tbuckley/cabot-search huggingface dataset:
Opportunistic pulmonary infections with fludarabine in previously treated patients with low‐grade lymphoid malignancies: A role for pneumocystis carinii pneumonia prophylaxis
Authors: John C. Byrd, Jeffrey B. Hargis, Kent E. Kester, Duane R. Hospenthal, Sarah W. Knutson, Louis F. Diehl
Journal: American Journal of Hematology (1995)

Abstract The high incidence of opportunistic pulmonary infections in fludarabine‐treated patients at Walter Reed Army Medical Center (WRAMC) and in the literature are described. A CancerLlt search of fludarabine from June 1983‐April 1994 with subsequent cross referencing and a retrospective review of all patients receiving fludarabine at WRAMC was performed. A total of 2,269 patients with low‐grade lymphoid malignancies who received 7,547 + cycles of fludarabine were identified from the literature. Seventy‐three (3.2%) of these patients developed opportunistic infections. Seventy‐one (97%) of these infections occurred in patients who were pretreated with alkylator regimens or corticosteroids. Forty‐five (2%) of these were of respiratory origin and associated with a 56% mortality rate. In contrast, 6 of the 21 patients (29%) treated with fludarabine at WRAMC developed opportunistic pulmonary infections which included three Pneumocystis carinii (PCP), one PCP/disseminated Candidiasis, one Mycobacterium avium intracellulare , and one Aspergillus niger pneumonia. These infections developed during and after treatment with fludarabine in alkylator‐resistant patients who had received corticosteroids before (n = 6), during (n = 1), or after (n = 4) fludarabine therapy. Lack of PCP prophylaxis was the only significant ( P = .018) variable that differentiated patients who developed opportunistic pulmonary infections. Corticosteroid treatment before, during, or after fludarabine treatment in patients with alkylator‐resistant, low‐grade lymphoid malignancies who have not received PCP prophylaxis is associated with an increased risk of opportunistic pulmonary infections. Aggressive work‐up of pulmonary syndromes and PCP prophylaxis in these patients should be considered during and after treatment with fludarabine. © 1995 Wiley‐Liss, Inc.
ANTI-VENEREAL MEASURES IN SCANDINAVIA
Authors: M. Rorke
Journal: BMJ (1938)

A Commission on Venereal Diseases, approved by Sir Kingsley Wood, the then Minister of Health, left London on July 12, 1937, to visit Scandinavia.The object was to investigate conditions following notification and treat- ment of venereal diseases in those countries, as the fall in the number of cases in Scandinavia of recent years had seemed to be striking compared with the number of cases returned to the Ministry of Health in this country as under treatment for venereal diseases.In the three Scandinavian countries visited-Sweden,
Initial experience with indium-111 autologous leucocyte imaging in patients with acute pancreatitis.
Authors: J R Anderson, R A Spence, J D Laird, W R Ferguson, T L Kennedy
Journal: BMJ (1983)

Indium-111 labelled autologous leucocyte imaging was used to assess severity in 13 patients with acute pancreatitis. All three patients with severe disease as judged by a prognostic factor grading system had a positive result on imaging. A fourth patient with mild disease as judged by prognostic factors had a positive imaging result and 14 days later developed a pseudocyst. There were no false positive or false negative scans. Evidence from three patients suggested that a positive 111In-leucocyte imaging result implies substantial fat necrosis. In this study imaging was as accurate as prognostic factor grading. The technique may be a useful method of separating mild from severe acute pancreatitis.
The Ischemic Leg
Authors: Carl Bredenberg
Journal: JAMA (1986)

This edition updates a volume originally published seven years ago. Its subject for the most part is chronic atherosclerotic occlusive disease of the legs. It also touches on less common chronic arterial occlusive disease of the legs, such as in diabetes mellitus, thromboangiitis obliterans, and popliteal artery entrapment. A single short chapter discusses acute arterial occlusion. There are excellent chapters on the natural history and anatomic patterns of atherosclerosis of the lower extremities as well as the relationship between atherosclerosis and diabetes mellitus. The section on diagnosis is heavily weighted toward technology and machinery, as is the current trend. Considering how valuable the history and physical examination are in not only diagnosing chronic arterial insufficiency of the lower extremity but also determining the indications for surgery, one might wish for a fuller discussion of clinical evaluation of the patient. Much of the book discusses the varieties of operations that can
A comparison of the pathological spectrum of hypertensive, diabetic, and hypertensive-diabetic heart disease.
Authors: K H van Hoeven, S M Factor
Journal: Circulation (1990)

The hearts obtained at autopsy of 67 patients with hypertension, diabetes mellitus, or both were examined microscopically and histochemically, and the amount of fibrosis was determined. Significant differences in heart weight, interstitial fibrosis, replacement fibrosis, and perivascular fibrosis were found among the groups. The mean heart weight of the hypertensive-diabetic patients was significantly greater than that of the hypertensive patients and the diabetic patients. The amount of microscopic fibrosis increased between the groups, the lowest in hypertensive hearts, midrange in diabetic hearts, and highest in hypertensive-diabetic hearts. Total fibrosis correlated with heart weight among diabetic and hypertensive-diabetic patients and was significantly greater among patients with congestive heart failure, most of whom had histories of both hypertension and diabetes. The microscopic grade of fibrosis correlated significantly (p less than 0.01) with a quantitative, histochemical determination of the amount of collagen per milligram of total noncollagenous protein in the heart tissue. Myocardial fibrosis may contribute to the diastolic dysfunction typical of hypertensive-diabetic cardiomyopathy, in which congestive heart failure is a common sequela. The importance of hypertension in the pathogenesis of severe diabetic heart disease is discussed.
Simple Scoring Scheme for Calculating the Risk of Acute Coronary Events Based on the 10-Year Follow-Up of the Prospective Cardiovascular Münster (PROCAM) Study
Authors: Gerd Assmann, Paul Cullen, Helmut Schulte
Journal: Circulation (2002)

Background — The absolute risk of an acute coronary event depends on the totality of risk factors exhibited by an individual, the so-called global risk profile. Although several scoring schemes have been suggested to calculate this profile, many omit information on important variables such as family history of coronary heart disease or LDL cholesterol. Methods and Results — Based on 325 acute coronary events occurring within 10 years of follow-up among 5389 men 35 to 65 years of age at recruitment into the Pro spective Ca rdiovascular Mü nster (PROCAM) study, we developed a Cox proportional hazards model using the following 8 independent risk variables, ranked in order of importance: age, LDL cholesterol, smoking, HDL cholesterol, systolic blood pressure, family history of premature myocardial infarction, diabetes mellitus, and triglycerides. We then derived a simple point scoring system based on the β-coefficients of this model. The accuracy of this point scoring scheme was comparable to coronary event prediction when the continuous variables themselves were used. The scoring system accurately predicted observed coronary events with an area under the receiver-operating characteristics curve of 82.4% compared with 82.9% for the Cox model with continuous variables. Conclusions — Our scoring system is a simple and accurate way of predicting global risk of myocardial infarction in clinical practice and will therefore allow more accurate targeting of preventive therapy.
Congenital Long-QT Syndromes
Authors: Charles I. Berul
Journal: Circulation (2008)

2][3] The principal events are syncope, seizures, and ventricular tachycardia, characteristically torsade de pointes.Most often, this arrhythmia is self terminating, producing a syncopal episode; however, LQTS is responsible for a significant proportion of sudden cardiac deaths (SCDs) in young people without structural heart disease, estimated to have an incidence of approximately 1 in 2500 and causing thousands of deaths annually. 4 -6 Characteristic ECG signs of LQTS include QT-interval prolongation and T-wave abnormalities.The heart rate-corrected QT interval (QTc) can range from 370 to Ͼ700 ms, clearly overlapping that of normal individuals, and a single ECG may not manifest the stereotypical features. 7-9Some patients have a normal or borderline QTc at rest but prolongation with exertion or ␤-adrenergic stimulation.Provocative testing with exercise or catecholamine infusion may improve the sensitivity of LQTS clinical detection. 9 -11 The inciting triggers are somewhat mutation-specific.Patients with potassium channel mutations typically have episodes during physical or emotional stress, whereas those with sodium channel defects have more events with bradycardia and during sleep. 12-15Symptoms, including syncope or SCD, can manifest anytime from the neonatal period to adulthood.Because risk stratification is still being refined, it is often recommended that most LQTS patients be treated with ␤-adrenergic blocking medications, but a diagnostic challenge is deciding who needs more specific or aggressive therapies.Interventions for LQTS include implantation of a permanent pacemaker or implantable cardioverter defibrillator (ICD), as well as consideration of left cardiac sympathetic denervation.If interventional therapy is warranted, what procedures are right for which patients, and when is the optimal time to intervene? 16The competing risks of the disease versus potential complications from the procedures or devices often increase the complexity of the clinical decisionmaking rationale.
General and Abdominal Obesity and Risk of Death among Black Women
Authors: Deborah A. Boggs, Lynn Rosenberg, Yvette C. Cozier, Lauren A. Wise, Patricia F. Coogan, Edward A. Ruiz-Narvaez, Julie R. Palmer
Journal: New England Journal of Medicine (2011)

Recent pooled analyses show an increased risk of death with increasing levels of the body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) of 25.0 or higher in populations of European ancestry, a weaker association among East Asians, and no association of an increased BMI with an increased risk of death among South Asians. The limited data available on blacks indicate that the risk of death is increased only at very high levels of BMI (≥35.0).We prospectively assessed the relation of both BMI and waist circumference to the risk of death among 51,695 black women with no history of cancer or cardiovascular disease who were 21 to 69 years of age at study enrollment. Our analysis was based on follow-up data from 1995 through 2008 in the Black Women's Health Study. Multivariable proportional-hazards models were used to estimate hazard ratios and 95% confidence intervals.Of 1773 deaths identified during follow-up, 770 occurred among 33,916 women who had never smoked. Among nonsmokers, the risk of death was lowest for a BMI of 20.0 to 24.9. For a BMI above this range, the risk of death increased as the BMI increased. With a BMI of 22.5 to 24.9 as the reference category, multivariable-adjusted hazard ratios were 1.12 (95% confidence interval [CI], 0.87 to 1.44) for a BMI of 25.0 to 27.4, 1.31 (95% CI, 1.01 to 1.72) for a BMI of 27.5 to 29.9, 1.27 (95% CI, 0.99 to 1.64) for a BMI of 30.0 to 34.9, 1.51 (95% CI, 1.13 to 2.02) for a BMI of 35.0 to 39.9, and 2.19 (95% CI, 1.62 to 2.95) for a BMI of 40.0 to 49.9 (P<0.001 for trend). A large waist circumference was associated with an increased risk of death from any cause among women with a BMI of less than 30.0.The risk of death from any cause among black women increased with an increasing BMI of 25.0 or higher, which is similar to the pattern observed among whites. Waist circumference appeared to be associated with an increased risk of death only among nonobese women. (Funded by the National Cancer Institute.).
DO GRAPE SEEDS CAUSE APPENDICITIS?
Authors: EDMUND ANDREWS
Journal: JAMA (1896)

The laity of Chicago have become infected with the idea that grapes are a dangerous fruit. They have received from some of our best physicians an opinion that grape seeds cause many, or perhaps nearly all of the cases of appendicitis occuring among us, and the occasional discovery of a seed in or near a perforated appendix adds to the alarm. Nearly all the grapes consumed in this city are eaten in the months of August, September, October and November. If they cause any large number of cases of appendicitis, we would expect that disease to be most frequent during the grape eating season, or at least within a reasonable period after its close. To settle this question, I have obtained statistics of the disease in Chicago for every month during the last fourteen years. My friend, Mr. Tracy H. Clark, a medical student, has been kind enough to examine
Rupture of the Heart
Authors: O. Grant
Journal: BMJ (1886)

Heemorrhage is not a very common symptom of tubal occlusion and distension, but, when present, is apt to be severe, and, when accom- panied by signs so nearly resembling nodular myoma of the uterus, may be specially misleading.I operated on a case presenting these features on December 10th of'last year.Excessive menstruation had
Risk of Intracranial Hemorrhage From Statin Use in Asians
Authors: Chia-Hsuin Chang, Chin-Hsien Lin, James L. Caffrey, Yen-Chieh Lee, Ying-Chun Liu, Jou-Wei Lin, Mei-Shu Lai
Journal: Circulation (2015)

Reports of statin usage and increased risk of intracranial hemorrhage (ICH) have been inconsistent. This study examined potential associations between statin usage and the risk of ICH in subjects without a previous history of stroke.Patients initiating statin therapy between 2005 and 2009 without a previous history of ischemic or hemorrhagic stroke were identified from Taiwan's National Health Insurance database. Participants were stratified by advanced age (≥70 years), sex, and diagnosed hypertension. The outcome of interest was hospital admission for ICH (International Classification of Diseases, Ninth Revision, Clinical Modification codes 430, 431, 432). Cox regression models were applied to estimate the hazard ratio of ICH. The cumulative statin dosage stratified by quartile and adjusted for baseline disease risk score served as the primary variable using the lowest quartile of cumulative dosage as a reference. There were 1 096 547 statin initiators with an average follow-up of 3.3 years. The adjusted hazard ratio for ICH between the highest and the lowest quartile was nonsignificant at 1.06 with a 95% confidence interval spanning 1.00 (0.94-1.19). Similar nonsignificant results were found in sensitivity analyses using different outcome definitions or model adjustments, reinforcing the robustness of the study findings. Subgroup analysis identified an excess of ICH frequency in patients without diagnosed hypertension (adjusted hazard ratio 1.36 [1.11-1.67]).In general, no association was observed between cumulative statin use and the risk of ICH among subjects without a previous history of stroke. An increased risk was identified among the nonhypertensive cohort, but this finding should be interpreted with caution.
Hippo/Mst1 Stimulates Transcription of the Proapoptotic Mediator <i>NOXA</i> in a FoxO1-Dependent Manner
Authors: Karel Valis, Lubomir Prochazka, Evzen Boura, Jaromira Chladova, Tomas Obsil, Jakub Rohlena, Jaroslav Truksa, Lan-Feng Dong, Stephen J. Ralph, Jiri Neuzil
Journal: Cancer Research (2011)

Abstract The proapoptotic protein Noxa, a member of the BH3-only Bcl-2 protein family, can effectively induce apoptosis in cancer cells, although the relevant regulatory pathways have been obscure. Previous studies of the cytotoxic effects of α-tocopheryl succinate (α-TOS) on cancer cells identified a mechanism whereby α-TOS caused apoptosis requiring the Noxa-Bak axis. In the present study, ab initio analysis revealed a conserved FoxO-binding site (DBE; DAF-16 binding element) in the NOXA promoter, and specific affinity of FoxO proteins to this DBE was confirmed by fluorescence anisotropy. FoxO1 and FoxO3a proteins accumulated in the nucleus of α-TOS–treated cells, and the drug-induced specific FoxO1 association with the NOXA promoter and its activation were validated by chromatin immunoprecipitation. Using siRNA knockdown, a specific role for the FoxO1 protein in activating NOXA transcription in cancer cells was identified. Furthermore, the proapoptotic kinase Hippo/Mst1 was found to be strongly activated by α-TOS, and inhibiting Hippo/Mst1 by specific siRNA prevented phosphorylation of FoxO1 and its nuclear translocation, thereby reducing levels of NOXA transcription and apoptosis in cancer cells exposed to α-TOS. Thus, we have demonstrated that anticancer drugs, exemplified by α-TOS, induce apoptosis by a mechanism involving the Hippo/Mst1-FoxO1-Noxa pathway. We propose that activation of this pathway provides a new paradigm for developing targeted cancer treatments. Cancer Res; 71(3); 946–54. ©2011 AACR.
Abstract 5112: Foxa1 and Foxa2 are essential for gender dimorphism in liver cancer
Authors: Zhaoyu Li, Geetu Tuteja, Jonathan Schug, Klaus H. Kaestner
Journal: Cancer Research (2012)

Abstract Hepatocellular carcinoma (HCC) is sexually dimorphic in both rodents and humans, with significantly higher incidence in males, an effect that is dependent on sex hormones. The molecular mechanisms by which estrogens prevent and androgens promote liver cancer remain unclear. Here, we discover that sexually-dimorphic HCC is completely reversed in Foxa1- and Foxa2-deficient mice after diethylnitrosamine-induced hepatocarcinogenesis. Co-regulation of target genes by Foxa1/a2 and either the estrogen receptor (ERalpha) or the androgen receptor (AR) was increased during hepatocarcinogenesis in normal female or male mice, respectively, but was lost in Foxa1/2-deficient mice. Thus, both estrogen-dependent resistance to and androgen-mediated facilitation of HCC depend on Foxa1/2. Strikingly, single nucleotide polymorphisms at FOXA2 binding sites reduce binding of both FOXA2 and ERalpha to their targets in human liver, and correlate with HCC development in women. Thus, Foxa factors and their targets are central for the sexual dimorphism of HCC. (Cell, accepted in press) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5112. doi:1538-7445.AM2012-5112
The Role of Erythroid Cell Membranes in Protein Synthesis.
Authors: Edward R. Burka
Journal: Annals of Internal Medicine (1968)

s1 May 1968The Role of Erythroid Cell Membranes in Protein Synthesis.Edward R. Burka, M.D., F.A.C.P.Edward R. Burka, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-68-5-1165_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe mammalian erythroid cell is a highly specialized element adapted to the synthesis of predominantly a single protein, hemoglobin. The cell membrane, in addition to maintaining the internal environment of the cell, participates actively in other metabolic activities. These studies define a role for the cell membrane in the metabolism of ribonucleic acid (RNA) and thus the control of protein synthesis in the cell. Approximately 25% of both nonribosomal RNA and ribosomal RNA is bound to the cell membrane. Ribosomes, the site of protein synthesis within the cell, exist in the mammalian reticulocyte in two forms: free and membrane-bound. The... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Edward R. Burka, M.D., F.A.C.P.Affiliations: Philadelphia, Pennsylvania PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1968Volume 68, Issue 5Page: 1165-1166KeywordsCell membranesCell metabolismHemoglobinMembrane proteinsProtein metabolismProtein synthesisRNAReticulocytesRibosomal RNARibosomes ePublished: 1 December 2008 Issue Published: 1 May 1968 PDF downloadLoading ...
Indeterminate cell histiocytosis-a clinicopathological entity with features of both X- and non-X histiocytosis
Authors: A. SIDOROFF, B. ZELGER, H. STEINER, N. SMITH
Journal: British Journal of Dermatology (1996)

An otherwise healthy 50-year-old woman presented with a 6-month history of having developed more than 100 generalized, non-confluent, reddish-brown, partially yellow-coloured papules. A non-epidemotropic, monomorphous infiltrate of vacuolated mononuclear, and occasionally multinuclear, histiocytes, positive for factor XIIIa and macrophage markers HAM56 and KiM1p, was consistent with the clinical impression of generalized eruptive histiocytomas. However, the additional reactivity for S100 protein, in the absence of features of histiocytosis X, suggested a diagnosis of indeterminate cell histiocytosis (ICH). Further immunohistochemical studies, performed on snap-frozen material, characterized the lesions as being diffusely positive with LN3 (HLA-DR), Leu4 (CD3) and Leu3 (CD4), the infiltrate in the upper dermis as reactive for OKT6 (CD1) and IOT6c (CD1c), and the infiltrate in the lower dermis as reactive for a variety of macrophage markers. Ultrastructural studies showed various non-specific features of histocytic disorders, but no Birbeck granules. Our findings confirm those of previous reports suggesting that ICH is a distinct histiocytic entity, characterized by immunophenotypic features of both X- and non-X histiocytoses. Generalized eruptive histiocytoma seems to be an early indeterminate stage of various non-X histiocytic syndromes including ICH, multicentric reticulohistiocytosis, xanthogranuloma and xanthoma disseminatum. The distribution pattern of the various X/non-X histiocytic markers suggests dermal arrest of antigen-presenting cells during their physiological trafficking from the skin to the lymph nodes.
SUNSHINE AND FRESH AIR VS. THE FINSE[unk] ULTRA-VIOLET RAYS AND THE ROENTGEN RAYS IN TUBERCULOSIS OF THE JOINTS AND BONES.
Authors: DE FOREST WILLARD
Journal: JAMA (1903)

The increasing use of the Finsen light and of the<i>x</i>-ray in the treatment of cancerous lesions of the skin and deeper tissues, and especially their use in lupus and other tubercular skin affections, naturally arouses the question of the utility of these rays in the cure of tuberculosis of the joints and bones. The results thus far obtained are certainly sufficient as regards tubercular lupus to warrant the continuance of our efforts in this direction, but the opportunities for noting the effect on deeper tissue in tubercular joints have not yet been sufficient to warrant definite conclusions. A large number of cases will be required to decide the question of benefit, since from the nature of the disease speedy conclusions will be unjustifiable. The course pursued by the tubercular process in joints is always slow, and there are such great difam ferences in the rapidity of progress that the
PROLONGED BENEFICIAL EFFECT OF BOSENTAN TREATMENT AND FOUR-YEAR SURVIVAL RATES IN ADULT PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION ASSOCIATED WITH CONGENITAL HEART DISEASE
Authors: Mark J. Schuuring, Jeroen C. Vis, Marielle G. Duffels, Pepijn Mulder, Rianne De Bruin-Bon, Berto J. Bouma, Rolf MF Berger, Elke S. Hoendernis, Arie PJ van Dijk, Barbara Mulder
Journal: Journal of the American College of Cardiology (2011)