tbuckley/cabot-search huggingface dataset:
Interleukin 2 and interferon-gamma augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis.
Authors: T Hibi, M Ohara, M Watanabe, T Kanai, H Takaishi, A Hayashi, Y Hosoda, H Ogata, Y Iwao, S Aiso
Journal: Gut (1993)

In vitro effects of cytokines and therapeutic drugs on antibody dependent cellular cytotoxicity (ADCC) mediated by anticolon antibody were investigated in serum samples from patients with ulcerative colitis. A 51Cr release assay was used to examine ADCC activity with the colon cancer cell line, colo 205, as the target and peripheral blood mononuclear cells as the effector. High ADCC activity was shown in 13 of 32 (41%) patients with ulcerative colitis. This ADCC activity was inhibited by protein A treatment of the serum samples. Interleukin 2 (IL2) activated effector cells could enhance ADCC activity, but interferon-gamma (IFN-gamma) or tumour necrosis factor-alpha (TNF-alpha) had no effect on the cytotoxic activity of effector cells. Treatment of target cells with IFN-gamma increased the vulnerability of these cells to ADCC with a large increase of intercellular adhesion molecule-1 (ICAM-1) expression on their surface. Monoclonal antibodies to ICAM-1 inhibited this IFN-gamma enhanced ADCC activity. Interestingly, prednisolone (PSL) reduced ADCC activity, but sulphasalazine (SASP) or 5-aminosalicylic acid (5-ASA) did not. These results suggest that IL2 and IFN-gamma could enhance colonic epithelial cell injury mediated by the ADCC mechanism in ulcerative colitis and that ADCC enhanced by cytokines is restored by PSL treatment.
Painful Lesions in the Genital Area of a Young Woman
Authors: Xiao Yang, Thomas S. Bander, Yolanda Rosi Helfrich
Journal: JAMA Dermatology (2014)

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 Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Dermatology journal
Pulmonary Edema after Pericardiocentesis for Cardiac Tamponade
Authors: W. H. Vandyke, J. Cure, C. S. Chakko, M. Gheorghiade
Journal: New England Journal of Medicine (1983)

DIAGNOSTIC and therapeutic aspiration of fluid from various body cavities is a common procedure. The amount of fluid that can be removed safely at one time is limited by potential complications. In patients with cirrhosis of the liver and ascites, a reduction in stroke volume and cardiac output can occur if more than 1500 ml of ascitic fluid is removed.1 Removal of more than 2000 ml of pleural fluid can result in unilateral pulmonary edema.2 We have not previously observed pulmonary edema as a complication of pericardiocentesis for cardiac tamponade. We describe a patient with cardiac tamponade caused by carcinomatous . . .
Immunohistochemical analyses of p63 expression in cutaneous tumours
Authors: Y. Takeuchi, A. Tamura, M. Kamiya, T. Fukuda, O. Ishikawa
Journal: British Journal of Dermatology (2005)

Journal Article Immunohistochemical analyses of p63 expression in cutaneous tumours Get access Y. Takeuchi, Y. Takeuchi Departments of Dermatology and Pathology, Graduate School of Medicine, Gunma University, 3‐39‐22 Showa‐machi, Maebashi, Gunma 371‐8511, Japan Search for other works by this author on: Oxford Academic Google Scholar A. Tamura, A. Tamura Departments of Dermatology and Pathology, Graduate School of Medicine, Gunma University, 3‐39‐22 Showa‐machi, Maebashi, Gunma 371‐8511, Japan Search for other works by this author on: Oxford Academic Google Scholar M. Kamiya, M. Kamiya Departments of Dermatology and Pathology, Graduate School of Medicine, Gunma University, 3‐39‐22 Showa‐machi, Maebashi, Gunma 371‐8511, Japan Search for other works by this author on: Oxford Academic Google Scholar T. Fukuda, T. Fukuda Division of Histopathology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Maebashi, Japan E‐mail: yukotake@showa.gunma‐u.ac.jp Search for other works by this author on: Oxford Academic Google Scholar O. Ishikawa O. Ishikawa Departments of Dermatology and Pathology, Graduate School of Medicine, Gunma University, 3‐39‐22 Showa‐machi, Maebashi, Gunma 371‐8511, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 153, Issue 6, 1 December 2005, Pages 1230–1232, https://doi.org/10.1111/j.1365-2133.2005.06952.x Published: 01 December 2005
Plasminogen‐dependent fibrinolytic activity in normal human lymphocytes: Diminished lymphocyte plasminogen activator in chronic lymphocytic leukemia
Authors: Stanley Zucker, Karen Mehling, Kanti Rai
Journal: American Journal of Hematology (1985)

Abstract Discrepancies in correlations between fibrinolytic activity and metastatic potential of malignant cells has resulted in speculation on the putative role of plasminogen activators (PA) in cancer. In this report we have compared lymphocyte PA from 40 patients with chronic lymphocytic leukemia (CLL) to normal human B‐ and T‐ lymphocytes. Lymphocytes were isolated from peripheral blood by Ficoll‐Hypaque centrifugation. The B‐ and T‐cells were further separated on nylon wool columns. Cell PA activity and cell membrane PA were determined using 3 H‐fibrin‐coated plates with added human plasminogen. Lymphocytes did not lyse 3 H‐fibrin in the absence of plasminogen. Plasminogen‐dependent fibrinolytic activities of normal B‐ and T‐ lymphocytes were comparable. The addition of protease inhibitors with trypsin or plasmin specificity to lymphocytes significantly inhibited normal PA, thus substantiating the serine protease spectrum of lymphocyte PA. Examination of lymphocytes from &gt; 95% of patients with chronic lymphocytic leukemia revealed a marked decrease in lymphocyte and cell membrane PA as compared to normals. No correlation between Stage of CLL and lymphocyte PA was observed. Likewise, an inhibitor of PA in CLL lymphocytes was not detected. The function of PA in normal B‐ lymphocyte physiology and the potential pathogenetic role of diminished PA in CLL lymphocytes remain to be explored.
Courts may not be able to rule on value of treatments when doctors and families clash
Authors: C. Dyer
Journal: BMJ (2013)

A Court of Protection judge who refused to grant declarations that three types of treatment should be withheld from a seriously ill man with limited consciousness got the law right, the UK Supreme Court has ruled unanimously.1

The five judges said that the Court of Appeal was also right to grant Aintree University Hospitals NHS Foundation Trust the declarations two weeks later when David James’s condition had deteriorated further, but its reasoning was wrong.2 James died on 31 December 2012, 10 days after the declarations were granted.

In its first case on the Mental Capacity Act 2005, the UK’s highest court laid down important guidance for doctors faced with family opposition to decisions to discontinue treatment on clinical grounds.

The …
Hepatitis B virus. Inappropriate reactions to transmission risks
Authors: Thomas W. Kiernan, Robert J. Powers
Journal: JAMA (1979)

Ten patients designated as hepatitis B surface antigen (HBsAg) carriers were screened for inappropriate reactions to their disease. Assessment with a 32-item questionnaire showed three carriers to have underreacted to the risks of HBsAg transmission through misunderstandings or denial concerning the disease. One carrier, through severe social withdrawal, showed overreaction to the possibilities of disease transmission. Counseling was provided regarding the risks of HBsAg transmission. At a one-month follow-up, all carriers appeared appropriately aware of the risks of transmission, and one of two carriers referred for psychotherapy showed greatly improved social adjustment. We recommend that persons treating HBsAg carriers screen routinely for inappropriate reactions to risks of disease transmission and provide counseling as needed.
A90: Pediatric Henoch-NSchöAdonlein Purpura: Can Length of Hospital Stay Be Predicted?
Authors: Neta Cohen, Francis Mimouni, Nadav Freidel, Gil Amarilyo
Journal: Arthritis & Rheumatology (2014)

Background/Purpose:

Henoch Schonlein purpura (HSP) is a common, usually benign, arthritis in childhood. However, at times, it follows a protracted course involving prolonged length of hospital stay (LOS).



Objective:

To determine clinical and laboratory characteristics that allow prediction of prolonged LOS in children with HSP.



Methods:

We retrospectively collected all consecutive cases of HSP that were admitted to the Dana-Duek Children's hospital between Jan. 1, 2000 and Sep. 30, 2013. All charts were thoroughly reviewed for demographic characteristics (e.g. age, gender), LOS (in days by date), presenting and later symptoms (abdominal pain, vomiting, GI bleeding, palpable purpura, arthralgia or periarthritis, fever) and laboratory data on admission and discharge (CBC, CRP, ESR, serum creatinine, urinalysis). In univariate analysis we studied the variables that were statistically related to LOS. Variables that significantly predicted LOS in univariate analysis or that were clinically relevant (i.e. Proteinuria (defined as positive protein in urinalysis in 2 consecutive tests), systemic fever (defined as rectal temperature ≥38.0°C), gastrointestinal (GI) bleeding, arthralgia, CRP concentration, age (years) and abdominal pain as sole presenting symptom on admission) were analyzed in stepwise backward multiple regression analysis. Variables that remained significant in the final analysis were correlated with LOS, were each given specific weight (according to their contribution to the final R square) and were used to assemble an HSP severity score. Discriminate analysis was used to determine the score best discriminating patients with prolonged LOS (4 or more days) from the others.



Results:

Eighty nine children (aged 9 months–17 years) were retrieved for analysis. In univariate analysis, variables that were associated with prolonged LOS were: abdominal pain as initial sole presentation (P < 0.001), CRP (P = 0.001) and systemic fever (P = 0.018). Four variables remained significant in the final stepwise multiple regression analysis, and were used as parameters in assembling the HSP severity score. The HSP severity score consisted of sole abdominal pain at presentation (0 or 3 points), Fever (0 or 2 points), CRP ≥45 (0 or 1 point) and Age ≥6 (0 or 0.5 points). A score of ≥3 predicted a prolonged LOS (4 or more days) with a sensitivity of 76%, a specificity of 79% and a positive predictive value of 93%.



Conclusion:

Four selected variables available on the day of admission allow predicting the severity (in terms of LOS) of HSP. This score will be validated in an ongoing prospective study.
CD39/Ectonucleoside Triphosphate Diphosphohydrolase 1 Provides Myocardial Protection During Cardiac Ischemia/Reperfusion Injury
Authors: David Köhler, Tobias Eckle, Marion Faigle, Almut Grenz, Michel Mittelbronn, Stefanie Laucher, Melanie L. Hart, Simon C. Robson, Christa E. Müller, Holger K. Eltzschig
Journal: Circulation (2007)

Extracellular adenosine, generated from extracellular nucleotides via ectonucleotidases, binds to specific receptors and provides cardioprotection from ischemia and reperfusion. In the present study, we studied ecto-enzymatic ATP/ADP-phosphohydrolysis by select members of the ectonucleoside triphosphate diphosphohydrolase (E-NTPDase) family during myocardial ischemia.As a first step, we used a murine model of myocardial ischemia and in situ preconditioning and performed pharmacological studies with polyoxometalate 1, a potent E-NTPDase inhibitor (Na6[H2W12O40]). Polyoxometalate 1 treatment increased infarct sizes and abolished beneficial effects of preconditioning. To define relative contributions of distinct E-NTPDases, we investigated transcriptional responses of E-NTPDases 1 to 3 and 8 to preconditioning. We noted robust and selective induction of E-NTPDase 1 (CD39) transcript and protein. Histological analysis of preconditioned myocardium localized CD39 induction to endothelia and myocytes. Cd39-/- mice exhibited larger infarct sizes with ischemia (cd39+/+ 43.0+/-3.3% versus cd39-/- 52%+/-1.8; P<0.05), and cardioprotection was abrogated by preconditioning (cd39+/+ 13.3%+/-1.5 versus cd39-/- 50.5%+/-2.8; P<0.01). Heightened levels of injury after myocardial ischemia and negligible preconditioning benefits in cd39-/- mice were corrected by infusion of the metabolic product (AMP) or apyrase. Moreover, apyrase treatment of wild-type mice resulted in 43+/-4.2% infarct size reduction (P<0.01).Taken together, these studies reveal E-NTPDase 1 in cardioprotection and suggest apyrase in the treatment of myocardial ischemia.
Use of haploid plants as bioassay for mutagens.
Authors: M L Christianson, M O Chiscon
Journal: Environmental Health Perspectives (1978)

Results of a pilot program show that suspension cultured polyhaploid Nicotiana tabacum cells can be used to bioassay the effects of mutagens. Reproducible survival curves with significant regression coefficients are obtained. Putative mutation conferring resistance to amino acid analogs is significantly more frequent after exposure to mutagens; in contrast, habituants, cytokinin-independent clones, are significantly less frequent (although the variance of clone size increases!). The maximum spontaneous mutation rate is estimated at 3 X 10(-8); the equilibrium frequency of habituant cells in an otherwise nonhabituated culture is estimated at 5 X 10(-7). An evaluation of the system suggests changes in several and further characterization of other of the parameters involved. The use of haploid tobacco as an in vivo mutagen screen is briefly described, as is the importance of similar in vivo diploid systems for discriminating between various kinds of mutational processes.
Adenovector-mediated gene transfer of active transforming growth factor-beta1 induces prolonged severe fibrosis in rat lung.
Authors: P J Sime, Z Xing, F L Graham, K G Csaky, J Gauldie
Journal: Journal of Clinical Investigation (1997)

Transforming growth factor (TGF)-beta1 has been implicated in the pathogenesis of fibrosis based upon its matrix-inducing effects on stromal cells in vitro, and studies demonstrating increased expression of total TGF-beta1 in fibrotic tissues from a variety of organs. The precise role in vivo of this cytokine in both its latent and active forms, however, remains unclear. Using replication-deficient adenovirus vectors to transfer the cDNA of porcine TGF-beta1 to rat lung, we have been able to study the effect of TGF-beta1 protein in the respiratory tract directly. We have demonstrated that transient overexpression of active, but not latent, TGF-beta1 resulted in prolonged and severe interstitial and pleural fibrosis characterized by extensive deposition of the extracellular matrix (ECM) proteins collagen, fibronectin, and elastin, and by emergence of cells with the myofibroblast phenotype. These results illustrate the role of TGF-beta1 and the importance of its activation in the pulmonary fibrotic process, and suggest that targeting active TGF-beta1 and steps involved in TGF-beta1 activation are likely to be valuable antifibrogenic therapeutic strategies. This new and versatile model of pulmonary fibrosis can be used to study such therapies.
Using patient and general practice characteristics to explain variations in cervical smear uptake rates
Authors: F A Majeed, D G Cook, H R Anderson, S Hilton, S Bunn, C Stones
Journal: BMJ (1994)

<b>Objectives</b>: To produce practice and patient20variables for general practices from census and family health services authority data, and to determine the importance of these variables in explaining variation in cervical smear uptake rates between practices. <b>Design</b>: Population based study examining variations in cervical smear uptake rates among 126 general practices using routine data. <b>Setting</b>: Merton, Sutton, and Wandsworth Family Health Services Authority, which covers parts of inner and outer London. <b>Main outcome measure</b>: Percentage of women aged 25-64 years registered with a general practitioner who had undergone a cervical smear test during the five and a half years preceding 31 March 1992. <b>Results</b>: Cervical smear uptake rates varied from 16.5% to 94.1%. The estimated percentage of practice population from ethnic minority groups correlated negatively with uptake rates (r=-0.42), as did variables associated with social deprivation such as overcrowding (r=-0.42), not owning a car (r=-0.41), and unemployment (r=-0.40). Percentage of practice population under 5 years of age correlated positively with uptake rate (r=0.42). Rates were higher in practices with a female partner than in those without (66.6% v 49.1%; difference 17.5% (95% confidence interval 10.5% to 24.5%)), and in computerised than in non- computerised practices (64.5% v 50.5%; 14.0% (6.4% to 21.6%)). Rates were higher in larger practices. In a stepwise multiple regression model that explained 52% of variation, five factors wre significant predictors of uptake rates: presence of a female partner; children under 5; overcrowding; number of women aged 35-44 as percentage of all women aged 25-64; change of address in past year. <b>Conclusions</b>: Over half of variation in cervical smear uptake rates can be explained by patient and practice variables derived from census and family health services authority data; these variables may have a role in explaining variations in performance of general practices and in producing adjusted measures of practice performance. Practices with a female partner had substantially higher uptake rates.
Safety (toxicity), pharmacokinetics, immunogenicity, and impact on elements of the normal immune system of recombinant human IL-15 in rhesus macaques
Authors: Thomas A. Waldmann, Enrico Lugli, Mario Roederer, Liyanage P. Perera, Jeremy V. Smedley, Rhonda P. Macallister, Carolyn K. Goldman, Bonita R. Bryant, Jean M. Decker, Thomas A. Fleisher, H. Clifford Lane, Michael C. Sneller, Roger J. Kurlander, David E. Kleiner, John M. Pletcher, William D. Figg, Jason L. Yovandich, Stephen P. Creekmore
Journal: Blood (2011)
REDUCTION IN EMBOLIC EVENTS WITH MULTIPOLAR DUTY-CYCLED RADIOFREQUENCY ISOLATION OF THE PULMONARY VEINS USING THE MODIFIED VERSION OF THE GENIUS™ ABLATOR
Authors: Edina Nagy-Balo, Alexandra Kiss, Levente Lanczi, Ervin Berenyi, Marcell Clemens, Istvan Edes, Zoltan Csanadi
Journal: Journal of the American College of Cardiology (2013)
Targeting lysosomal degradation induces p53-dependent cell death and prevents cancer in mouse models of lymphomagenesis
Authors: Kirsteen H. Maclean, Frank C. Dorsey, John L. Cleveland, Michael B. Kastan
Journal: Journal of Clinical Investigation (2007)

Despite great interest in cancer chemoprevention, effective agents are few. Here we show that chloroquine, a drug that activates the stress-responsive Atm-p53 tumor-suppressor pathway, preferentially enhances the death of Myc oncogene–overexpressing primary mouse B cells and mouse embryonic fibroblasts (MEFs) and impairs Myc-induced lymphomagenesis in a transgenic mouse model of human Burkitt lymphoma. Chloroquine-induced cell death in primary MEFs and human colorectal cancer cells was dependent upon p53, but not upon the p53 modulators Atm or Arf. Accordingly, chloroquine impaired spontaneous lymphoma development in Atm-deficient mice, a mouse model of ataxia telangiectasia, but not in p53-deficient mice. Chloroquine treatment enhanced markers of both macroautophagy and apoptosis in MEFs but ultimately impaired lysosomal protein degradation. Interestingly, chloroquine-induced cell death was not dependent on caspase-mediated apoptosis, as neither overexpression of the antiapoptotic protein Bcl-2 nor deletion of the proapoptotic Bax and Bak affected chloroquine-induced MEF death. However, when both apoptotic and autophagic pathways were blocked simultaneously, chloroquine-induced killing of Myc-overexpressing cells was blunted. Thus chloroquine induces lysosomal stress and provokes a p53-dependent cell death that does not require caspase-mediated apoptosis. These findings specifically demonstrate that intermittent chloroquine use effectively prevents cancer in mouse models of 2 genetically distinct human cancer syndromes, Burkitt lymphoma and ataxia telangiectasia, suggesting that agents targeting lysosome-mediated degradation may be effective in cancer prevention.
The ontogeny of liver copper metabolism in the guinea pig: Clues to the etiology of Wilson's disease
Authors: Surjit K. S. Srai, Andrew K. Burroughs, Bernard Wood, Owen Epstein
Journal: Hepatology (1986)

The normal human neonate has a copper profile indistinguishable from Wilson's disease, and we have previously postulated that this disease is caused by genetic failure to switch from the fetal to adult mode of copper metabolism. This study validates the developing guinea pig as a suitable animal in which to study copper ontogeny. At birth, liver copper concentrations are 7 times higher than in adults and serum copper and ceruloplasmin are 27 and 21% of adult values, respectively. A 53% fall in liver copper occurs in the 4 days after birth. This is associated with a marked increase in bile copper output, which does not parallel increasing bile flow. Liver copper falls, and serum copper and ceruloplasmin increase to near adult levels in the 30 days after birth. Until the sixtieth day of gestation, liver copper was significantly increased in copper-stressed littermates, although paradoxically at birth, concentrations were significantly lower. In copper-stressed fetal animals, bile copper output increased markedly before birth. Metallothionein was the dominant copper-binding protein in the fetal liver but a minor component in the adult. Superoxide dismutase activity only developed after birth. We conclude that the postnatal switch from the fetal to adult mode of copper metabolism involves activation of biliary excretion and ceruloplasmin export as well as changes in the association of copper with hepatic copper proteins. Similarities between the fetus and Wilson's disease suggest that this disease is caused by failure of this postnatal adaptation process.
VTD combination therapy with bortezomib–thalidomide–dexamethasone is highly effective in advanced and refractory multiple myeloma
Authors: M Pineda-Roman, M Zangari, F van Rhee, E Anaissie, J Szymonifka, A Hoering, N Petty, J Crowley, J Shaughnessy, J Epstein, B Barlogie
Journal: Leukemia (2008)
Symptoms and signs: physical disease or illness behaviour?
Authors: G Waddell, M Bircher, D Finlayson, C J Main
Journal: BMJ (1984)

The amount of treatment received by 380 patients with backache was found to have been influenced more by their distress and illness behaviour than by the actual physical disease. Patients showing a large amount of inappropriate illness behaviour had received significantly more treatment (p less than 0.001). The symptoms and signs of illness behaviour need to be clearly distinguished from those of physical disease, and better assessment of illness behaviour is essential if everyday clinical practice is to fulfil the ideal of treating patients as well as diseases.