tbuckley/cabot-search huggingface dataset:
Tricalcium Phosphate Crystallosis
Authors: Hobart A. Reimann, Thelma Ducanes, Leonard K. Supple
Journal: JAMA (1964)

Three years of inadvertent excessive inhalation and ingestion of the dust from a dentifrice resulted in the systemic accumulation of tricalcium phosphate crystals and granulomatous lesions in a patient who died from carcinomatosis apparently unrelated to the crystallosis. Dyspnea and cough were the only symptoms. Crystals detected in the tissues by high magnification and polarized light and identified by x-ray-diffraction analysis matched those of the dentifrice, and of standard tricalcium phosphate. Continual heedless exposure to minute, insoluble, airborne crystals dispersed from widely used powdery abrasive substances may have caused other instances of systemic or pulmonic granulomas.
Autoimmune Response in Chronic Ongoing Myocarditis Demonstrated by Heterotopic Cardiac Transplantation in Mice
Authors: Hiroshi Nakamura, Taisei Yamamura, Seiji Umemoto, Shinji Fukuta, Tetsuo Shioi, Akira Matsumori, Shigetake Sasayama, Masunori Matsuzaki
Journal: Circulation (1996)

Background Autoimmune mechanisms have been implicated in the pathogenesis of chronic ongoing myocarditis. To investigate this relation, we used an A/J mouse model inoculated with coxsackievirus B3 and determined whether myocarditis would be transferred to normal hearts that were heterotopically transplanted. Methods and Results Inbred 3-week-old A/J mice were inoculated intraperitoneally with coxsackievirus B3 (Nancy strain; 2×10 4 plaque-forming units) and housed for &gt;60 days. The presence of the viral genome in the myocardium was determined by the polymerase chain reaction with primers specific for the 5′ end of the coxsackievirus B3 genome performed at 40, 50, or 60 days after inoculation. Normal A/J mouse hearts were transplanted into the same strain of mice without myocarditis (group A) and into mice with chronic ongoing myocarditis (group B). The hearts were evaluated histologically 2 weeks after transplantation. Conventional histological examination of infiltrated T cells and macrophages was performed, and the expression of intercellular adhesion molecule-1, major histocompatibility complex (MHC) class I antigen, and MHC class II antigen was evaluated by immunoenzymatic staining. The concentrations of interleukin-1α (IL-1α) and tumor necrosis factor (TNF-α) in the grafts were measured with an ELISA. The viral RNA genomes were not detected in the mice with chronic ongoing myocarditis, but their transplanted hearts did show myocarditis. In the hearts with induced myocarditis, infiltrated mononuclear cells consisted of CD4+ T cells, CD8+ T cells (CD4+ cell number &gt;CD8+ cell number), and macrophages. Intercellular adhesion molecule-1, MHC class I antigen, and MHC class II antigen were expressed in the vascular endothelial cells and myocardial cells in and around the infiltrated lesions. The concentrations of IL-1α and TNF-α in group B were significantly higher than those in group A (group A versus group B: IL-1α, 125±35 versus 180±34 pg/mL; TNF-α, 45±15 versus 96±40 pg/mL; P &lt;.05). Conclusions Results suggest that an autoimmune response may play a key role in the progression of chronic ongoing myocarditis.
Interpretation of myocardial contraction recorded from local segments
Authors: K. MATRE, E. HEXEBERG, J. LEKVEN
Journal: Cardiovascular Research (1985)

An attempt to quantify the influence of extra-segmental contraction upon external mechanical work of a segment was made in cat hearts. By placing four ultrasound crystals across a borderline between normal and ischaemic myocardium, the pressure-length loop area of segments with different ischaemic contents were recorded. The relation between a normalised segment work index and the amount of ischaemic tissue within the segment showed a negative correlation. Assuming that the contributions to the segment work index from ischaemic and normal tissue coupled in series within the segment add up by cancelling each other, the extra-segmental influence of adjacent fibre contraction could be established. In six cats the extra-segmental influence which affected a typical segment of 10.0 mm corresponded to 1.5 to 3.7 mm of adjacent myocardial musculature on either side of the segment.
Effect of graded coronary flow reduction on ionic, electrical, and mechanical indexes of ischemia in the pig.
Authors: I Watanabe, T A Johnson, J Buchanan, C L Engle, L S Gettes
Journal: Circulation (1987)

This study was performed to determine the relative sensitivities of ionic, electrical, and mechanical indexes of myocardial ischemia. We used ion-selective and bipolar plunge electrodes, epicardial unipolar electrodes, a suction electrode, and ultrasonic crystals to determine the changes in intramyocardial extracellular potassium ([K+]e) and extracellular pH (pHe), local activation, epicardial TQ-ST segment, monophasic action potential duration (MAPD), and regional contractility during graded coronary flow reduction in open-chest pigs. A carotid-to-coronary shunt was created to perfuse the left anterior descending coronary artery via a roller pump. The shunted coronary flow was reduced in a stepwise fashion at 5-min intervals. In 25 pigs, the approximate myocardial blood flow associated with the initial changes in each variable was as follows: midmyocardial [K+]e, pHe, and TQ-ST segment, 0.7 to 0.8 ml/min/g; subepicardial [K+]e and TQ-ST segment, 0.6 to 0.7 ml/min/g; segmental shortening, 0.5 to 0.6 ml/min/g; local activation and epicardial TQ-ST segment, 0.3 to 0.4 ml/min/g; epicardial MAPD, 0.15 to 0.2 ml/min/g. Our results indicate that changes in [K+]e, pHe, and TQ-ST segment provide the most sensitive means of detecting myocardial ischemia and of determining the effect of interventions capable of influencing the ischemic process.
The marginal plasma zone in the retinal microcirculation
Authors: C. J. Bulpitt, C. T. Dollery, E. M. Kohner
Journal: Cardiovascular Research (1970)

The marginal plasma zone of retinal vessels has been measured by a photographic technique. The mean arterial plasma zone of the pig retina was 9·7% of the internal diameter and the mean venous plasma zone 8·0%. The arterial and venous plasma zones increased with the diameter of the vessel. Changes in arterial oxygen tension and perfusion pressure produced changes in the arterial and venous plasma zone proportional to the changes in vessel size. With increases in arterial carbon dioxide tension, the arterial plasma zone became wider than would be expected from the increase in diameter.
Straddling a Hobby: Avocational Books by Canadian Physicians
Authors: Charles G. Roland
Journal: JAMA (1965)

To the physician who is a book collector, nonmedical books written by other physicians have an appeal out of all proportion to their literary merits. No matter whether written by a friend, a classmate, or some forgotten practitioner of a previous century, a special interest invests the publications of a colleague. To a doctor in practice, book writing (exclusive of medical texts) is usually a hobby. This hobby may be not an end in itself but a way of expressing interest in more compelling avocations. As considered here, these range from a book about birds, reflecting an interest in ornithology and birdwatching, to a novel. And, in the middle ground, I discuss volumes of poetry and mysticism and a collection of letters. None of the books are well known now; some never enjoyed great popularity. Yet all have merit, and all have interesting things to say. <h3>Birdwatching</h3> Alexander Milton Ross
645. Combination of Oncolytic Adenovirotherapy and Bax Gene Therapy Does Not Augments Antitumor Efficacy
Authors: Masayoshi Hioki, Shunsuke Kagawa, Toshiya Fujiwara, Yoshihiro Ikeda, Toru Kojima, Ryo Sakai, Futoshi Uno, Fuminori Teraishi, Yoshiko Shirakiya, Yuichi Watanabe, Yuuri Hashimoto, Yasuo Urata
Journal: Molecular Therapy (2006)

Cancer gene therapy and oncolytic virotherapy have been studied extensively. However, the clinical application is hampered by its weak anticancer activity. We constructed a replicating adenovirus (OBP-301, Telomelysin), in which the human telomerase reverse transcriptase (hTERT) promoter drives expression of the adenoviral E1 genes, could replicate in and causes selective lysis of human cancer cells. We hypothesized that combination adenoviral therapy containing OBP-301 and a non-replicating E1-deleted adenovirus expressing the proapoptotic Bax gene (Ad/Bax) could overcome the weakness and augment anticancer efficacy of each modality. The human cancer cell line A549, SW620, DU145, MKN28, MKN45 were treated with OBP-301 with Ad/Bax, and cell viability, transgene expression, viral replication were assessed in vitro. To test the antitumor effects of combination treatment in vivo, subcutaneous tumors and pleural dissemination of A549 cells were generated in nude mice. Each mouse underwent intratumoral or intrapleural administration of viruses and the growth of implanted tumors were observed after trearment. Combination treatment resulted in marked Bax protein expression, and enhanced efficay in in vitro cell viability assay, as compared with either single treatment. Unexpectedly, combination treatment was not so effective in suppressing both subcutaneous and pleural disseminated tumors compared with OBP-301 treatment alone. Further investigation revealed that combination treatment resulted in suppressed E1A protein expression due to reduced viral replication. Our results suggest that Bax gene therapy may interfere with viral production and thus be antagonistic to oncolytic virotherapy.
Rhinoplastic Operation after Complete Destruction of the Nose
Authors: J. W. Cousins
Journal: BMJ (1884)

i Ma clilition to rosist geioiiral itivasion of the cireulationa.The pois1on is wiore or less Ioealilmsl or slent upon tte 0loodl ill tllejM, llvic vesel, or i te jiteioe wallsl.In tlho first *ase, the iiigeat.tfloisi.nIiet as a j,rerillitant t 'rion the hylwrinotic blood anll( lylpth, au,ll we have clot.tilOg *r thmromnlosis ; that im, thronabotic pmerixral fever, Or pblegimlmasi fidlellus.hit the other cseo, tilo invadling selptic ettill, imiore Or 1!.%f opposRed in its progress, vauses ilnflainmniiatioii ill the Teins, lYn1lhjhtifss, ai1id tither tisslies Ofo the uteris andii btronad ligmnonts4, which is Almost sure to ex teiid to the uterine and jolvi IOfrito)nCihn; hicnce we have tho various formus of metritis, pelvic cellutlitis or larainetritis, andl of writonitis.Thoeseaach, iii some iiistasecii , rietain their indlividuality, folint Itiire frrqiuenltly thlly illi'go illto COl hibillttiiom, almi theem rs.ult inctro.lieritoniiti54,ilflntiiitnatioui of the hiroal ligJ1,metut.ts1a(1 other t15.411(5.8ominetines tho ingeated poison IreaeJks hbouinds, andl affects thle etiol ime of the ciretlation.There aro at lefast two conditiouin obs(rveul.Ill one, thio poison peitvades tihe whole systeflm, caulsing fever, without arny tangible tissue-change or inflamnmation.This may end in recovery, but not seldonm it Iresilts in deati.In tho other con- dlition, thero is at first pelvic inflatnmation, tentritis, or johlegmasia dolens; hut under tho continiuous4 imnbibition or generation of fr'eh poison, anl(d the degraded condition of tho blood1, thie rscal harriers that resisted tho first impuIse of the invading poison yiel]l, andi general tix.X.i':iii elsuisi .'I' lis ngain may issue1 in death at no listuitt (lay, or, if thiero renmain a fair degreo of resisting force, distant inifliinmatiomim may arisc, as synovitis, pileuriXsy, pneumonia, dlifuse celhihitis and Supilphurations in variouiOs organs ana tissuies, sonietiunis designateel Then we come to the lieterogenctic fevers.These miay be (livide(l into two classes.
Hypersensitivity reaction after barium meal examination
Authors: B. Nagi, M. Mandal, R. Kochhar, S. K. Mehta
Journal: Allergy (1988)

Hypersensitivity reactions can occur after the administration of barium products and all caused by one of the many additives. These reactions are extremely unusual. Authors report on a patient who developed urticaria shortly after a conventional barium examination.
Neoadjuvant chemoradiation treatment impairs accuracy of MRI staging in rectal carcinoma
Authors: J Jonas
Journal: Gut (2005)

This study aimed to determine whether the changes in practice in the management of asthma since the early 1980s have improved standards (as assessed by higher actual/best function) and reduced the need for oral corticosteroids. All asthmatic outpatients were reviewed in 1980, 1983, 1988/89 and 1993/94. Therapeutic step, defined by suppressive medication alone, actual and best peak expiratory flow (PEF) were recorded. Cohorts from 1980, 1983 and 1988/89 were identified in whom best function was established on all subsequent occasions. Changes in practice demonstrated by cross-sectional review of all subjects were interpreted with the aid of longitudinal analysis of the cohorts. Attendance increased from 463 in 1980 to 772 in 1993/94. Between 1983 and 1993/94, the proportion maintained on inhaled corticosteroids increased from 49 to 84% with increased use of higher doses. Mean actual/best PEF rose from 80 to 87%, improving at each therapeutic step. The proportion needing rescue oral corticosteroids fell from 47 to 35% and maintenance oral corticosteroids from 20 to 9%. In the cohorts, there was a similar reduction in use of rescue corticosteroids, but not of maintenance oral corticosteroids. The study confirmed an increase in the use and dose of inhaled corticosteroids, and a better outcome at all treatment steps. The fall in the proportion of subjects dependent on oral corticosteroids was due to attrition, rather than weaning in later years.
Extensor expansion in the rheumatoid hand.
Authors: K M Backhouse
Journal: Annals of the Rheumatic Diseases (1968)

the right-hand side in a right-handed man, suggesting some correlation with use.In general, therefore, it may be that minor trauma, causing increase in vascular perme- ability, is a localizing factor, not only in relation to skin lesions, but possibly in relation to joint lesions also.DR. GOLDING: I do not think that the skin lesions were, in fact, more severe on the right than on the left side.
Systematic Musculoskeletal Examinations
Authors: Lisa Ann DiPonio
Journal: JAMA (2012)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
miR-29 Inhibits Bleomycin-induced Pulmonary Fibrosis in Mice
Authors: Jun Xiao, Xiao-Ming Meng, Xiao R Huang, Arthur CK Chung, Yu-Lin Feng, David SC Hui, Cheuk-Man Yu, Joseph JY Sung, Hui Y Lan
Journal: Molecular Therapy (2012)

Loss of microRNA-29 (miR-29) is known to be a mechanism of transforming growth factor-β (TGF-β)-mediated pulmonary fibrosis, but the therapeutic implication of miR-29 for pulmonary fibrosis remains unexplored. The present study investigated whether miR-29 had therapeutic potential for lung disease induced by bleomycin in mice. In addition, the signaling mechanisms that regulated miR-29 expression were investigated in vivo and in vitro. We found that miR-29 was a downstream target gene of Smad3 and negatively regulated by TGF-β/Smad signaling in fibrosis. This was evidenced by the findings that mice or pulmonary fibroblasts null for Smad3 were protected against bleomycin or TGF-β1-induced loss of miR-29 along with fibrosis in vivo and in vitro. Interestingly, overexpression of miR-29 could in turn negatively regulated TGF-β and connective tissue growth factor (CTGF) expression and Smad3 signaling. Therefore, Sleeping Beauty (SB)-mediated miR-29 gene transfer into normal and diseased lung tissues was capable of preventing and treating pulmonary fibrosis including inflammatory macrophage infiltration induced by bleomycin in mice. In conclusion, miR-29 is negatively regulated by TGF-β/Smad3 and has a therapeutic potential for pulmonary fibrosis. SB-mediated miR-29 gene therapy is a non-invasive therapeutic strategy for lung disease associated with fibrosis. Loss of microRNA-29 (miR-29) is known to be a mechanism of transforming growth factor-β (TGF-β)-mediated pulmonary fibrosis, but the therapeutic implication of miR-29 for pulmonary fibrosis remains unexplored. The present study investigated whether miR-29 had therapeutic potential for lung disease induced by bleomycin in mice. In addition, the signaling mechanisms that regulated miR-29 expression were investigated in vivo and in vitro. We found that miR-29 was a downstream target gene of Smad3 and negatively regulated by TGF-β/Smad signaling in fibrosis. This was evidenced by the findings that mice or pulmonary fibroblasts null for Smad3 were protected against bleomycin or TGF-β1-induced loss of miR-29 along with fibrosis in vivo and in vitro. Interestingly, overexpression of miR-29 could in turn negatively regulated TGF-β and connective tissue growth factor (CTGF) expression and Smad3 signaling. Therefore, Sleeping Beauty (SB)-mediated miR-29 gene transfer into normal and diseased lung tissues was capable of preventing and treating pulmonary fibrosis including inflammatory macrophage infiltration induced by bleomycin in mice. In conclusion, miR-29 is negatively regulated by TGF-β/Smad3 and has a therapeutic potential for pulmonary fibrosis. SB-mediated miR-29 gene therapy is a non-invasive therapeutic strategy for lung disease associated with fibrosis.
George Somerville Welch
Authors: Richard Baker, Paul Neary
Journal: BMJ (2006)

of medicine at Oxford, Emory, Yale, and Washington, who discovered the pathology of fever in infections and advocated death with dignity At the height of the brain drain, when Britain was haemorrhaging researchers to the United States, Paul Beeson left a chair of medicine at Yale to become Nuffield professor of medicine at Oxford.He reformed the curriculum, edited two textbooks and the Oxford Companion to Medicine, and laid the foundations for Oxford's pre-eminence in infectious diseases.He was awarded an honorary KBE.Beeson inspired generations of students with his concern for patients.He showed that hepatitis could be transmitted by blood transfusion, and brought new insights into the causes of high persistent fevers.He also discovered the cytokine interleukin-1.During the second world war he was one of the volunteer US doctors who staffed Harvard Hospital in Salisbury.He was professor of medicine at three US universities: Emory, Yale, and Washington.Although he started as a conservative who intended to follow a career in private practice, he ended as a liberal concerned with the uninsured and old, medical ethics, and the medical consequences of nuclear warfare.Professor John Stein of Oxford University told the BMJ, "Paul Beeson was a wonderful clinician, and incredibly kind to young people like me."Paul Beeson was born in rural Montana, United States, and brought up in Anchorage, Alaska, where
Visualization of Metastatic Liver Disease on Technetium-99m Bone Scintigraphy
Authors: ANTONIE M. ROMYN, DAVID L. BUSHNELL, MAYNARD L. FREEMAN, ERVIN KAPLAN
Journal: Clinical Nuclear Medicine (1987)

To determine the frequency with which liver metastases are visualized on bone scintigraphy, 425 pairs of liver and bone scans, performed within one month of each other, were reviewed. Sixty-three of the 425 liver scans showed metastases. Of these 63, five cases of carcinoma of the colon and six cases of carcinoma of the lung also visualized by Tc-99m MDP scintigraphy. This represented 46% of colon metastases and 15% of lung metastases detected on liver scan. Liver metastases from other primary tumors were not detected on bone scan, but the numbers for these tumors were small. The liver metastases which were detected on bone scan were significantly larger than those which were not. The literature was reviewed and the primary and secondary tumors of liver with uptake of Tc-99m phosphate compounds listed.
Gene Transfer of Inducible Nitric Oxide Synthase Affords Cardioprotection by Upregulating Heme Oxygenase-1 Via a Nuclear Factor-κB-Dependent Pathway
Authors: Qianhong Li, Yiru Guo, Qinghui Ou, Chuanjue Cui, Wen-Jian Wu, Wei Tan, Xiaoping Zhu, Lilibeth B. Lanceta, Santosh K. Sanganalmath, Buddhadeb Dawn, Ken Shinmura, Gregg D. Rokosh, Shuyan Wang, Roberto Bolli
Journal: Circulation (2009)

Background— Although inducible nitric oxide synthase (iNOS) is known to impart powerful protection against myocardial infarction, the mechanism for this salubrious action remains unclear. Methods and Results— Adenovirus-mediated iNOS gene transfer in mice resulted 48 to 72 hours later in increased expression not only of iNOS protein but also of heme oxygenase (HO)-1 mRNA and protein; HO-2 protein expression did not change. iNOS gene transfer markedly reduced infarct size in wild-type mice, but this effect was completely abrogated in HO-1 −/− mice. At 48 hours after iNOS gene transfer, nuclear factor-κB was markedly activated. In transgenic mice with cardiomyocyte-restricted expression of a dominant negative mutant of IκBα (IκBα S32A,S36A ), both basal HO-1 levels and upregulation of HO-1 by iNOS gene transfer were suppressed. Chromatin immunoprecipitation analysis of mouse hearts provided direct evidence that nuclear factor-κB subunits p50 and p65 were recruited to the HO-1 gene promoter (−468 to −459 bp) 48 hours after iNOS gene transfer. Conclusions— This study demonstrates for the first time the existence of a close functional coupling between cardiac iNOS and cardiac HO-1: iNOS upregulates HO-1 by augmenting nuclear factor-κB binding to the region of the HO-1 gene promoter from −468 to −459 bp, and HO-1 then mediates the cardioprotective effects of iNOS. These results also reveal an important role of nuclear factor-κB in both basal and iNOS-induced expression of cardiac HO-1. Collectively, the present findings significantly expand our understanding of the regulation of cardiac HO-1 and of the mechanism whereby iNOS exerts its cardioprotective actions.