tbuckley/cabot-search huggingface dataset:
Hemolytic Transfusion Reaction Due to Inter-Donor Incompatibility
Authors: F Skov, E Dybkjaer, E Taaning, V Thygesen, O Drachmann
Journal: JAMA (1963)

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
<i>Wollschlaeger v. Governor of Florida</i>— The First Amendment, Physician Speech, and Firearm Safety
Authors: Wendy E. Parmet, Jason A. Smith, Matthew J. Miller
Journal: New England Journal of Medicine (2016)

An appeals court case challenges a law regulating physicians' speech related to patients' gun ownership. The decision may have broad implications for states' ability to regulate physicians' speech and physicians' efforts to protect patients from firearm-related injuries.
Need for Safety Goggles for Endoscopy
Authors: T. Benter, L. Klühs, U. Teichgräber, F. Riechert, W. Ludwig, B. Dörken
Journal: Endoscopy (2003)

Although new techniques such as spectroscopy have been developed for endoscopy and have found their way into clinical application, endoscopists' eyes are still the most important tool in everyday work [1]. However, the eyes are the instrument that is most at risk during an endoscopist's career. Macular damage after intensive light exposure during endoscopy has been described [2]. It has also been suspected that exposure to ionizing radiation during endoscopic retrograde cholangiopancreatography (ERCP) may cause injury to the lenses of endoscopists' eyes [3].
High Day 28 ST2 Biomarker Levels Predict Severe Day 100 Acute Graft-Versus-Host Disease and Day 180 Transplant-Related Mortality After Double-Unit Cord Blood Transplantation
Authors: Doris M Ponce, Patrick Hilden, Christy Mumaw, Sean Devlin, Marissa N Lubin, Katherine L Evans, Susan Prockop, Andromachi Scaradavou, Nancy A. Kernan, Sergio A Giralt, Marcel R.M. van den Brink, Sophie Paczesny, Juliet N Barker
Journal: Blood (2013)
Influenza outbreaks in nursing homes with high vaccination coverage in Navarre, Spain, 2011/12
Authors: J Castilla, F Cía, J Zubicoa, G Reina, V Martínez-Artola, C Ezpeleta
Journal: Eurosurveillance (2012)

In the 2011/12 season, three influenza outbreaks were studied in nursing homes with high vaccination coverage in Navarre, Spain. Attack rates ranged from 2.9% to 67%. Influenza A/Stockholm/18/2011(H3N2) virus strain was isolated from the three outbreaks. Vaccination should be complemented with other hygiene measures in nursing homes. Early detection of influenza outbreaks in nursing homes can aid in their control.
Shifting priorities in the aftermath of a Q fever epidemic in 2007 to 2009 in the Netherlands: from acute to chronic infection
Authors: W van der Hoek, P M Schneeberger, T Oomen, M C Wegdam-Blans, F Dijkstra, D  W Notermans, H A Bijlmer, K Groeneveld, C J Wijkmans, A Rietveld, L M Kampschreur, Y van Duynhoven
Journal: Eurosurveillance (2012)

From 2007 to 2009, the Netherlands faced large seasonal outbreaks of Q fever, in which infected dairy goat farms were identified as the primary sources. Veterinary measures including vaccination of goats and sheep and culling of pregnant animals on infected farms seem to have brought the Q fever problem under control. However, the epidemic is expected to result in more cases of chronic Q fever among risk groups in the coming years. In the most affected area, in the south of the country, more than 12% of the population now have antibodies against Coxiella burnetii. Questions remain about the follow-up of acute Q fever patients, screening of groups at risk for chronic Q fever, screening of donors of blood and tissue, and human vaccination. There is a considerable ongoing research effort as well as enhanced veterinary and human surveillance.
New Metabolites of &lt;italic&gt;N&lt;/italic&gt;-3-Fluorenylacetamide&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Elizabeth K. Weisburger
Journal: JNCI Journal of the National Cancer Institute (1961)

Two new metabolites, N-(7-hydroxy-3-fluorenyl)acetamide and N-(2,7-dihydroxy - 3 - fluorenyl)acetamide, were identified in the urine of rats receiving an injection of N-3-fluorenylacetamide, These compounds were present chiefly as glucuronic acid conjugates, but were also excreted as sulfates. N-(7-Hydroxy-3-fluorenyl)acetamide was made from 7-methoxy-2-fluorenamine by an eight-step synthesis, while N-(2,7-dihydroxy-3 - fluorenyl)acetamide was prepared from the same starting material in six steps.
Production of RANKL by Memory B Cells: A Link Between B Cells and Bone Erosion in Rheumatoid Arthritis
Authors: Nida Meednu, Hengwei Zhang, Teresa Owen, Wen Sun, Victor Wang, Christopher Cistrone, Javier Rangel‐Moreno, Lianping Xing, Jennifer H. Anolik
Journal: Arthritis & Rheumatology (2015)

Objective Rheumatoid arthritis (RA) is a systemic autoimmune disease that often leads to joint damage. The mechanisms of bone damage in RA are complex, involving activation of bone‐resorbing osteoclasts (OCs) by synoviocytes and Th17 cells. This study was undertaken to investigate whether B cells play a direct role in osteoclastogenesis through the production of RANKL, the essential cytokine for OC development. Methods RANKL production by total B cells or sorted B cell subpopulations in the peripheral blood and synovial tissue from healthy donors or anti–cyclic citrullinated peptide–positive patients with RA was examined by flow cytometry, real‐time polymerase chain reaction, enzyme‐linked immunosorbent assay, and immunohistochemical analysis. To define direct effects on osteoclastogenesis, B cells were cocultured with CD14+ monocytes, and OCs were enumerated by tartrate‐resistant acid phosphatase staining. Results Healthy donor peripheral blood B cells were capable of expressing RANKL upon stimulation, with switched memory B cells (CD27+IgD−) having the highest propensity for RANKL production. Notably, switched memory B cells in the peripheral blood from RA patients expressed significantly more RANKL compared to healthy controls. In RA synovial fluid and tissue, memory B cells were enriched and spontaneously expressed RANKL, with some of these cells visualized adjacent to RANK+ OC precursors. Critically, B cells supported OC differentiation in vitro in a RANKL‐dependent manner, and the number of OCs was higher in cultures with RA B cells than in those derived from healthy controls. Conclusion These findings reveal the critical importance of B cells in bone homeostasis and their likely contribution to joint destruction in RA.
Glucose Variability in a 26-Week Randomized Comparison of Mealtime Treatment With Rapid-Acting Insulin Versus GLP-1 Agonist in Participants With Type 2 Diabetes at High Cardiovascular Risk
Journal: Diabetes Care (2016)

A1C is associated with diabetes complications but does not reflect glycemic variability (GV), which may worsen outcomes by inducing inflammation, oxidative stress, and cardiac arrhythmias. We tested whether a glucagon-like peptide 1 agonist-based regimen can reduce GV and cardiometabolic risk markers while maintaining similar A1C levels in people with insulin-requiring type 2 diabetes and high cardiovascular risk.After run-in on metformin and basal-bolus insulin (BBI), 102 participants continued metformin and basal insulin and were randomized to exenatide dosing before the two largest meals (glucacon-like peptide-1 receptor agonist and insulin [GLIPULIN group]) or continuation of rapid-acting insulin analogs (BBI group). Indices of GV by continuous glucose monitoring (CGM), hypoglycemia, weight, risk markers, and cardiac arrhythmias were assessed. The primary end point was change in glucose coefficients of variation (CV) by CGM from baseline to 26 weeks.At randomization, the median A1C was 7.3% (57 mmol/mol) for GLIPULIN and 7.4% (56.3 mmol/mol) for BBI, and glucose CVs were 30.3 for BBI and 31.9 for GLIPULIN. At 26 weeks, A1C levels were similar (7.1% [54 mmol/mol] vs. 7.2% [55 mmol/mol]), whereas mean CV improved with GLIPULIN (-2.4 vs. 0.4, P = 0.047). Other GV indices followed similar nonsignificant patterns of improvement with GLIPULIN. There were no differences in hypoglycemic events during CGM or arrhythmias during electrocardiographic monitoring. On-trial changes in body weight (-4.8 kg vs. +0.7 kg, P < 0.001), alanine aminotransferase (P = 0.0002), and serum amyloid A (P = 0.023) favored GLIPULIN.GLIPULIN reduced GV, weight, and some cardiometabolic risk markers while maintaining equivalent A1C levels versus BBI and might improve clinical outcomes in a larger trial.
Abstract IA31: Mechanisms of resistance to EGFR inhibitors in lung cancer
Authors: Pasi Jänne
Journal: Cancer Research (2016)

Abstract Epidermal Growth Factor Receptor (EGFR) tyrosine kinase inhibitors (TKIs), including geftinib, erlotinib and afatinib are the standard of care for patients with advanced EGFR mutant non-small cell lung cancer. Treatment with an EGFR TKI leads to a response rate of ~60% and a median progression free survival ranging from 9 to 11 months. Acquired drug resistance inevitably develops in most of not all EGFR mutant lung cancer patients treated with EGFR inhibitors. The most common mechanism of acquired resistance is the development of a secondary EGFR T790M mutation. Other mechanism of resistance include activation of bypass signaling pathways (such as MET or HER2) and histological transformation. Over the last few years a series of new structurally distinct EGFR inhibitors have been identified and entered the clinic that are capable of inhibiting EGFR T790M. This class of mutant selective EGFR TKIs are effective both against the activating EGFR mutation and the drug resistant T790M but spare inhibition of wild type (WT) EGFR. This has enormous potential therapeutic implications as the side effects of all approved EGFR inhibitors is derived from inhibition of WT EGFR. Several of these agents, including AZD9291 and rociletinib (CO-1686) are in advanced stage clinical development. Both agents have been granted FDA’s breakthrough designation. In EGFR inhibitor resistant patients who have developed resistance to current clinical EGFR inhibitors through T790M, the response rates to either AZD9291 or rociletinib is over 60% with median progression free survivals of ~ 10 months. Current research efforts and clinical studies are focusing on a.) understanding mechanisms of drug resistance to this new class of EGFR inhibitors, b.) the development of rationale combination therapies and c.) use of these agents as initial treatment (instead of currently approved EGFR inhibitors) for patients with advanced EGFR mutant NSCLC. Citation Format: Pasi Jänne. Mechanisms of resistance to EGFR inhibitors in lung cancer. [abstract]. In: Proceedings of the Fourth AACR International Conference on Frontiers in Basic Cancer Research; 2015 Oct 23-26; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2016;76(3 Suppl):Abstract nr IA31.
Frontal leukotomy and related psychosurgical procedures in the era before antipsychotics (1935-1954): a historical overview
Authors: V W Swayze
Journal: American Journal of Psychiatry (1995)

This article provides an overview of the history of psychosurgery as a treatment for psychiatric illnesses.The author reviewed articles describing psychosurgery between 1935 and 1954 in order to summarize surgical techniques, clinical indications for surgery, patient selection, complications, and outcome.Patients were operated on for a wide variety of psychiatric illnesses. Initially, a large number of uncontrolled studies reported considerable therapeutic benefit in at least one-third of the patients operated on. Complications with the early surgical techniques included hemorrhage, seizures, infection, and personality changes. Surgical techniques proliferated in hopes of achieving greater therapeutic benefit while minimizing detrimental side effects. As psychosurgery became more widely accepted, its principal supporters began to use it as a routine therapy. A number of uncontrolled and controlled short-term studies supported the efficacy of psychosurgery, but long-term controlled studies showed mixed results.Psychosurgery was promoted as a treatment for patients who had shown little or no response to less drastic therapies. In the context of an era when no efficacious treatments were available for psychosis, its use was understandable. However, its history illustrates the importance of critical evaluation of new treatments in the context of long-term controlled outcome studies, the natural course of specific illnesses, and an understanding of brain physiology.
Differences between Streptococcal Infections of the Throat and of the Skin
Authors: Lewis W. Wannamaker
Journal: New England Journal of Medicine (1970)

Antibody ResponseVariation in the streptococcal immune response related to the site of infection (Tables 1 and 4) is supported by a growing body of information with pervasive implications, both practical and theoretical. The report of Burnett20 contains perhaps the first observations that certainly in retrospect can be interpreted as a warning not to rely on the antistreptolysin-O (ASO) test to exclude a streptococcal etiology in pyoderma. A mild immune response was also postulated lor streptococcal pyoderma on the basis of ASO findings by Markowitz et al.29 Interpretation of the ASO levels in these two studies was hampered by the . . .
Association between low plasma levels of dexamethasone and elevated levels of cortisol in psychiatric patients given dexamethasone
Authors: G W Arana, R J Workman, R J Baldessarini
Journal: American Journal of Psychiatry (1984)

In psychiatric inpatients, positive results on 40 dexamethasone suppression tests (elevated cortisol levels) were strongly associated with low plasma levels of dexamethasone. Bioavailability or pharmacokinetic factors may contribute importantly to the outcome of the dexamethasone suppression test.
Brown Adipose Tissue Activation Is Linked to Distinct Systemic Effects on Lipid Metabolism in Humans
Authors: Maria Chondronikola, Elena Volpi, Elisabet Børsheim, Craig Porter, Manish K. Saraf, Palam Annamalai, Christina Yfanti, Tony Chao, Daniel Wong, Kosaku Shinoda, Sebastien M. Labbė, Nicholas M. Hurren, Fernardo Cesani, Shingo Kajimura, Labros S. Sidossis
Journal: Cell Metabolism (2016)
Brief Report: HLA–DRB1, DQA1, and DQB1 in Juvenile‐Onset Systemic Sclerosis
Authors: Anne M. Stevens, Sami B. Kanaan, Kathryn S. Torok, Thomas A. Medsger, Maureen D. Mayes, John D. Reveille, Marisa Klein‐Gitelman, Ann M. Reed, Tzielan Lee, Suzanne C. Li, Gretchen Henstorf, Christine Luu, Tessa Aydelotte, J. Lee Nelson
Journal: Arthritis & Rheumatology (2016)

Objective Systemic sclerosis (SSc) is a rare disease that is particularly uncommon in children. Specific HLA alleles have been associated with SSc in adults. This study was undertaken to investigate HLA class II alleles in juvenile‐onset SSc. Methods DRB1, DQA1, and DQB1 alleles were determined by DNA‐based HLA typing. Analyses were conducted comparing Caucasian patients with juvenile‐onset SSc (n = 76) to healthy Caucasian controls (n = 581). Results Initial analyses focused on HLA class II associations previously reported in adult Caucasian patients with SSc. The frequency of DRB1*11 was not significantly increased in juvenile‐onset SSc (22.4% of patients with juvenile‐onset SSc versus 17.6% of controls; odds ratio [OR] 1.35, P = 0.34), nor were the specific DRB1*11:01 or *11:04 alleles. DQA1*05, a risk factor previously identified in adult men with SSc, was increased in patients with juvenile‐onset SSc versus controls (57.9% versus 44.1%; OR 1.76, P = 0.027), as was DRB1*03 (34.2% versus 22.5%; OR 1.79, P = 0.031). Secondary analyses of all DRB1 allele groups revealed an association with DRB1*10 (10.5% of patients with juvenile‐onset SSc versus 1.5% of controls; OR 7.48, P = 0.0002). As this is a new observation, correction was made for multiple comparisons of 13 different DRB1 allele groups; results nevertheless remained significant ( P = 0.003). Also, a lower frequency of DRB1*01 was observed in patients with juvenile‐onset SSc who were younger at disease onset (OR 0.06, P = 0.01) and in those with antibodies to topoisomerase (OR 0.14, P = 0.024). Conclusion Associations of HLA alleles with juvenile‐onset SSc differed from associations with SSc in women, but were similar to associations with SSc in men. Additionally, a novel association with DRB1*10 was observed in children. The greatest proportion of genetic risk of SSc is contributed by the HLA complex, and the current study reveals the importance of the association of HLA class II genes in juvenile‐onset SSc.
A prospective follow-up and family study of somatization in men and women
Authors: C R Cloninger, R L Martin, S B Guze, P J Clayton
Journal: American Journal of Psychiatry (1986)

The authors evaluated alternative criteria for somatization disorder in 277 female and 129 male psychiatric outpatients. In women, the diagnosis of somatization disorder based on DSM-III criteria was highly concordant with the diagnosis of Briquet's syndrome based on Guze's original criteria. There was familial aggregation for Briquet's syndrome in women but none among individuals of either sex who had somatization disorder without the full Briquet's syndrome. In men, the diagnosis of somatization disorder was rarer and less stable than in women. The findings show that somatization usually has a different clinical picture and different familial antecedents in men than in women.
Abstract B05: Mechanism for enhanced 5-aminolevulinic acid fluorescence in isocitrate dehydrogenase 1 mutant malignant gliomas
Authors: Kim Ja Eun, Hye Rim Cho, Wen Jun Xu, Young-Hoon Kim, Ji Hoon Phi, Seung Hong Choi, Sunghyouk Park, Chul-Kee Park
Journal: Cancer Research (2015)

Abstract Fluorescence-guided surgery using 5-aminolevulinic acid (5-ALA) and the discovery of IDH1 mutations are major recent advances in glioma management and research. However, the mechanism underlying the selective intracellular accumulation of the 5-ALA derivative protoporphyrinogen IX (PpIX) and the metabolic effect of IDH1 mutations in malignant glioma cells are still not fully understood. Based on clinical experience, we hypothesized an association between enhanced 5-ALA fluorescence and IDH1 mutations in WHO grade III gliomas. Using genetically engineered malignant glioma cells harboring wild type (U87MG-IDH1WT) or mutant (U87MG-IDH1R132H) versions of IDH1, we confirmed a lag in 5-ALA metabolism and a temporary accumulation of PpIX in U87MG-IDH1R132H cells. To investigate the metabolic aspects of the mechanism responsible, we used liquid chromatography–mass spectrometry (LC-MS) to screen for tricarboxylic acid (TCA) cycle-related metabolite changes resulting from 5-ALA exposure. We observed low baseline levels of NADPH, an essential cofactor for the rate-limiting step of heme degradation, in U87MG-IDH1R132H cells. Abundant levels of NADPH are required to metabolize excessive 5-ALA, giving a plausible reason for the temporary enhanced 5-ALA fluorescence in mutant IDH1 cells. This hypothesis was supported by the results of metabolic screening in human malignant glioma samples. We discovered a relationship between enhanced 5-ALA fluorescence and IDH1 mutations in malignant gliomas and investigated the metabolic aspects of the mechanism responsible, identifying significantly different levels of NADPH between wild type and mutant IDH1 malignant glioma cells. Citation Format: Kim Ja Eun, Hye Rim Cho, Wen Jun Xu, Young-Hoon Kim, Ji Hoon Phi, Seung Hong Choi, Sunghyouk Park, Chul-Kee Park. Mechanism for enhanced 5-aminolevulinic acid fluorescence in isocitrate dehydrogenase 1 mutant malignant gliomas. [abstract]. In: Proceedings of the AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2015;75(23 Suppl):Abstract nr B05.
A first-in-human, phase Ib combination study to assess safety, pharmacokinetics (PK), and pharmacodynamics (PD) of a hedgehog inhibitor, GDC-0449, with a Notch inhibitor, RO4929097, in patients with advanced sarcoma.
Authors: Mrinal M. Gounder, Mark Andrew Dickson, Nian Wu, S. Percy Ivy, Richard D. Carvajal, Sandra P. D'Angelo, Mary Louise Keohan, Li-Xuan Qin, Joseph Patrick Erinjeri, Naoko Takebe, Lanier Tanner, Rita Morales, Mercedes M Condy, Yelena Ustoyev, Robert G. Maki, William D. Tap, Gary K. Schwartz
Journal: Journal of Clinical Oncology (2012)

10004 Background: Aberrant Hedgehog and Notch signaling is seen in sarcoma and anti-tumor activity is enhanced by inhibiting both pathways. This first in man Phase Ib study evaluated safety and efficacy of the combination of GDC-0449 (G), a smoothened inhibitor with RO4929097 (R), a gamma-secretase/notch inhibitor. Methods: The study evaluated fixed dose G (150 mg qd) for 21 days followed by G + R at either 10 mg (level 1) or 15 mg (level 2) QD. At MTD pts were evaluated with G + R (without “lead in” G) or single agent R. Pre and post treatment tumor biopsies were obtained to assess notch and hedgehog inhibition. PK was assessed for each drug. Key eligibility: advanced sarcoma, ECOG ≤ 2, age ≥ 18 and prior therapies ≤ 4. RECIST response was assessed Q6 wks. Results: 34 pts had a median age of 53 yrs (23-78), median priors 3 and various histologies [liposarcoma (7), chondrosarcoma (7), leiomyosarcoma (4), osteosarcoma (2), GIST (2) and other (12)]. No DLT was seen. Common (≥10 %) grade ≤3 toxicity was hypophosphatemia (18%). Systemic exposure (AUC 0-24 and C max ) of G was similar to established studies (not shown). AUC 0-24 and C max of R was significantly lower (~70%) when administered with G (Table). However, measurement of unbound, free drug (C free ) of R showed comparable levels between single agent R and G + R, but not when G was a “lead in” (Table). Target inhibition of the notch pathway (cleaved notch) and pAkt was observed in matched tumor biopsies with both arms. Durable SD was seen in both arms: myxoid chondrosarcoma (56 wks), liposarcoma (24+ wks), clear cell (21+ wks), desmoid (17+ wks), spindle cell (15+ wks) and chondrosarcoma (13+ wks). Conclusions: The combination of G+R is well tolerated and the RP2D is G 150 mg qd and R 15 mg qd without a “lead in” G. Despite reduction in total levels of R in the combination, free drug was similar and inhibits target. Disease stability was seen with R and R + G. Further clinical development of notch and hedgehog inhibitors in sarcomas is warranted. [Table: see text]
Phenotypic and Functional Evidence for the Expression of CXCR4 Receptor During Megakaryocytopoiesis
Authors: Christel Rivière, Frédéric Subra, Karine Cohen-Solal, Véronique Cordette-Lagarde, Remi Letestu, Christian Auclair, William Vainchenker, Fawzia Louache
Journal: Blood (1999)
Neuro-ophthalmic systemic lupus erythematosis misdiagnosed as hysterical blindness
Authors: A Stoudemire, M Stork, D Simel, J L Houpt
Journal: American Journal of Psychiatry (1982)

The authors present a case of neuro-ophthalmic systemic lupus erythematosus in which an initial diagnosis of "hysteria" was made. The authors review the ophthalmic symptoms of systemic lupus erythematosus and technical aspects of the ophthalmic examination useful in differentiating organic from functional blindness.