tbuckley/cabot-search huggingface dataset:
Morbid obesity and hypersomnolence in several members of an ancient royal family
Authors: A Michalopoulos
Journal: Thorax (2003)

Revision of BTS guidelines for treatment of asthmaThe paper by Ward et al 1 confirms the findings of Laitinen et al 2 showing that airways inflammation is present even in patients with mild asthma.This emphasises the importance of using anti-inflammatory drugs (steroids) as soon as the diagnosis of asthma has been confirmed, even in patients thought to have only "mild asthma".Without antiinflammatory treatment, symptoms resulting from bronchial hyperresponsiveness are never controlled and optimal lung function is never attained.Over time, structural changes (remodelling) occur leading to a progressive decline in lung function 3 and the risk of fixed obstruction (chronic obstructive pulmonary disease).The present widespread dependence on bronchodilators in the UK may contribute to the fact that we have one of the highest respiratory death rates in Europe. 4The use of bronchodilators alone as in step 1 of the BTS guidelines should be discouraged, and treatment started at step 2 with regular inhaled corticosteroids to control symptoms and maximise peak flow rate.Bronchodilators should be used only as necessary for breakthrough wheezing.These principles have been used in Finland since 1994 with remarkable success in treating asthma. 5 The new BTS guidelines would do well to follow their example.
Pesticide Exposure and Self-Reported Gestational Diabetes Mellitus in the Agricultural Health Study
Authors: Tina M. Saldana, Olga Basso, Jane A. Hoppin, Donna D. Baird, Charles Knott, Aaron Blair, Michael C.R. Alavanja, Dale P. Sandler
Journal: Diabetes Care (2007)

To examine the association between pesticide use during pregnancy and gestational diabetes mellitus (GDM) among wives of licensed pesticide applicators.
Guidelines of care for the management of atopic dermatitis
Authors: Lawrence F. Eichenfield, Wynnis L. Tom, Timothy G. Berger, Alfons Krol, Amy S. Paller, Kathryn Schwarzenberger, James N. Bergman, Sarah L. Chamlin, David E. Cohen, Kevin D. Cooper, Kelly M. Cordoro, Dawn M. Davis, Steven R. Feldman, Jon M. Hanifin, David J. Margolis, Robert A. Silverman, Eric L. Simpson, Hywel C. Williams, Craig A. Elmets, Julie Block, Christopher G. Harrod, Wendy Smith Begolka, Robert Sidbury
Journal: Journal of the American Academy of Dermatology (2014)
Addressing Spiritual Care: Calling for Help
Authors: C. John Steer, Chris Lee
Journal: Journal of Clinical Oncology (2004)

Discussion Oncologists recognize that a diagnosis of cancer challenges a patient and family in many ways: physical, psychological, practical, and spiritual. While most oncologists have an understanding of how to address the first three issues, they may be less likely to know how to ask for help with the fourth. Using the above scenario as background, this article offers advice on when and how to call on the services of a religious minister or a chaplain. Spirituality, a cardinal feature of human life, relates to an individual’s capacity to seek meaning and purpose in life. It allows a person to be able to see beyond the present situation, to have faith, to be able to worship, and to be able to love and forgive other individuals. Cancer commonly affects the spiritual dimension of patients with cancer. Religious beliefs and practices, a subset of the spirituality domain, play a significant part in the way that some patients cope with their disease and how they make sense of what is happening to them. A physician or health care professional who shows interest in spiritual care expresses concern for the “whole person” who has cancer. The simple screening question, “What role does faith play in your life?” could be all that is needed to assess the dimension of faith in a patient, and to point the way for future support. Physicians should have the same confidence in referring their patients to clergy as they do in referring them to other colleagues. The first step is to understand the distinctions between clergy and chaplaincy.
Treatment of the Acute Alcohol Withdrawal State: A Comparison of Four Drugs
Authors: S. C. KAIM, C. J. KLETT, BENJAMIN ROTHFELD
Journal: American Journal of Psychiatry (1969)

A double-blind study of 537 patients evaluated the relative efficacy of four drugs—chlordiazepoxide, chlorpromazine, hydroxyzine, and thiamine—commonly used in treating alcohol withdrawal symptoms, specifically to prevent delirium tremens and convulsions. Of the 55 patients who developed these symptoms, two percent were in the chlordiazepoxide group; the incidence ranged from ten to 16 percent in the other treatment groups. The authors conclude that chlordiazepoxide appears to be the drug of choice among those tested.
Case of Accidental Poisoning by Tincture of Cantharides
Authors: W. R. S. Jefferiss
Journal: BMJ (1876)

On one point I have reason to congratulate myself, and that is the liberal tone which the medical press, with few exceptions, has observed towards me.Our science, theoretic and practical, is an organism every part of which shares the life of the whole.Isolate any portion of it from the general circulation, and that portion is doomed to atrophy and death.That the ph'sician and the physicist are mutually helpful units in this organism, will become more and more evident as time moves on.Though the apparatus is now in disarray, I should willingly, if it were thought desirable, make arrangements to enable medical men to see my infusions, protected and unprotected.Words can scarcely con- vey a clear notion of the contrast between the hyaline purity of the one and the muddy turbidity of the other.
Illegitimate WNT Pathway Activation by β-Catenin Mutation or Autocrine Stimulation in T-Cell Malignancies
Authors: Richard W.J. Groen, Monique E.C.M. Oud, Esther J.M. Schilder-Tol, Marije B. Overdijk, Derk ten Berge, Roel Nusse, Marcel Spaargaren, Steven T. Pals
Journal: Cancer Research (2008)

Abstract Recent studies in mice have shown a role for the canonical WNT pathway in lymphocyte development. Because cancers often arise as a result of aberrant activation of signaling cascades that normally promote the self-renewal and expansion of their progenitor cells, we hypothesized that activation of the WNT pathway might contribute to the pathogenesis of lymphoproliferative disease. Therefore, we screened a large panel (n = 162) of non–Hodgkin lymphomas (NHL), including all major WHO categories, for nuclear expression of β-catenin, a hallmark of “active” WNT signaling. In 16 lymphomas, mostly of T-lineage origin, nuclear localization of β-catenin was detected. Interestingly, some of these tumors contained established gain-of-function mutations in the gene encoding β-catenin (CTNNB1); however, in the majority, mutations in either CTNNB1 or APC were not detected. Functional analysis of WNT signaling in precursor T-lymphoblastic lymphomas/leukemias, the NHL subset in which β-catenin accumulation was most prevalent (33% positive), revealed a constitutively activated, but still responsive, WNT pathway, which controlled T-cell factor–mediated gene transcription and cell growth. Our data indicate that activation of the WNT pathway, either by CTNNB1 mutation or autocrine stimulation, plays a role in the pathogenesis of a subset of NHLs, in particular, those of T-cell origin. [Cancer Res 2008;68(17):6969–77]
Future for Ovarian Cancer Screening: Novel Markers From Emerging Technologies of Transcriptional Profiling and Proteomics
Authors: G. B. Mills, R. C. Bast, S. Srivastava
Journal: JNCI Journal of the National Cancer Institute (2001)

The completion of the human genome project and the burgeoning use of genomic, transcriptional profiling, and proteomic technologies to investigate DNA, RNA, and protein levels in tumors, serum, plasma, and urine offer the exciting potential of identifying novel and effective cancer-specific screening markers. If the markers are secreted or released from tumor cells and migrate to serum, plasma, urine, or other accessible sites, they may be useful as screening markers either alone or in combination with currently identified tumor markers or screening approaches. Thus, these technologies potentially provide for a rapid advance in the identification of novel tumor markers comparable to that initiated by the introduction of monoclonal antibody technology. In this issue of the Journal, Mok et al. (1), using transcriptional profiling of ovarian cancer cell lines, found that messenger RNA (mRNA) levels of prostasin (a serine protease, previously identified in prostatic secretions), osteopontin (a secreted bone morphogen), and creatine kinase B (a marker for renal and lung cancers) are higher in ovarian cancer cell lines than in normal ovarian epithelial lines. Prostasin mRNA and protein levels subsequently were found to be markedly elevated in ovarian cancer cell lines and in ovarian cancer tissue. The preliminary data presented by Mok et al. (1) suggest that prostasin is released from ovarian cancer cells, migrates to the bloodstream, and may be a novel marker for the diagnosis or management of ovarian cancer. This is exciting evidence that global, nondirected screening approaches at the level of DNA, RNA, or protein may identify a series of markers complementing those found previously by antibody-based or candidate gene approaches. Prostasin has low sensitivity in early-stage disease and lower sensitivity than CA 125, the best characterized marker for advanced epithelial ovarian cancers. Similar to CA 125 (2–4), prostasin levels were frequently elevated in serum from patients with serous epithelial ovarian cancers, with limited increases in serum from patients with mucinous tumors or serous borderline tumors. A lack of correlation between CA 125 and prostasin suggested that combining the two markers could increase the sensitivity. Indeed, in a screen of 37 patients and 100 control subjects, Mok et al. (1) reported that this combination resulted in 92% sensitivity (95% confidence interval [CI] 78.1% to 98.3%) and 94% specificity (95% CI 87.4% to 97.7%), compared with a sensitivity of 64.9% (95% CI 47.5% to 79.8%) for CA 125 and of 51.4% (95% CI 34.4% to 68.1%) for prostasin at a specificity of 94% for prostatin in the same set of samples.
Ustekinumab improves nail disease in patients with moderate‐to‐severe psoriasis: results from <scp>PHOENIX</scp> 1
Authors: P. Rich, M. Bourcier, H. Sofen, S. Fakharzadeh, Y. Wasfi, Y. Wang, U. Kerkmann, P.‐D. Ghislain, Y. Poulin
Journal: British Journal of Dermatology (2013)

Most patients with psoriasis have nail changes, and treating nail psoriasis is challenging.To assess improvement in fingernail psoriasis with ustekinumab treatment in the PHOENIX 1 trial.Patients received ustekinumab 45 mg or 90 mg, or placebo at weeks 0 and 4. Ustekinumab-randomized patients continued maintenance dosing every 12 weeks, while patients receiving placebo crossed over to receive ustekinumab 45 mg or 90 mg at weeks 12/16 followed by dosing every 12 weeks. At week 40, initial responders [those with ≥ 75% improvement from baseline in Psoriasis Area and Severity Index (PASI 75)] were rerandomized either to continue maintenance dosing or to withdraw from treatment. Nail involvement was evaluated using the Nail Psoriasis Severity Index (NAPSI) on a target fingernail, Nail Physician's Global Assessment (Nail PGA) and mean number of nails involved.Of 766 randomized patients, 545 (71·1%) had nail psoriasis. At week 24, the percentage improvement from baseline NAPSI score was 46·5% (ustekinumab 45 mg) and 48·7% (ustekinumab 90 mg). Percentage improvements in NAPSI ranged from 29·7% (PASI < 50) to 57·3% (PASI ≥ 90). Mean NAPSI scores improved from 4·5 at baseline to 2·4 at week 24 (45 mg) and from 4·4 to 2·2 (90 mg). Nail PGA scores and the mean number of psoriatic nails improved by week 24. Further improvement was observed for all end points among initial responders continuing maintenance treatment through week 52.Ustekinumab significantly improves nail psoriasis, and improvements continue over time until up to 1 year of treatment in those receiving maintenance treatment.
Quantitative HER2 and p95HER2 levels in primary breast cancers and matched brain metastases
Authors: R. Duchnowska, J. Sperinde, A. Chenna, W. Huang, J. M. Weidler, J. Winslow, M. Haddad, A. Paquet, Y. Lie, T. Trojanowski, T. Mandat, A. Kowalczyk, B. Czartoryska-Ar ukowicz, B. Radecka, B. Jarosz, R. Staszkiewicz, E. Kalinka-Warzocha, M. Chudzik, W. Biernat, J. Jassem
Journal: Neuro-Oncology (2015)

Patients with advanced breast cancer positive for human epidermal growth factor receptor 2 (HER2) are at high risk for brain metastasis (BM). The prevalence and significance of expression of HER2 and its truncated form p95HER2 (p95) in BM is unknown.Seventy-five pairs of formalin-fixed paraffin-embedded samples from matched primary breast cancers (PBCs) and BM were assayed for quantitative p95 and HER2-total (H2T) protein expression using the p95 VeraTag and HERmark assays, respectively.There was a net increase in p95 and H2T expression in BM relative to the matched PBC (median 1.5-fold, P = .0007 and 2.1-fold, P < .0001, respectively). Cases with H2T-positive tumors were more likely to have the largest (≥5-fold) increase in p95 (odds ratio = 6.3, P = .018). P95 positivity in PBC correlated with progression-free survival (hazard ratio [HR] = 2.2, P = .013), trended with shorter time to BM (HR = 1.8, P = .070), and correlated with overall survival (HR = 2.1, P = .042). P95 positivity in BM correlated with time to BM (HR = 2.0, P = .016) but did not correlate with overall survival from the time of BM diagnosis (HR = 1.2, P = .61).This is the first study of quantitative p95 and HER2 expression in matched PBC and BM. BM of breast cancer shows significant increases in expression of both biomarkers compared with matched PBC. These data provide a rationale for future correlative studies on p95 and HER2 levels in BM.
Therapeutic potency of IL2-caspase 3 targeted treatment in a murine experimental model of inflammatory bowel disease
Authors: S Shteingart, M Rapoport, I Grodzovski, O Sabag, M Lichtenstein, R Eavri, H Lorberboum-Galski
Journal: Gut (2008)

<h3>Background:</h3> Inflammatory bowel disease (IBD) comprises primarily the two disorders – ulcerative colitis and Crohn’s disease – that involve deregulated T cell responses. The ever-increasing incidence rate of Crohn’s disease and ulcerative colitis during recent decades, combined with the limited efficacy and potential adverse effects of current treatments, explain the real need for seeking more specific and selective methods for treating these diseases. <h3>Aim:</h3> To investigate the ability of interleukin 2 (IL2)–caspase 3 chimeric protein, designed to target activated T lymphocytes that express the high-affinity IL2 receptor, to ameliorate the clinical symptoms of acute murine experimental colitis, using a mouse model of dextran sodium sulfate (DSS)-induced colitis. <h3>Methods:</h3> Mice with DSS-induced colitis were treated with IL2–caspase 3 for 7 days and disease severity was assessed in parallel to control, non-treated mice, receiving only daily injections of phosphate-buffered saline. IL2–caspase 3 was tested both for its ability to prevent the development of colitis, and for its therapeutic potential to cure on-going, active acute disease. In addition, colon tissue samples were used for myeloperoxidase assays and RNA isolation followed by polymerase chain reaction to determine mRNA expression levels of specific genes. <h3>Results:</h3> Treatment with IL2–caspase 3 dose-dependently ameliorated the disease activity index (DAI) of mice colitis. We achieved up to 78% improvement in DAI with intravenous injections of 15 μg/mouse/day. Furthermore, IL2–caspase 3 decreased neutrophil and macrophage infiltration to the inflamed tissue by up to 57%. IL2–caspase 3 was proven as a therapeutic reagent in another model, where treatment begins only after disease onset. Here we demonstrated a 70% decrease in DAI when compared to non-treated sick mice. A reduction in mRNA expression levels of both IL1β and tumour necrosis factor α was found in lysates of total colon tissue of treated mice, as compared to sick, untreated mice. We also found that expression levels of Bcl2 were significantly decreased after treatment, while Bax was upregulated in comparison to non-treated mice. Moreover, the Bcl2/Bax ratio, which is elevated in both experimental colitis and in human Crohn’s disease, decreased dramatically after treatment. <h3>Conclusions:</h3> IL2–caspase 3 chimeric protein may provide a novel approach to the therapy of human IBD, and a possible suggested treatment for other pathological conditions that involve uncontrolled expansion of activated T cells.
Intratumoral heterogeneity of HER2/neu expression and its consequences for the management of advanced breast cancer
Authors: P.H. Cottu, J. Asselah, M. Lae, J.-Y. Pierga, V. Diéras, L. Mignot, B. Sigal-Zafrani, A. Vincent-Salomon
Journal: Annals of Oncology (2008)
Prospective Analysis Of Plasma Cholesterol and Triglycerides In Patients (pts) With Chronic Phase (CP)-Chronic Myeloid Leukemia (CML) During Treatment With The 2nd Generation Tyrosine Kinase Inhibitor (TKI) Nilotinib
Authors: Delphine Rea, Tristan Mirault, Jean-Francois Gautier, Francois Guilhot, Emmanuel Messas, Herve Dombret
Journal: Blood (2013)
In Vitro Tests for Immediate Hypersensitivity
Authors: A I Terr
Journal: Annual Review of Medicine (1988)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Intracellular Delivery of Bioactive Cargos to Hard‐to‐Transfect Cells Using Carbon Nanosyringe Arrays under an Applied Centrifugal <i>g</i>‐Force
Authors: Minsuk Choi, Sang Ho Lee, Won Bae Kim, Vipul Gujrati, Daejin Kim, Jinju Lee, Jae‐Il Kim, Hyungjun Kim, Phei Er Saw, Sangyong Jon
Journal: Advanced Healthcare Materials (2015)

There is considerable interest in developing a common, universal platform for delivering biomacromolecules such as proteins and RNAs into diverse cells with high efficiency. Here, it is shown that carbon nanosyringe arrays (CNSAs) under an applied centrifugal g ‐force ( cf ‐CNSAs) can deliver diverse bioactive cargos directly into the cytosol of hard‐to‐transfect cells with relatively high efficiency and reproducibility. The cf ‐CNSA platform, an optimized version of a previous CNSA‐mediated intracellular delivery platform that adds a g ‐force feature, exhibits more rapid and superior delivery of cargos to various hard‐to‐transfect cells than is the case in the absence of g ‐force. Active species, including small interfering RNAs, plasmids, and proteins are successfully transported across plasma membrane barriers into various cells. By overcoming the limitations of currently available transfection methods, the cf ‐CNSA platform paves the way to universal delivery of a variety of cargos, facilitating the analysis of cellular responses in diverse cell types.
Resolution of Pulmonary Edema. Thirty Years of Progress
Authors: Michael A. Matthay
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

In the last 30 years, we have learned much about the molecular, cellular, and physiological mechanisms that regulate the resolution of pulmonary edema in both the normal and the injured lung. Although the physiological mechanisms responsible for the formation of pulmonary edema were identified by 1980, the mechanisms that explain the resolution of pulmonary edema were not well understood at that time. However, in the 1980s several investigators provided novel evidence that the primary mechanism for removal of alveolar edema fluid depended on active ion transport across the alveolar epithelium. Sodium enters through apical channels, primarily the epithelial sodium channel, and is pumped into the lung interstitium by basolaterally located Na/K-ATPase, thus creating a local osmotic gradient to reabsorb the water fraction of the edema fluid from the airspaces of the lungs. The resolution of alveolar edema across the normally tight epithelial barrier can be up-regulated by cyclic adenosine monophosphate (cAMP)-dependent mechanisms through adrenergic or dopamine receptor stimulation, and by several cAMP-independent mechanisms, including glucocorticoids, thyroid hormone, dopamine, and growth factors. Whereas resolution of alveolar edema in cardiogenic pulmonary edema can be rapid, the rate of edema resolution in most patients with acute respiratory distress syndrome (ARDS) is markedly impaired, a finding that correlates with higher mortality. Several mechanisms impair the resolution of alveolar edema in ARDS, including cell injury from unfavorable ventilator strategies or pathogens, hypoxia, cytokines, and oxidative stress. In patients with severe ARDS, alveolar epithelial cell death is a major mechanism that prevents the resolution of lung edema.
Electrophoretic Analysis of P-glycoproteins Produced by Mouse J774.2 and Chinese Hamster Ovary Multidrug-Resistant Cells
Authors: L. M. Greenberger, S. S. Williams, E. Georges, V. Ling, S. B. Horwitz
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article Electrophoretic Analysis of P-glycoproteins Produced by Mouse J774.2 and Chinese Hamster Ovary Multidrug-Resistant Cells Get access Lee M. Greenberger, Lee M. Greenberger 3Departments of Molecular Pharmacology and Cell Biology, Albert Einstein College of Medicine1300 Morris Park Ave., Bronx, NY 10461 Search for other works by this author on: Oxford Academic PubMed Google Scholar Scott S. Williams, Scott S. Williams 3Departments of Molecular Pharmacology and Cell Biology, Albert Einstein College of Medicine1300 Morris Park Ave., Bronx, NY 10461 Search for other works by this author on: Oxford Academic PubMed Google Scholar Elias Georges, Elias Georges 4Department of Medical Biophysics, The Ontario Cancer Institute, University of TorontoToronto, ON, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Victor Ling, Victor Ling 4Department of Medical Biophysics, The Ontario Cancer Institute, University of TorontoToronto, ON, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Susan Band Horwitz Susan Band Horwitz 3Departments of Molecular Pharmacology and Cell Biology, Albert Einstein College of Medicine1300 Morris Park Ave., Bronx, NY 10461 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 80, Issue 7, 1 June 1988, Pages 506–510, https://doi.org/10.1093/jnci/80.7.506 Published: 01 June 1988 Article history Received: 26 February 1988 Accepted: 08 March 1988 Published: 01 June 1988