tbuckley/cabot-search huggingface dataset:
Do Male Lymphoma Survivors Have Impaired Sexual Function?
Authors: Cecilie E. Kiserud, Leslie R. Schover, Alv A. Dahl, Alexander Fosså, Trine Bjøro, Jon Håvard Loge, Harald Holte, Ying Yuan, Sophie D. Fosså
Journal: Journal of Clinical Oncology (2009)

Sexual function in male lymphoma survivors was examined and compared with that of age-matched controls.This cross-sectional study included serum gonadal hormone levels (testosterone, sex hormone-binding globulin, luteinizing hormone [LH], and follicle-stimulating hormone) and responses to questionnaires assessing sexual function (Brief Sexual Function Inventory [BSFI]), socioeconomic factors, quality of life, emotional distress, and fatigue. The lymphoma group included 246 men < or = 50 years old at diagnosis who were diagnosed from 1980 to 2002 and treated at the Norwegian Radium Hospital. For each lymphoma survivor, two age-matched controls (n = 492) were drawn from a normative sample with BSFI scores.The lymphoma survivors had a mean age at survey of 47.4 years, the mean duration of follow-up was 14.8 years, and 79% lived in committed relationships. All BSFI domain scores decreased significantly with age. Lymphoma survivors having low testosterone and/or elevated LH had lower BSFI scores than survivors with normal gonadal hormones. Multivariate analyses showed that increasing age, more emotional distress, poor physical health, and low testosterone and/or elevated LH were significantly associated with reduced sexual function within the lymphoma group. Lymphoma survivors had significantly lower BSFI domain scores than did controls on erection, ejaculation, and sexual satisfaction.Lymphoma survivors had significantly poorer sexual function than normative controls. It is unclear whether the abnormal hormone levels directly cause the reduced sexual function within the lymphoma group or if a mediating factor is involved, such as aging, emotional distress, or perceived health status.
Effect of membrane depolarization on binding of [3H]nitrendipine to rat cardiac myocytes.
Authors: F J Green, B B Farmer, G L Wiseman, M J Jose, A M Watanabe
Journal: Circulation Research (1985)

Binding of the dihydropyridine calcium antagonist [3H]nitrendipine was studied in cardiac myocytes incubated in normal and high potassium buffer so that we might examine the voltage dependence of dihydropyridine binding. Hearts were obtained from adult male Wistar rats, and isolated calcium tolerant myocytes were dissociated by enzymatic dispersion. Cells in 5.6 mM extracellular potassium showed specific binding of [3H]nitrendipine with KD 587 +/- 50 (mean +/- SE) pM and maximum receptor density, Bmax, 10.8 +/- 1.3 fmol/mg wet weight. Cells depolarized in 50 mM potassium showed no change in KD, 661 +/- 77 pM, but approximate doubling of Bmax 25.6 +/- 3.7 fmol/mg wet weight. Binding equilibrium was reached within 5 minutes at 37 degrees C, and the KD determined by kinetic analysis was in good agreement with KD determined by saturation experiments. Unlabeled nitrendipine and nifedipine completely inhibited [3H]nitrendipine binding with slope factors less than one, whereas verapamil and diltiazem only partially inhibited binding with slope factors substantially less than one. As a function of increasing extracellular potassium concentration from 2.4-54.1 mM, the number of nitrendipine-binding sites increased gradually 115%. Aconitine also produced a 58% increase in binding sites over a concentration range of 1-30 micrograms/ml. The potassium-induced changes in number of binding sites occurred rapidly and were rapidly reversible with changes in extracellular potassium concentration. There was no change in the number of [3H]nitrendipine-binding sites as a function of potassium or aconitine concentration in dead or digitonin-treated myocytes. We conclude that nitrendipine receptor density in viable myocytes is voltage dependent, but we detect no change in KD as a function of voltage.
Inspiratory crackles--early and late
Authors: A. R. Nath, L. H. Capel
Journal: Thorax (1974)

<b>Nath, A. R. and Capel, L. H. (1974).</b><i>Thorax</i>, <b>29</b>, 223-227. <b>Inspiratory crackles early and late.</b> Inspiratory crackles were recorded simultaneously with the inspiratory flow rate in patients with airways obstruction and in those with a restrictive defect. Early inspiratory crackles were associated with severe airways obstruction and late inspiratory crackles with a restrictive defect.
Three month treatment of reactive arthritis with azithromycin: a EULAR double blind, placebo controlled study
Authors: T K Kvien, J S H Gaston, T Bardin, I Butrimiene, B A C Dijkmans, M Leirisalo-Repo, P Solakov, M Altwegg, P Mowinckel, P-A Plan, T Vischer
Journal: Annals of the Rheumatic Diseases (2004)

<b>Objective:</b> To determine the efficacy of weekly treatment with oral azithromycin for 13 weeks on the severity and resolution of reactive arthritis (ReA). <b>Methods:</b> 186 patients from 12 countries were enrolled in a randomised, double blind, placebo controlled trial. Inclusion criteria were inflammatory arthritis of ⩽6 swollen joints, and disease duration of ⩽2 months. All patients received a single azithromycin dose (1 g) as conventional treatment for possible <i>Chlamydia</i> infection, and were then randomly allocated to receive weekly azithromycin or placebo. Clinical assessments were made at 4 week intervals for 24 weeks. <b>Results:</b> 152 patients were analysable (34 failed entry criteria), with a mean (SD) age of 33.8 (9.4) and duration of symptoms 30.7 (17.5) days. Mean C reactive protein (CRP) was 48 mg/l, and ∼50% of those typed were HLA-B27+, suggesting that the inclusion criteria successfully recruited patients with acute ReA. Treatment and placebo groups were well matched for baseline characteristics. There were no statistical differences for changes in any end point (swollen and tender joint count, joint pain, back pain, heel pain, physician and patient global assessments, and CRP) between the active treatment and placebo groups, analysed on an intention to treat basis or according to protocol completion. The time to resolution of arthritis and other symptoms or signs by life table analyses was also not significantly different. Adverse events were generally mild, but were more commonly reported in the azithromycin group. <b>Conclusions:</b> This large trial has demonstrated that prolonged treatment with azithromycin is ineffective in ReA.
P282 A Prospective Study To Determine The Accuracy Of Self-reported Smoking Habits In Patients With Tuberculosis
Authors: A. Carver, R. Whitfield, M. Soobratty, G. O'Donovan, G. Grove, G. Cope, H. Milburn
Journal: Thorax (2014)

<h3>Background</h3> Smoking is an independent risk factor for tuberculosis infection, disease and mortality. It is therefore important that clinicians can identify patients who are actively smoking in order to provide optimal care. The reliability of self-reported smoking habits is often questioned but the development of biochemical assays that measure the nicotine metabolite cotinine, allow for an objective assessment of smoking status. Here we assess the accuracy of self-reported smoking habits in patients with tuberculosis by comparing these with urinary cotinine levels. <h3>Methods</h3> Patients were recruited from two London tuberculosis clinics. Self-reported smoking habits were obtained from an interviewer administered questionnaire. Urinary cotinine levels were measured using a SmokeScreen<b><sup>®</sup></b> test kit (GFC Diagnostics, Oxfordshire, UK), a semi-quantitative colorimetric assay. <h3>Results</h3> One hundred patients attending clinic for treatment of active tuberculosis or latent tuberculosis infection completed the study (Table 1). Nineteen reported using tobacco and had either smoked or chewed tobacco the day before testing, the quantity of which was representative of a standard day’s consumption. Duration of smoking ranged from 3 to 40 years with a mean of 13.4+10.5 and a median of 10.0. Eight further patients recorded stopping smoking between a few days and 6 years prior to testing, with a mean cessation period of 2.0+2.1 years. Two of these had later started chewing tobacco. Although nineteen patients reported either smoking or chewing tobacco, a further six patients’ urine tested positive for cotinine, i.e. 24% of tobacco users failed to report its use (Table 1). Furthermore, nine patients produced the colour change indicating heavy smoking (11–15/day) and ten patients produced a result indicating very heavy smoking (&gt;16/day), although only two reported smoking 11–15 cigarettes the previous day and a further two must have chewed an equivalent amount of tobacco. This corresponds to 79% of heavy to very heavy tobacco users under-reporting its use. <h3>Conclusion</h3> Discrepancies exist between objective and subjective assessments of smoking habits amongst patients with TB which may be attributable to an under-reporting of tobacco use, suggesting further avenues of research in this patient cohort.
XIAP variants in male Crohn's disease
Authors: Yvonne Zeissig, Britt-Sabina Petersen, Snezana Milutinovic, Esther Bosse, Gabriele Mayr, Kenneth Peuker, Jelka Hartwig, Andreas Keller, Martina Kohl, Martin W Laass, Susanne Billmann-Born, Heide Brandau, Alfred C Feller, Christoph Röcken, Martin Schrappe, Philip Rosenstiel, John C Reed, Stefan Schreiber, Andre Franke, Sebastian Zeissig
Journal: Gut (2014)

The genetic basis of inflammatory bowel disease (IBD) is incompletely understood. The aim of this study was to identify rare genetic variants involved in the pathogenesis of IBD.Exome sequencing and immunological profiling were performed in a patient with early onset Crohn's disease (CD). The coding region of the gene encoding X-linked inhibitor of apoptosis protein (XIAP) was sequenced in samples of 275 paediatric IBD and 1047 adult-onset CD patients. XIAP genotyping was performed in samples of 2680 IBD patients and 2864 healthy controls. Functional effects of the variants identified were investigated in primary cells and cultured cell lines.Our results demonstrate the frequent occurrence of private variants in XIAP in about four percent of male patients with paediatric-onset CD. While XIAP mutations are known to be associated with the primary immunodeficiency (PID) X-linked lymphoproliferative disease type 2 (XLP2), CD patients described here exhibited intestinal inflammation in the absence of XLP2 and harboured a spectrum of mutations partially distinct from that observed in XLP2. The majority of XIAP variants identified was associated with a selective defect in NOD1/2 signalling, impaired NOD1/2-mediated activation of NF-κB, and altered NF-κB-dependent cytokine production.This study reveals the unanticipated, frequent occurrence of XIAP variants in male paediatric-onset CD. The link between XIAP and NOD1/2, and the association of XIAP variants with XLP2, support the concept of PID in a subset of IBD patients. Moreover, these studies provide a rationale for the implementation of XIAP sequencing in clinical diagnostics in male patients with severe CD.
Phospholipase A2 in inflammatory bowel disease Reply
Authors: T BERTSCH, J AUFENANGER, J PETERSON, G KLIMPEL, A CHOPRA, S SAINI, W DICKEY, W GOURLEY
Journal: Gut (1997)

Phospholipase A 2 in inflammatory bowel disease EDITOR,-Increased release of proinflammatory eicosanoids such as prostaglandin E 2 and thromboxane B 2 from mononuclear cells occurs during relapse in patients with inflammatory bowel disease (IBD). 1 The key enzyme in eicosanoid synthesis is phospholipase A 2 (PLA 2 ).Raised serum concentrations of the PLA 2 group II isoenzyme can be detected by immunoassay during the acute stages of IBD. 2 We read with interest the recent article by Peterson et al about the role of a phospholipase A 2 activating protein, PLAP (Gut 1996; 39: 698-704).The authors showed clearly that PLAP can be detected in monocytes and granulocytes originating from intestinal mucosa of patients with Crohn's disease and ulcerative colitis.In addition to this finding, extracellular deposits of PLAP antigen were associated with blood vessels and oedematous fluid from the inflamed tissue.Peterson et al postulated that PLAP may be involved in increasing PLA 2 activity with consecutive eicosanoid generation in IBD.We propose a further possible mechanism of PLA 2 activation during acute IBD in which the pro-inflammatory cytokine interleukin-6 (IL-6) is a key mediator.Peripheral blood concentrations of this cytokine are raised during acute IBD. 3 We showed recently that recombinant human IL-6 alone can increase serum concentrations of PLA 2 group II isoenzyme in humans. 4 Therefore, we suggest that increased IL-6 concentrations during relapse of IBD are also able to induce PLA 2 by a diVerent mechanism from PLA 2 activation via PLAP.The important role of cytokines in the induction of PLA 2 was confirmed by Crowl et al, 5 who showed that IL-6 could induce PLA 2 in vitro.The molecular mechanism of this induction was further elucidated by detection of an IL-6 response element in the promoter region of the PLA 2 gene. 5 In conclusion, activation of PLA 2 by PLAP could be a possible mechanism for increased eicosanoid synthesis in IBD but direct induction of PLA 2 gene transcription by pro-inflammatory cytokines should be taken into account.Therefore, we suggest a study with parallel measurements of IL-6 and PLA 2 serum concentrations during acute relapse of IBD to correlate these parameters and to determine the profiles of occurrence of these inflammation markers.We have developed a radiometric assay which may be useful as a sensitive and reliable method for absolute measurements of the true PLA 2 group II enzyme activity in serum. 6 Parallel measurements using a PLA 2 group II immunoassay may also indicate whether activation or inhibitory factors of PLA 2 are also present in peripheral blood.
Vascular density and survival in cutaneous melanoma
Authors: J. Marcoval, A. Moreno, J. Graells, A. Vidal, J.M. Escriba, J. Peyri, A. Fabra
Journal: British Journal of Dermatology (1996)

Journal Article Vascular density and survival in cutaneous melanoma Get access J. Marcoval, J. Marcoval Department of Dermatology, CSIU Bellvitge, Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar A. Moreno, A. Moreno Department of Pathology, CSIU Bellvitge, Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar J. Graells, J. Graells Department of Dermatology, CSIU Bellvitge, Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar A. Vidal, A. Vidal Department of Pathology, CSIU Bellvitge, Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar J.M. Escriba, J.M. Escriba Department of Epidemilogy of Cancer, CSIU Bellvitge, Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar J. Peyri, J. Peyri Department of Dermatology, CSIU Bellvitge, Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar A. Fabra A. Fabra Department of Càncer i Metàstasi, Institut de Recerca Oncologica, Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 134, Issue 4, 1 April 1996, Pages 809–810, https://doi.org/10.1111/j.1365-2133.1996.tb07001.x Published: 01 April 1996
Age- and Sex-Specific Prevalence of Diabetes and Impaired Glucose Regulation in 11 Asian Cohorts
Authors: Qing Qiao, Gang Hu, Jaako Tuomilehto, Tomoko Nakagami, Beverley Balkau, Knut Borch-Johnsen, A Ramachandran, V Mohan, S Ramnathan Iyer, Makoto Tominaga, Yutaka Kiyohara, Isao Kato, Ken Okubo, Masaki Nagai, Satomi Shibazaki, Ze Yang, Zhifu Tong, Qinying Fan, Binzhi Wang, Suok Kai Chew, Bee Yian Tan, Derrick Heng, Shanta Emmanuel, Naoko Tajima, Yasuhiko Iwamoto, C Snehalatha, V Vijay, A Kapur, Yanhu Dong, Hairong Nan, Weiguo Gao, Haiyan Shi, Fangming Fu
Journal: Diabetes Care (2003)

OBJECTIVE—To report the age- and sex-specific prevalence of diabetes and impaired glucose regulation (IGR) according to revised World Health Organization criteria for diabetes in Asian populations. RESEARCH DESIGN AND METHODS—We performed 11 studies of 4 countries, comprising 24,335 subjects (10,851 men and 13,484 women) aged 30–89 years who attended the 2-h oral glucose tolerance test and met the inclusion criteria for data analysis. RESULTS—The prevalence of diabetes increased with age and reached the peak at 70–89 years of age in Chinese and Japanese subjects but peaked at 60–69 years of age followed by a decline at the 70 years of age in Indian subjects. At 30–79 years of age, the 10-year age-specific prevalence of diabetes was higher in Indian than in Chinese and Japanese subjects. Indian subjects also had a higher prevalence of IGR in the younger age-groups (30–49 years) compared with that for Chinese and Japanese subjects. Impaired glucose tolerance was more prevalent than impaired fasting glycemia in all Asian populations studied for all age-groups. CONCLUSIONS—Indians had the highest prevalence of diabetes among Asian countries. The age at which the peak prevalence of diabetes was reached was ∼10 years younger in Indian compared with Chinese and Japanese subjects. Diabetes and IGR will be underestimated in Asians based on the fasting glucose testing alone.
Projecting Absolute Invasive Breast Cancer Risk in White Women With a Model That Includes Mammographic Density
Authors: Jinbo Chen, David Pee, Rajeev Ayyagari, Barry Graubard, Catherine Schairer, Celia Byrne, Jacques Benichou, Mitchell H. Gail
Journal: JNCI Journal of the National Cancer Institute (2006)

To improve the discriminatory power of the Gail model for predicting absolute risk of invasive breast cancer, we previously developed a relative risk model that incorporated mammographic density (DENSITY) from data on white women in the Breast Cancer Detection Demonstration Project (BCDDP). That model also included the variables age at birth of first live child (AGEFLB), number of affected mother or sisters (NUMREL), number of previous benign breast biopsy examinations (NBIOPS), and weight (WEIGHT). In this study, we developed the corresponding model for absolute risk.We combined the relative risk model with data on the distribution of the variables AGEFLB, NUMREL, NBIOPS, and WEIGHT from the 2000 National Health Interview Survey, with data on the conditional distribution of DENSITY given other risk factors in BCDDP, with breast cancer incidence rates from the Surveillance, Epidemiology, and End Results program of the National Cancer Institute, and with national mortality rates. Confidence intervals (CIs) accounted for variability of estimates of relative risks and of risk factor distributions. We compared the absolute 5-year risk projections from the new model with those from the Gail model on 1744 white women.Attributable risks of breast cancer associated with DENSITY, AGEFLB, NUMREL, NBIOPS, and WEIGHT were 0.779 (95% CI = 0.733 to 0.819) and 0.747 (95% CI = 0.702 to 0.788) for women younger than 50 years and 50 years or older, respectively. The model predicted higher risks than the Gail model for women with a high percentage of dense breast area. However, the average risk projections from the new model in various age groups were similar to those from the Gail model, suggesting that the new model is well calibrated.This new model for absolute invasive breast cancer risk in white women promises modest improvements in discriminatory power compared with the Gail model but needs to be validated with independent data.
Mammography in management of breast lesions
Authors: W. B. James, R. W. Irvine
Journal: BMJ (1969)

Comparison of the clinical and mammography findings in 101 histologically proved breast lesions showed that the accuracy of each method in diagnosing carcinoma was about 90%, but when taken together an accuracy of 98% was reached. Though mammography was less accurate in the diagnosis of benign lesions, it was found to be a valuable complement in the management of a lesion in the large atrophic breast and for showing an impalpable carcinoma. In mammography of the young dense breast a negative result must be interpreted with caution.
Synthesis and biological evaluation of immunoconjugates of adriamycin and a human IgM linked by poly[N5-2-hydroxyethyl)-l-glutamine]
Authors: C.J.T. Hoes, M. Ankoné, J. Grootoonk, J. Feijen, E. van der Struik, A. van Doornmalen, D. Pham, A. de Man, A. van Ettekoven, I. Schlachter, P.J. Boon, F. Kaspersen, E.S. Bos
Journal: Journal of Controlled Release (1996)
Airway Smooth Muscle Cell Proliferation Is Increased in Asthma
Authors: PETER R. A. JOHNSON, MICHAEL ROTH, MICHAEL TAMM, MARGARET HUGHES, QI GE, GREG KING, JANETTE K. BURGESS, JUDITH L. BLACK
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Increased airway smooth muscle (ASM) within the bronchial wall of asthmatic patients has been well documented and is likely to be the result of increased muscle proliferation. We have for the first time been able to culture ASM cells from asthmatic patients and to compare their proliferation rate with that of nonasthmatic patients. Asthmatic ASM cell cultures (n = 12) were established from explanted lungs and endobronchial biopsies. Nonasthmatic ASM cells (n = 10) were obtained from explanted tissue from patients with no airway disease, emphysema, carcinoma, and fibrosing alveolitis. Cell counts, tritiated thymidine incorporation, and cell cycle analysis were conducted over 7 d. Asthmatic ASM cell numbers at Days 3, 5, and 7 were significantly higher than corresponding values for nonasthmatic cells (p < 0.05). Tritiated thymidine incorporation was increased 3.2-fold in asthmatic cells compared with nonasthmatic cells within the first 24 h (p = 0.026). Flow cytometric analysis of DNA content on Days 1 and 2 revealed that a significantly greater percentage of asthmatic ASM cells were in the G2 + M phase (p < 0.05). This study shows for the first time that proliferation of ASM cells is increased in patients with asthma and provides evidence for an intrinsic abnormality in the ASM cell in this disease.Keywords: asthma; human airway smooth muscle; cell culture; cell proliferation; hyperplasia
EMOTIONAL FACTORS IN ORGANIC DISEASE OF THE CENTRAL NERVOUS SYSTEM
Authors: GEORGE WILSON, CHARLES RUPP, HARVEY BARTLE
Journal: American Journal of Psychiatry (1943)

A series of cases of diverse organic diseases of the central nervous system such as chronic encephalitis with Parkinsonism, multiple sclerosis, pseudo-sclerosis, dystonia musculorum deformans, and brain tumor is presented. In these cases, the initial symptoms became manifest either during or immediately subsequent to some severe emotional disturbance or psychic trauma and the objective neurologic signs were at first minimal. As a result, the symptoms were attributed to emotional causes and only later after the objective neurologic signs had progressed was the correct diagnosis established. The possible role of the emotional disturbances as an etiological factor in the production of the structural changes is discussed. It is suggested that the emotional trauma precipitates both physiologic and psychologic alterations which lead to the appearance of objective neurologic signs.