.Cost-effectiveness articles published between January 1989 and March 2002.Studies were identified by using MEDLINE and the National Health Service Economic Evaluation Database. The authors included research on screening after age 65 years conducted from a societal or government perspective; reviews and analyses of other technologies were excluded.115 studies were identified and 10 met inclusion criteria. One study modeled age-dependent assumptions of disease biology. No study fully captured the potential harms of screening, including anxiety associated with false-positive results, overdiagnosis, and previous knowledge of cancer or living longer with the consequences of treatment. Studies differed in the specific strategies compared and in analytic approaches. On average, extending biennial screening to age 75 or 80 years was estimated to cost 34 000 dollars to 88 000 dollars (2002 U.S. dollars) per life-year gained, compared with stopping screening at age 65 years. Two studies suggested that it was more cost-effective to target healthy women than those with several competing risks for death.Current estimates suggest that biennial breast cancer screening after age 65 years reduces mortality at reasonable costs for women without clinically significant comorbid conditions. More data are needed on disease biology and preferences for benefits and harms in older women.
Intravital Staining of the Atrioventricular Bundle with Iodine Compounds during Cardiopulmonary Bypass
Authors: DELMONTE BITTENCOURT, DAVID M. LONG, YUNG K. LEE, C. WALTON LILLEHEI, JOHNSON THOMAS
Journal: Circulation Research (1959)

Complete atrioventricular dissociation occurring as a result of intracardiac reparative surgery has been a relatively infrequent, hut serious complication. Important advances have been made in its treatment through use of isoproterenol (Isuprel) and by use of the myocardial electrode. The next obvious goal is to prevent completely, if possible, the occurrence of heart block and this depends upon an accurate and safe method of identifying the bundle at the time of cardiotomy. Solutions containing free iodine very effectively identified the conduction system at the time of cardiotomy in dogs, but produced lasting interference with cardiac conduction in most all of the animals.
Doublecortin-Like Kinases Promote Neuronal Survival and Induce Growth Cone Reformation via Distinct Mechanisms
Authors: Homaira Nawabi, Stephane Belin, Romain Cartoni, Philip R. Williams, Chen Wang, Alban Latremolière, Xuhua Wang, Junjie Zhu, Daniel G. Taub, Xiaoqin Fu, Bin Yu, Xiaosong Gu, Clifford J. Woolf, Judy S. Liu, Christopher V. Gabel, Judith A. Steen, Zhigang He
Journal: Neuron (2015)
Modulation of the Secretory Pathway Rescues Zebrafish Polycystic Kidney Disease Pathology
Authors: Stéphanie Le Corre, David Eyre, Iain A. Drummond
Journal: Journal of the American Society of Nephrology (2014)

Mutations in polycystin 1 and polycystin 2 are responsible for autosomal dominant polycystic kidney disease, the most common heritable human disease. Polycystins function as calcium ion channels, but their impact on cell physiology is not fully known. Recent findings suggest that polycystins could function in the maintenance of extracellular matrix integrity. In zebrafish, polycystin 2 knockdown induces kidney cysts, hydrocephalus, left/right asymmetry defects, and strong dorsal axis curvature. Here, we show that increased notochord sheath collagen deposition in polycystin 2–deficient embryos is directly linked to axis defects. Increased collagen II protein accumulation did not associate with increased col2a1 mRNA or a decrease in matrix metalloproteinase activity but, instead, it associated with increased expression of the endoplasmic reticulum/Golgi transport coat protein complex II Sec proteins. sec24D knockdown prevented dorsal axis curvature and kidney cystogenesis in polycystin 2 morphants. Nontoxic doses of brefeldin A also prevented the dorsal axis curvature formation in polycystin 2 morphants and curly up polycystin 2 mutants. Brefeldin A treatment after the onset of polycystin deficiency phenotypes reversed the curved axis phenotype but not kidney cyst progression. Our results suggest that polycystin 2 deficiency causes increased collagen II synthesis with upregulation of secretory pathway coat protein complex II components. Restoration of normal rates of secretory protein synthesis and secretion may be a new target in the treatment of autosomal dominant polycystic kidney disease.
A novel mutation in ICOS presenting as hypogammaglobulinemia with susceptibility to opportunistic pathogens
Authors: Janet Chou, Michel J. Massaad, Brittney Cangemi, Wayne Bainter, Craig Platt, Yousef R. Badran, Bram P. Raphael, Daniel S. Kamin, Jeffrey D. Goldsmith, Sung-Yun Pai, Waleed Al-Herz, Raif S. Geha
Journal: Journal of Allergy and Clinical Immunology (2015)
Evidence for the Direct Binding of Phosphorylated p53 to Sites of DNA Breaks <i>In vivo</i>
Authors: Shahnaz T. Al Rashid, Graham Dellaire, Andrew Cuddihy, Farid Jalali, Mita Vaid, Carla Coackley, Melvyn Folkard, Yang Xu, Benjamin P.C. Chen, David J. Chen, Lothar Lilge, Kevin M. Prise, David P. Bazett Jones, Robert G. Bristow
Journal: Cancer Research (2005)

Abstract Despite a clear link between ataxia-telangiectasia mutated (ATM)–dependent phosphorylation of p53 and cell cycle checkpoint control, the intracellular biology and subcellular localization of p53 phosphoforms during the initial sensing of DNA damage is poorly understood. Using G0-G1 confluent primary human diploid fibroblast cultures, we show that endogenous p53, phosphorylated at Ser15 (p53Ser15), accumulates as discrete, dose-dependent and chromatin-bound foci within 30 minutes following induction of DNA breaks or DNA base damage. This biologically distinct subpool of p53Ser15 is ATM dependent and resistant to 26S-proteasomal degradation. p53Ser15 colocalizes and coimmunoprecipitates with γ-H2AX with kinetics similar to that of biochemical DNA double-strand break (DNA-dsb) rejoining. Subnuclear microbeam irradiation studies confirm p53Ser15 is recruited to sites of DNA damage containing γ-H2AX, ATMSer1981, and DNA-PKcsThr2609 in vivo. Furthermore, studies using isogenic human and murine cells, which express Ser15 or Ser18 phosphomutant proteins, respectively, show defective nuclear foci formation, decreased induction of p21WAF, decreased γ-H2AX association, and altered DNA-dsb kinetics following DNA damage. Our results suggest a unique biology for this p53 phosphoform in the initial steps of DNA damage signaling and implicates ATM-p53 chromatin-based interactions as mediators of cell cycle checkpoint control and DNA repair to prevent carcinogenesis.
Dynamic Expression Profile of p21<sup><i>WAF1/CIP1</i></sup> and Ki-67 Predicts Survival in Rectal Carcinoma Treated With Preoperative Radiochemotherapy
Authors: Beate Rau, Isrid Sturm, Hermann Lage, Stefan Berger, Ulrike Schneider, Steffen Hauptmann, Peter Wust, Hanno Riess, Peter M. Schlag, Bernd Dörken, Peter T. Daniel
Journal: Journal of Clinical Oncology (2003)

We investigated p53 and its downstream effectors p21WAF1/CIP1, BAX, and hMSH2 as well as the proliferation marker Ki-67 (mki-67/MIB-1) in patients undergoing preoperative radiochemotherapy for rectal carcinoma to identify prognostic and predictive factors. The focus of this study was on the dynamics of these genetic markers in a longitudinal study-that is, before and after radiochemotherapy.Expression of p53, BAX, p21WAF1/CIP1, Ki-67, and hMSH2 was investigated by immunohistochemistry in pre- and posttherapeutic tumor samples in 66 patients. Tumor DNA was screened for p53 mutations by single-strand conformation polymorphism-polymerase chain reaction (SSCP-PCR). Paired tumor samples (pretherapy and posttherapy) were collected prospectively.Patients with a decrease in p21 expression following radiochemotherapy had better disease-free survival (P =.03). Similarly, patients with an increase in proliferative activity as measured by increased Ki-67 expression posttherapy had better disease-free survival (P <.005). In addition, we observed a significantly better prognosis for patients with high hMSH2 expression. In contrast, pretherapeutic levels of p53, BAX, or p21 expression and p53 mutation had no prognostic value, indicating that the combination of radiotherapy and chemotherapy might override defects in these genes.These findings are novel and support the clinical relevance of p21 in the suppression of both proliferation and apoptosis. Thus, the dynamic induction of p21WAF1/CIP1 was associated with a lower proliferative activity but an ultimately worse treatment outcome following neoadjuvant radiochemotherapy and tumor resection. Induction of p21, therefore, represents a novel resistance mechanism in rectal cancer undergoing preoperative radiochemotherapy.