tbuckley/cabot-search huggingface dataset:
Urinary Monoclonal Immunoglobulin in Multiple Myeloma
Authors: R. PEREZ-SOLER
Journal: Annals of Internal Medicine (1981)

Letters1 January 1981Urinary Monoclonal Immunoglobulin in Multiple MyelomaR. PEREZ-SOLER, M.D., R. ESTEBAN, M.D., J. GUARDIA, M.D.R. PEREZ-SOLER, M.D.Search for more papers by this author, R. ESTEBAN, M.D.Search for more papers by this author, J. GUARDIA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-94-1-140_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The paper by Border and Cohen (1) reported four cases of clinically silent myeloma presenting as acute renal failure and diagnosed by renal biopsy. We were very surprised that no mention was made of what is a rather exceptional feature. Multiple myeloma may present, although rarely, as acute renal failure. The finding of an M-protein in the serum protein electrophoresis makes renal biopsy unnecessary in most cases. In Bence-Jones myeloma, however, as no M-protein is found in serum and the usual hypogammaglobulinemia may not be readily taken into account, renal biopsy in some cases may not be...References1. BORDER W and COHEN A. Renal biopsy diagnosis of clinically silent multiple myeloma. Ann Intern Med. 1980;93(Part 1):43-6. LinkGoogle Scholar2. OOI B, PESCE A, POLLAK V, and MANDALENAKIS N. Multiple myeloma with massive proteinuria and terminal renal failure. Am J Med. 1972;52:538-46. CrossrefMedlineGoogle Scholar3. HARRISON J, BLAINEY J, HARDWICKE J, ROWE D, and SOOTHILL J. Proteinuria in multiple myeloma. Clin Sci. 1966;31:95. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: R. PEREZ-SOLER, M.D.; R. ESTEBAN, M.D.; J. GUARDIA, M.D.Affiliations: Departamento Medicina Interna Ciudad Sanitaria Seg. Social Universidad Autónoma Barcelona Spain PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1981Volume 94, Issue 1Page: 140-140KeywordsAcute renal failureBiopsyMultiple myelomaMyelomaSerum proteins ePublished: 1 December 2008 Issue Published: 1 January 1981 PDF downloadLoading ...
The Concept of Behavioral Specificity: Three Concepts
Authors: Chase Patterson Kimball
Journal: Psychotherapy and Psychosomatics (1982)

A brief review of specificity theories in relationship to illness is identified. Psychosomatic medicine has gradually moved from unitary-specificity relationships to multi-specificity ones. This movement has been determined by the increasing number of factors that are temporally and sequentially related to illness. The relationship of specific factors to disease is seen as derivative, generative or coincidental. Particular attention is addressed to the social life field in which illness develops, is responded to by the patient and treated by the physician. The emerging field of behavioral analysis allows for the identification of discrete factors which may be correlated with specific behaviors. Such relationships are amenable to behavioral interventions which are specific. Change is measurable. The patient takes an active part in the therapy by noting the relationship of environmental events to specific reactions. As these are recognized through encouragement, relaxation, desensitization and reinforcement, maladaptive responses are replaced by adaptive ones.
Inducible nitric oxide synthase in rat hepatic lipocytes and the effect of nitric oxide on lipocyte contractility.
Authors: D C Rockey, J J Chung
Journal: Journal of Clinical Investigation (1995)

In liver injury, perisinusoidal cells known as lipocytes (Ito cells) undergo "activation," acquiring smooth muscle-like features and a contractile phenotype. To assess whether contraction of these cells is regulated by nitric oxide (NO), we examined the production of NO by lipocytes and the effect of NO on lipocyte contractility. Cultured lipocytes were exposed to cytokines and/or LPS. Single agents had little or no effect on the level of inducible NO synthase (iNOS) mRNA. However, interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), or LPS in combination with interferon-gamma (IFN-gamma) stimulated iNOS mRNA, which was present within 4 h after exposure. iNOS mRNA levels were paralleled by changes in nitrite (a metabolic product of NO). Intraperitoneal administration of IFN-gamma, TNF-alpha, and LPS led to rapid induction of iNOS mRNA in lipocytes, confirming in vivo the culture findings. Ligation of the common hepatic bile duct, which induces periportal-based liver injury, stimulated iNOS mRNA in lipocytes. Transforming growth factor-beta 1 decreased IFN-gamma/TNF-alpha--stimulated iNOS mRNA and nitrite. Finally, the effect of NO on lipocyte contractility was examined. In cells incubated with IFN-gamma and TNF-alpha, the contractile response to either serum or endothelin-1 was blocked. Contraction was restored entirely by an inhibitor of NO synthase, NG-monomethylarginine. Furthermore, 8-bromoguanosine 3':5'-cyclic monophosphate and sodium nitroprusside inhibited lipocyte contractility, consistent with the effect of NO induced by cytokines. We conclude that NO is a potent modulator of lipocyte contractility and may regulate this function by autocrine (or intracrine) mechanisms. Moreover, NO may play an important role in liver injury, countering the effect of contractile agonists on lipocytes.
Press: Writers' views on September 11
Authors: J. Collee
Journal: BMJ (2002)

For most of us, who knew no one in or near the twin towers, September 11 was just like the worst kind of summer blockbuster—like Godzilla or Independence Day or Pearl Harbor —impossible by its scale to ignore, but equally impossible to see the point of. Why did it happen? What did it mean?

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“What occurred that terrible day in Manhattan is no more significant, more tragic, nor more meaningful than … the much larger massacres … you hardly ever read about”

(Credit: CHAO SOI CHEONG/AP PHOTO)

It is this—the quest for meaning—which has us picking through the rubble for months, working through the powdered concrete of ground zero in the hope of finding a recognisable smear of DNA. And when that hope evaporates it is presumably the quest for meaning that prompts the New York Times to run a series of potted biographies on all of those who perished, searching for the common …

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Case of Hour-Glass Stomach and Pyloric Stenosis: Gastro-Enterostomy: Death
Authors: S. Martin, B. Pollard
Journal: BMJ (1900)

tox D. F. 39 Hour-glass stomach; the narrow con-Ten years ago an illness characterised by profound aniemia.Seven R. For a month after then Aug., striction being near the middle of the months ago clear symptoms of ulcer of the stomach, but neither operation pain at.899 stomach, and adherent to the anterior then nor at any time any acute illness suggestive of perforation.times, and loss8 ot apabdominal wall over an area equal to a Now vomits after all ordinary food, and more often than not petite.Since the& crown piece.On each side of this the even after small quantities of fluid food.Pain after food is ex- has been free fromb stomach dilated, and seemed to be ceedingly severe.On examination of abdomen a dilated stomach pain, and in excellent6 anchored by the adhesion.On separat-can be felt.At one point, a little to the left of the middle line, health.Appetite and.ing the stomach from the abdominal and slightly below the ensiform cartilage is an area 2 ins. in dia-digestion good.wall, an opening into the viscus was ex-meter, which is markedly tender, and offers increased resistance posed, and stomach contents escaped.on palpatioD.This area was found, at the operation, to corre- rhis opening was enlarged transversely, spoujd precisely with the area of stomach adhesion.Patient has and the wound and filstula stitched up lost weight, and deteriorated seriously in general health duringvertically.An omental graft was the last few months brought to cover in the sutured area, in order to guard against future anchoring M.P. F. 27 Hour-glass stomach.The constriction No history of gastric ulcer.Has complained of irregular attacks R. Vomiting for 5 daysApril, was about 4 in 8, from pylorus, the pas-of pain in epigastric region for it months, always associated after the operation.1900 sage between the two sacs equalled a witn the taking of food, and coming on about one hour after a blood-stained.Sincev No. I2 catheterin diameter.There was meal.Vomiting occasional and irregular, in rather large quan- then perfectly welL marked induration and puckering, but tities: no blood.On examinatlon, stomach distended and no adhesion to the abdominal wall splashy; contractions seen when distended.Medical treat- or elsewhere.The strictured neck was ment has proved unavailing
Abstract 2357: Novel transgenic animal model of salivary gland tumors
Authors: Zobeida Cruz-Monserrate, Baoan Ji, Adel K. El-Naggar, Craig D. Logsdon
Journal: Cancer Research (2012)

Abstract Background: Salivary gland malignancies represent 1-2% of human head and neck cancers with approximately 3,300 new cases per year in the United States. Surgery is the best treatment, however must tumors are too advanced at discovery and are unresectable. Furthermore, many surgeries are not margin negative and thus they recur. In addition, advanced tumors metastasize, which makes them fatal. The lack of research tools and the limited number of cases per year makes it difficult for investigators to study the development and progression of these tumors. The aim of this study was to characterize a novel inducible mouse model of salivary gland tumors, which develops by the activation of oncogenic K-RasG12V. Methods: We developed transgenic mice with Cre regulated mutant K-RasG12D and a specific tamoxifen regulated Cre (Ela-CreER). Double transgenic animals and littermate controls were treated with tamoxifen over 3 consecutive days and after 3, 8, and 15 days they were sacrificed and analyzed histologically. Results: Tamoxifen fed animals with mutant K-RasG12D expression in the salivary gland develop tumors with intense fibrosis and inflammatory cell infiltration. Histologically the tumors resembled human high grade salivary sarcomas. Conclusions: Our results show the development of a new animal model to study the role of K-Ras in the progression of salivary gland tumors and could be a useful tool for future salivary gland tumor studies. In particular it should serve as a useful preclinical model to test for drugs against inflammatory response pathways induced by activated K-RasG12V in salivary gland tumors. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2357. doi:1538-7445.AM2012-2357
Population-Based Comparison of CEF and AC/T, Two Adjuvant Chemotherapy 'Standards' for Early Stage Breast Cancer.
Authors: A. Al-Tourah, R. Woods, B. Norris, C. Speers, H. Kennecke
Journal: Cancer Research (2009)

Abstract Introduction: Anthracyclines and taxanes in adjuvant therapy have improved the outcomes of women with early stage breast cancer. The first analysis of the phase III NCIC-MA21 trial comparing the three 6 month adjuvant regimens CEF, AC followed by q3weekly paclitaxel(AC/T) and dose dense EC followed by paclitaxel (EC/T) revealed inferior Relapse Free Survival for AC/Tversus CEF (HR 1.49[1.12,1.99]) and EC/T (HR1.68 [1.25-2.27]). The purpose of this population based analysis is to evaluate the characteristics and outcome of women with high-risk breast cancer treated with CEF vs q3weekly AC/T.Methods: The British Columbia Breast Cancer Outcomes Unit (BCOU) and Pharmacy databases were used to identify patients with node positive or high-risk node negative breast cancer between years 2000-2004 treated with adjuvant chemotherapy with either CEF or AC/T. Both regimens were available and recommended for high risk breast cancer during the time of the study. Patients with cTx, pTx tumours, previous or synchronous breast cancer and those with with locally advanced/inflammatory breast cancer were excluded. Patient and tumour characteristics were compared across study cohorts.Univariate comparisons of overall survival (OS) and breast cancer specific survival (BCSS) were performed using the Kaplan-Meier method. Propensity score models were used to compare outcomes in the two cohorts, adjusting for differences in prognostic and other treatment variables.Results: Between 2000-2004, 774 (CEF=557, AC/T=217)women with breast cancer met the inclusion criteria. Median follow-up for CEF was 4.7 years and for AC-T was 3.0 years. CEF-treated patients had more LVI (p=0.0001) and node +ve disease (p&amp;lt;0.0001), were younger (p&amp;lt;0.0001), more likely ER+ (p&amp;lt;0.0001), less likely to have grade 3 tumours (p&amp;lt;0.0001) and received higher rates of both hormones (p&amp;lt;0.0001) and radiation therapy to regional nodes (p&amp;lt;0.0001). Univariate analyses showed better outcomes for the CEF-treated cohort for both OS (p=0.0056) and BCSS (p=0.0012). Propensity score models also favoured the CEF cohort with adjusted HR's of 0.47 (95% CI: 0.27, 0.83; p=0.0086) and 0.40 (95% CI: 0.22, 0.71; p=0.0020) for OS and BCSS respectively.Conclusion: Between 2000 and 2004, women in British Columbia treated with adjuvant CEF had higher risk breast cancer than patients who received AC/T. However, CEF-treated patients have better outcomes than those receiving AC/T. Both univariate and adjusted analyses favour the CEF cohort. These population-based outcomes are consistent with the finding of the NCIC-MA21 randomized trial. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 2084.
Effects of Targeting Higher vs Lower Arterial Oxygen Saturations on Death or Disability in Extremely Preterm Infants
Authors: Barbara Schmidt, Robin K. Whyte, Elizabeth V. Asztalos, Diane Moddemann, Christian Poets, Yacov Rabi, Alfonso Solimano, Robin S. Roberts, for the Canadian Oxygen Trial (COT) Group
Journal: JAMA (2013)

The goal of oxygen therapy is to deliver sufficient oxygen to the tissues while minimizing oxygen toxicity and oxidative stress. It remains uncertain what values of arterial oxygen saturations achieve this balance in preterm infants.To compare the effects of targeting lower or higher arterial oxygen saturations on the rate of death or disability in extremely preterm infants.Randomized, double-blind trial in 25 hospitals in Canada, the United States, Argentina, Finland, Germany, and Israel in which 1201 infants with gestational ages of 23 weeks 0 days through 27 weeks 6 days were enrolled within 24 hours after birth between December 2006 and August 2010. Follow-up assessments began in October 2008 and ended in August 2012.Study participants were monitored until postmenstrual ages of 36 to 40 weeks with pulse oximeters that displayed saturations of either 3% above or below the true values. Caregivers adjusted the concentration of oxygen to achieve saturations between 88% and 92%, which produced 2 treatment groups with true target saturations of 85% to 89% (n = 602) or 91% to 95% (n = 599). Alarms were triggered when displayed saturations decreased to 86% or increased to 94%.The primary outcome was a composite of death, gross motor disability, cognitive or language delay, severe hearing loss, or bilateral blindness at a corrected age of 18 months. Secondary outcomes included retinopathy of prematurity and brain injury.Of the 578 infants with adequate data for the primary outcome who were assigned to the lower target range, 298 (51.6%) died or survived with disability compared with 283 of the 569 infants (49.7%) assigned to the higher target range (odds ratio adjusted for center, 1.08; 95% CI, 0.85 to 1.37; P = .52). The rates of death were 16.6% for those in the 85% to 89% group and 15.3% for those in the 91% to 95% group (adjusted odds ratio, 1.11; 95% CI, 0.80 to 1.54; P = .54). Targeting lower saturations reduced the postmenstrual age at last use of oxygen therapy (adjusted mean difference, -0.8 weeks; 95% CI, -1.5 to -0.1; P = .03) but did not alter any other outcomes.In extremely preterm infants, targeting oxygen saturations of 85% to 89% compared with 91% to 95% had no significant effect on the rate of death or disability at 18 months. These results may help determine the optimal target oxygen saturation.ISRCTN Identifier: 62491227; ClinicalTrials.gov Identifier: NCT00637169.
P2-274: Clinical benefits of pemetrexed 500 mg/m2 and 1000 mg/m2 in a randomized phase II study for pretreated patients with locally advanced or metastatic non–small cell lung cancer (NSCLC)
Authors: Kaoru Kubota, Tomohide Tamura, Nobuyuki Yamamoto, Kazuhiko Nakagawa, Satoshi Morita, Yoshihiro Nambu, Susumu Adachi, Yutaka Nishiwaki, Nagahiro Saijo, Masahiro Fukuoka
Journal: Journal of Thoracic Oncology (2007)
Notch signaling regulates murine atrioventricular conduction and the formation of accessory pathways
Authors: Stacey Rentschler, Brett S. Harris, Laura Kuznekoff, Rajan Jain, Lauren Manderfield, Min Min Lu, Gregory E. Morley, Vickas V. Patel, Jonathan A. Epstein
Journal: Journal of Clinical Investigation (2011)

Ventricular preexcitation, which characterizes Wolff-Parkinson-White syndrome, is caused by the presence of accessory pathways that can rapidly conduct electrical impulses from atria to ventricles, without the intrinsic delay characteristic of the atrioventricular (AV) node. Preexcitation is associated with an increased risk of tachyarrhythmia, palpitations, syncope, and sudden death. Although the pathology and electrophysiology of preexcitation syndromes are well characterized, the developmental mechanisms are poorly understood, and few animal models that faithfully recapitulate the human disorder have been described. Here we show that activation of Notch signaling in the developing myocardium of mice can produce fully penetrant accessory pathways and ventricular preexcitation. Conversely, inhibition of Notch signaling in the developing myocardium resulted in a hypoplastic AV node, with specific loss of slow-conducting cells expressing connexin-30.2 (Cx30.2) and a resulting loss of physiologic AV conduction delay. Taken together, our results suggest that Notch regulates the functional maturation of AV canal embryonic myocardium during the development of the specialized conduction system. Our results also show that ventricular preexcitation can arise from inappropriate patterning of the AV canal-derived myocardium.
Drug Problems and the Philadelphia Plan
Authors: Thomas M. Durant
Journal: JAMA (1965)

The need for communication in human affairs has become increasingly apparent in the rapidly expanding complex of modern life. In the health sciences, problems relating to drug therapy have made such a need especially apparent. With this in mind, the College of Physicians of Philadelphia has established under its aegis a committee made up of representatives of the five medical and two pharmacy schools of the city and five of the leading pharmaceutical concerns of the area (Figure). This committee is charged with the establishment and maintenance of a working relationship between its members directed toward solution of some of the most serious of the problems having to do with drug production and utilization and has been called the Greater Philadelphia Committee for Medical-Pharmaceutical Sciences. <h3>Historical</h3> The first meeting of the Committee was held on April 18, 1963. From that date until the present (November 1964) there have been 12
Mortality in hereditary antithrombin-III deficiency—1830 to 1989
Authors: F.R Rosendaal, K de Bruin, J.P Vandenbroucke, E Briët, F.R Rosendaal, H Heijboer, H.R Buller, D.P.M Brandjes, D.W Hommes
Journal: The Lancet (1991)
Reduced Coronary Flow Reserve in Hypercholesterolemic Patients Without Overt Coronary Stenosis
Authors: Ikuo Yokoyama, Tohru Ohtake, Shin-ichi Momomura, Junichi Nishikawa, Yasuhito Sasaki, Masao Omata
Journal: Circulation (1996)

Reduced coronary flow reserve (CFR) in hypercholesterolemic patients without evidence of ischemia has been reported. However, it remains uncertain whether this abnormality occurs without overt coronary atherosclerosis. This study aimed to clarify whether CFR is impaired even in anatomically normal coronary arteries in hypercholesterolemic patients and to compare CFR between familial hypercholesterolemic (FH) patients and secondary hypercholesterolemic (SH) patients.Twenty-two patients with hypercholesterolemia (11 FH, 11 SH) and 11 control subjects were studied. Baseline myocardial blood flow (MBF) and MBF during dipyridamole loading were measured in segments perfused by angiographically normal coronary arteries with the use of positron emission tomography and 13N-ammonia, and CFR was calculated. Baseline MBF (mL/min per 100 g heart wt) in FH (81.3 +/- 31.4) and SH (70.0 +/- 20.7) patients was not different from that in control subjects (75.0 +/- 34.9). However, MBF during dipyridamole loading was significantly lower in FH patients (129 +/- 19.1) than in control subjects (322 +/- 174, P < .01) and SH patients (210 +/- 71.2, P < .01). CFR in FH patients (1.59 +/- 0.41) was also significantly lower compared with both control subjects (4.22 +/- 1.42, P < .01) and SH patients (3.00 +/- 0.96, P < .01). CFR in SH patients was also significantly lower than that in control subjects (P < .05). CFR correlated significantly with both plasma total cholesterol (r = .67, P < .01) and LDL cholesterol concentrations (r = .69, P < .01).CFR was decreased even in anatomically normal coronary arteries in hypercholesterolemic patients. This abnormality was more prominent in FH patients.
B cell depletion in immune thrombocytopenia reveals splenic long-lived plasma cells
Authors: Matthieu Mahévas, Pauline Patin, François Huetz, Marc Descatoire, Nicolas Cagnard, Christine Bole-Feysot, Simon Le Gallou, Mehdi Khellaf, Olivier Fain, David Boutboul, Lionel Galicier, Mikael Ebbo, Olivier Lambotte, Mohamed Hamidou, Philippe Bierling, Bertrand Godeau, Marc Michel, Jean-Claude Weill, Claude-Agnès Reynaud
Journal: Journal of Clinical Investigation (2012)

Primary immune thrombocytopenia (ITP) is a disorder caused by autoantibody-mediated platelet destruction and decreased platelet production. Rituximab, a B cell–depleting agent, has become the first-line treatment for ITP; however, patients with refractory disease usually require splenectomy. We identified antibody-secreting cells as the major splenic B cell population that is resistant to rituximab. The phenotype, antibody specificity, and gene expression profile of these cells were characterized and compared to those of antibody-secreting cells from untreated ITP spleens and from healthy tissues. Antiplatelet-specific plasma cells (PC) were detected in the spleens of patients with ITP up to 6 months after rituximab treatment, and the PC population displayed a long-lived program similar to the one of bone marrow PC, thus explaining for most of these patients the absence of response to rituximab and the response to splenectomy. When analyzed by multiplex PCR at the single-cell level, normal splenic PC showed a markedly different gene expression profile, with an intermediate signature, including genes characteristic of both long-lived PC and proliferating plasmablasts. Surprisingly, long-lived PC were not detected in untreated ITP spleens. These results suggest that the milieu generated by B cell depletion promotes the differentiation and settlement of long-lived PC in the spleen.