tbuckley/cabot-search huggingface dataset:
"M.D., Indianapolis."
Authors: Fred Byron Robinson
Journal: JAMA (1891)

<h3>To the Editor:</h3> —During the past few weeks a case was brought up in the courts of this city which induced very free remarks relative to the requisite standing of a man in the States to possess the title M.D. S. E. L. Smith, of this town, was registered as a licentiate of the Society of Apothecaries, which gave him rights to practice. But said Smith assumed the title of "M.D., Indianapolis," and he was summoned into court, fined the maximum fee of $100, with probably a quarter as much costs. Mr. Smith produced in court, during the trial, a document which gave him the title of " M.D., Indianapolis." It was said to have cost him $30. The medical man who prosecuted the case said that such a title could only be one of those foreign or American titles which could be got for a dollar or two. It might
A Perfect Place to Die, Revisited
Authors: Carolyn C Cannuscio
Journal: JAMA (2010)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
The Role of the Addictive Process as a Key Step in Causation of All Tobacco-Related Diseases
Authors: William Pollin
Journal: JAMA (1984)

Two circumstances—the fact that cigarette smoking is the single largest preventable cause of disease and death in the country<sup>1</sup>and the rapid development of a new body of knowledge concerning the addictive process—combine to provide an unparalleled opportunity for American medicine to fulfill its primary responsibility—"the reduction of suffering and death."<sup>2</sup> The magnificent neuroadaptability of our species at times becomes dangerous and expensive. We can, unfortunately, come to accept familiar and well-known situations as givens, a part of the landscape. As a result of this adaptability, we frequently overlook important factors that have become so familiar they have lost their saliency. Applied to cigarette smoking, we need to see relative burdens of mortality and morbidity more clearly again, as for the first time. The 350,000 excess deaths per year attributable to cigarette smoking constitute more than all other drug and alcohol abuse deaths combined, seven times more than
SF3B1 haploinsufficiency leads to formation of ring sideroblasts in myelodysplastic syndromes
Authors: Valeria Visconte, Heesun J. Rogers, Jarnail Singh, John Barnard, Manoj Bupathi, Fabiola Traina, James McMahon, Hideki Makishima, Hadrian Szpurka, Anna Jankowska, Andres Jerez, Mikkael A. Sekeres, Yogen Saunthararajah, Anjali S. Advani, Edward Copelan, Haruhiko Koseki, Kyoichi Isono, Richard A. Padgett, Sami Osman, Kazunori Koide, Christine O'Keefe, Jaroslaw P. Maciejewski, Ramon V. Tiu
Journal: Blood (2012)
THE IMPROVED OUTLOOK FOR THE DIABETIC PATIENT
Authors: Edwin L. Rippy
Journal: JAMA (1952)

One of the most dramatic human interest stories of our times is the story of diabetes. It has the elements of early tragedy, scientific lethargy and confusion, magnificent effort, and a great triumph. It is a story to which many persons have contributed immortal chapters. It is an unfinished story to which a challenged mind will someday dictate a fitting conclusion. It is a story that will inspire medical imagination and effort for all time to come.  EARLY CONTRIBUTIONS  The story began a long time ago, but we may begin at a chapter in the 1870's as A. Trousseau lectures to a medical class in Paris. He was presenting a 36-year-old man who was obviously afflicted with severe symptomatic diabetes in a stage of early acidosis. In the courtly style of the day, he remarked: Gentlemen, his glycosuria is of a bad kind, against which medical treatment cannot prevail. Whatever
Aging of the liver: Age-associated mitochondrial damage in intact hepatocytes
Authors: J Sastre, F V Pallardó, R Plá, A Pellín, G Juan, J E O'Connor, J M Estrela, J Miquel, J Viña
Journal: Hepatology (1996)

Mitochondrial damage may be a major cause of cellular aging. So far, this hypothesis had only been tested using isolated mitochondria. The aim of this study was to investigate the involvement of mitochondria in aging using whole liver cells and not isolated mitochondria only. Using flow cytometry, we found that age is associated with a decrease in mitochondrial membrane potential (30%), an increase in mitochondrial size, and an increase in mitochondrial peroxide generation (23%). Intracellular peroxide levels were also increased. The number of mitochondria per cell and inner mitochondrial membrane mass did not change. Gluconeogenesis from glycerol or fructose (mitochondrial- independent) did not change with age, whereas it did from lactate (mitochondrial-dependent). The change in the rate of gluconeogenesis was not accompanied by changes in any of the following parameters: phosphoenolpyruvate carboxykinase or pyruvate carboxylase activities or mitochondrial ATP/ADP or cytosolic NADH/NAD+ ratios. This was caused by a decreased rate of malate export (to 20% of the controls) from mitochondria. The impairment of the mitochondrial malate transporter is posttranscriptional because its expression in Xenopus oocytes using polyadenylated RNA from livers of young or old animals did not change. Ketogenesis from oleate also fell in hepatocytes from old rats. Our results show, for the first time in intact cells, a correlation between age-associated impairment of cell metabolism and specific changes in mitochondrial function and morphology, supporting the hypothesis that mitochondrial damage plays a key role in aging.
An engineered 3D human airway mucosa model based on an SIS scaffold
Authors: Maria Steinke, Roy Gross, Heike Walles, Rainer Gangnus, Karin Schütze, Thorsten Walles
Journal: Biomaterials (2014)

To investigate interrelations of human obligate airway pathogens, such as Bordetella pertussis, and their hosts test systems with high in vitro/in vivo correlation are of urgent need. Using a tissue engineering approach, we generated a 3D test system of the airway mucosa with human tracheobronchial epithelial cells (hTEC) and fibroblasts seeded on a clinically implemented biological scaffold. To investigate if hTEC display tumour-specific characteristics we analysed Raman spectra of hTEC and the adenocarcinoma cell line Calu-3. To establish optimal conditions for infection studies, we treated human native airway mucosa segments with B. pertussis. Samples were processed for morphologic analysis. Whereas our test system consisting of differentiated epithelial cells and migrating fibroblasts shows high in vitro/in vivo correlation, hTEC seeded on the scaffold as monocultures did not resemble the in vivo situation. Differences in Raman spectra of hTEC and Calu-3 were identified in distinct wave number ranges between 720 and 1662 cm−1 indicating that hTEC do not display tumour-specific characteristics. Infection of native tissue with B. pertussis led to cytoplasmic vacuoles, damaged mitochondria and destroyed epithelial cells. Our test system is suitable for infection studies with human obligate airway pathogens by mimicking the physiological microenvironment of the human airway mucosa.
KCl cotransport mediates abnormal sulfhydryl-dependent volume regulation in sickle reticulocytes
Authors: Clinton H. Joiner, R. Kirk Rettig, Maorong Jiang, Robert S. Franco
Journal: Blood (2004)

Abstract KCl cotransport (KCC) activation by cell swelling and pH was compared in sickle (SS) and normal (AA) red blood cells (RBCs). KCC fluxes had the same relationship to mean corpuscular hemoglobin concentration (MCHC) in SS and AA RBCs when normalized to the maximal volume-stimulated (VSmax) flux (MCHC &amp;lt; 270 g/L [27 g/dL]). Acid-stimulated (pH 6.9) KCC flux in SS RBCs was 60% to 70% of VSmax KCC versus 20% in AA RBCs. Density gradients were used to track changes in reticulocyte MCHC during KCC-mediated regulatory volume decrease (RVD). Swelling to MCHC of 260 g/L (26 g/dL) produced Cl-dependent RVD that resulted in higher MCHC in SS than AA reticulocytes. In acid pH, RVD was also greater in SS than AA reticulocytes. Sulfhydryl reduction by dithiothreitol (DTT) lowered VSmax KCC flux in AA and SS RBCs by one third but did not alter swelling-induced RVD. DTT lowered acid-activated KCC in SS RBCs by 50% and diminished acid-induced RVD in SS reticulocytes. Thus, swelling activation of KCC is normal in SS RBCs but KCC-mediated RVD produces higher MCHC in SS than AA reticulocytes. Acid activation of KCC is exaggerated in SS RBCs and causes dehydration in SS reticulocytes. KCC response to acid stimulation was mitigated by DTT, suggesting that it arises from sulfhydryl oxidation.
Discovery of new cause for fractures among children who were adopted has "painful" lessons for doctors
Authors: C. Dyer
Journal: BMJ (2009)

A case in which new medical evidence shows that three children who were taken into care and adopted may have been wrongly removed from their parents is a “painful learning experience” for the medical profession, according to a senior Court of Appeal judge.

The case of Mark and Nicky Webster is “a further illustration of the proposition that things may not always be what they seem,” said Lord Justice Wall.

The judge said that the case had been “a disaster” for the Websters, whose three children, named only as A, B, and C, were adopted in December 2005 after B was found to have fractures that doctors said could only be the result of intentional injuries.

But later evidence from several experts, including one described by the judge as “arguably, it is …
Mini‐BEAM and autologous hematopoietic stem‐cell transplant for treatment of post‐transplant lymphoproliferative disorders
Authors: Rami S. Komrokji, Jamie L. Oliva, Martin Zand, Raymond Felgar, Camille N. Abboud
Journal: American Journal of Hematology (2005)

Abstract Post‐transplant lymphoproliferative disorder (PTLD) represents a spectrum of lymphoid proliferative diseases seen as result of immunosuppression in recipients of solid organ or hematopoietic stem‐cell transplantation. Options of treatment include reduction or discontinuation of immunosuppressive agents, antiviral drugs, rituximab, chemotherapy, and radiation. We report two unique cases of PTLD (CNS and plasmacytoma‐like) treated successfully with salvage chemotherapy, mini‐BEAM chemotherapy, and autologous stem‐cell transplant. In both cases, patients were also treated with sirolimus and prednisone as immunosuppression, and neither patient rejected their solid organ transplants. With over 30 months of follow‐up, both patients remain in complete remission with excellent allograft function. Am. J. Hematol. 79:211–215, 2005. © 2005 Wiley‐Liss, Inc.
Ofloxacin and Ursodeoxycholic Acid Versus Ursodeoxycholic Acid Alone to Prevent Occlusion of Biliary Stents: A Prospective, Randomized Trial
Authors: U. Halm, I. Schiefke, W. E. Fleig, J. Mössner, V. Keim
Journal: Endoscopy (2001)

Background and Study Aims: Biliary plastic stents are highly effective in the treatment of malignant biliary obstruction, but may become occluded over time, leading to jaundice and cholangitis. Stent occlusion is thought to be caused by bacterial adhesion and formation of biofilm. This study was carried out to assess whether treatment with ofloxacin in combination with ursodeoxycholic acid is superior to ursodeoxycholic acid alone in preventing stent occlusion.
<i>RNAi</i>-Mediated Silencing of Nuclear Factor Erythroid-2–Related Factor 2 Gene Expression in Non–Small Cell Lung Cancer Inhibits Tumor Growth and Increases Efficacy of Chemotherapy
Authors: Anju Singh, Swetlana Boldin-Adamsky, Rajesh K. Thimmulappa, Srikanta K. Rath, Hagit Ashush, Jonathan Coulter, Amanda Blackford, Steven N. Goodman, Fred Bunz, Walter H. Watson, Edward Gabrielson, Elena Feinstein, Shyam Biswal
Journal: Cancer Research (2008)

Abstract Nuclear factor erythroid-2–related factor 2 (Nrf2) is a redox-sensitive transcription factor that regulates the expression of electrophile and xenobiotic detoxification enzymes and efflux proteins, which confer cytoprotection against oxidative stress and apoptosis in normal cells. Loss of function mutations in the Nrf2 inhibitor, Kelch-like ECH-associated protein (Keap1), results in constitutive activation of Nrf2 function in non–small cell lung cancer. In this study, we show that constitutive activation of Nrf2 in lung cancer cells promotes tumorigenicity and contributes to chemoresistance by up-regulation of glutathione, thioredoxin, and the drug efflux pathways involved in detoxification of electrophiles and broad spectrum of drugs. RNAi-mediated reduction of Nrf2 expression in lung cancer cells induces generation of reactive oxygen species, suppresses tumor growth, and results in increased sensitivity to chemotherapeutic drug–induced cell death in vitro and in vivo. Inhibiting Nrf2 expression using naked siRNA duplexes in combination with carboplatin significantly inhibits tumor growth in a subcutaneous model of lung cancer. Thus, targeting Nrf2 activity in lung cancers, particularly those with Keap1 mutations, could be a promising strategy to inhibit tumor growth and circumvent chemoresistance. [Cancer Res 2008;68(19):7975–84]
Points from Letters: Nursing Home or Hospital?
Authors: R. Binning
Journal: BMJ (1966)

that thoughtless minority who are out to claim all they can without concern for their doctor's discomfiture.Rather than embark on propaganda designed to prevent abuse of a tottering ser- vice I look forward to the day when a more positive approach becomes evident-namely, providing the general practitioner with the proper premises and facilities so badly needed to cope adequately with the sort of medicine required of him in this modern age.If distributing leaflets is the best that can be done I hope the planners find other means of so doing rather than through us.-Iam, etc., Resolven, Glam.
Myc controls transcriptional regulation of cardiac metabolism and mitochondrial biogenesis in response to pathological stress in mice
Authors: Preeti Ahuja, Peng Zhao, Ekaterini Angelis, Hongmei Ruan, Paavo Korge, Aaron Olson, Yibin Wang, Eunsook S. Jin, F. Mark Jeffrey, Michael Portman, W. Robb MacLellan
Journal: Journal of Clinical Investigation (2010)

In the adult heart, regulation of fatty acid oxidation and mitochondrial genes is controlled by the PPARgamma coactivator-1 (PGC-1) family of transcriptional coactivators. However, in response to pathological stressors such as hemodynamic load or ischemia, cardiac myocytes downregulate PGC-1 activity and fatty acid oxidation genes in preference for glucose metabolism pathways. Interestingly, despite the reduced PGC-1 activity, these pathological stressors are associated with mitochondrial biogenesis, at least initially. The transcription factors that regulate these changes in the setting of reduced PGC-1 are unknown, but Myc can regulate glucose metabolism and mitochondrial biogenesis during cell proliferation and tumorigenesis in cancer cells. Here we have demonstrated that Myc activation in the myocardium of adult mice increases glucose uptake and utilization, downregulates fatty acid oxidation by reducing PGC-1alpha levels, and induces mitochondrial biogenesis. Inactivation of Myc in the adult myocardium attenuated hypertrophic growth and decreased the expression of glycolytic and mitochondrial biogenesis genes in response to hemodynamic load. Surprisingly, the Myc-orchestrated metabolic alterations were associated with preserved cardiac function and improved recovery from ischemia. Our data suggest that Myc directly regulates glucose metabolism and mitochondrial biogenesis in cardiac myocytes and is an important regulator of energy metabolism in the heart in response to pathologic stress.
Sources of Errors in Diagnosis of Acute Rheumatic Fever in Children
Authors: Burton J. Grossman, Balu Athreya
Journal: JAMA (1962)

The history and clinical and laboratory findings in 455 patients referred with a possible diagnosis of rheumatic fever but found to have no rheumatic or related disease were studied with reference to the Jones criteria (modified) for the diagnosis of rheumatic fever. The interpretation of the data by the referring physician was compared with the interpretation arrived at by the hospital staff after a thorough evaluation of the patient. Common sources of error were (1) an innocent murmur or the murmur of acyanotic congenital heart disease interpreted as the murmur of rheumatic heart disease, (2) arthralgia interpreted as arthritis, (3) abnormal movements interpreted as chorea, (4) low-grade, persistent fever interpreted as rheumatic fever, (5) clinical evidence of sore throat interpreted as β hemolytic streptococcal pharyngitis, and (6) a rise in antistreptolysin O titer interpreted as indicating presence of rheumatic fever.
14 DUAL ORAL THERAPY WITH THE NS5A INHIBITOR DACLATASVIR (BMS-790052) AND NS3 PROTEASE INHIBITOR ASUNAPREVIR (BMS-650032) IN HCV GENOTYPE 1B-INFECTED NULL RESPONDERS OR INELIGIBLE/INTOLERANT TO PEGINTERFERON/RIBAVIRIN
Authors: F. Suzuki, K. Ikeda, J. Toyota, Y. Karino, T. Ohmura, K. Chayama, S. Takahashi, Y. Kawakami, H. Ishikawa, H. Watanabe, W. Hu, F. McPhee, E. Hughes, H. Kumada
Journal: Journal of Hepatology (2012)
Effective Dystrophin Restoration by a Novel Muscle-Homing Peptide–Morpholino Conjugate in Dystrophin-Deficient mdx Mice
Authors: Xianjun Gao, Jingwen Zhao, Gang Han, Yajie Zhang, Xue Dong, Limin Cao, Qingsong Wang, Hong M Moulton, HaiFang Yin
Journal: Molecular Therapy (2014)

Antisense oligonucleotide (AO)–mediated splice correction therapy for Duchenne muscular dystrophy has shown huge promise from recent phase 2b clinical trials, however high doses and costs are required and targeted delivery can lower both of these. We have previously demonstrated the feasibility of targeted delivery of AOs by conjugating a chimeric peptide, consisting of a muscle-specific peptide and a cell-penetrating peptide, to AOs in mdx mice. Although increased uptake in muscle was observed, the majority of peptide–AO conjugate was found in the liver. To search for more effective muscle-homing peptides, we carried out in vitro biopanning in myoblasts and identified a novel 12-mer peptide (M12) showing preferential binding to skeletal muscle compared to the liver. When conjugated to phosphorodiamidate morpholino oligomers, ~25% of normal level of dystrophin expression was achieved in body-wide skeletal muscles in mdx mice with significant recovery in grip strength, whereas <2% in corresponding tissues treated with either muscle-specific peptide–phosphorodiamidate morpholino oligomer or unmodified phosphorodiamidate morpholino oligomer under identical conditions. Our data provide evidences for the first time that a muscle-homing peptide alone can enhance AO delivery to muscle without appreciable toxicity at 75 mg/kg, suggesting M12-phosphorodiamidate morpholino oligomer can be an alternative option to current AOs. Antisense oligonucleotide (AO)–mediated splice correction therapy for Duchenne muscular dystrophy has shown huge promise from recent phase 2b clinical trials, however high doses and costs are required and targeted delivery can lower both of these. We have previously demonstrated the feasibility of targeted delivery of AOs by conjugating a chimeric peptide, consisting of a muscle-specific peptide and a cell-penetrating peptide, to AOs in mdx mice. Although increased uptake in muscle was observed, the majority of peptide–AO conjugate was found in the liver. To search for more effective muscle-homing peptides, we carried out in vitro biopanning in myoblasts and identified a novel 12-mer peptide (M12) showing preferential binding to skeletal muscle compared to the liver. When conjugated to phosphorodiamidate morpholino oligomers, ~25% of normal level of dystrophin expression was achieved in body-wide skeletal muscles in mdx mice with significant recovery in grip strength, whereas <2% in corresponding tissues treated with either muscle-specific peptide–phosphorodiamidate morpholino oligomer or unmodified phosphorodiamidate morpholino oligomer under identical conditions. Our data provide evidences for the first time that a muscle-homing peptide alone can enhance AO delivery to muscle without appreciable toxicity at 75 mg/kg, suggesting M12-phosphorodiamidate morpholino oligomer can be an alternative option to current AOs.
An Operation for the Destruction of Varicose Veins
Authors: C. Steele
Journal: BMJ (1875)

chills by coming on deck to get cool ; and, though acute inflammation of the lungs is by no means uncommon, yet I thinkl he will find it hard to prove they are more liable to ague than the otlher seamen oni board.The most deadly spot in the world probably, excee(ling even the coast of Africa in the intensity of its malaria, is the " Terai"-that belt of jungle runiiningalong the foot of the Himalayas; for an European to enlter it at certain seasons of the year, is almost certai death.Here is a true example of malaria produced by the well known factors, vegetable dlecomnposition, moistuLre to saturation, subsoil-water almost at the surface, anl. a high temperature.Here it is not nlecessary to be chilled, and no niumber of blankets will keep off the deadly malaria ; but, twen-ty miles off, one may sleep in the openi w,Nith almost perfect safety, exceptinig, perhaps, at the end of the rainis, wheni, all the factors of malaria being present in a greater or less degree, every part of the continen-t of Hindostan is more or less malarious.I fear I have been Inot only prolix, but egotistic, in the above re- marl-s ; but experience in one's own persoii is imiore valuable than the parlour argumenits of a mani who tries to upset the conclusions arrived at by such men as Dr. Maclean, who have spenit their lives not oiily in seeinig, but in suffering from, the effects of malaria.
Stress: Medical and Legal Analysis of Late Effects of World War II Suffering in The Netherlands
Authors: Eugene V. Boisaubin
Journal: JAMA (1989)

Born of a postgraduate course in May of 1988, this volume delivers what its title purports. The intent of the course and text was to integrate the fields of medicine, history, and legislation around the catastrophic events of World War II in western Europe. It was hoped that trends and lessons for the future could be identified. First, a historical background of medical care in the Netherlands before, during, and after the war is provided. The medical aspects of the Nazi invasion and occupation, primarily focusing on stress, form the more interesting corpus of the work. Introducing the medical section are brief and somewhat cursory overviews of the neuroendocrine and immunologic aspects of stress as well as starvation. Subsequent chapter titles, however, such as "The Pathophysiology of Imprisonment, Deportation, and Resistance," reflect some of the difficulty of hybridizing basic medical science with history. Some of the theories presented, such as