tbuckley/cabot-search huggingface dataset:
Phase II study of combination of hyperCVAD with ponatinib in frontline therapy of patients (pts) with Philadelphia chromosome (Ph) positive acute lymphoblastic leukemia (ALL).
Authors: Susan Mary O'Brien, Elias Jabbour, Deborah A. Thomas, Farhad Ravandi, Jorge E. Cortes, Naveen Pemmaraju, Tapan M. Kadia, Rebecca Garris, Vicky Jeanis, Guillermo Garcia-Manero, Gautam Borthakur, William G. Wierda, Hagop M. Kantarjian
Journal: Journal of Clinical Oncology (2014)

7064 Background: Combination of chemotherapy (CTX) with TKI is effective in the treatment of Ph+ ALL. Ponatinib is a more potent BCR-ABL inhibitor. The combination of CTX + ponatinib may be associated with better outcome. Methods: Pts with newly diagnosed Ph+ ALL received 8 cycles of hyperCVAD every 21 days. Ponatinib was given at 45 mg po daily for the first 14 days of cycle 1 then continuously for the subsequent cycles. Pts in CR received maintenance with ponatinib 45 mg po daily with vincristine/prednisone monthly for 2 yrs followed by ponatinib indefinitely. Results: 34 pts with untreated Ph+ ALL and 3 previously treated (1 course) have received a median of 6 cycles; 12 pts are receiving maintenance in CR. Median age was 51 yrs. All pts were in CR after cycle 1. CCyR rates were 94% and 100% after 1 and 2 cycles, respectively. To date, 35 pts (95%) achieved MMR and 26 (70%) CMR. MRD is negative in 35/36 (97%) pts, in whom a sample was sent for assessment. 8 pts received ASCT after a median of 4 courses. Grade ≥ 3 toxicity included infections during induction in 18 pts (49%), increased LFT’s in 13 (35%), thrombotic events in 3 (8%), myocardial infarction (MI) in 3 (8%, 2 unexplained, 1 in the context of sepsis ), skin rash in 4 (11%), and pancreatitis in 6 (16%). With a median follow up of 13 months, 31 pts are alive and in CR; 1 pt died in CR from an unrelated cardiac event after being taken off therapy and placed on imatinib, 1 from MOF (C2D13), 1 from NSTEMI (C2D41), 1 from potential MI (C4D42), 1 from head injury sustained after a fall (C4D13), and 1 from sepsis post ASCT. At the last follow-up, 7 pts (19%) are alive post ASCT; 15 pts (41%) on ponatinib at 15 mg daily in 14, and 30 mg daily in 1; Of the other 9 alive pts, 7 were switched to dasatinib, 1 was switched to imatinib, and 1 is no longer receiving treatment. The 1-year PFS and OS rates were 100% and 86%, respectively. Conclusions: Combination of hyperCVAD + ponatinib is highly effective in pts with Ph+ ALL. Due to the vascular events observed, some pts switched to alternative TKI; in the remaining, ponatinib dose was modified to 30 mg daily during consolidation with subsequent reduction to 15 mg in pts in CMR. Clinical trial information: NCT01424982.
Differences between Men and Women in Risk for Death after a Heart Attack
Journal: Annals of Internal Medicine (2001)

Summaries for Patients6 February 2001Differences between Men and Women in Risk for Death after a Heart AttackSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-134-3-200102060-00003 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail What is the problem and what is known about it so far?Acute myocardial infarction, more commonly known as heart attack, is a condition in which the blood vessels that supply blood to the heart muscle become blocked. If blood flow is blocked for long enough, a part of the heart muscle dies and is replaced by scar tissue. When large areas of the heart or special areas that control heart rhythms are involved, heart attacks can be deadly. Women younger than 60 years of age are more likely than men younger than 60 years of age to die while ... Author, Article, and Disclosure InformationAffiliations: The summary below is from the full report titled “Sex Differences in 2-Year Mortality after Hospital Discharge for Myocardial Infarction.” It is in the 6 February 2001 issue of Annals of Internal Medicine (volume 134, pages 173-181). The authors are V Vaccarino, HM Krumholz, J Yarzebski, JM Gore, and RJ Goldberg.Summaries for Patients are a service provided by Annals to help patients better understand the complicated and often mystifying language of modern medicine.Summaries for Patients are presented for informational purposes only. These summaries are not a substitute for advice from your own medical provider. If you have questions about this material, or need medical advice about your own health or situation, please contact your physician. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoSex Differences in 2-Year Mortality after Hospital Discharge for Myocardial Infarction Viola Vaccarino , Harlan M. Krumholz , Jorge Yarzebski , Joel M. Gore , and Robert J. Goldberg Metrics 6 February 2001Volume 134, Issue 3Page: I-74KeywordsBlood flowBlood vesselsDeath ratesHospitalizationsLongitudinal studiesMedical risk factorsMortalityMyocardial infarctionMyocardiumScars ePublished: 6 February 2001 Issue Published: 6 February 2001 Copyright & PermissionsCopyright © 2001 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Functional Rescue of Dystrophin-Deficient mdx Mice by a Chimeric Peptide-PMO
Authors: HaiFang Yin, Hong M. Moulton, Corinne Betts, Thomas Merritt, Yiqi Seow, Shirin Ashraf, QingSong Wang, Jordan Boutilier, Matthew J.A. Wood
Journal: Molecular Therapy (2020)

(Mol Therapy. 18, 1822–1829; October 2010) The authors have discovered that the original article has errors in Figures 1 and 4 that were introduced when a graduate student used the wrong shared image folder when putting together the figures. In the original Figure 1a, which shows expression of dystrophin-positive fibers in body-wide muscles, control images for wild-type C57 and untreated mdx mice were repeatedly used instead of the right images corresponding to the mice used for this manuscript. The control images have been replaced and a corrected Figure 1a now appears below. In the original Figure 4b, which shows histological staining of liver and kidney, control images for wild-type C57 and untreated mdx mice (kidney) were repeatedly used instead of the right images corresponding to the mice used for this manuscript. The control images have been replaced and a corrected Figure 4b now appears below. These corrections do not change the conclusions of the paper and the authors apologize for the error and any confusion they may have caused.Figure 4bInvestigation of systemic immunotoxicity in mdx mice treated with the multiple B-MSP-PMO conjugate administrationView Large Image Figure ViewerDownload Hi-res image Download (PPT) Functional Rescue of Dystrophin-deficient mdx Mice by a Chimeric Peptide-PMOYin et al.Molecular TherapyOctober, 2010In BriefSplice modulation using antisense oligonucleotides (AOs) has been shown to yield targeted exon exclusion to restore the open reading frame and generate truncated but partially functional dystrophin protein. This has been successfully demonstrated in dystrophin-deficient mdx mice and in Duchenne muscular dystrophy (DMD) patients. However, DMD is a systemic disease; successful therapeutic exploitation of this approach will therefore depend on effective systemic delivery of AOs to all affected tissues. Full-Text PDF Open Archive
THE USE AND ABUSE OF EXPERT MEDICAL AND SURGICAL TESTIMONY AND SOME RECOMMENDATIONS FOR INCREASING THE VALUE OF SUCH TESTIMONY.
Authors: ROBERT MATHER
Journal: JAMA (1897)

Expert testimony has no logical place in the common law theory of trial by jury. The admission of it, indeed, violates one of the cardinal principles on which the system is founded. The legitimate function of testimony in courts of law is to make known the facts relative to the cause in controversy. Inasmuch as these facts in general rest in the knowledge and recollection of persons, the ordinary medium for the ascertainment of them is the living witness. Owing to the infirmities of human nature, it results that the facts made known in a legal controversy through this medium are often, if not always, uncertain, confusing and contradictory. To deduce from this mass of uncertainty, confusion and contradiction a just conclusion as to the truth of the matter is the proper province of the jury. It is the theory of the law that in the process by which the
Fate of the human liver after hemihepatic portal vein embolization: Cell kinetic and morphometric study.
Authors: H Harada
Journal: Hepatology (1997)

The favorable therapeutic effect of preoperative portal vein embolization (PVE) was analyzed by assessing various volumetric, cell kinetic and morphometric parameters and examining histologically the embolized and nonembolized lobes of 15 patients who underwent extended right lobectomy 2 to 3 weeks after PVE. Each lobar volume was calculated from computed tomography (CT) images, hepatocyte proliferation was evaluated by assessing proliferative cell nuclear antigen (PCNA) expression and mitosis, hepatocyte apoptosis was evaluated by the terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and the hepatocyte numerical density as well as the sinusoidal volumetric ratio (Vvs) and the mean hepatocyte volume (Cv) were calculated using morphometric methods. PVE induced hepatocyte apoptosis and atrophy of the embolized lobe (from 798 +/- 213 to 708 +/- 222 cm3; P < .05). The increased sinusoidal volume in this lobe (17.7% +/- 4.5% and 21.7% +/- 5.7%, periportal and pericentral area, respectively) may have been attributable to hepatocyte deletion. Cells in the nonembolized lobe entered a highly active phase of proliferation within 2 weeks after PVE. Further evidence of cellular proliferation was provided by the increased nonembolized lobar volume (from 379 +/- 132 to 545 +/- 130 cm3; P < .01) and numerical density of hepatocyte nuclei (Nv) (5.38 +/- 1.26 vs. 3.11 +/- 0.85 x 10(5)/mm3; P < .01, nonembolized vs. embolized lobe, respectively). In conclusion, these results indicate that the favorable effect of PVE is attributable to a net gain of functional hepatocyte mass and/or early induction of hepatocyte proliferation following hepatectomy.
HIV Treatment Guidelines
Journal: JAMA (1999)

In response to the rapidly changing treatment options for HIV, the Federal government issued draft guidelines for using HIV drugs in adults and adolescents. The main points of the new guidelines are described. No study has yet definitively determined the best time to start anti-HIV treatment, although the drugs have been shown to help people with AIDS live longer. People with AIDS or symptomatic HIV should begin treatment immediately, monitoring progress through viral load and T4 cell testing. Viral load and T4 cell counts, used to measure progress in reducing the amount of HIV in the body to the lowest possible levels for the longest time, are described. For maximum antiviral action, combination therapy is recommended, using two nucleoside analog reverse transcriptase inhibitors with a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor. Guidelines are given for determining when a treatment should be changed or discontinued. Anti-HIV treatments in pregnant women should be based on the health of the mother.
Defensive Medicine
Authors: Clifford L. Graves
Journal: JAMA (1974)

<h3>To the Editor.—</h3> Mr. Bergen seems to think that a doctor need only order plenty of tests to keep out of trouble. It isn't as simple as that. A patient has a lump in the breast. You are sure it is benign. Normally, you would leave it alone. But you can't do that any more because if the patient should develop cancer in that breast at any time in the future, the doctor can be sued for negligence. It's happening to a friend of mine right now—even though three years elapsed between the time he saw the patient and the appearance of the cancer. So you take out all lumps. Good medicine? No. A patient has a bellyache. It could be appendicitis, and it could be a gas bubble. Normally, you would watch. But you can't do that any more because if the patient should develop appendicitis while you are
Abstract 3185: CAR-T cells can eradicate human uveal melanoma and immune-therapy resistant malignant melanoma in IL-2 transgenic NOD/SCID IL2 receptor gamma knockout mice
Authors: Elin Forsberg, Mattias Lindberg, Henrik Jespersen, Samuel Alsén, Roger Olofsson Bagge, Marco Donia, Inge Marie Svane, Ola Nilsson, Lars Ny, Lisa Nilsson, Jonas Nilsson
Journal: Cancer Research (2019)

Abstract Immune therapies including checkpoint blockade and adoptive T cell transfer show great promise for the treatment of melanoma, with long-term effects in some patients. However, not all patients respond to current immune therapies and are in need of other treatment strategies. For example, around half of the patients with metastatic malignant melanoma will not be cured with available therapies today. For metastatic uveal melanoma (a rare melanoma of the eye) available immune therapies have less effect, and there is currently no approved therapy for these patients. Our objective is to find novel immune therapies with the potential to treat immune-therapy resistant melanoma, with the use of chimeric antigen receptor T cells (CAR-T). So far, no CAR-T therapy is approved for use in solid tumors. We have previously developed a humanized mouse model, where tumor cells and T cells from the same patient are grafted in IL-2 transgenic NOD/SCID IL2 receptor gamma knockout (NOG) mice, and found that responses in the mouse model correlated to responses in the corresponding patients in a clinical trial of adoptive T cell transfer (Jespersen et al, Nature Communications, 2017). In order to test the potential for CAR-T therapy in immune-therapy resistant melanoma in this mouse model, we used TCGA to determine the expression in melanoma biopsies of targets for commercially available CAR-T cells. Interestingly, we were able to use this model to treat immune-therapy resistant malignant melanoma and uveal melanoma patient-derived xenografts with human CAR-T cells and obtain curative responses, but only in IL-2 transgenic mice and not in regular NOG mice. These findings prove potential for the use of CAR-T cell therapy in immune-therapy resistant melanoma, and indicate the utility of this mouse model in the translation of CAR-T therapies. We are currently working on the development of CAR-T cells derived from patient-specific T cells. Citation Format: Elin Forsberg, Mattias Lindberg, Henrik Jespersen, Samuel Alsén, Roger Olofsson Bagge, Marco Donia, Inge Marie Svane, Ola Nilsson, Lars Ny, Lisa Nilsson, Jonas Nilsson. CAR-T cells can eradicate human uveal melanoma and immune-therapy resistant malignant melanoma in IL-2 transgenic NOD/SCID IL2 receptor gamma knockout mice [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 3185.
Authors’ Reply
Authors: Tadao Akizawa, Manabu Iwasaki, Yusuke Yamaguchi, Yoshikatsu Majikawa, Michael Reusch
Journal: Journal of the American Society of Nephrology (2021)

In a letter to the editor regarding the recently published article titled "Phase 3, randomized, double-blind, active-comparator (darbepoetin alfa) study of oral roxadustat in CKD patients with anemia on hemodialysis in Japan,"[1][1] Liu et al. [2][2] note that our manuscript does not provide
The Yale Students' Infirmary.
Journal: JAMA (1892)

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
SYMPOSIUM ON THE THERAPY OF RHEUMATIC DISEASES: Aix-les-Bains, France, June, 1964
Journal: Annals of the Rheumatic Diseases (1964)

DR. WEST: The only patient I can recollect was one who had been on cortisone and then prednisolone for 6 to 7 years and who had only just started ACTH.I do not think that we have had any in-patients on long-term ACTH therapy.Measurement of Effective Concentrations of Cortisol available to Cells affected by Rheumatic Diseases.The renal handling of cortisol was studied in the hope of deducing the effective (non-protein bound) plasma con- centration from the amount filtered in the kidney and the G.F.R.The passive tubular reabsorbtion could easily be allowed for, but it was difficult to account for or eliminate the cortisol that was specifically reabsorbed- which under standardized morning conditions was approximately 80 per cent.Corticosterone was found copyright.
A CASE OF HEREDITARY GLAUCOMA.
Authors: HERBERT HARLAN
Journal: JAMA (1898)

Before this Section, at the New Orleans meeting in 1885, I reported a case of glaucoma, the patient being one of the fifth successive generation in which the disease had appeared. That case, C. E. B., aged 17, consulted me in March of that year. The following is the family history taken from the previous report: ''Her mother, who accompanied her, is 49 years and absolutely blind. Both anterior chambers are obliterated and the pupils closed. She states that at 19 her eyesight began gradually to waste away. She saw halos around the lamp. A year later she had inflammation in the eyes which the doctors called cold and treated with drops and blisters. After a while the eyes got better. Then another attack of inflammation came on, and she has been blind ever since. Never at any time was there much pain. The mother's father lost his eyes in the
Anaphylaxis
Authors: Bruce S. Bochner, Lawrence M. Lichtenstein
Journal: New England Journal of Medicine (1991)

SYSTEMIC anaphylaxis represents the most dramatic and potentially catastrophic manifestation of immediate hypersensitivity. This syndrome can affect virtually any organ in the body, although reactions involving the pulmonary, circulatory, cutaneous, neurologic, and gastrointestinal systems are the most common. Reactions range widely in severity from mild pruritus and urticaria to shock and death. Despite recent advancements in our understanding of the mechanisms and mediators involved in these events, the typically explosive and unforeseen nature of severe reactions often hampers treatment. As a result, anaphylaxis occurs in the United States at rates estimated to be as high as once in every 3000 . . .
The Neostriatal Mosaic: Multiple Levels Of Compartmental Organization In The Basal Ganglia
Authors: C. Gerfen
Journal: Annual Review of Neuroscience (1992)

The brain's default mode network consists of discrete, bilateral and symmetrical cortical areas, in the medial and lateral parietal, medial prefrontal, and medial and lateral temporal cortices of the human, nonhuman primate, cat, and rodent brains. Its ...Read More
Book Listings
Journal: Annals of Internal Medicine (2001)

Book Listings21 August 2001Book ListingsSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-135-4-200108210-00001 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Alternative MedicineAlternative and Complementary Treatment in Neurologic IllnessMI Weintraub, ed. 325 pages. Philadelphia: WB Saunders; 2001. $45.00. ISBN 0443065586. Order phone 215-238-7800.Clinician's Guide to Holistic MedicineRA Anderson. 421 pages. New York: McGraw-Hill; 2001. $35.00. ISBN 0071347143. Order phone 800-262-4729.Health Care and Spirituality: Listening, Assessing, CaringRB Gilbert, ed. 313 pages. Amityville, NY: Baywood; 2001. $37.00. ISBN 0895032503. Order phone 800-638-7819.Integrated Cancer Care: Holistic, Complementary, and Creative ApproachesJ Barraclough, ed. 292 pages. New York: Oxford Univ Pr; 2001. $45.00. ISBN 0192630954. Order phone 800-451-7556.CardiologyAtrial Flutter: From Mechanism to TreatmentAL Waldo. 64 pages. Armonk, NY: Futura; 2001. ... Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 21 August 2001Volume 135, Issue 4Page: B1KeywordsComputed axial tomography ePublished: 21 August 2001 Issue Published: 21 August 2001 Copyright & PermissionsCopyright © 2001 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Silent retroperitoneal fibrosis associated with methysergide therapy
Authors: A. H. Elkind
Journal: JAMA (1968)

Intravenous urography was performed in 114 asymptomatic patients who had been treated with methysergide maleate for six months or longer. There were 13 abnormal urograms; 5 revealed congenital anomalies, and 5 showed medial deviation of the ureter but no other abnormalities. In three there was the characteristic picture of retroperitoneal fibrosis; two of these showed marked roentgenographic improvement after methysergide therapy was stopped, while in the third there was only partial improvement. Withdrawal of methysergide did not affect the medial deviation of the ureter. We recommend that a urogram be obtained at the start of methysergide therapy, and that urography be repeated at six-month intervals during therapy. Early recognition of silent ureteral obstruction may prevent renal damage, since the fibrosis usually regresses with drug withdrawal.
Plasma cell dyscrasias and cryoglobulins
Authors: K. J. Bloch
Journal: JAMA (1982)

<h3>PLASMA CELL DYSCRASIAS</h3> SEVERAL disorders characterized by the uncontrolled monoclonal proliferation of cells synthesizing antibody (immunoglobulin) are generally included in the group of plasma cell dyscrasias. Their morphological and clinical features, taken together with the type of protein produced by the neoplastic cells, permits their grouping into the three following major categories: (1) multiple myeloma, IgG, A, D, and E; (2) Waldenström's macroglobulinemia, IgM; and (3) heavy-chain diseases, gamma, alpha, and mu. A closely related variant, now more frequently encountered due to the widespread use of serum protein electrophoresis, is benign monoclonal gammopathy, a condition in which a serum protein abnormality is noted in the absence of a significant plasma cell neoplasm. As is true of most other neoplasms, the etiology of these tumors remains unknown. <h3>Multiple Myeloma—Clinical Picture</h3> Multiple myeloma, the most common of the plasma cell dyscrasias, is characterized by the infiltration of the marrow by neoplastic plasma