tbuckley/cabot-search huggingface dataset:
Clinical evaluation of atenolol in hypertensive patients.
Authors: M M Ibrahim, R Mossallam
Journal: Circulation (1981)

Atenolol, a cardioselective beta-adrenergic blocking agent, was given as the sole hypotensive drug for 8-12 weeks to 20 patients with hypertension of varying degrees of severity. Initial systolic blood pressure ranged from 162-238 mm Hg (mean +/- SEM 196 +/- 5.5 mm Hg) and diastolic blood pressure ranged from 105-143 mm Hg (118 +/- 2.5 mm Hg). Three patients had accelerated hypertension, six had cardiomegaly with recent exertional dyspnea and three were diabetics. Atenolol, 100-300 mg once daily, controlled both the supine and standing blood pressure and markedly attenuated the initial hypertensive response to severe exercise. In 17 patients (85%), atenolol therapy reduced blood pressure more than 20/10 mm Hg; however, adequate blood pressure control was not achieved in severe hypertension. A significant hypotensive action developed within 2 weeks of treatment, and control of hypertension was maintained for 2 weeks after sudden interruption of therapy. No patient had postural or postexercise hypotension. The drug appeared to exert its maximum hypotensive effect at the 100-mg dosage. The magnitude of the hypotensive response was related to the initial systolic blood pressure (r = 0.77, p less than 0.01) and the degree of inhibition of exercise tachycardia (r = 0.66, p less than 0.01). The atenolol plasma level and its hypotensive action were not related. Except for impairment of glucose tolerance in diabetic patients, atenolol had minimal side effects.
Maintenance Treatment with Recombinant Interferon Alfa-2b in Patients with Multiple Myeloma Responding to Conventional Induction Chemotherapy
Authors: Franco Mandelli, Giuseppe Avvisati, Sergio Amadori, Mario Boccadoro, Angela Gernone, Vito M. Lauta, Filippo Marmont, Maria T. Petrucci, Maurizio Tribalto, Maria L. Vegna, Franco Dammacco, Alessandro Pileri
Journal: New England Journal of Medicine (1990)

The use of interferon for the induction treatment of multiple myeloma has been shown to be effective in about 20 percent of patients. We studied its effects on long-term survival when it was used for maintenance treatment. Between April 1985 and May 1988, 101 patients with symptomatic multiple myeloma who had had a substantial objective response or a lesser objective response with disappearance of symptoms ("disease stabilization") after 12 courses of induction chemotherapy were randomly assigned to receive recombinant interferon alfa-2b as maintenance therapy (n = 50) or to receive no treatment (n = 51).
Gastric Ulcer in the Preschool Child
Authors: John J. Goldsberry
Journal: New England Journal of Medicine (1951)

GASTRIC ulcer is unusual in children. This symptom complex, although first reported by Rufz1 as early as 1843, was not successfully recognized and treated until 1909.2 , 3 The purpose of this article is to review the literature and report a case of gastric ulcer in the preschool child. According to Proctor's4 criteria, 41 cases of chronic gastric ulcer in children four months to fourteen years of age have been recorded in the literature.4 5 6 7 8 9 Five occurred in preschool children (one to six years of age, inclusive) (Fig. 1C).Although the etiology of gastric ulcer in children is unknown, in the 41 . . .
Clinical detection of the hepatic lesion of pericentral sclerosis in chronic alcoholics.
Authors: Y Kaku, Y Hasumura, J Takeuchi
Journal: Gut (1982)

It has been shown that a specific liver lesion--that is, pericentral sclerosis associated with pericellular fibrosis--is the precursor of alcoholic liver sclerosis. It is, however, difficult to diagnose this hepatic lesion in chronic alcoholics, using only clinical data without liver biopsy. To investigate the possibility of a clinical test reflecting the presence of this hepatic lesion, ethanol (0.75 g/kg body weight) was given orally to chronic alcoholics, and serum glycoprotein levels (prealbumin, alpha HS glycoprotein, haptoglobin, alpha 2-macroglobulin) were measured before and six hours after. Chronic alcoholics were divided into three groups according to the histological findings in the liver at the time of study. Group I (alcoholic fatty liver or non-specific change) consisted of seven cases without pericentral sclerosis. Group II (alcoholic hepatic fibrosis or alcoholic hepatitis) consisted of five cases with pericentral sclerosis and pericellular fibrosis. Group III consisted of five cases with alcoholic liver cirrhosis. After the ethanol administration, serum glycoprotein levels decreased significantly in group I (P less than 0.05), whereas they increased in group II and group III. Their alternative ratios (see text) apparently differed (P less than 0.005) between group I and group II, and between group I and group III. These results indicate that the determination of serum glycoprotein levels before and after oral ethanol administration is useful way of discriminating alcoholic patients with hepatic pericentral sclerosis and pericellular fibrosis from alcoholics without such lesions.
USP9X Downregulation Renders Breast Cancer Cells Resistant to Tamoxifen
Authors: Hendrika M. Oosterkamp, E. Marielle Hijmans, Thijn R. Brummelkamp, Sander Canisius, Lodewyk F.A. Wessels, Wilbert Zwart, René Bernards
Journal: Cancer Research (2014)

Abstract Tamoxifen is one of the most widely used endocrine agents for the treatment of estrogen receptor α (ERα)–positive breast cancer. Although effective in most patients, resistance to tamoxifen is a clinically significant problem and the mechanisms responsible remain elusive. To address this problem, we performed a large scale loss-of-function genetic screen in ZR-75-1 luminal breast cancer cells to identify candidate resistance genes. In this manner, we found that loss of function in the deubiquitinase USP9X prevented proliferation arrest by tamoxifen, but not by the ER downregulator fulvestrant. RNAi-mediated attenuation of USP9X was sufficient to stabilize ERα on chromatin in the presence of tamoxifen, causing a global tamoxifen-driven activation of ERα-responsive genes. Using a gene signature defined by their differential expression after USP9X attenuation in the presence of tamoxifen, we were able to define patients with ERα-positive breast cancer experiencing a poor outcome after adjuvant treatment with tamoxifen. The signature was specific in its lack of correlation with survival in patients with breast cancer who did not receive endocrine therapy. Overall, our findings identify a gene signature as a candidate biomarker of response to tamoxifen in breast cancer. Cancer Res; 74(14); 3810–20. ©2014 AACR.
Molecular Predictors of Locoregional Recurrence in Breast Cancer: Ready for Prime Time?
Authors: Bruce G. Haffty, Thomas A. Buchholz
Journal: Journal of Clinical Oncology (2010)

tumor recurrence and locoregional recurrences in patients treated by breastconserving therapy in five national surgical adjuvant breast and bowel project protocols of node-negative breast cancer. J Clin Oncol 27:2466-2473, 2009 20. Fisher B, Dignam J, Wolmark N, et al: Tamoxifen and chemotherapy for lymph node-negative, estrogen receptor-positive breast cancer. J Natl Cancer Inst 89:1673-1682, 1997 21. Chagpar A, Kuerer HM, Hunt KK, et al: Outcome of treatment for breast cancer patients with chest wall recurrence according to initial stage: Implications for post-mastectomy radiation therapy. Int J Radiat Oncol Biol Phys 57:128-135, 2003 22. Cefaro GA, Genovesi D, Marchese R, et al: Predictors of local recurrence after conservative surgery and whole-breast irradiation. Breast Cancer Res Treat 98:329-335, 2006 23. Horst KC, Smitt MC, Goffinet DR, et al: Predictors of local recurrence after breast-conservation therapy. Clin Breast Cancer 5:425-438, 2005 24. Nuyten DS, Kreike B, Hart AA, et al: Predicting a local recurrence after breast-conserving therapy by gene expression profiling. Breast Cancer Res 8:R62, 2006 25. Carlson RW, Brown E, Burstein HJ, et al: NCCN Task Force Report: Adjuvant Therapy for Breast Cancer. J Natl Compr Canc Netw 4:S1-S26, 2006 (suppl 1) 26. Simes RJ, Coates AS: Patient preferences for adjuvant chemotherapy of early breast cancer: How much benefit is needed? J Natl Cancer Inst Monogr 30:146-152, 2001 27. Sparano JA: TAILORx: Trial assigning individualized options for treatment (Rx). Clin Breast Cancer 7:347-350, 2006 28. Mongan JJ, Ferris TG, Lee TH: Options for slowing the growth of health care costs. N Engl J Med 358:1509-1514, 2008 29. Iglehart JK: Prioritizing comparative-effectiveness research: IOM recommendations. N Engl J Med 361:325-328, 2009 30. Asad J, Jacobson AF, Estabrook A, et al: Does Oncotype DX recurrence score effect management of patients with early stage breast cancer. Am J Surg 196:527-529, 2008 31. Oratz R, Paul D, Cohn AL, Sedlacek SM: Impact of a commercial reference laboratory test recurrence score on decision making in early-stage breast cancer. Journal of Oncology Practice 3:182-186, 2007 32. Lyman GH, Cosler LE, Kuderer NM, et al: Impact of a 21-gene RT-PCR assay on treatment decisions in early-stage breast cancer: An economic analysis based on prognostic and predictive validation studies. Cancer 109: 1011-1018, 2007 33. Goldstein LJ, Gray R, Badve S, et al: Prognostic utility of the 21-gene assay in hormone receptor-positive operable breast cancer compared with classical clinicopathologic features. J Clin Oncol 26:4063-4071, 2008 34. Paik S, Tang G, Fumagalli D: An ideal prognostic test for estrogen receptor-positive breast cancer? J Clin Oncol 26:4058-4059, 2008
Disparate effects of adhesion and degranulation of platelets on myocardial and coronary function in postischaemic hearts
Authors: Bernhard Heindl, Stefan Zahler, Ulrich Welsch, Bernhard F Becker
Journal: Cardiovascular Research (1998)

Objective: Beside the major effect of acute thrombus formation, little is known about the interaction of platelets with the coronary endothelium in an ischaemia–reperfusion situation. The present study was designed to investigate, separately, the consequences of platelet adhesion and degranulation during myocardial reperfusion. Methods: Isolated guinea pig hearts perfused with Krebs–Henseleit buffer and performing pressure–volume work were used. We infringed myocardial function by imposing ischaemia (20 min of low-flow perfusion with 1 ml/min and 10 min of global ischaemia) and reperfusion (15 min with 5 ml/min). During low-flow perfusion, the coronary endothelium was stimulated by thrombin before and during infusion of a bolus: 108 washed human platelets±the Arg–Gly–Asp (RGD) analogon lamifiban, the supernatant of 108 thrombin-stimulated platelets, fibrinogen (2 μM), lamifiban (2 μM) or Tyrode's solution (control group). The parameter external heart work (EHW), determined pre- and postischaemically, served as criterion for recovery of myocardial function. Additionally, the formation of capillary transudate was measured during the reperfusion phase to assess coronary permeability. Coronary perfusion pressure was monitored continuously and myocardial production of lactate and consumption of pyruvate were measured. Electron microscopy of hearts was performed after platelet application to verify platelet adhesion in the coronary system. Results: Recovery of EHW by hearts without platelet application was 64±3% and was significantly reduced to 49±5% by platelet infusion (n=8 each). Infusion of supernatant of thrombin-stimulated platelets did not impair recovery of heart work. In the reperfusion phase (6th–10th min), hearts that either had received platelets or supernatant of platelets exhibited a significantly reduced production of capillary transudate (70 μl/min vs. 180 μl/min for the controls). Intracoronary bolus application of fibrinogen or lamifiban also reduced coronary leak. Coronary perfusion pressure and metabolic parameters were not statistically different between the groups at any time. Conclusions: Platelet adhesion to the coronary endothelium in a situation of myocardial ischaemia impairs cardiac recovery, whereas constituents released by platelets may have beneficial effects on the integrity of the coronary endothelium. In particular, fibrinogen seems to contribute to the permeability reducing effect, possibly by interaction with endothelial receptors recognising the RGD sequence.
Relation of vagotomy to subsequent risk of lung cancer: population based cohort study
Authors: A. Ekbom, G. Lundegardh, J. K McLaughlin, O. Nyren
Journal: BMJ (1998)

<h3>Abstract</h3> Smoking increases the risk of peptic ulcer disease and also adversely affects its course.1 Both pharmacological and surgical treatments will lead to a relief from the symptoms of the disease.23 We analysed to what extent such potential relief would affect the subsequent risk of lung cancer in patients who had had a vagotomy for peptic ulcer disease, compared with patients with the disease who were treated without surgery.
Spirometry in healthy elderly Chinese.
Authors: J Woo, J Pang
Journal: Thorax (1988)

Forced expiratory volume (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF) were measured in healthy subjects (129 men, 210 women) aged 60 years and above who were leading an independent and active life in the community. Women but not men showed an age related decline in FEV1 and FVC. Correlations of FEV1 and FVC with height were weaker than those reported for all age groups. Male ex-smokers had lower FEV1 values than current smokers and non-smokers. Regression equations are derived for men and women for predicting values appropriate to Chinese elderly people. These values are slightly lower than those for white people, but the difference is not as great as in values derived from surveys of all age groups.
Genome-wide association study to identify novel loci associated with therapy-related myeloid leukemia susceptibility
Authors: Jeffrey A. Knight, Andrew D. Skol, Abhijit Shinde, Darcie Hastings, Richard A. Walgren, Jin Shao, Thelma R. Tennant, Mekhala Banerjee, James M. Allan, Michelle M. Le Beau, Richard A. Larson, Timothy A. Graubert, Nancy J. Cox, Kenan Onel
Journal: Blood (2009)
Pathogenic importance of fibronectin in the superficial region of articular cartilage as a local factor for the induction of pannus extension on rheumatoid articular cartilage.
Authors: S Shiozawa, R Yoshihara, Y Kuroki, T Fujita, K Shiozawa, S Imura
Journal: Annals of the Rheumatic Diseases (1992)

To identify the local factors in cartilage that are responsible for the induction of pannus invasion, a 14 day organ culture study in which rheumatoid synovium was grown in contact with cartilage pieces was carried out. Rheumatoid synovium preferentially extended over hyaluronidase treated cartilage pieces, but detached from untreated pieces. Rheumatoid synovium extended over hyaluronidase treated cartilage surfaces containing fibronectin more extensively than over surfaces treated with hyaluronidase only. Extension over hyaluronidase treated cartilage surfaces containing immune complexes was small. The adherence of synovial cells to hyaluronidase treated cartilage slices in vitro was specifically inhibited by the synthetic peptide, Gly-Arg-Gly-Asp-Ser-Pro, which is the adhesive portion of the fibronectin molecule. Furthermore, synovial fibroblast-like cellular extension, morphologically similar to rheumatoid pannus, was observed in the organ culture experiments in which rheumatoid synovium grew over hyaluronidase treated cartilage surfaces containing fibronectin. Synovial tissue extension over fibronectin coated surfaces was inhibited when hyaluronic acid and chondroitin-4-sulphate, major components of cartilage proteoglycans, were present on the cartilage surface. These findings suggest that fibronectin present in the superficial region of cartilage potentiates rheumatoid synovial extension and proteoglycans and immune complexes inhibit rheumatoid synovial extension. It is likely that fibronectin deposited on the eroded surface of articular cartilage induces pannus formation in rheumatoid arthritis.
Evidence based case report Managing an elderly patient with a fractured femur
Authors: M. J Parker
Journal: BMJ (2000)

My patient, an elderly woman, had been admitted to the trauma ward via the accident and emergency department on the previous day because she had sustained a trochanteric fracture of the left hip after a simple fall at home. She was in average health for someone of 82 and had a medical history that included hypertension, a myocardial infarction (three years previously), and a fractured wrist (eight years before). Since her husband's death she had lived alone in sheltered accommodation.

I needed to establish the extent to which her management could be evidence based and, where possible, to determine the optimum management using evidence based medicine. I also decided that I could spare no more than four hours to identify the evidence and that I should be able to do this from my office computer.

I used Medline, the Cochrane Library 1 and Best Evidence 2 (both on CD Rom), and the following internet sites: the NHS Centre for Reviews and Dissemination (nhscrd.york.ac.uk), the American Academy of Orthopedic Surgeons (www.aaos.org), Omni (www.omni.ac.uk), the Trip Database (http://www.ceres.uwcm.ac.uk/frameset.cfm?section=trip), the Scottish Intercollegiate Guidelines Network (SIGN; www.show.scot.nhs.uk/sign/home.htm), and Bandolier (www.jr2.ox.ac.uk/Bandolier). Unless otherwise indicated, I used the search term “hip fracture.” I found …
Fibrinolysis and Hemorrhage in a Fatal Case of Heat Stroke
Authors: A. Wayne Meikle, John R. Graybill
Journal: New England Journal of Medicine (1967)

WIDESPREAD hemorrhage is common in fatal heat stroke.1 Before 1962, hemorrhage was generally attributed to increased capillary fragility, thrombocytopenia and hypoprothrombinemia.1 2 3 4 However, in that year hemorrhage associated with significant fibrinolysis was first reported in a fatal case of heat stroke by Shibolet et al.5 These authors also observed 2 additional cases with afibrinogenemia in which studies for fibrinolysis were not performed.The present case of fatal heat stroke with severe hemorrhage is the second in which severe hypofibrinogenemia and fibrinolysis are clearly documented.Case ReportA 45 year-old roofer was admitted to Vanderbilt University Hospital on July 13, 1966, an . . .
Nuclear DNA fragmentation and expression of Bcl-2 in primary biliary cirrhosis
Authors: H Koga, S Sakisaka, M Ohishi, M Sata, K Tanikawa
Journal: Hepatology (1997)

It is uncertain whether or not apoptosis is involved in the pathogenesis of primary biliary cirrhosis (PBC). The aims of this study were to assess the nuclear DNA fragmentation and expression of Bcl-2 in the biliary epithelial cells (BECs) and in the hepatocytes of PBC. Additionally, the effects of ursodeoxycholic acid (UDCA) on DNA fragmentation and Bcl-2 expression in PBC were evaluated. Liver tissue specimens from 35 PBC patients were examined by in situ nick-end labeling to detect any nuclear DNA fragments, and by immunohistochemistry for Bcl-2. Ten of these patients underwent a second liver biopsy after the treatment with UDCA. Sixteen histologically normal liver tissues and 17 chronic viral hepatitis C (CVHC) samples were chosen as controls. DNA fragmentation in BECs was more frequently found in PBC than in CVHC and more frequently than in the normal controls (both P < .05), and fragmentation in the hepatocytes of PBC more frequently than in normal controls (P < .01). Bcl-2 expression was more frequently found in both the BECs and hepatocytes of PBC than in the controls. UDCA significantly decreased the DNA fragmentation in BECs (P < .05) and the positivity for Bcl-2 in BECs (P < .01), although no significant decrease was found in hepatocytes. In conclusion, de novo Bcl-2 expression in hepatocytes of PBC was shown, and the increased nuclear DNA fragmentation and the Bcl-2 expression both in BECs and in hepatocytes may reflect apoptotic stress, although nuclear DNA fragmentation in BECs did not necessarily represent apoptosis. UDCA showed a potential effect of reducing nuclear DNA fragmentation in BECs.
Association Between Mediterranean Diet and Late-Life Cognition
Authors: Pascale Barberger-Gateau
Journal: JAMA (2009)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Cutaneous malignant melanoma and human immunodeficiency virus (HIV) infection: a report of three cases
Authors: J.M. McGREGOR, M. NEWELL, J. ROSS, N. KIRKHAM, D.H. McGIBBON, C. DARLEY
Journal: British Journal of Dermatology (1992)

Cutaneous malignant melanoma was diagnosed in three patients suffering from human immunodeficiency virus (HIV) infection. Staging at presentation inversely correlated with absolute CD4 count. In addition, a notably sparse lymphocytic inflammatory response to the melanoma was observed in two cases. Established data on melanoma in non-HIV immunosuppressed patients suggests a poor prognosis for melanoma in HIV disease.
Neurodegenerative Diseases: An Overview of Environmental Risk Factors
Authors: Rebecca C. Brown, Alan H. Lockwood, Babasaheb R. Sonawane
Journal: Environmental Health Perspectives (2005)

The population of the United States is aging, and an ever-increasing number of Americans are afflicted with neurodegenerative diseases. Because the pathogenesis of many of these diseases remains unknown, we must consider that environmental factors may play a causal role. This review provides an overview of the epidemiologic evidence for environmental etiologies for neurodegenerative diseases such as Alzheimer disease, Parkinson disease, parkinsonian syndromes (multiple system atrophy and progressive supranuclear palsy), and amyotrophic lateral sclerosis. Epidemiologic evidence for an association between environmental agents' exposure and neurodegenerative diseases is not conclusive. However, there are indications that there may be causal links, and the need for more research is obvious.