tbuckley/cabot-search huggingface dataset:
CathKIT: improving quality in the cardiac catheterization laboratory
Authors: Gregory J Dehmer, John W Hirshfeld, William J Oetgen, Kristi Mitchell, April Wells Simon, MaryAnne Elma, Mirle A Kellett, Ralph G Brindis, Richard A Chazal, Gregory J Dehmer, Ralph G Brindis, Charles E Chambers, Mary Heisler, Frederick A Heupler, John W Hirshfeld, Mirle A Kellett, Thomas D Lane, William J Oetgen, Roger Siegfried, April Wells Simon, C.Michael Valentine
Journal: Journal of the American College of Cardiology (2004)
Abstract A24: Epigenetic silencing of ID4 (inhibitor of DNA binding 4) is associated with prostate cancer
Authors: Pankaj Sharma, Swathi Chinaranagari, Divya Patel, Jaideep Chaudhary
Journal: Cancer Research (2012)

Abstract Introduction: Inhibitor of DNA binding/differentiation protein 4 (Id4) is dominant negative regulator of basic helix loop helix (bHLH) family of transcription factors. Id4 shares the homology of HLH domain with other Ids and lack the basic DNA binding region. Previous studies from our lab had shown that unlike Id1, Id2 and Id3, Id4 acts as a tumor suppressor in prostate cancer by attenuating cell proliferation and promote apoptosis. Consistent with these observations Id4 is epigenetically silenced in Du145 prostate cancer cell line. In this study we investigated whether Id4 is also epigenetically silenced in prostate cancer. We also examined association between Id4 promoter hypermethylation and its expression in prostate cancer cell lines. Experimental procedures: Id4 protein expression was analyzed on human prostate adenocarcinoma samples by Immunhistochemistry. Id4 promoter methylation pattern on prostate cancer cell lines (C33, C81, DU145, LNCaP, DU145+ID4, and PC3) was examined. In addition, we performed Laser capture microdisection (LCMD) on the human prostate tissues and methylation specific PCR to correlate our cell line studies with clinical studies. Results: IHC demonstrated decreased Id4 protein expression in human prostate tissue samples whereas higher nuclear Id4 expression was found in normal prostate tissues.Id4 methylation specific PCR (MSP) on prostate cancer cell lines, showed Id4 methylation in DU145 cell and but not in LNCaP and C33 cells. In C81 and PC3 cells it showed partial methylation. C81 are derivatives of LNCaP cell lines and are Androgen independent and are more metastatic. Increased Id4 methylation in C81 as compared to LNCaP suggests its epigenetic silencing as cells acquire androgen independence. Tumors with Id4 promoter hypermethylation showed distinct loss of Id4 expression. Conclusions: Id4 appears as a potential tumor suppressor gene that is epigenetically silenced during cancer development.Id4 promoter hypermethylation had been reported in breast, colorectal cancer and chronic lymphocytic leukemia Thus, loss of Id4 expression due to promoter hypermethylation. Id4 methylation status could serve as a prognostic biomarker in human prostate cancer. Acknowledgement: The research was supported by NIH/NCI-RO1CA128914 and in part by NIH/NCRR/RCMI G12RR03062. Citation Format: Pankaj Sharma, Swathi Chinaranagari, Divya Patel, Jaideep Chaudhary. Epigenetic silencing of ID4 (inhibitor of DNA binding 4) is associated with prostate cancer [abstract]. In: Proceedings of the AACR Special Conference on Advances in Prostate Cancer Research; 2012 Feb 6-9; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2012;72(4 Suppl):Abstract nr A24.
Clues to understanding the role of estrogen receptors in mediating cardiovascular protection
Authors: X Du
Journal: Cardiovascular Research (2002)

See article by Molero et al. [14] ( pages 43 -51) in this membrane ERs through several pathways, including issue.tyrosine kinase, mitogen-activated protein kinase (MAPK), Gender-related differences in the risk of cardiovascular adenylyl cyclase / cAMP, and guanylyl cyclase / cGMP diseases have been well recognized with premenopausal [1,7].Estrogen is a key regulator of growth, differentiation women exhibiting a lower risk compared to age-matched or apoptosis, and function of vascular smooth muscle cells, men [1].Estrogen is implicated as the factor responsible endothelial cells, fibroblasts and cardiomyocytes [2].Exfor this gender difference due to the facts that the female pression of a number of proteins, that are important in the advantage over male in cardiovascular morbidity disap-development of cardiovascular diseases, is either up-regpears following menopause and that administration of ulated (e.g., metalloproteinases, nitric oxide synthase, 17a-estradiol (E ) is protective against cardiovascular prostaglandin synthase, vascular endothelial growth factor, 2 injury.In addition to changes in lipid metabolism, E at Akt, atrial natriuretic factor, coagulation factors, tissue
Homeless Persons and Health Care
Authors: PHILIP W. BRICKNER
Journal: Annals of Internal Medicine (1986)

Health care is generally unavailable for the homeless. This heterogeneous group of men and women, including long-term street dwellers, residents of shelters, the chronically mentally ill, the economically debased, and alienated youth, are subject to a broad range of acute and chronic diseases, intensified by unsuitable living conditions, stress, and sociopathic behavior. Trauma, pulmonary tuberculosis, infestations, and peripheral vascular disease are common problems among the homeless; incomplete and fragmentary medical care permits exacerbation of chronic disorders. Outreach programs imaginatively constructed by teams of physicians, nurses, and social workers can effectively reestablish and maintain health services for these disenfranchised persons.
Correlation of myocardial echo contrast disappearance rate (“Washout”) and severity of experimental coronary stenosis
Authors: Chuwa Tei, Shuji Kondo, Samuel Meerbaum, Kenneth Ong, Gerald Maurer, Frederick Wood, Tatsuo Sakamaki, Keicho Shimoura, Eliot Corday, Pravin M. Shah
Journal: Journal of the American College of Cardiology (1984)
THE MAINTENANCE OF THE HONOUR AND INTERESTS OF THE MEDICAL PROFESSION
Authors: S. Crawshaw
Journal: BMJ (1907)

Serial cranial computed tomograms were carried out in 136 children with acute lymphoblastic leukaemia who were receiving 24 Gy or 18 Gy of cranial irradiation and continuing treatment with doses of methotrexate given weekly orally or intramuscularly. The findings were correlated with treatment variables, the development of fits, and the intelligence quotient (IQ). Reversible brain shrinkage, attributed to treatment with steroids, was found on 87 of 114 initial scans (76%); 14 showed changes in white matter during treatment (10%), and calcification was found in 13 either during or after treatment (10%). Eight children (6%) had fits, and in six of the eight there were changes in white matter or calcification on the scans. Comparison of the two radiotherapy dosages showed no difference in the incidence of abnormalities seen on computed tomography, fits, or serial IQ measurements, but children receiving intramuscular methotrexate had a higher incidence of calcification and a lower mean IQ at one year than those who received the drug orally, although this difference was not apparent later. Younger children were more likely to develop changes on computed tomograms and fits, and to have low IQs on completion of treatment, with changes most apparent in those less than 2 years of age. There were highly significant correlations between abnormalities on computed tomography, fits, and IQ. These findings confirm the neurological vulnerability of younger children with acute lymphoblastic leukaemia, show an association between abnormalities on computed tomography and intellectual deficit, and suggest that methotrexate is more toxic when given intramuscularly than orally. They provide no evidence that 18 Gy of cranial irradiation is less toxic than 24 Gy, and indicate the need for alternative treatment regimens.
Effects of Congestive Heart Failure on Ca<sup>2+</sup>Handling in Skeletal Muscle During Fatigue
Authors: Per Kristian Lunde, Ole M. Sejersted, Hanne-Mari Schiøtz Thorud, Theis Tønnessen, Unni Lie Henriksen, Geir Christensen, Håkan Westerblad, Joseph Bruton
Journal: Circulation Research (2006)

Skeletal muscle weakness and decreased exercise capacity are major symptoms reported by patients with congestive heart failure (CHF). Intriguingly, these skeletal muscle symptoms do not correlate with the decreased heart function. This suggests that CHF leads to maladaptive changes in skeletal muscles, and as reported most markedly in slow-twitch muscles. We used rats at 6 weeks after infarction to measure expression of key proteins involved in SR Ca(2+) release and uptake in slow-twitch soleus muscles. We also measured force and myoplasmic free [Ca(2+)] ([Ca(2+)](i)) in intact single fibers of soleus muscles. CHF rats showed clear signs of severe cardiac dysfunction with marked increases in heart weight and left ventricular end-diastolic pressure compared with sham operated rats (Sham). There were small, but significant, changes in the content of proteins involved in cellular Ca(2+) handling in CHF muscles: slight increases in SR Ca(2+) release channels (ie, the ryanodine receptors) and in SR Ca(2+)-ATPase. Tetanic force and [Ca(2+)](i) were not significantly different between CHF and Sham soleus fibers under resting conditions. However, during the stimulation period there was a decrease in tetanic force without changes in [Ca(2+)](i) in CHF fibers that was not observed in Sham fibers. The fatigue-induced changes recovered rapidly. We conclude that CHF soleus fibers fatigue more rapidly than Sham fibers because of a reversible fatigue-induced decrease in myofibrillar function.
The chemokines RANTES, MCP-3, MCP-4, eotaxin-1 and eotaxin-2 are associated with eosinophil recruitment into the airways of asthmatic children
Authors: Luis M Teran, Enrique Rojas-Ramos, Ana Francisca Avalos, Lorenzo Perez-Fernandez, Francisco Cuevas
Journal: Journal of Allergy and Clinical Immunology (2002)
Cytoplasmic localization of FAC is essential for the correction of a prerepair defect in Fanconi anemia group C cells.
Authors: H Youssoufian
Journal: Journal of Clinical Investigation (1996)

Mutations in the gene defective in Fanconi anemia complementation group C, FAC, are responsible for a subset of Fanconi anemia, a group of autosomal recessive disorders characterized by chromosomal instability, hypersensitivity to cross-linking agents, and cancer susceptibility. Although abnormalities in DNA repair have been suspected, localization of the FAC gene product to the cytoplasm has cast doubt on such a mechanism. Monitoring of interstrand DNA cross-linking shows that the predominant defect in group C cells is in the initial induction of cross-links, not in repair synthesis. Both the cross-linking defect and the enhanced cytotoxicity of cross-linkers on Fanconi anemia group C cells are corrected completely by cytoplasmic isoforms of the FAC protein, but not by an isoform targeted to the nucleus. The ability of FAC to correct these phenotypic abnormalities reaches a maximum threshold despite overexpression leading to higher levels of cytosolic protein. These results demonstrate that cytoplasmic localization is essential for the intracellular activity of the FAC protein. It is proposed that this activity is coupled to a cytoplasmic defense mechanism against a specific class of genotoxic agents.
Hematopoietic cell transplantation in patients with intermediate and high-risk AML: results from the randomized Study Alliance Leukemia (SAL) AML 2003 trial
Authors: J Schetelig, M Schaich, K Schäfer-Eckart, M Hänel, W E Aulitzky, H Einsele, N Schmitz, W Rösler, M Stelljes, C D Baldus, A D Ho, A Neubauer, H Serve, J Mayer, W E Berdel, B Mohr, U Oelschlägel, S Parmentier, C Röllig, M Kramer, U Platzbecker, T Illmer, C Thiede, M Bornhäuser, G Ehninger
Journal: Leukemia (2014)
Magnetic resonance imaging may be alternative to necropsy
Authors: R. Bisset
Journal: BMJ (1998)

EDITOR—Certification of the cause of death is a valuable source ofinformation about illness in the community. When a death is unexplained thecase is referred to the coroner in England and Wales and the procurator fiscal in Scotland. Although Scottish law does not demand explanation of a non-suspicious death, in England a cause of death (or mode of death under certain circumstances) must …
VITAMIN A IN DARIER'S DISEASE
Authors: Z. A. LEITNER, T. MOORE
Journal: British Journal of Dermatology (1948)

Journal Article VITAMIN A IN DARIER'S DISEASE Get access Z. A. LEITNER, M.D.Berlin. L.R.C.P.E., Z. A. LEITNER, M.D.Berlin. L.R.C.P.E. St. Mary's Hospital, London Search for other works by this author on: Oxford Academic Google Scholar T. MOORE, D.Sc.Belfast, Ph. D.Cambridge T. MOORE, D.Sc.Belfast, Ph. D.Cambridge Dunn Nutritional Laboratory, University of Cambridge, and Medical Research Council Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 60, Issue 2, 1 February 1948, Pages 41–50, https://doi.org/10.1111/j.1365-2133.1948.tb10989.x Published: 01 February 1948
The Saccharin Controversy
Authors: Ronald K Kalkhoff, Marvin E Levin
Journal: Diabetes Care (1978)

Saccharin and its salts are the most extensively consumed artificial sweeteners in the United States today. The current controversy about the risks of their use to human health has surfaced from research findings that report an increased incidence of cancer, primarily of the urinary bladder, in certain animal species and man chronically exposed to these agents. The April 1977 proposal by the Food and Drug Administration to restrict use of saccharin was based on these investigations. The intense public response against any ban has led to Congressional deliberations over the fate of saccharin during the present moratorium and information-gathering period. Since diabetic patients are among the principal users of this compound, it appears timely to review the evidence for and against its carcinogenic potential.
Prevalence of Hepatitis B in Pregnant Women-Reply
Authors: Neil Silverman
Journal: JAMA (1992)

<h3>In Reply.</h3> —We appreciate Dr Krause's comments. Variations in the hepatitis B vaccine worldwide, in both cost and dosing recommendations, prevented us from constructing a useful cost-effectiveness algorithm within the discussion section of the article. However, in view of the long-term costs associated with chronic hepatitis B-related disease, it would seem that prophylactic neonatal vaccination could be cost-beneficial. This view has also been espoused in the recent recommendation for widened hepatitis B vaccination from the ACIP.<sup>1</sup> We agree with Waters and Cook that other risk factors may be predictive of maternal hepatitis B status. This study was designed to look at the lack of prenatal care as a possible risk factor in itself and showed unregistered status to be linked to maternal drug use. The existence of other associated risks in these women speaks even more strongly to a need for widened neonatal vaccination. Finally, this study was not
P3-137: XPD 312 single nucleotide polymorphism (SNP) predicts survival in stage IIIA–B non–small–cell lung cancer (NSCLC) patients (p) &lt;59 years (y) treated with chemotherapy followed by surgery
Authors: Carmen Santarpia, José-Luis González-Larriba, Pilar Azagra, Blanca Cantos, Pilar Garrido, José M. Sánchez, Itziar de Aguirre, Maria Sánchez-Ronco, Miguel Tarón, Rafael Rosell
Journal: Journal of Thoracic Oncology (2007)
Oral Administration of Aureomycin in the Treatment of Certain Dermatoses
Authors: Jacob L. Grund
Journal: New England Journal of Medicine (1950)

ORAL administration of aureomycin was first employed in dermatologic disorders in 1949. A report of its effectiveness in penicillin-resistant staphylococcal infections appeared from the Mayo Clinic,1 shortly after an article by O'Leary et al.2 describing encouraging results in the treatment of late cutaneous syphilis. Baer and Miller3 found it of specific value in quickly healing and preventing the spread of the cutaneous lesions of disseminated cutaneous herpes simplex (Kaposi's varicelliform eruption). Penicillin-resistant stomatitis ulceromembranosa acuta,4 a condition synonymous with acute infectious stomatitis or gingivostomatitis, has also been successfully treated with aureomycin by mouth. The latter condition and Kaposi's varicelliform eruption . . .
Low free serum histidine concentration in rheumatoid arthritis. A measure of disease activity.
Authors: D A Gerber
Journal: Journal of Clinical Investigation (1975)

A study of sera from 285 patients with definite or classical rheumatoid arthritis (including 37 patients receiving no anti-inflammatory drugs) and sera from 67 healthy subjects has confirmed 10 published reports of a statistically significant decreased blood histidine concentration in patients with rheumatoid arthritis. Contrastingly, in sera from 231 patients with a variety of acute and chronic illnesses other than rheumatoid arthritis, no statistically significant hypohistidinemia was observed either in the group as a whole or in association with the administration of aspirin, prednisone, indomethacin, phenylbutazone, or dextropropoxyphene. In the patients with rheumatoid arthritis there was a statistically significant correlation between the serum histidine concentration and the following: Westergren sedimentation rate (r=-0.33, P smaller than 10- minus 9), grip strength (r=0.26, P smaller than 10- minus 9), hematocrit (r=0.23, P smaller than 10- minus 9), duration of morning stiffness (r=-0.14, P=10- minus 5), walking time (r=-0.13, P=10- minus 4), latex titer of rheumatoid factor (r=-0.11, P=0.001), and the duration of arthritis (r=-0.06, P=0.05). There was no statistically significant association between the serum histidine concentration and the duration of rheumatoid arthritis in the 151 patients with disease of 0-10-yr duration (r=0.02, P=0.5), the sex of the patient, or the presence of antinuclear antibody (R=0.007, P=0.9). The serum histidine concentration was less in rheumatoid patients receiving steroids (P=0.00001), gold (P=0.009), and aspirin (P=0.15) than in rheumatoid patients not receiving these drugs. This study indicates that histidine determinations on properly preserved casual serum samples can be helpful in the diagnosis of rheumatoid arthritis and in the evaluation of the activity of the disease.
Inducer and Suppressor T–Cells in Hepatitis B Virus–Induced Liver Disease
Authors: Howard C. Thomas, David Brown, Guitaine Routhier, George Janossy, Patrick C. Kung, Gideon Goldstein, Sheila Sherlock
Journal: Hepatology (1982)

During acute type B hepatitis, the proportion of inducer to cytotoxic/suppressor T-cells is decreased due to an increase in the concentration of suppressor cells. Similar changes are seen in chronically infected subjects with evidence of active viral replication (HBeAg positive) and chronic hepatitis of varying severity. This imbalance of the regulatory cells returns to normal when viral replication decreases during the recovery phase of acute hepatitis and in patients who become chronic carriers with minimal liver disease (HBeAb positive patient). Patients in whom viral replication has subsided (HBeAb positive) but who continue to exhibit chronic active liver disease have increased inducer to cytotoxic/suppressor cell ratios due to a decrease in the concentration of the cytotoxic/suppressor cell population. Further studies are needed to determine whether these alterations of the regulatory cells of the immune system are a causal factor influencing the duration of active hepatitis B virus replication and the degree of inflammatory liver damage, or merely changes secondary to the presence of a replicating virus.
Artesunate and Malaria
Authors: Tracy Hampton
Journal: JAMA (2010)

The results of an open-label, randomized trial that included 5425 children in 9 African countries suggest that intravenous artesunate should replace quinine for treating severe malaria (Dondorp AM et al for the AQUAMAT group. Lancet. 2010;376[9753]:1647-1657).
Reciprocal regulation of ZEB1 and AR in triple negative breast cancer cells.
Authors: TR Graham, R Yacoub, T Liu, V Odero-Marah, K Kimbro, RM O'Regan
Journal: Cancer Research (2009)

Abstract Abstract #3054 Introduction: Approximately 60-80% of breast tumors are positive for androgen receptor (AR) and negative for estrogen receptor (ER) and progesterone (PR) (Isola et al. J Pathol. 1993). This suggests that AR may function independently of ER and PR to cross-talk with other factors such as Zinc-finger enhancer binding protein (ZEB1). ZEB1 is a transcription factor involved in the progression of breast cancer primarily through promoting epithelial to mesenchymal transition (EMT). ZEB1 represses the expression of E-cadherin by binding to E-box sequences in the promoter, thus decreasing epithelial differentiation and promotes cell migration.&amp;#x2028; Methods: We established a stable control and ZEB1 knockdown using shRNA in MDA-MB-231 cells, a highly metastatic triple negative breast cancer cell line with mesechymal morphology. The stable cell lines were characterized by immunoblot and RT-PCR analysis and were stimulated with synthetic androgens or an androgen antagonist and cell growth and migration were monitored.&amp;#x2028; Results: ZEB1 regulated the expression of AR in triple breast cancer cell lines. AR promoter contains two E-boxes, which may be critical to the transcriptional regulation of this gene. ZEB1 suppression by stably transfecting shRNA in MDA-MB-231 cells resulted in a decrease of AR mRNA, protein and AR downstream targets. In addition, ZEB1 suppression reduced the protein expression of Cyclin D1 and decreased cell proliferation. Conversely, blockade of AR signaling with bicalutamide resulted in suppression of ZEB1 protein expression in two triple negative breast cancer cell lines. ZEB1 knockdown in MDA-MB-231 cells sensitized the cells to bicalutamide by inducing a greater amount of cell death and a reduction in migration compared to the control cells.&amp;#x2028; Conclusions: Taken together, these results indicate that ZEB1 and AR regulate each other to promote cell growth and cell migration in triple negative breast cancer cells. Inhibition of AR signaling could decrease cell proliferation via ZEB1 in a subset of triple negative breast cancers. The growth of triple negative breast cancers that express ZEB1 and AR could be inhibited by antiandrogen treatment. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 3054.
THYROID FUNCTION IN EXPERIMENTAL STREPTOCOCCAL PNEUMONIA IN THE RAT
Authors: Seymour Reichlin, Robert J. Glaser
Journal: The Journal of Experimental Medicine (1958)

In order to study the effects of a severe bacterial infection on thyroid function rats were subjected to group A streptococcal pneumonia, and thyroid activity determined by measurement of the rate of discharge of I(131) from the thyroid gland. Decreased thyroid activity of moderate to marked degree was observed in the majority of infected animals. Infected animals ate less than normal animals. Since fasting leads to decreased thyroid function, I(131) release rates were measured in control animals pair-fed with infected animals and in control and infected animals force-fed a normal intake. The reduction in thyroid activity seen in acute infection was found to be partly but not entirely due to the associated voluntary food restriction. Although the adrenal glands of rats dying of pneumonia were very large, the thyroid inhibition occurring during the course of experimental pneumonia was not secondary to increased adrenocortical function since infected, adrenalectomized animals, receiving injections of cortisone, showed thyroid inhibition comparable to that observed in intact infected animals. The possible influence of the level of thyroid activity on resistance was evaluated. In two experiments a total of 80 rats in 3 groups was pretreated with propylthiouracil and injected daily with 3 dosage levels of 7-thyroxine for 3 weeks prior to inoculation. Under these conditions mortality rates in infected animals fell with decreasing levels of thyroid function. However, induced hypothyroidism was found to afford no protective effect in comparison with untreated infected animals.