tbuckley/cabot-search huggingface dataset:
Plasma Angiopoietin-1, Angiopoietin-2, Angiopoietin Receptor Tie-2, and Vascular Endothelial Growth Factor Levels in Acute Coronary Syndromes
Authors: Kaeng W. Lee, Gregory Y.H. Lip, Andrew D. Blann
Journal: Circulation (2004)

Angiopoietin (Ang) -1 and -2, their receptor Tie-2, and vascular endothelial growth factor (VEGF) regulate angiogenesis and may be important in myocardial collateral development. Elevated levels of growth factors and their receptors are reported in myocardial infarction (MI), but changes after an acute coronary event are unknown.Plasma Ang-1, Ang-2, Tie-2, and VEGF levels were measured on admission (baseline) and at 48 hours (acute stage) in 126 patients with acute coronary syndrome (82 MI, 44 unstable angina pectoris). Baseline levels were compared with those of 40 patients with stable angina and 40 healthy controls. Measurements were repeated in 38 MI patients at 6 and 18 weeks (chronic stage). Baseline Ang-2 and Tie-2 levels were highest in MI patients (P<0.001). Patients with MI and unstable angina pectoris had higher VEGF levels compared with stable angina patients and healthy control subjects (P<0.001). In patients with acute MI, serial changes in all indexes from baseline to 18 weeks were observed (all P<0.001). Ang-1 levels were unchanged from baseline to 6 weeks but were elevated at 18 weeks. Ang-2 changes followed a biphasic pattern, being higher at baseline and 6 weeks but lower at 48 hours and 18 weeks. Tie-2 levels increased from baseline and remained elevated in the chronic phase. VEGF peaked at 6 weeks and then decreased toward baseline at 18 weeks.Plasma Ang-2, Tie-2, and VEGF levels but not Ang-1 levels were increased in patients with acute coronary syndrome. Serial changes in the plasma levels and interrelationships among Ang-1, Ang-2, Tie-2, and VEGF levels from the acute to the chronic stages in MI may reflect the progressive stages of angiogenesis activity in the ischemic-necrotic myocardium in vivo.
N-Methylpurine DNA Glycosylase and OGG1 DNA Repair Activities: Opposite Associations With Lung Cancer Risk
Authors: Yael Leitner-Dagan, Ziv Sevilya, Mila Pinchev, Ran Kramer, Dalia Elinger, Laila C. Roisman, Hedy S. Rennert, Edna Schechtman, Laurence Freedman, Gad Rennert, Zvi Livneh, Tamar Paz-Elizur
Journal: JNCI Journal of the National Cancer Institute (2012)

Only a minority of smokers develop lung cancer, possibly due to genetic predisposition, including DNA repair deficiencies. To examine whether inter-individual variations in DNA repair activity of N-methylpurine DNA glycosylase (MPG) are associated with lung cancer, we conducted a blinded, population-based, case–control study with 100 lung cancer case patients and 100 matched control subjects and analyzed the data with conditional logistic regression. All statistical tests were two-sided. MPG enzyme activity in peripheral blood mononuclear cells from case patients was higher than in control subjects, results opposite that of 8-oxoguanine DNA glycosylase (OGG1) DNA repair enzyme activity. For lung cancer associated with one standard deviation increase in MPG activity, the adjusted odds ratio was 1.8 (95% confidence interval [CI] = 1.2 to 2.6; P = .006). A combined MPG and OGG1 activities score was more strongly associated with lung cancer risk than either activity alone, with an odds ratio of 2.3 (95% CI = 1.4 to 3.6; P < .001). These results form a basis for a future panel of risk biomarkers for lung cancer risk assessment and prevention.
Tympanostomy Tubes and Developmental Outcomes at 9 to 11 Years of Age
Authors: Jack L. Paradise, Heidi M. Feldman, Thomas F. Campbell, Christine A. Dollaghan, Howard E. Rockette, Dayna L. Pitcairn, Clyde G. Smith, D. Kathleen Colborn, Beverly S. Bernard, Marcia Kurs-Lasky, Janine E. Janosky, Diane L. Sabo, Rollanda E. O'Connor, William E. Pelham
Journal: New England Journal of Medicine (2007)

Developmental impairments in children have been attributed to persistent middle-ear effusion in their early years of life. Previously, we reported that among children younger than 3 years of age with persistent middle-ear effusion, prompt as compared with delayed insertion of tympanostomy tubes did not result in improved cognitive, language, speech, or psychosocial development at 3, 4, or 6 years of age. However, other important components of development could not be assessed until the children were older.We enrolled 6350 infants soon after birth and evaluated them regularly for middle-ear effusion. Before 3 years of age, 429 children with persistent effusion were randomly assigned to undergo the insertion of tympanostomy tubes either promptly or up to 9 months later if effusion persisted. We assessed literacy, attention, social skills, and academic achievement in 391 of these children at 9 to 11 years of age.Mean (+/-SD) scores on 48 developmental measures in the group of children who were assigned to undergo early insertion of tympanostomy tubes did not differ significantly from the scores in the group that was assigned to undergo delayed insertion. These measures included the Passage Comprehension subtest of the Woodcock Reading Mastery Tests (mean score, 98+/-12 in the early-treatment group and 99+/-12 in the delayed-treatment group); the Spelling, Writing Samples, and Calculation subtests of the Woodcock-Johnson III Tests of Achievement (96+/-13 and 97+/-16; 104+/-14 and 105+/-15; and 99+/-13 and 99+/-13, respectively); and inattention ratings on visual and auditory continuous performance tests.In otherwise healthy young children who have persistent middle-ear effusion, as defined in our study, prompt insertion of tympanostomy tubes does not improve developmental outcomes up to 9 to 11 years of age. (ClinicalTrials.gov number, NCT00365092 [ClinicalTrials.gov].).
Phase II study of docetaxel–vinorelbine in platinum-resistant, paclitaxel-pretreated ovarian cancer
Authors: G. Aravantinos, D. Bafaloukos, G. Fountzilas, C. Christodoulou, C. Papadimitriou, N. Pavlidis, H.P. Kalofonos, H. Gogas, P. Kosmidis, M.A. Dimopoulos
Journal: Annals of Oncology (2003)
Reporting and preventing medical mishaps: lessons from non-medical near miss reporting systems
Authors: P. Barach
Journal: BMJ (2000)

Reducing mishaps from medical management is central to efforts to improve quality and lower costs in health care. Nearly 100 000 patients are estimated to die preventable deaths annually in hospitals in the United States, with many more incurring injuries at an annual cost of $9 billion. Underreporting of adverse events is estimated to range from 50%-96% annually.1–3 This annual toll exceeds the combined number of deaths and injuries from motor and air crashes, suicides, falls, poisonings, and drownings.4 Many stakeholders in health care have begun to work together to resolve the moral, scientific, legal, and practical dilemmas of medical mishaps. To achieve this goal, an environment fostering a rich reporting culture must be created to capture accurate and detailed data about nuances of care.

Outcomes in complex work depend on the integration of individual, team, technical, and organisational factors. 5 6 A continuum of cascade effects exists from apparently trivial incidents to near misses and full blown adverse events. 7 8 Consequently, the same patterns of causes of failure and their relations precede both adverse events and near misses. Only the presence or absence of recovery mechanisms determines the actual outcome.9 The National Research Council defines a safety “incident” as an event that, under slightly different circumstances, could have been an accident.10 Focusing on data for near misses may add noticeably more value to quality improvement than a sole focus on adverse events.

Schemes for reporting near misses, “close calls,” or sentinel (“warning”) events have been institutionalised in aviation,w1 w2 nuclear power technology,w3 w4 petrochemical processing, steelw5 production,w6 military operations, and air transportation.w7-w11 In health care, efforts are now being made to create incident reporting systems for medical near misses 8 11–15 to supplement the limited …
Adrenergic Component of Renin Release Induced by Vasodilating Antihypertensive Drugs in the Rat
Authors: WILLIAM A. PETTINGER, WILLIAM B. CAMPBELL, KENT KEETON
Journal: Circulation Research (1973)

The capacity of the vasodilating drugs, minoxidil and hydralazine, for inducing renin release was characterized in rats according to chronology and dose response. Propranolol inhibition of this renin release was also characterized and related to serum levels of propranolol. Minoxidil and hydralazine (1.0 mg/kg) induced sevenfold elevations of serum renin activity. Treatment with propranolol, resulting in plasma propranolol concentrations as low as 50 ng/ml, impaired vasodilatory drug-induced renin release. The propranolol inhibition suggests a beta-adrenergic component to this type of renin release and the potential for a clinically efficacious drug interaction.
Immunoreconstitution by Peripheral Blood Leukocytes in Adenosine Deaminase-deficient Severe Combined Immunodeficiency
Authors: Kenneth C. Rich, Carol M. Richman, Edwin Mejias, Peter Daddona
Journal: Journal of Clinical Investigation (1980)

Transplantation of histocompatible allogeneic peripheral blood leukocytes resulted in successful reconstitution of an adenosine deaminase (ADA)-deficient, severe combined immune-deficient patient. Erythrocyte transfusions before the transplant were associated with a rise of serum immunoglobulin concentration to normal without improvement in T cell function. The patient received 5 x 10(7) peripheral blood mononuclear leukocytes/kg obtained from the histocompatible father by leukopheresis. 3 wk after the transplant the lymphocyte count, proportion of E rosetting lymphocytes, and the ADA content of the patient's mononuclear leukocytes became normal while the phytohemagglutinin-stimulated blastogenic responses improved and became normal 52 d after the transplant. Antibody response to diphtheria immunization and response to naturally acquired herpes simplex infection were normal while isohemagglutinins progressively increased. Immunization with a neoantigen, bacteriophage phiX 174, resulted in a small but definite antibody response but no amplification of the response after secondary immunization. A positive reaction to a skin test for Candida albicans developed. Erythrocyte deoxy ATP (dATP) concentration decreased during the course of erythrocyte transfusions. 9 mo after the transplant, the erythrocyte dATP was elevated to twice pretransfusion levels while mononuclear leukocyte dATP varied from normal to elevated during the first 4 mo of the posttransplant period, but remained normal during the last 8 mo. The improvement in immune function persisted during the 12-mo posttransplant observation period while the mononuclear leukocyte ADA concentration stabilized at approximately 0.25 of normal, which is similar to the enzyme activity of the donor cells. This in vivo study supports the hypothesis that lymphoid precursor cells are present in peripheral blood which may partially reconstitute an immune-deficient recipient.
Duodenal and antral mucosal prostaglandin E2 synthesis in a study of normal subjects and all stages of duodenal ulcer disease treated by H2 receptor antagonists.
Authors: S Pugh, S E Williams, M R Lewin, M Ishaque, T P Barton, K Bose, K D Bardhan, C G Clark
Journal: Gut (1989)

We tested the hypothesis that the production of prostaglandin E2 (PGE2) is impaired in duodenal ulcer disease and affected by treatment and healing. This was investigated by a study of maximal PGE2 synthesis rates in duodenal and antral mucosal biopsies obtained at endoscopy. The patients were divided into three groups. Group (a): endoscopically normal controls (n = 56); group (b): treatment controls (non-DU disease: gastric ulcer or oesophagitis treated by histamine H2 receptor antagonists) (n = 41); and group (c): patients with DU disease (n = 183) further subdivided into group (c1) active ulcer not on treatment (n = 47), (c2) treated active ulcer (n = 35), (c3) healed ulcer on treatment (n = 86), and (c4) healed ulcer not on treatment (n = 15). Group (a) synthesised (mean (SD] 106.6 (39.0) pg PGE2/mg wt of tissue from the duodenal bulb and 129.9 (56.9) from the second part of the duodenum. No difference was found between group (a) and (b) at either site. Group (c1) ulcer rim made 49.8 (22.7) and at all stages ulcer rim and scar made less than the control duodenal bulb (p less than 0.02). Uninvolved duodenal bulb form groups (c1) (63.4 (31.0], (c2) (83.6 (38.5], and (c3) (81.5 (31.1], however, also made significantly less than controls (p less than 0.02) and a similar though non-significant trend was seen in group (c4). Biopsies from the second part of the duodenum did not synthesise significantly less than the control group but a similar trend was noticed at each stage of ulcer treatment. Biopsies of control antrum synthesised 124.5 (32.2) but only 93.7 (44.2) in group (cl) (p < 0.005). All stages of duodenal ulcer healing were associated with a decreased capacity to synthesise the major prostaglandin PGE2 at the ulcer site and the uninvolved duodenal bulb and, in acute untreated duodenal ulcer, the uninvolved antrum. This decreased capacity may be the consequence of the disease process itself and not secondary to the treatment, indicating a basic pathophysiological abnormality which may explain the characteristic tendency of the disease to relapse.
Synchronous neuroblastoma and von Recklinghausen's disease: a review of the literature.
Authors: B H Kushner, S I Hajdu, L Helson
Journal: Journal of Clinical Oncology (1985)

We report an unusual case of progressive disseminated neuroblastoma occurring in a child with a family history and stigmata of von Recklinghausen's disease. A review of the literature confirms the extreme rarity of finding these two neurocristopathies in a single individual and thus undermines the widely held notion of an association--genetic or otherwise--between these two entities. We propose that synchronous neuroblastoma and von Recklinghausen's disease is accounted for by chance alone and therefore represents a randomly occurring phenomenon.
Inactivating All Three Rb Family Pocket Proteins Is Insufficient to Initiate Cervical Cancer
Authors: Myeong-Kyun Shin, Julien Sage, Paul F. Lambert
Journal: Cancer Research (2012)

Abstract Human papillomavirus-16 (HPV-16) is associated etiologically with many human cervical cancers. It encodes 3 oncogenes E5, E6, and E7. Of these oncogenes, E7 has been found to be the dominant driver of cervical cancer in mice. More than 100 cellular proteins have been reported to associate with HPV-16 E7, which is thought to dysregulate the cell cycle in part by binding and inducing the degradation of pRb and its related pocket protein family members, p107 and p130. The ability of E7 to inactivate the pRb family correlates with its ability to induce head and neck cancers in mice. We previously showed that the inactivation of pRb is itself not sufficient to recapitulate the oncogenic properties of E7 in cervical carcinogenesis. In this study, we evaluated mice that were deficient in multiple pocket proteins, including mice that lacked pRb, p107, and p130. Strikingly, combined loss of two or all 3 pocket proteins resulted in development of high-grade cervical intraepithelial neoplasia, but not frank cervical carcinoma. These findings strongly argue that the oncogenic properties of HPV-16 E7 in human cervical carcinogenesis may involve disruption of E7 binding proteins beyond simply the pRb family members. Cancer Res; 72(20); 5418–27. ©2012 AACR.
Novel P53 mutations detected by FAMA in colorectal cancers
Authors: F. De Galitiis, K. Cannita, A. Tessitore, F. Martella, Z.C. Di Rocco, A. Russo, V. Adamo, S. Iacobelli, S. Martinotti, P. Marchetti, C. Ficorella, E. Ricevuto
Journal: Annals of Oncology (2006)
Insulin resistance and sleep-disordered breathing in healthy humans.
Authors: R A Stoohs, F Facchini, C Guilleminault
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

Fifty healthy, normotensive individuals (34 women) with a mean age of 44.3 +/- 13.2 yr and a mean body mass index of 27.1 +/- 5.4 kg/m2 were tested for the presence or absence of insulin resistance and sleep-disordered breathing. The hypothesis of this investigation was that insulin resistance is associated with sleep-disordered breathing. In vivo insulin action with determination of steady-state plasma glucose (SSPG) and insulin was measured using simultaneous intravenous infusion of somatostatin, glucose, and insulin via a Harvard pump. Determination of sleep-disordered breathing was performed through clinical assessment and portable nocturnal monitoring using a validated sleep apnea recorder. Individuals with > or = 10 hypoxic respiratory events per hour of sleep were significantly more insulin-resistant than subjects without sleep-breathing disorders. After adjusting the relationship between insulin resistance and sleep-disordered breathing for potential confounding variables, it was found that this relationship was entirely dependent on body mass.
Hemodynamic Effects of Quantitatively Varied Experimental Aortic Regurgitation
Authors: GEORGE H. WELCH, EUGENE BRAUNWALD, STANLEY J. SARNOFF
Journal: Circulation Research (1957)

A canine preparation was devised in which aortic regurgitant flow could be acutely produced, metered and controllably varied. Aortic regurgitant flows in excess of the dog's resting cardiac output resulted in a marked decrease of effective cardiac output, a substantial rise of peripheral resistance and left ventricular end-diastolic pressure, and a marked depression of the left ventricular function curve, with little change in the mean left atrial pressure. When mitral regurgitation was added to aortic regurgitation, effective cardiac output, stroke work and left ventricular end-diastolic pressure fell, while left atrial pressure rose.
The Anatomy of Medical School Patenting
Authors: Pierre Azoulay, Ryan Michigan, Bhaven N. Sampat
Journal: New England Journal of Medicine (2007)

Although issues related to patenting by faculty at academic medical centers have been the source of much controversy, there is little systematic evidence of the growth of these activities, their distribution among academic departments, and their relationship to faculty research efforts.We pooled data on medical school faculty, National Institutes of Health (NIH) grant activity, and patenting to examine changes in the propensity to apply for a patent during the period from 1981 through 2000 that was subsequently granted, the distribution of these activities among departments, and the relationships between patenting and variables associated with individual faculty members. These variables included sex, academic degree, years since the last academic degree was earned, patenting by departmental peers, and NIH funding history. In addition to basic descriptive statistics, we estimated Poisson regression models based on the number of patents a faculty member applied for as a function of these variables.Applications for patents that were subsequently granted per medical school faculty increased dramatically during the period from 1981 through 2000. Although most patenting activity was carried out by faculty members in clinical departments, their rate of patents was low relative to that of faculty members in basic science departments. Regression results showed that persons were more likely to patent if they had recent NIH funding, were male, had Ph.D. degrees, were more experienced faculty members, and worked in departments with higher patenting rates.Although the number of patents granted to medical school faculty increased dramatically during this period, patent activity was concentrated among a small number of departments and faculty members. Moreover, persons who had recently received NIH funding were more likely to apply for a patent than those who had not received such funding.
Discriminating Risk and Resilience Endophenotypes From Lifetime Illness Effects in Familial Major Depressive Disorder
Authors: Bradley S. Peterson, Zhishun Wang, Guillermo Horga, Virginia Warner, Bret Rutherford, Kristin W. Klahr, Barbara Graniello, Priya Wickramaratne, Felix Garcia, Shan Yu, Xuejun Hao, Phillip B. Adams, Ming Qian, Jun Liu, Andrew Gerber, Myrna M. Weissman
Journal: JAMA Psychiatry (2013)

The neural systems that confer risk or vulnerability for developing familial depression, and those that protect against or confer resilience to becoming ill, can be disentangled from the effects of prior illness by comparing brain imaging measures in previously ill and never ill persons who have either a high or low familial risk for depression.To distinguish risk and resilience endophenotypes for major depression from the effects of prior lifetime illness.We used functional magnetic resonance imaging to measure and compare brain function during performance of an attentional, self-regulatory task across a large sample of multigenerational families ascertained specifically to be at either high or low risk for developing major depression. Study procedures were performed in a university setting. A total of 143 community participants were followed up prospectively for more than 20 years in a university setting. The sample was enriched with persons who were at higher or lower familial risk for developing depression based on being biological offspring of either a clinical sample of persons with major depression or a community control sample of persons with no discernible lifetime illness.Task-related change in blood oxygen level-dependent functional magnetic resonance imaging signal.A risk endophenotype included greater activation of cortical attention circuits. A resilience endophenotype included greater activation of the dorsal anterior cingulate cortex. The effects of prior lifetime illness were common to both risk groups and included greater deactivation of default-mode circuits.These findings identify neural systems that increase risk for depression, those that protect from illness, and those that endure following illness onset, and they suggest circuits to target for developing novel preventive and therapeutic interventions.
Confidentiality in Medicine
Authors: Sharon Kling
Journal: New England Journal of Medicine (1983)

ceivably be playing a part in the aetiology of other disease entities,9 and halogenated salicylanilides and related compounds may not be the only drugs retained in this manner.'0Dr. R. H. Champion, in the article "Diseases of the Skin: Drug Therapy of Urticaria" (22 December 1973, p. 730) states that "antihistamine drugs may, if necessary, be continued for months or years with safety."How can he be sure of this?How can we be certain that any of the photosensitizing drugs which cover a wide therapeutic range and include several anti- histamines are not retained in the dermis for long periods, eventually playing a part in the production of actinic reticuloid in sus- ceptible subjects?Promethazine, an anti- histamine, and chlorpromazine, a tran- quillizer, two phenothiazine derivatives, may cause persistent photodermatitis which depends upon concomitant oral administration and external application."'3The active photocontact sensitizers cause multiple cross- sensitivities'4 and it is conceivable that one or several photosensitizing drugs retained in the dermis might be immunologically activated by an external powerful sensitizer such as fenticlor, leading to actinic reticu- loid.-Iam, etc.,