tbuckley/cabot-search huggingface dataset:
Dysphagia. Initial symptom of an ectopic hyperfunctioning parathyroid adenoma
Authors: Bruce S. Trippe, Jay R. Shapiro, John L. Doppman
Journal: JAMA (1976)

ACUTE pancreatitis, acute arthritis, or features of the multiple endocrine adenoma syndrome may be the initial manifestations of hyperparathyroidism. It is rare, however, for the simple bulk of a parathyroid adenoma, or its ectopic location, to dominate a patient's initial complaints. In the case reported here, none of the expected symptoms of hyperparathyroidism were present, but the unusual tumor location led to its discovery and to the subsequent chemical verification of primary hyperparathyroidism. <h3>Report of a Case</h3> A 35-year-old woman, previously in excellent health, had a two-year history of increasing difficulty in swallowing and a five-month history of intermittent aching pain radiating from the angle of the right mandible to the right ear. Fatigue, polyuria, polydypsia, constipation, renal calculi, or fractures had not occurred. Family history was noncontributory. Blood pressure was 140/90 mm Hg, funduscopic and slit lamp examination results were normal, hair and nails were normal, and neurofibromata were
Clinical Critical Care Medicine
Authors: Jeffrey S. Groeger
Journal: Annals of Internal Medicine (2007)

Medical Writings: Book Notes20 November 2007Clinical Critical Care MedicineJeffrey S. Groeger, MDJeffrey S. Groeger, MDFrom Memorial Sloan Kettering Cancer Center, New York, New York.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-147-10-200711200-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Albert RK, Slutsky A, Ranieri M, et al. 722 pages. Philadelphia: Mosby; 2006. $139.00. ISBN 0323028446. Order at us.elsevierhealth.com.Field of medicine: Critical care.Format: Hardcover book with CD-ROM.Audience: Physicians (critical care specialists, as well as any discipline, including physicians in training), nurses, respiratory therapists, or any other individuals who are interested in the pathophysiology and care of patients requiring intensive care unit management.Purpose: To provide an overview of critical care medicine.Content: A group of international authors gives an overview of the discipline of critical care medicine. The scope of clinical scenarios covered is broad and clinically ... Author, Article, and Disclosure InformationAffiliations: From Memorial Sloan Kettering Cancer Center, New York, New York. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 20 November 2007Volume 147, Issue 10Page: 744KeywordsCritical careDrugsIntensive care unitsPatientsPrimary careSoftware tools ePublished: 20 November 2007 Issue Published: 20 November 2007 Copyright & PermissionsCopyright © 2007 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
A New Disease.
Authors: W. E. Clark
Journal: JAMA (1907)

Frederick, S. D., Sept. 9, 1907. <h3>To the Editor:</h3> —In the northeastern part of South Dakota and the southeastern part of North Dakota during the last few weeks an epidemic has appeared of what is apparently a new infectious disease. I have seen about sixty cases and other physicians have had a similar experience. None of them, so far as I know, has made a definite diagnosis, and those with whom I have conversed have considered it a new disease. The malady attacks children and young adults by preference; I have seen but three cases in people over 35. The symptoms seem to be more severe in patients from 20 to 35 years of age. The proportion of females attacked to that of males is as three to one. Many more cases occur during the hot, dry days than during the moist, cool ones. As to condition of life, there
Obesity, weight change, and risk of adenoma recurrence: a prospective trial
Authors: A. Laiyemo, C. Doubeni, D. Badurdeen, G. Murphy, P. Marcus, R. Schoen, E. Lanza, D. Smoot, A. Cross
Journal: Endoscopy (2012)

Obesity is a risk factor for colorectal neoplasia. Lifestyle modifications, including weight loss, have been advocated to reduce the risk. However, no prospective study has evaluated whether weight loss actually affects adenoma recurrence. The aim of this study was to examine whether weight change (loss or gain) over 4 years is associated with adenoma recurrence.A total of 1826 patients with colorectal adenoma in the Polyp Prevention Trial had their height and weight measured at baseline. Adenoma recurrence was determined by end of trial colonoscopy 4 years after study entry when patients' weights were re-measured. Poisson regression models were used to evaluate body mass index (BMI), weight change over 4 years, and the risk of any adenoma and advanced adenoma recurrence.Adenoma recurrence was observed in 723 patients (39.6%), 118 (6.5%) of whom had advanced adenoma recurrence. Among those with baseline BMI < 25 kg/m² (n = 466), BMI 25-29 kg/m² (n = 868), and BMI ≥ 30 kg/m² (n = 492), the recurrence rate was 34.5%, 41.0%, and 41.9%, respectively. Obesity was associated with an increased risk of adenoma recurrence (RR = 1.19; 95%CI 1.01-1.39) and advanced adenoma recurrence (RR = 1.62; 95%CI 1.01-2.57). However, when compared with those with relatively stable weight (weight change < 5 lb) over the 4-year trial, weight gain or loss was not associated with adenoma recurrence. This was consistent, regardless of the baseline BMI.Weight loss or gain over 4 years does not affect adenoma recurrence. This study does not support weight loss alone as an effective intervention for reducing adenoma recurrence.
Vasodilator Therapy — A Physiologic Approach to the Treatment of Heart Failure
Authors: Eugene Braunwald
Journal: New England Journal of Medicine (1977)

Experiments on isolated cardiac tissue have established that myocardial-fiber shortening is dependent on three factors: the preload, which determines the muscle fiber's end-diastolic length; the contractile or inotropic state of the myocardium; and the afterload (i.e., the myocardial systolic tension). At any level of the contractile state and preload, the extent of shortening varies inversely with the afterload: when afterload is progressively raised, an increasing proportion of the muscle's contractile activity is expended in the generation of tension, and a smaller fraction is expended in fiber shortening. Although the geometric arrangement of myocardial fibers is far more complex in the . . .
Treatment of Experimental (Trinitrobenzene Sulfonic Acid) Colitis by Intranasal Administration of Transforming Growth Factor (Tgf)-β1 Plasmid
Authors: Atsushi Kitani, Ivan J. Fuss, Kazuhiko Nakamura, Owen M. Schwartz, Takashi Usui, Warren Strober
Journal: The Journal of Experimental Medicine (2000)

In this study, we show that a single intranasal dose of a plasmid encoding active transforming growth factor beta1 (pCMV-TGF-beta1) prevents the development of T helper cell type 1 (Th1)-mediated experimental colitis induced by the haptenating reagent, 2,4, 6-trinitrobenzene sulfonic acid (TNBS). In addition, such plasmid administration abrogates TNBS colitis after it has been established, whereas, in contrast, intraperitoneal administration of rTGF-beta1 protein does not have this effect. Intranasal pCMV-TGF-beta1 administration leads to the expression of TGF-beta1 mRNA in the intestinal lamina propria and spleen for 2 wk, as well as the appearance of TGF-beta1-producing T cells and macrophages in these tissues, and is not associated with the appearances of fibrosis. These cells cause marked suppression of interleukin (IL)-12 and interferon (IFN)-gamma production and enhancement of IL-10 production; in addition, they inhibit IL-12 receptor beta2 (IL-12Rbeta2) chain expression. Coadministration of anti-IL-10 at the time of pCMV-TGF-beta1 administration prevents the enhancement of IL-10 production and reverses the suppression of IL-12 but not IFN-gamma secretion. However, anti-IL-10 leads to increased tumor necrosis factor alpha production, especially in established colitis. Taken together, these studies show that TGF-beta1 inhibition of a Th1-mediated colitis is due to: (a) suppression of IL-12 secretion by IL-10 induction and (b) inhibition of IL-12 signaling via downregulation of IL-12Rbeta2 chain expression. In addition, TGF-beta1 may also have an inhibitory effect on IFN-gamma transcription.
PWE-018 Hspc1 Inhibitors Potentiate The Effect Of 5-fu In Primary Colorectal Cancer Cell Model
Authors: SL Lee, NC Dempsey-Hibbert, P Sutton, D Vimalachandran, TD Wardle, J Williams
Journal: Gut (2014)

<h3>Introduction</h3> Colorectal cancer (CRC) is the fourth most common cancer in the UK and was responsible for more than 15,000 deaths in 2011.<sup>1</sup> Less than 50% of patients with Dukes stage C and D survive more than 5 years.<sup>2</sup> Molecular chaperone Heat shock protein (HSP) C1 is elevated in CRC.<sup>3</sup> HSPC1’s client proteins (e.g., HER2, pNF-ĸB, Akt etc.) are involved in key cellular pathways and apoptosis. HSPC1 inhibitors recently showed positive clinical results in breast cancer<sup>4</sup> and non-small cell lung carcinoma.<sup>5</sup> This study aims to explore the effect of combining HSPC1 inhibitors with 5-fluorouracil (5-FU), the mainstay chemotherapy, in CRC. <h3>Methods</h3> CRC cell line HT29 were treated with HSPC1 inhibitors 17-DMAG and NVP-AUY922 as single agent and in combination with 5-FU. Six primary CRC samples were obtained immediately following surgical resection with consent and treated with HSPC1 inhibitors. Four subsequent samples were treated with a combination of HSPC1 inhibitors and 5-FU. Following treatment, cell metabolism rate and apoptosis were assessed using MTS and caspase-3 assay. <h3>Results</h3> In HT29, 17-DMAG was effective in inducing apoptosis and reducing cell proliferation whereas NVP-AUY922 did not. When combined with 5-FU, 17-DMAG showed additive effect. In primary CRC cells, a 50% reduction in cell metabolism rate was observed in 2/6 samples for 17-DMAG and 1/5 samples for NVP-AUY922. When subsequent primary samples were treated with 5-FU and HSPC1 inhibitors, significant decrease in cell metabolism rate and increase in apoptosis were observed in 1/4 samples. <h3>Conclusion</h3> HSPC1 inhibitors are able to potentiate the chemotherapeutic effect of 5-FU in CRC cell line and this result may be replicated in primary colorectal cancer cells obtained from surgical specimen. HSPC1 inhibitors have different mode of actions which is evident in the different response observed in both HT29 and primary cells. In addition, CRC cells have individual response to HSPC1 inhibitors and some were not responsive. Although a small sample size, this study encouraged our next phase of research combining HSPC1 inhibitors with current chemotherapeutic agents including oxaliplatin and irinotecan. Further studies will also focus on identifying potential biomarkers to select susceptible patients. <h3>References</h3> Cancer Research UK, 2013 National Cancer Intellidence Network (NCIN), 2009 Milicevic, Z, <i>et al</i>. <i>International Journal of Oncology</i> 2008. 32(6):p. 1169–1178 Modi, S, <i>et al</i>. <i>Clin Cancer Res</i> 2011;17(15):5132–9 Sequist, LV, <i>et al</i>. <i>J Clin Oncol</i> 2010:28(33):4953–60 <h3>Disclosure of Interest</h3> None Declared.
Pregnant rat uterus expresses high levels of the type 3 iodothyronine deiodinase
Authors: Valerie Anne Galton, Elena Martinez, Arturo Hernandez, Emily A. St. Germain, Joanne M. Bates, Donald L. St. Germain
Journal: Journal of Clinical Investigation (1999)

Although thyroid hormones are critically important for the coordination of morphogenic processes in the fetus and neonate, premature exposure of the embryo to levels of the hormones present in the adult is detrimental and can result in growth retardation, malformations, and even death. We report here that the pregnant rat uterus expresses extremely high levels of the type 3 iodothyronine deiodinase (D3), which inactivates thyroxine and 3,3′,5-triiodothyronine by 5-deiodination. Both D3 mRNA and activity were present at the implantation site as early as gestational day 9 (E9), when expression was localized using in situ hybridization to uterine mesometrial and antimesometrial decidual tissue. At later stages of gestation, uterine D3 activity remained very high, and the levels exceeded those observed in the placenta and in fetal tissues. After days E12 and E13, as decidual tissues regressed, D3 expression became localized to the epithelial cells lining the recanalized uterine lumen that surrounds the fetal cavity. These findings strongly suggest that the pregnant uterus, in addition to the placenta, plays a critical role in determining the level of exposure of the fetus to maternal thyroid hormones.
Abstract LB-425: An NF-κB pathway mediated positive feedback loop amplifies Ras activity to pathological levels in mice
Authors: Baoan Ji, Jaroslaw Daniluk, Yan Liu, Defeng Deng, Haojie Huang, Huamin Wang, Craig D. Logsdon
Journal: Cancer Research (2012)

Abstract Elevated Ras activity is critical for Ras induced tumorigenesis. However, the underlying mechanisms that lead to pathological levels of Ras activity are unclear. Here, we found that stimulation of Ras signaling by typical inflammatory stimuli was transient and had no long term sequelae in wild-type mice. In contrast, these stimuli generated prolonged Ras signaling and led to chronic inflammation and precancerous lesions (PanINs) in mice expressing endogenous levels of oncogenic K-Ras. The effects of inflammatory stimuli on oncogenic Ras expressing mice were disrupted by deleting IKK2 or inhibiting Cox-2. Likewise, the expression of active IKK2 or Cox-2, or treatments with LPS generated chronic inflammation and PanINs only in mice expressing oncogenic Ras. The data support that in the presence of oncogenic Ras, inflammatory stimuli trigger an NF-κB mediated positive feedback mechanism involving Cox-2 that amplifies Ras activity to pathological levels. Because a large portion of the adult human population possesses Ras mutations in tissues including colon, pancreas, and lung, disruption of this positive feedback loop may be an important strategy for cancer prevention. 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 LB-425. doi:1538-7445.AM2012-LB-425
Atrial Ischemia Promotes Atrial Fibrillation in Dogs
Authors: Hani Sinno, Katayoun Derakhchan, Danielle Libersan, Yahye Merhi, Tack Ki Leung, Stanley Nattel
Journal: Circulation (2003)

Coronary artery disease is a significant risk factor for atrial fibrillation (AF), but the basis for this association is incompletely understood. The present study evaluated the hypothesis that atrial ischemia can create a substrate for AF maintenance.Atrial ischemia was induced by occlusion of an atrial arterial branch that did not provide blood flow to the ventricles. Atrial-arterial occlusion increased the duration of AF induced by burst pacing from 57+/-32 seconds (control) to 803+/-214 seconds (P<0.001) after 0.5 hour of occlusion and to 887+/-209 seconds (P<0.001) after 3 hours of occlusion. Prolonged AF (>20 minutes) was induced in 0 of 16 dogs (0%) under control conditions, 7 of 16 (44%, P<0.01) at 0.5 to 3 hours, and 5 of 13 (38%, P<0.01) 3 to 5 hours after occlusion. Atrial conduction was slowed substantially within the ischemic zone: eg, conduction delay was 8+/-1 ms at a cycle length of 200 ms, control, versus 22+/-5 ms (P<0.01) after 0.5 hours and 27+/-5 ms (P<0.001) after 3 hours of ischemia. Refractoriness was initially unaffected but was prolonged 5 hours after occlusion. Phase-delay analysis and high-density mapping confirmed severe conduction slowing in the ischemic zone. Histological examination confirmed the location of ischemic regions and revealed extensive ischemia-induced necrosis at sites of conduction delay.Experimental atrial ischemia creates a substrate for AF maintenance, apparently by causing local conduction slowing that promotes reentry. These results suggest that atrial ischemia may significantly promote AF, and may be relevant to AF mechanisms in association with coronary artery disease.
1001-18 Determinants of natural regression of pulmonary vein stenosis secondary to radiofrequency catheter ablation for atrial fibrillation
Authors: Yong-Mei Cha, Samuel J Asirvathom, Thomas M Munger, Paul A Friedman, Luiz Leite, Laura Peterson, Christie Bluhm, Douglas L Packer
Journal: Journal of the American College of Cardiology (2004)
The Association Between Midlife Cardiorespiratory Fitness Levels and Later-Life Dementia
Authors: Laura F. DeFina, Benjamin L. Willis, Nina B. Radford, Ang Gao, David Leonard, William L. Haskell, Myron F. Weiner, Jarett D. Berry
Journal: Annals of Internal Medicine (2013)

Chinese translation Background: Primary prevention of Alzheimer disease and other types of dementia (all-cause dementia) is an important public health goal. Evidence to date is insufficient to recommend any lifestyle change to prevent or delay the onset of dementia. Objective: To assess the association between objectively measured midlife cardiorespiratory fitness (“fitness”) levels and development of all-cause dementia in advanced age. Design: Prospective, observational cohort study. Setting: Preventive medicine clinic. Patients: 19 458 community-dwelling, nonelderly adults who had a baseline fitness examination. Measurements: Fitness levels, assessed using the modified Balke treadmill protocol between 1971 and 2009, and incident all-cause dementia using Medicare Parts A and B claims data from 1999 to 2009. Results: 1659 cases of incident all-cause dementia occurred during 125 700 person-years of Medicare follow-up (median follow-up, 25 years [interquartile range, 19 to 30 years]). After multivariable adjustment, participants in the highest quintile of fitness level had lower hazard of all-cause dementia than those in the lowest quintile (hazard ratio, 0.64 [95% CI, 0.54 to 0.77]). Higher fitness levels were associated with lower hazard of all-cause dementia with previous stroke (hazard ratio, 0.74 [CI, 0.53 to 1.04]) or without previous stroke (hazard ratio, 0.74 [CI, 0.61 to 0.90]). Limitations: Dementia diagnoses were based on Medicare claims, and participants generally were non-Hispanic white, healthy, and well-educated and had access to preventive health care. This study evaluated fitness levels, so a specific exercise prescription cannot be generated from results and the findings may not be causal. Conclusion: Higher midlife fitness levels seem to be associated with lower hazards of developing all-cause dementia later in life. The magnitude and direction of the association were similar with or without previous stroke, suggesting that higher fitness levels earlier in life may lower risk for dementia later in life, independent of cerebrovascular disease. Primary Funding Source: The Cooper Institute; University of Texas Southwestern Medical Center; National Heart, Lung, and Blood Institute; and American Heart Association.
The Effects of Noise on Man
Authors: Aram Glorig
Journal: JAMA (1966)

Althoughre is still much to be learned about L the relations of hearing loss to noise exposure, we have accumulated enough information through experience and research to enable us to organize and conduct hearing conservation programs. This basic information is, in brief: Many noise exposures can produce a permanent hearing loss that may affect communication by speech. Noise-induced hearing loss may be temporary, permanent, or a combination of temporary and permanent. Permanent noise-induced hearing loss is due to destruction of certain inner ear structures which cannot be replaced or repaired. The amount of hearing loss produced by a given noise exposure varies from person to person. Noise-induced hearing loss first affects man's hearing of sounds higher in frequency than those essential for communication by speech. Therefore, most early noise-induced hearing losses pass unnoticed unless they are detected by suitable hearing tests. Four major factors
New Intravenous Fat Emulsion
Authors: Isidore Cohn, W. Sidney Singleton, Quentin L. Hartwig, M. Atik
Journal: JAMA (1963)

A NEW INTRAVENOUS FAT EMULSION has satisfactorily passed extensive animal testing, and preliminary clinical testing has been initiated. This emulsion, designated the SR emulsion, has been administered to dogs in massive doses over extended periods with minimum toxicity. Animal studies were conducted at a dosage level 4 to 6 times that recommended clinically, because earlier work showed that any toxic effects could be brought out more rapidly with this massive dosage.<sup>1</sup> <h3>Materials and Methods</h3> Mongrel dogs were infused through an indwelling polyethylene cannula in the external jugular vein.<sup>1</sup>The animals received 30 infusions at the rate of 5 a week. The dogs were allowed food and water throughout the experimental period. Some of the dogs were killed and autopsy was performed immediately after the 30th infusion. Others were kept for long-term observations. Autopsy was performed on all dogs that died during the infusion period. Tissue specimens were sent
Thrombolysis in patients with unstable angina improves the angiographic but not the clinical outcome. Results of UNASEM, a multicenter, randomized, placebo-controlled, clinical trial with anistreplase.
Authors: F W Bär, F W Verheugt, J Col, P Materne, J P Monassier, P G Geslin, J Metzger, P Raynaud, J Foucault, C de Zwaan
Journal: Circulation (1992)

BACKGROUND The value of thrombolytic therapy in unstable angina is unclear. METHODS AND RESULTS To study this problem, 159 patients were studied in a double-blind, placebo-controlled multicenter trial. Patients without a previous myocardial infarction, with a typical history of unstable angina, and ECG abnormalities indicative of ischemia were included. After baseline angiography, study medication (anistreplase or placebo) was given. Angiography was repeated after 12-28 hours. A significant decrease occurred in diameter stenosis between the first and second angiogram in the anistreplase group compared with the placebo group (11% versus 3%, p = 0.008). This difference was caused by reopening of occluded vessels in the thrombolytic group. However, no beneficial clinical effects of thrombolytic treatment were found. Bleeding complications were significantly higher in patients who received thrombolytic therapy (21 versus seven patients, p = 0.001). CONCLUSIONS Thus, angiographic but no clinical improvement after thrombolytic treatment with anistreplase was found in patients with unstable angina with an excess of bleeding complications. Therefore, thrombolytic treatment cannot be recommended in patients diagnosed as having unstable angina until proven otherwise.
IMPORTANCE OF NEGATIVE PRESSURE PHASE IN MECHANICAL RESPIRATORS
Authors: J. V. Maloney
Journal: JAMA (1953)

The management of medical emergencies involving respiratory failure remains an important challenge in clinical medicine. Despite many years of vigorous controversy, the question of which is the best mechanical method of artificial respiration is still unsettled. The problem concerns in part the respective merits of respirators producing intermittent positive pressure and those producing alternating positive-negative pressure. Thompson,<sup>1</sup>and Birnbaum and Thompson<sup>2</sup>have stood almost alone in claiming for positive-negative pressure a desirable effect on the circulation. These workers found that alternating positive-negative pressure stimulates the return of normal respiration and produces some degree of passive circulation in the dead animal. Other investigators believe that a negative pressure phase during expiration serves no useful purpose.<sup>3</sup>The opinions of those opposed to the use of any type of mechanical breathing machine, especially those employing a negative pressure phase, have been clearly stated by Henderson.<sup>4</sup>As Schwerma and Ivy