tbuckley/cabot-search huggingface dataset:
A Survey of the Effects of Oral Contraceptive Patient Information
Authors: Louis A. Morris
Journal: JAMA (1977)

A nationwide survey of 1,720 current and 949 former oral contraceptive (OC) users gathered information about receipt, readership, knowledge, opinions, and reported behavioral changes induced by two forms of patient-oriented OC information. A substantial majority of women said they received and read the patient insert dispensed with the drug. However, only about one third of pill users said that they received the longer informational brochure supplied by physicians on patient request. Directions for use and side effects were the most often recalled information. Physician-patient contact patterns were reported as generally unaffected by written patient information. Respondents preferred the longer informational brochure to the insert. Survey results have implications for recently proposed changes in required OC patient information and for the development of patient information on additional prescription drugs.
Abstract LB-50: Overexpression of <i>PBX1</i> is associated with recurrence and worse clinical outcome in patients with recurrent ovarian high-grade serous carcinoma
Authors: Elisabetta Kuhn, Joon T. Park, Ben Davidson, Robert J. Kurman, Ie-Ming Shih, Tian-Li Wang
Journal: Cancer Research (2010)

Abstract PBX1 has been initially identified as a proto-oncogene in human leukemia in a form of the E2A-PBX1 fusion protein. PBX1 is currently known as a regulator of self renewal of stem cells which contributes to maintenance of a “stemness” phenotype mainly through TGF-ß signaling. PBX1 was recently shown to be elevated in ovarian cancer and its locus was found to be frequently amplified in many cancer types including ovarian carcinoma. In order to further understand the clinicopathological and prognostic significance of PBX1 in ovarian carcinoma, we investigated the gene expression of PBX1 in patients with ovarian high-grade serous carcinoma (HGSC). PBX1 mRNA levels were analyzed in a panel of 78 ascites from patients with HGSC (including 36 primaries and 42 recurrences) by quantitative RT-PCR. Moreover, we performed immunohistochemical staining for PBX1 in 25 pairs of matched primary and recurrent HGSCs from the same patients. The results were correlated with clinicopathological data. Kaplan-Meier analysis demonstrated higher PBX1 levels in ascites from patients with recurrent/chemoresistant HGSC and an association with worse overall survival (p=0.026) as well as disease-free survival (p=0.024). Patients’ effusions with high PBX1 levels (based on median cut-off, n=22) had a mean overall survival of 26 months vs. 39 months for patients whose effusions showed low PBX1 expression (n=20). Patients’ effusions with high PBX1 expression (n=21) also had a mean progression-free survival of 4 months vs. 10 months for patients whose effusions showed low PBX1 levels (n=20). Furthermore, we found more intense PBX1 immunoreactivity in recurrent HGSCs than in matched primaries (Paired t test, p=0.024). Finally, PBX1 expression in primary HGSCs did not demonstrate any significant correlation with patients’ clinical outcome. This study is the first one demonstrating that PBX1 expression correlates with recurrent disease and is associated with worse clinical outcome in patients who develop recurrent HGSC. Future studies will aim at determining the usefulness of PBX1 immunoreactivity as a biomarker to predict patient treatment response and whether it can be a potential molecule for drug-targeted treatment in patients with recurrent HGSC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-50.
THE PRODUCTION OF EXPERIMENTAL PLAUT-VINCENT'S ANGINA IN THE DOG
Authors: Helene Wallace, E. W. Wallace, O. H. Robertson
Journal: Journal of Clinical Investigation (1933)

Since the original description of Plaut-Vincent's angina some fifty years aigo, a voluminous literature on this subject has accumulated.It is not the purpose of this paper to review the literature in any detail as this has been done elsewhere (1, 2).However, it may be stated briefly that the disease was described in 1883 by Miller (18), in 1894 by Plaut (3), and in 1896 by Vincent (4), as manifested by sore and bleeding gums, foul breath, and, in severe cases, by eventual ulceration of the mouth.They dlescribed the causative micro-organisms as a spirochete and a fusiform l)acillus.Since then, these organisms have been found associated with pathological lesions in practically every part of the body, but especially in the upper digestive system, the lungs, and the genitalia.Upon the isolation of the etiological agents the question was immedi- ately raised as to whether they were separate entities or different forms of the same micro-organism.Weaver and Tunicliff (5) succeeded early in cultivating the fusiform bacillus from a patient with Vincent's angina, and on the basis of further work, Tunicliff (6) has stated that she believes the spirochete and bacillus are the same organism in different stages of a definite life cycle.Some workers (7) have supported her, but others (8), and in particular, Pratt (9), have come to the conclusion that these are two distinct micro-organisms.The early literature stressed the infectious nature of the disease, but more recent observations indicate that the causative organisms are found in the normal mouth rather constantly and that the inception of infection depends on the presence of certain predisposing factors.Pratt found fusiform bacilli in 100 per cent of the two hundred people routinely ex- amined at a large hospital.She also found the fusiform bacillus constantly and the spirochete occasionally in normal monkeys, guinea pigs, and rabbits.Other workers have reported analogous findings in these and other animals (2).Thus it would seem that the fusiform bacillus at least is present in the healthy mouth and is not in itself pathogenic.This is borne out by our work.Of forty dogs examined, thirty-eight showed the bacillus, and in those with poor teeth, spirochetes were usually present in the teeth pockets.'
Decline and Rise of Psychoanalysis
Authors: Virginia C. Saft
Journal: JAMA (1974)

To the Editor.—  As a practicing psychoanalyst and psychiatrist, my own experience does not support Dr. Conn's conclusions as to the current status of psychoanalysis. Local, national, and international society membership and meeting attendance suggest quite the opposite.  Statistics from the Chicago Institute for Psychoanalysis, compiled a little over a year ago, indicate that of the roughly 250 graduates, two thirds hold academic appointments in medical schools, ranging from lecturers to department heads to medical school deans. I have no reason to believe that other psychoanalytic training centers have not also made equivalent contributions to the training of future physicians and psychiatrists. How can such statistics be squared with the statement that psychoanalysis is on the way out?  Psychoanalytic theory continues to evolve. It has not stopped, as Dr. Conn implies, with the reification of the id, superego, and ego, nor is it content with increasingly questioned energic metaphors of
Autoantibodies to nucleolar antigens in systemic scleroderma: clinical correlations
Authors: MARIA BLASZCZYK, MARIA JARZABEK-CHORZELSKA, STEFANIA JABLONSKA, T. CHORZELSKI, ZOFIA KOLACINSKA-STRASZ, E.H. BEUTNER, V. KUMAR
Journal: British Journal of Dermatology (2006)

Journal Article Autoantibodies to nucleolar antigens in systemic scleroderma: clinical correlations Get access MARIA BLASZCZYK, MARIA BLASZCZYK Department of Dermatology, Warsaw School of Medicine, Poland Dr Maria Blaszczyk, Department of Dermatology, Warsaw School of Medicine, Koszykowa 82a, 02–008 Warsaw, Poland. Search for other works by this author on: Oxford Academic Google Scholar MARIA JARZABEK‐CHORZELSKA, MARIA JARZABEK‐CHORZELSKA Department of Dermatology, Warsaw School of Medicine, Poland Search for other works by this author on: Oxford Academic Google Scholar STEFANIA JABLONSKA, STEFANIA JABLONSKA Department of Dermatology, Warsaw School of Medicine, Poland Search for other works by this author on: Oxford Academic Google Scholar T. CHORZELSKI, T. CHORZELSKI Department of Dermatology, Warsaw School of Medicine, Poland Search for other works by this author on: Oxford Academic Google Scholar ZOFIA KOLACINSKA‐STRASZ, ZOFIA KOLACINSKA‐STRASZ Department of Dermatology, Warsaw School of Medicine, Poland Search for other works by this author on: Oxford Academic Google Scholar E.H. BEUTNER, E.H. BEUTNER Department of Microbiology, State University of New York at Buffalo, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar V. KUMAR V. KUMAR Department of Microbiology, State University of New York at Buffalo, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 123, Issue 4, 1 October 1990, Pages 421–430, https://doi.org/10.1111/j.1365-2133.1990.tb01445.x Published: 01 October 1990
Blockade of NF-κB ameliorates myocardial hypertrophy in response to chronic infusion of angiotensin II
Authors: S KAWANO, T KUBOTA, Y MONDEN, N KAWAMURA, H TSUTSUI, A TAKESHITA, K SUNAGAWA
Journal: Cardiovascular Research (2005)

Nuclear factor (NF)-kappaB is a key transcription factor that regulates inflammatory processes. In the present study, we assessed the hypothesis that blockade of NF-kappaB may ameliorate ventricular hypertrophy in response to chronic infusion of angiotensin II.Mice with targeted disruption of the p50 subunit of NF-kappaB (KO) were used to block the activation of NF-kappaB. Male KO and age-matched wild-type (WT) mice were chronically infused with angiotensin II at the rate of 0.2 (low dose) or 2 microg/kg/min (high dose) for 4 weeks.High- but not low-dose angiotensin II significantly increased systemic blood pressure and left ventricular weight in WT mice. In contrast, although the pressor response was slightly but significantly augmented, the hypertrophic effect of angiotensin II was significantly attenuated in KO mice. The attenuated hypertrophic responsiveness was confirmed histologically (cross-sectional area) and transcriptionally (atrial natriuretic peptide). Echocardiography revealed no evidence of cardiac dysfunction in angiotensin II-treated KO mice. Although phosphorylation of MAPKs, including ERK, JNK, or p38-MAPK, was not affected after 4 weeks of angiotensin II treatment in WT mice, phosphorylation of JNK was specifically abrogated in KO mice. Angiotensin II increased myocardial expression of proinflammatory cytokines and chemokines in WT mice, while expression of TNF-alpha and RANTES was paradoxically augmented in KO mice.Blockade of NF-kappaB activation attenuated myocardial hypertrophy without deteriorating cardiac function. NF-kappaB may play an important role in cardiac hypertrophy and remodeling besides promoting inflammation.
Release of angiopoietin-1 by primary human acute myelogenous leukemia cells is associated with mutations of nucleophosmin, increased by bone marrow stromal cells and possibly antagonized by high systemic angiopoietin-2 levels
Authors: K J Hatfield, R Hovland, A M Øyan, K H Kalland, A Ryningen, B T Gjertsen, Ø Bruserud
Journal: Leukemia (2007)
Disulfiram, a Clinically Used Anti-Alcoholism Drug and Copper-Binding Agent, Induces Apoptotic Cell Death in Breast Cancer Cultures and Xenografts via Inhibition of the Proteasome Activity
Authors: Di Chen, Qiuzhi Cindy Cui, Huanjie Yang, Q. Ping Dou
Journal: Cancer Research (2006)

Abstract Disulfiram (DSF), a member of the dithiocarbamate family capable of binding copper and an inhibitor of aldehyde dehydrogenase, is currently being used clinically for the treatment of alcoholism. Recent studies have suggested that DSF may have antitumor and chemosensitizing activities, although the detailed molecular mechanisms remain unclear. Copper has been shown to be essential for tumor angiogenesis processes. Consistently, high serum and tissue levels of copper have been found in many types of human cancers, including breast, prostate, and brain, supporting the idea that copper could be used as a potential tumor-specific target. Here we report that the DSF-copper complex potently inhibits the proteasomal activity in cultured breast cancer MDA-MB-231 and MCF10DCIS.com cells, but not normal, immortalized MCF-10A cells, before induction of apoptotic cancer cell death. Furthermore, MDA-MB-231 cells that contain copper at concentrations similar to those found in patients, when treated with just DSF, undergo proteasome inhibition and apoptosis. In addition, when administered to mice bearing MDA-MB-231 tumor xenografts, DSF significantly inhibited the tumor growth (by 74%), associated with in vivo proteasome inhibition (as measured by decreased levels of tumor tissue proteasome activity and accumulation of ubiquitinated proteins and natural proteasome substrates p27 and Bax) and apoptosis induction (as shown by caspase activation and apoptotic nuclei formation). Our study shows that inhibition of the proteasomal activity can be achieved by targeting tumor cellular copper with the nontoxic compound DSF, resulting in selective apoptosis induction within tumor cells. (Cancer Res 2006; 66(21): 10425-33)
Provident Medical Societies in Relation to the Midwifery of the Poor
Authors: T. W. Thursfield
Journal: BMJ (1869)

THE BRITISH MEDICAL _OURNAL.,85the upper, inflating the cheeks, and suddenly compressing them with the tips of the fingers.It is both curious and interesting to witness the constant use which a person, suffering from this affection, is ever making of his fingers in aid of the muscles of the face._N NN N Palsy of the face may result from lesion of the nerve in three different parts of its course-namely, (a) at its origin, from effusion of blood into the brain substance, as in apoplexy; (b) during its course through the petrous bone, from direct injury as fracture, or from disease, as abscess Fj'g. 2. and necrosis; (c) at its peripheral distribution to the muscles of the face from the application of cold, etc.These various lesions, the effects of various causes, offer various prospects of recovery; for, while the first is possibly and the last perhaps certainly, the second is impossibly curable.Itis to this second class that the present case belongs ; for the nerve, having shared in the ulceration going on in the contiguous bone, ultimately suf- fered destruction.The accurate location of the disease involves little or no difficulty; for it is not probable that it exists at the internal auditory foramen, inasmuch as the intimate relation in which the facial there stands to the auditory nerve would, doubtless, have led to the destruction of the latter.Again, it is not probable that the lesion exists posteriorly to the origin of the nervous petrosus superficialis major, for in that case the muscles of the palatine arches would have escaped pa- ralysis, which they have not.It is probable, however, from a positive argument, that the disease exists between these two points ; for during five years it so encroached upon the trunk of the portio mollis as to cause very considerable deafness.
John Bunnell Davis and the Universal Dispensary for Children.
Authors: I S Loudon
Journal: BMJ (1979)

Until 1850, England lagged behind the Continent in the provision of charitable institutions for sick children.'The first was George Armstrong's Dispensary for the Infant Poor, established in 1769.Because it was the first of its kind it has attracted much attention.It was, however, a small single-handed institution run mostly at the founder's own expense,3 which ceased soon after he died in January 1789.3Certainly, the Dispensary for the Infant Poor was smaller and much shorter lived than the general dispensaries that followed it-for example, the Aldersgate (1770), the Westminster General (1774), and the Surrey (1777)-which were larger, influential institutions, and the first three of many general dispensaries that followed in rapid succession.Only a few children were seen at these dispensaries, and, while children's hospitals were being established in all the major cities on the Continent, nothing happened in England until the Universal Dispensary for Children at St Andrew's Hill, Doctors' Commons, was estab- lished in 1816.Other dispensaries also evolved into hospitals and changed their names in the process, but none so con- fusingly as the Universal, which became known as: the Universal Dispensary for Children (1816) and the Royal Universal Dispensary for Children (1821)-both at St Andrew's Hill.
Trophoblast migration during human placental implantation
Authors: T. Burrows
Journal: Human Reproduction Update (1996)

During the process of implantation in humans, fetal trophoblast cells invade and migrate into the maternal decidua. During this migration, trophoblast cells destroy the wall of the maternal spiral arteries, converting them from muscular vessels into flaccid sinusoidal sacs. This vascular transformation is important to ensure an adequate blood supply to the feto-placental unit. Both cell-cell and cell-matrix interactions are important for trophoblast invasion of the decidual stroma and decidual spiral arteries. Cell-matrix adhesions are mediated by specific receptors, mostly belonging to the family of integrins. Signals transduced to the cells from the matrix via integrins could play a pivotal role in the control of cellular behaviour and gene expression, such as metalloproteinases that facilitate matrix degradation and tissue remodelling. This review focuses on the role of integrins and extracellular matrix in trophoblast cell migration, trophoblast invasion of the decidual spiral arteries and matrix degradation by trophoblast during implantation. Keywords: extracellular matrix/integrins/metalloproteinases/trophoblast
Abnormal gastrocolonic response in patients with ulcerative colitis.
Authors: W J Snape, S A Matarazzo, S Cohen
Journal: Gut (1980)

The purpose of these studies is to determine the colonic myoelectrical and contractile response after eating a 1000 calorie meal in patients with active ulcerative colitis. During fasting, slow waves are identifiable significantly more in patients with ulcerative colitis than in normal subjects (p &lt; 0 . 01). The predominant slow wave frequency is 6 . 1 +/- 0 . 2 cycles/min, which is similar to the normal subjects. The slow waves are not altered by eating in either group. Minimal spike or contractile activity occurs during the fasting period both in patients with ulcerative colitis and in normal subjects. In patients with ulcerative colitis, spike activity increases rapidly after eating the 1000 calorie meal (P &lt; 0 . 01), but the maximal response is decreased and shorter in duration than in normal subjects. There is no simultaneous increase in colonic contractility above fasting levels after the meal in patients with ulcerative colitis. This is strikingly different from the simultaneous increase in contractile and spike activity (P &lt; 0 . 01) that occurs after eating in normal subjects. These studies suggest that in ulcerative colitis (1) the colonic smooth muscle slow wave activity is intact; and (2) a disturbance in the normal colonic contractile response to eating is present despite an adequate spike response. This lack of colonic contractility may contribute to the increase in diarrhoea that occurs in these patients after eating.
New Insights in Chronic Obstructive Pulmonary Disease and Comorbidity
Authors: Fiona Cleutjens, Filip Triest, Sarah Wilke, Lowie E. G. W. Vanfleteren, Frits M. E. Franssen, Daisy J. A. Janssen, Erica P. Rutten, Martijn A. Spruit, Emiel F. M. Wouters
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Interest in cognitive impairment in patients with chronic obstructive pulmonary disease (COPD) was raised long ago (2). Yet, it has not been investigated extensively whether COPD is a risk factor for any mild cognitive impairment (MCI), the earliest symptomatic phase of dementia. Singh and colleagues (1) conducted a prospective, population-based study to examine whether diagnosis and duration of COPD are associated with an increased risk for incident MCI and MCI subtypes (amnestic MCI [A-MCI] and nonamnestic MCI [NA-MCI]). A total of 1,425 cognitively normal individuals, including individuals with a medical record–based diagnosis of COPD (n = 171), aged 70 to 89 years, underwent assessment with a nurse interview (including questions about memory and the Clinical Dementia Rating Scale), neurologic examination (including the Short Test of Mental Status and the Unified Parkinson’s Disease Rating Scale), and neuropsychological testing (including nine cognitive tests to assess the cognitive domains of memory, language, executive function, and visuospatial skills) at baseline and every 15 months thereafter. Normal cognition, MCI, or dementia was diagnosed according to published criteria and was based on a consensus agreement among the multidisciplinary staff, taking into account all the information collected. MCI cases were classified into A-MCI or NA-MCI, depending on whether the memory domain was impaired. Three hundred seventy out of 1,425 patients developed incident MCI, of whom 230 (62.2%) had A-MCI, 97 (26.2%) NA-MCI, 27 (7.3%) MCI of unknown type, and 16 (4.3%) progressed from normal cognition at one visit to having dementia at the next. The median duration of follow-up was 5.1 years. After adjusting for covariates, a diagnosis of COPD significantly increased the risk for NA-MCI by 83% but not of any MCI or A-MCI in multivariate analyses. A dose–response relationship was found, such that individuals with COPD duration of longer than 5 years at baseline had the greatest risk for any MCI and NA-MCI. The current study is limited by its lack of data on spirometry and data on smoking duration. In summary, MCI, and particularly NA-MCI, is increased in individuals diagnosed with COPD, and a dose–response relationship was found with the duration of COPD. These findings stress the importance of COPD as a risk factor for MCI and may provide a substrate for early intervention or to treat COPD more aggressively at earlier points to prevent or delay the onset and progression of MCI. n
Overexpression of sarcolipin decreases myocyte contractility and calcium transient
Authors: G BABU, Z ZHENG, P NATARAJAN, D WHEELER, P JANSSEN, M PERIASAMY
Journal: Cardiovascular Research (2004)

Sarcolipin (SLN) is a novel 31-amino-acid protein associated with the sarcoplasmic reticulum (SR) whose function in cardiac muscle is poorly defined. In this study, we tested the hypothesis that SLN is a regulator of SR Ca(2+) transport function by overexpressing SLN in adult rat ventricular myocytes which express low levels of SLN.Expression of SLN mRNA in rat tissues was analyzed by Northern blot as well by RT-PCR analysis. To define the role of SLN in cardiac muscle contractility, we overexpressed SLN in adult rat ventricular myocytes using adenoviral gene transfer techniques. Localization of SLN in the adult rat ventricular myocytes was determined using confocal microscopy. Myocyte contractility and calcium transients were measured using edge detection and Fura 2AM.Our results demonstrate that overexpression of SLN decreased the cell shortening significantly when compared to control myocytes, whereas the time to peak contraction was not altered. In addition, SLN overexpression prolonged the time of 50% relaxation. Calcium transient analysis shows that time to 50% decay of [Ca(2+) ]i was markedly prolonged in SLN-overexpressing myocytes (control -245.0+/-3.78 vs. SLN -199.0+/-3.25 ms, p<0.001). However, there were no significant differences in peak amplitudes of [Ca(2+)](i) between SLN-overexpressing and control myocytes. We further demonstrate that SLN is localized within the SR membrane similar to PLB and SR Ca(2+) ATPase. Co-immunoprecipitation studies indicate that SLN can physically interact with phospholamban.We conclude that SLN may play an important role in regulating the SR calcium ATPase pump, possibly by interacting with phospholamban.