tbuckley/cabot-search huggingface dataset:
Losartan-induced hepatotoxicity
Authors: X. Bosch
Journal: JAMA (1997)

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
Obstruction of extrahepatic bile ducts by lymphocytes is regulated by IFN-γ in experimental biliary atresia
Authors: Pranavkumar Shivakumar, Kathleen M. Campbell, Gregg E. Sabla, Alexander Miethke, Greg Tiao, Monica M. McNeal, Richard L. Ward, Jorge A. Bezerra
Journal: Journal of Clinical Investigation (2004)

The etiology and pathogenesis of bile duct obstruction in children with biliary atresia are largely unknown. We have previously reported that, despite phenotypic heterogeneity, genomic signatures of livers from patients display a proinflammatory phenotype. Here, we address the hypothesis that production of IFN-γ is a key pathogenic mechanism of disease using a mouse model of rotavirus-induced biliary atresia. We found that rotavirus infection of neonatal mice has a unique tropism to bile duct cells, and it triggers a hepatobiliary inflammation by IFN-γ–producing CD4+ and CD8+ lymphocytes. The inflammation is tissue specific, resulting in progressive jaundice, growth failure, and greater than 90% mortality due to obstruction of extrahepatic bile ducts. In this model, the genetic loss of IFN-γ did not alter the onset of jaundice, but it remarkably suppressed the tissue-specific targeting of T lymphocytes and completely prevented the inflammatory and fibrosing obstruction of extrahepatic bile ducts. As a consequence, jaundice resolved, and long-term survival improved to greater than 80%. Notably, administration of recombinant IFN-γ led to recurrence of bile duct obstruction following rotavirus infection of IFN-γ–deficient mice. Thus, IFN-γ–driven obstruction of bile ducts is a key pathogenic mechanism of disease and may constitute a therapeutic target to block disease progression in patients with biliary atresia.
'Benign' monoclonal gammopathy. A misnomer?
Authors: R. A. Kyle
Journal: JAMA (1984)

A series of 241 patients with monoclonal protein but no evidence of multiple myeloma, macroglobulinemia, amyloidosis, or lymphoma (benign monoclonal gammopathy) were followed up for more than ten years. The patients were classified as follows: group 1, patients without increase of monoclonal serum protein during follow-up (benign) (37%); group 2, patients with greater than 50% increase of monoclonal protein or development of monoclonal urine protein (5%); group 3, patients who died of unrelated causes (39%); and group 4, patients in whom myeloma, macroglobulinemia, amyloidosis, or related diseases developed (19%). The median interval from recognition of the monoclonal protein to diagnosis of multiple myeloma was 98 months; macroglobulinemia, 115 months; and systemic amyloidosis, 92 months. No laboratory or clinical data initially differentiated patients with benign gammopathy from those in whom serious diseases developed. Consequently, serial measurement of serum monoclonal protein is essential. (<i>JAMA</i>1984;251:1849-1854)
Anogenital (Extramammary) Paget's Disease: Clinicopathologic Study
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
Unfunded Research? I Am Shocked, Shocked!
Authors: Michael Phillips
Journal: JAMA (1993)

<h3>To the Editor.</h3> —Remember Claude Raines in<i>Casablanca</i>? In his role as a policeman he exclaimed, "I am shocked, shocked!" to discover that there was gambling in a nightclub, while he stuffed a large wad of winnings in his pocket. Stein et al<sup>1</sup>appear to be shocked, shocked, to discover that some physicians actually perform medical research without financial support, while they acknowledge no funding for their own publication. They hint at dark scandals, of "procedures that presumably were performed for research purposes and not as part of routine patient care... part of the cost may have been passed on to study participants or their third-party payers, perhaps unknowingly." Presumably? May have been? Perhaps? If this is an exposé of "Researchgate," the authors should have presented some hard data to support their speculations. The truth of the matter is that unfunded medical research has always been the rule rather than
In Reply:
Authors: Eric J. Small
Journal: Journal of Clinical Oncology (2004)

THE EDITOR:The study by Small et al 1 showed that pamidronate disodium failed to demonstrate a significant overall treatment benefit compared with placebo in palliation of bone pain or reduction of skeletal-related events in metastatic prostate cancer patients.They also observed that the most frequently reported adverse events in both treatment groups were bone pain, nausea, anorexia, and fatigue.Interestingly, they did not observe any hypocalcemia, which may be explained in two ways: one is that they did not measure serum calcium levels 3 to 7 days later after the administration of pamidronate in which time the hypocalcemia is more frequently seen, second is that they added calcium and vitamin D supplementation throughout the study but did not mention this in the treatment plan.
THE REDUCTION OF THE ARMY MEDICAL DEPARTMENT.
Journal: JAMA (1894)

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
Dog Bite Wounds
Authors: Michael Callaham
Journal: JAMA (1981)

<h3>To the Editor.—</h3> I have noted an erroneous impression given by my recent article in<i>JAMA</i>on dog bite wounds (1980;244:2327) that I would like to correct. The statement was made that anaerobic bacteria "are common but apparently do not cause infection." This was based on an early report by Goldstein et al<sup>1</sup>in which only aerobes were found in seven patients with cellulitis, while aerobes and anaerobes were common in wounds without cellulitis. The same author has recently published a more detailed description of this series<sup>2</sup>in which approximately 75% of cultures of infected wounds grew mixed cultures of both aerobes and anaerobes. Some 22 anaerobic strains were identified. Approximately 25% of infected wounds grew pure aerobic cultures; none grew pure anaerobes. However, the frequency of their occurrence suggests that when cultures are obtained for the indications outlined in my article, both aerobes and anaerobes should be
Pyridoxine antagonism of levodopa in parkinsonism
Authors: A. S. Leon
Journal: JAMA (1971)

Since the decarboxylation of dopa to form dopamine is dependent upon pyridoxal phosphate, Duvoison and co-workers<sup>1</sup>hypothesized that pyridoxine might enhance the therapeutic effects of levodopa. Accordingly, they administered pyridoxine hydrochloride to patients with parkinsonism who were receiving maintenance doses of levodopa. They found that large doses of pyridoxine completely eliminated the clinical effects of levodopa, while smaller doses reduced or abolished its therapeutic activity or only dyskinetic side effects. This was associated with a reduced rise in plasma dopa levels following levodopa administration. Other workers have also reported reduced clinical activity of levodopa following pyridoxine.<sup>2-3</sup>The purpose of the present study was to correlate the effects of pyridoxine on the therapeutic activity of levodopa with its effects on absorption and metabolism. <h3>Materials and Methods</h3> The study population consisted of three men and one woman with parkinsonism who had achieved stable improvement (Table 1). Maintenance levels of levodopa
Jack O'Health and Peg O'Joy. A Fairy-Tale.
Journal: JAMA (1921)

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
BIOLOGICAL PROBLEMS OF DEATH.
Journal: JAMA (1893)

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
Abstract 4043: Application of high complexity flow cytometry for Monitoring activated T-cells, T and B regulatory subsets in combination immunotherapy trials, melanoma case study
Authors: Jennifer Tsau, Michael Abadier, Brittney Atzmiller, Christine Vaupel, Naveen Dakappagari, Ghanashyam Sarikonda, Ahmad Tarhini
Journal: Cancer Research (2019)

Abstract Background Ever increasing knowledge of the interplay between immune composition and a novel drugs’ treatment efficacy or the lack thereof leads to continual advancements in immunotherapies. Given the exponential increase in combination therapies, tools to determine the most promising regimens are critical. Immunotherapeutic agents either reverse T-cell inhibitory pathways (e.g., PD-1) or activate the immune system to induce cytotoxic T-cell activation and proliferation through agonistic stimulation (e.g., Cytokines). These treatment strategies have proven to be efficacious by enhancing the balance between immune-effector and suppressive/regulatory cells that can directly affect the outcome of immunotherapy. To concurrently monitor multiple immune cell subsets responsible for either immuno-suppression or activation, we developed a high-complexity (13-color) flow cytometry panel to reliably enumerate activated T-cells, Tregs (A &amp; B subsets) and Bregs for clinical trial application. Methods The panel includes CD3, CD4, CD8, CD19, FoxP3, CD25, CD127, CD45RA, HLA-DR, CD38, CD24, and CD27 to monitor total Tregs, Treg-subsets, Bregs and T-cell activation. After robust analytical method validation following industry guidelines for exploratory biomarker assessments, we confirmed the clinical utility of this panel in stage III or IV melanoma patients (N= 14) enrolled in a randomized phase II clinical trial receiving high-dose of IL-2 with or without Afliberecept (VEGF inhibitor). Results We observed up-to 20-fold increase in activated CD8+ T-cells following treatment. Interestingly, while no discernible change was observed in the naive Treg-A cells (CD45RAhiFoxp3lo), a remarkable 5-fold expansion of effector Treg-B cells (CD45RAloFoxp3hi) was observed following treatment. Additionally, frequencies of Bregs (CD24hiCD38hi) remained unchanged after treatment. Conclusions In summary, we demonstrated the utility of a powerful high complexity clinical flow cytometry tool for precisely monitoring immune cell subsets involved in tumor escape such as Tregs and Bregs or those involved in tumor killing like CD8+ cytotoxic T-cells. More notably, this tool may be utilized to deprioritize agents that cause immunosuppression and focus on combination agents that lead to additive immune activation. Citation Format: Jennifer Tsau, Michael Abadier, Brittney Atzmiller, Christine Vaupel, Naveen Dakappagari, Ghanashyam Sarikonda, Ahmad Tarhini. Application of high complexity flow cytometry for Monitoring activated T-cells, T and B regulatory subsets in combination immunotherapy trials, melanoma case study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4043.
Transcription cofactor GRIP1 differentially affects myeloid cell–driven neuroinflammation and response to IFN-β therapy
Authors: Sanda Mimouna, David A. Rollins, Gayathri Shibu, Bowranigan Tharmalingam, Dinesh K. Deochand, Xi Chen, David Oliver, Yurii Chinenov, Inez Rogatsky
Journal: The Journal of Experimental Medicine (2020)

Macrophages (MФ) and microglia (MG) are critical in the pathogenesis of multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). Glucocorticoids (GCs) and interferon β (IFN-β) are frontline treatments for MS, and disrupting each pathway in mice aggravates EAE. Glucocorticoid receptor–interacting protein 1 (GRIP1) facilitates both GR and type I IFN transcriptional actions; hence, we evaluated the role of GRIP1 in neuroinflammation. Surprisingly, myeloid cell–specific loss of GRIP1 dramatically reduced EAE severity, immune cell infiltration of the CNS, and MG activation and demyelination specifically during the neuroinflammatory phase of the disease, yet also blunted therapeutic properties of IFN-β. MФ/MG transcriptome analyses at the bulk and single-cell levels revealed that GRIP1 deletion attenuated nuclear receptor, inflammatory and, interestingly, type I IFN pathways and promoted the persistence of a homeostatic MG signature. Together, these results uncover the multifaceted function of type I IFN in MS/EAE pathogenesis and therapy, and an unexpectedly permissive role of myeloid cell GRIP1 in neuroinflammation.
The Pharmacology and Toxicology of the Interferons: An Overview
Authors: G. Mannering
Journal: The Annual Review of Pharmacology and Toxicology (1986)

Heme oxygenases (HO) catabolize free heme, that is, iron (Fe) protoporphyrin (IX), into equimolar amounts of Fe2+, carbon monoxide (CO), and biliverdin. The stress-responsive HO-1 isoenzyme affords protection against programmed cell death. The mechanism ...Read More
Infectious Hepatitis
Authors: Saul Krugman
Journal: JAMA (1984)

The identification of two types of infectious hepatitis with distinctive clinical, epidemiological, and immunological features provided an explanation for the occurrence of second attacks of the disease. One type resembled classical infectious hepatitis (IH); it was characterized by an incubation period of 30 to 38 days, a relatively short period of abnormal serum transaminase activity (3 to 19 days), a consistently abnormal thymol turbidity, and a high degree of contagion. The other type resembled serum hepatitis (SH); it was characterized by a longer incubation period (41 to 108 days), a longer period of abnormal transaminase activity (35 to 200 days) and a relatively normal thymol turbidity. Contrary to commonly accepted concepts, the SH type was moderately contagious. Patients with IH type were later proved to be immune to the same type. Patients with the SH type were not immune to the IH type infection.
Die Urogenitalerkrankungen der Kinder.
Journal: JAMA (1925)

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 present status of parathyroid thermography
Authors: B. I. Samuels
Journal: JAMA (1975)

THE PURPOSES of this communication are to (1) demonstrate the usefulness of parathyroid thermography in the localization of parathyroid adenomas, (2) stress that this technique is only partly efficacious in patients with parathyroid hyperplasia, and (3) underline the advantages of this noninvasive technique and suggest that it may be acceptable as a screening procedure in patients with hypercalcemia. Because of the increased use of multiphasic screening, the need exists for a simple screening procedure in individuals with asymptomatic hypercalcemia. Although parathyroid thermography is an incompletely tested procedure, preliminary studies suggest that it may prove efficacious in the presurgical localization of parathyroid adenomas.<sup>1-4</sup> Approximately 80% to 90% of parathyroid adenomas lie in the neck, with the inferior parathyroid glands affected in more than 75%. In spite of the established efficacy of selective catheterization of the thyroid venous plexus with radioimmunoassay of the samples for parathyroid hormone concentration, the catheterization may
Efficacy of lower-limb muscle training modalities in severely dyspnoeic individuals with COPD and quadriceps muscle weakness: response from the authors
Authors: Maurice J H Sillen, Frits M E Franssen, Jeannet M L Delbressine, Anouk W Vaes, Emiel F M Wouters, Martijn A Spruit
Journal: Thorax (2014)

Efficacy of lower-limb muscle training modalities in severely dyspnoeic individuals with COPD and quadriceps muscle weakness: response from the authorsWe thank Chaplin and Latimer for their interest in the DICES study. 1 The correspondents question the validity of the power calculation, and in turn, state that we cannot conclude that high-frequency neuromuscular electrical stimulation (HF-NMES) and strength training have equivalent effects in severely dyspnoeic patients with COPD and quadriceps muscle weakness at baseline. 1 At the time of the start of the preparations of the DICES study in September 2009, we were not able to find statistical formulas where results from studies comparing two groups can be used for power calculations for three groups.Therefore, for the initial power calculation, we have used a power calculation of two groups to estimate the sample size for a three-arm study design.Initially, we did not expect a difference in change in isokinetic quadriceps peak torque between HF-NMES and strength training.A posteriori analyses revealed that an extra ±15 patients per group would be needed to detect a significant difference for the primary outcome, with HF-NMES being superior.To conclude, future trials are needed to investigate optimal strategies for exercise training in pulmonary rehabilitation for specific subgroups of patients with COPD, to enable development of exercise guidelines. 2 Based on the results of the DICES study, 1 we still believe that HF-NMES may be a good alternative for strength training in severely dyspnoeic COPD patients with quadriceps muscle weakness.