tbuckley/cabot-search huggingface dataset:
Review of the Health Effects of Sulfur Oxides
Authors: David P. Rall
Journal: Environmental Health Perspectives (1974)

The pollution in the air is a complex mixture of chemical substances of varying toxicity of which the sulfur oxides are a principal component. Those components which pose the primary hazards to human health have not yet been fully identified, nor have their respective contributions to human disease been fully determined. Efficient and effective control strategies are dependent upon the identification and understanding of these toxic components. Ultimately, the goal of standard-setting should be the development of composite pollution indices rather than control of individual pollutants.Concentrations of SO2 in the ambient air twice the current standards are associated with adverse health effects. A considerable body of evidence suggests that there may be discernible human health effects from exposure to concentrations approximating the current standards. There is therefore no basis for relaxation of the present standards for sulfur oxides at this time. Since the scientific basis for this judgment is incomplete, further scientific information will be required either to validate the present standards or to justify alteration of these standards.
session C: early and advanced breast cancer
Authors: Fabio Puglisi, Enrico Pegolo, Cinzia Puppin, Claudia Andreetta, Stefania Russo, Gaetano Pascoletti, Alessandro Minisini, Mauro Mansutti, Barbara Alessi, Giovanni Cardellino, Andrea Piga, Gianpiero Fasola, Carla Di, Paolo Marchetti, Federica Mazzuca, M Ionta, S Barni, F Atzori, M Cremonesi, A Trogu, B Frau, M Murgia, L Minerba, B Massidda, Polimeni Ma, P Matera, I Lista, R Facilissimo, Dubois Rw
Journal: Annals of Oncology (2007)
MISCELLANY.
Journal: JAMA (1890)

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
Department of Error
Authors: Edward Carr, Mary Wu, Ruth Harvey, Roseanne Billany, Emma Wall, Gavin Kelly, Covid-19 Consortium, Michael Howell, George Kassiotis, Charles Swanton, Sonia Gandhi, David Bauer, Matthew Graham-Brown, Rachel Jones, Rona Smith, Stephen Mcadoo, Michelle Willicombe, Rupert Beale
Journal: The Lancet (2022)
NFB-14. PSYCHOSOCIAL OUTCOMES IN CHILDREN WITH NEUROFIBROMATOSIS TYPE 1 AND PLEXIFORM NEUROFIBROMAS
Authors: Sudarshawn Damodharan, Paige Mission, Diane Puccetti
Journal: Neuro-Oncology (2020)

Abstract OBJECTIVE This case series seeks to examine neurocognitive outcomes, social-emotional functioning, and family burden in young children diagnosed with Neurofibromatosis, type 1 (NF1) with early growing plexiform neurofibromas (PNFs). BACKGROUND Neurofibromatosis, type 1 (NF1) is a common predisposing chronic disease arising in early childhood, with an incidence of approximately 1:3000. Though NF1 displays a wide range of phenotypic variability, the primary feature of the disease is peripheral nerve sheath tumors called neurofibromas. Less is well known regarding the broader neurocognitive and social-emotional profile in presentations with more complex tumor growths, namely PNFs, which are present in at least half of the NF1-affected population. METHODS Participants with NF1 and PNFs (n=2) aged 6-7years completed comprehensive neuropsychological evaluations and parents completed measures of quality of life, social-emotional/behavioral functioning of child, parental stress, family adaptability, and family cohesion. RESULTS Outcomes suggest broad neurocognitive dysfunction (e.g., executive functioning deficits, attention problems, visual-motor delays, and poor motor coordination), social-emotional challenges (e.g., symptoms of anxiety and depression, and poor social skills), and familial distress. CONCLUSIONS Findings indicate the value of early and frequent monitoring of children with PNFs in medical systems and multi-disciplinary teams, and the importance of early intervention for both children and families.
Bioactive glass selectively promotes cytotoxicity towards giant cell tumor of bone derived neoplastic stromal cells and induces MAPK signalling dependent autophagy
Authors: Joerg Fellenberg, Sarina Losch, Burkhard Lehner, Marcela Arango-Ospina, Aldo R. Boccaccini, Fabian Westhauser
Journal: Bioactive Materials (2022)

Giant cell tumors of bone (GCTB) are associated with massive bone destructions and high recurrence rates. In a previous study, we observed cytotoxic effects of three different compositions of bioactive glasses (BGs) towards GCTSC but not bone marrow derived stromal cells (BMSC) indicating that BGs represent promising candidates for the development of new therapeutic approaches. In the current study we aimed to investigate the molecular mechanisms that are involved in BG induced cytotoxicity. We observed, that BG treatment was not associated with any signs of apoptosis, but rather led to a strong induction of mitogen activated protein kinases (MAPK) and, as a consequence, upregulation of several transcription factors specifically in GCTSC. Genome wide gene expression profiling further revealed a set of fifteen genes that were exclusively induced in GCTSC or induced significantly stronger in GCTSC compared to BMSC. BG treatment further induced autophagy that was significantly more pronounced in GCTSC compared to BMSC and could be inhibited by MAPK inhibitors. Together with the known osteogenic properties of BGs our findings support the suitability of BGs as therapeutic agents for the treatment of GCTB. However, these data have to be verified under in vivo conditions.
Book Review Erdmann's Clinics . Stenographic Reports of the Clinics of John F. Erdmann, M.D., F.A.C.S., Professor of Surgery in Columbia University; Executive Officer in the Department of Surgery, New York Post-Graduate Medical School; Director of the Department of Surgery, New York Post-Graduate Hospital. Edited by J. William Hinton, M.D., F.A.C.S., Associate Professor of Surgery, New York Post-Graduate Medical School (Columbia University); Associate Visiting Surgeon to Bellevue Hospital, New …
Journal: New England Journal of Medicine (1933)
Lost in metrication
Authors: S. Vaisrub
Journal: JAMA (1977)

Old-times who trained before the metric era caught up with medicine remember well how difficult it was to adapt to the early inroads of the metric system. With drams, ounces, minims, and grains ingrained in the mind, it was a struggle to engram into it grams, milligrams, and cubic centimeters. Conversions were a chore. But the metric system was the wave of the future, and to resist its onward surge was patently futile. It was equally futile to resist its lateral motion when milliequivalents began to replace milligrams percent. This too was taken in stride as a necessary step in the march of progress. In grappling with the metric system, the physician could not count on sympathy from the layman to whom the old English units of prescribed drugs meant little. The patient about to receive a hypodermic injection of morphine could not care less whether the dose was 1/4
Therapeutic Success in Paget Disease
Journal: JAMA (1973)

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
New Medical College.
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
Env-independent protection of intrarectal SIV challenge by vaccine induction of Gag/Vif-specific CD8+ T cells but not CD4+ T cells
Authors: Hiroshi Ishii, Kazutaka Terahara, Takushi Nomura, Midori Okazaki, Hiroyuki Yamamoto, Tsugumine Shu, Hiromi Sakawaki, Tomoyuki Miura, David I. Watkins, Tetsuro Matano
Journal: Molecular Therapy (2022)

Effective T cell induction is an important strategy in HIV-vaccine development. However, it has been indicated that vaccine-induced HIV-specific CD4+ T cells, the preferential targets of HIV infection, might increase viral acquisition after HIV exposure. We have recently developed an immunogen (CaV11), tandemly connected overlapping 11-mer peptides spanning the simian immunodeficiency virus (SIV) Gag capsid and Vif proteins, to selectively induce Gag- and Vif-specific CD8+ T cells but not CD4+ T cells. Here, we show protective efficacy of a CaV11-expressing vaccine against repeated intrarectal low-dose SIVmac239 challenge in rhesus macaques. Eight of the twelve vaccinated macaques were protected after eight challenges. Kaplan-Meier analysis indicated significant protection in the vaccinees compared to the unvaccinated macaques. Vaccine-induced Gag-specific CD8+ T cell responses were significantly higher in the protected than the unprotected vaccinees. These results suggest that classical CD8+ T cell induction by viral Env-independent vaccination can confer protection from intrarectal SIV acquisition, highlighting the rationale for this immunogen design to induce virus-specific CD8+ T cells but not CD4+ T cells in HIV-vaccine development. Effective T cell induction is an important strategy in HIV-vaccine development. However, it has been indicated that vaccine-induced HIV-specific CD4+ T cells, the preferential targets of HIV infection, might increase viral acquisition after HIV exposure. We have recently developed an immunogen (CaV11), tandemly connected overlapping 11-mer peptides spanning the simian immunodeficiency virus (SIV) Gag capsid and Vif proteins, to selectively induce Gag- and Vif-specific CD8+ T cells but not CD4+ T cells. Here, we show protective efficacy of a CaV11-expressing vaccine against repeated intrarectal low-dose SIVmac239 challenge in rhesus macaques. Eight of the twelve vaccinated macaques were protected after eight challenges. Kaplan-Meier analysis indicated significant protection in the vaccinees compared to the unvaccinated macaques. Vaccine-induced Gag-specific CD8+ T cell responses were significantly higher in the protected than the unprotected vaccinees. These results suggest that classical CD8+ T cell induction by viral Env-independent vaccination can confer protection from intrarectal SIV acquisition, highlighting the rationale for this immunogen design to induce virus-specific CD8+ T cells but not CD4+ T cells in HIV-vaccine development.
RTID-01. RADIOSURGERY FOLLOWED BY TUMOR TREATING FIELDS FOR BRAIN METASTASES (1-10) FROM NSCLC IN THE PHASE 3 METIS TRIAL
Authors: Minesh Mehta, Vinai Gondi, Paul Brown, Manmeet Ahluwalia
Journal: Neuro-Oncology (2020)

Abstract BACKGROUND Tumor Treating Fields (TTFields) are non-invasive, loco-regional, anti-mitotic treatment modality comprising alternating electric fields. TTFields have demonstrated efficacy in preclinical non-small cell lung cancer (NSCLC) models. TTFields treatment to the brain was safe and extended overall survival in newly-diagnosed glioblastoma. The objective of the METIS study [NCT02831959] is evaluation of the efficacy and safety of TTFields in NSCLC patients with brain metastases. METHODS NSCLC patients (N=270) with 1-10 brain metastases were randomized 1:1 to stereotactic radio surgery (SRS) followed by continuous TTFields ((150 kHz, &amp;gt; 18 hours/day) within 7 days of SRS or supportive care. The portable device delivered TTFields to the brain using 4 transducer arrays, while patients received the best standard-of-care for systemic disease. Patients were followed every two months until second intracranial progression. Key inclusion criteria: KPS ≥70, new diagnosis of 1 inoperable or 2–10 supra- and/or infratentorial brain metastases from NSCLC amenable to SRS; and optimal therapy for extracranial disease. Prior WBRT, surgical resection of metastases, or recurrent brain metastases were exclusionary. Primary endpoint was time to 1st intracranial progression. Secondary endpoints included time to neurocognitive failure (HVLT, COWAT and TMT), overall survival, radiological response rate (RANO-BM and RECIST V1.1); quality-of-life; adverse events; time to first/second intracranial progression for patients with 1–4 and 5–10 brain metastases; bi-monthly intracranial progression rate from 2–12 months; and time to second intracranial and distant progression. The sample size (N=270) was calculated using a log-rank test (Lakatos 1988 and 2002) with 80% power at two sided alpha of 0.05 to detect a hazard ratio of 0.57. On September, 2019, an independent Data Monitoring Committee (DMC) reviewed METIS trial data collected to that point. The DMC concluded that no unexpected safety issues had emerged and recommended continuation of the METIS study as planned.
Phase I Clinical and Pharmacodynamic Evaluation of Oral CI-1033 in Patients with Refractory Cancer
Authors: Ralph G. Zinner, John Nemunaitis, Irene Eiseman, Hyung Ju C. Shin, Stephen C. Olson, James Christensen, Xin Huang, Peter F. Lenehan, Nicholas J. Donato, Dong M. Shin
Journal: Clinical Cancer Research (2007)

To determine the tolerability and pharmacokinetics of CI-1033 given daily for 7 days of a 21-day cycle. Tumor response and changes in erbB receptor tyrosine kinase activity in tumor and skin tissue were examined, and modulation of potential biomarkers in plasma was explored.This was a dose-finding phase I study in patients with advanced solid malignancies. Patients were evaluated for safety, pharmacokinetics, and tumor response. Pharmacodynamic markers, such as Ki67, p27, and erbB receptor status, were assessed in tumor and skin tissue using immunohistochemical and immunoprecipitation methodologies. Plasma biomarkers HER2, vascular endothelial growth factor, interleukin-8, and matrix metalloproteinase-9 were evaluated using immunologic techniques.Fifty-three patients were enrolled in the study. Dose-limiting toxicity (emesis, persistent rash, and mouth ulcer) was observed at 750 mg. The maximum tolerated dose was 650 mg. There were no confirmed objective responses. CI-1033 treatment showed down-regulation of epidermal growth factor receptor, HER2, and Ki67 in a variety of tumor tissues and up regulation of p27 in skin tissue. Plasma HER2 was reduced following CI-1033 administration, but no consistent change in vascular endothelial growth factor, interleukin-8, or matrix metalloproteinase-9 was noted. CI-1033 plasma concentrations were proportional to dose.The safety and pharmacokinetic profile of CI-1033 was favorable for multidose oral administration. Evidence of modulation of erbB receptor activity in tumor and skin tissue was accompanied by changes in markers of proliferation and cell cycle inhibition. Additional clinical trials are warranted in defining the role of CI-1033 in the treatment of cancer and further assessing the utility of antitumor markers.
Nederlands Tijdschr Geneeskunde, Amsterdam
Journal: JAMA (1964)

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
Lead-Poisoning and Lead Absorption.
Journal: JAMA (1913)

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
Loss of ATRX suppresses anti-tumor immunity
Authors: Aaron A Diaz
Journal: Neuro-Oncology (2022)

Alpha-thalassemia/mental retardation syndrome X-linked (ATRX) is a chromatin-modifying enzyme that suffers from loss-of-function in most isocitrate dehydrogenase (IDH)-mutant astrocytomas.ATRX has long been recognized as a chaperone for histone core H3.3, a variant associated with heterochromatin and enriched in telomeres. 1ATRX mutations correlate with telomere lengthening via the alternative lengthening of telomeres (ALT) pathway in several cancers, where it appears ATRX loss is necessary but not sufficient for ALT. 2 ATRX loss also inhibits DNA-damage repair, 3 as H3.3 likewise plays a role during strand synthesis.However, while histone H3.3 is also deposited throughout the genome, 4 less is known about the impact of ATRX mutations on gene expression.In this issue, Hu et al 5 show that ATRX knockdown (KD) induces an immunosuppressive gene expression program in IDH-mutant glioma, including the upregulation of the immune-checkpoint programmed death-ligand 1 (PD-L1) and the secretion of immunosuppressive cytokines.Cytokine expression in ATRX-KD gliomas was further enhanced by chemo-radiation.ATRX-KD cells were more resistant to T-cell killing in vitro and induced T-cell apoptosis at significantly higher rates than controls.These effects could be abrogated, however, by pre-treatment with anti-PD-L1 antibodies.Likewise, elaborated contact with ATRX-KD cells polarized macrophages toward an M2 expression program.Macrophages treated with conditioned media from ATRX-KD cells inhibited T-cell proliferation.In vivo, ATRX-KD gliomas continued to over-express PD-L1 and the immunosuppressive cytokines observed in vitro.Orthotopic ATRX-KD tumors were more heavily infiltrated by macrophages.Moreover, macrophages in ATRX-KD tumors expressed higher levels of arginase and immunosuppressive cytokines.PD-L1 and cytokine expression could be regressed in ATRX-KD gliomas by targeting bromo-and extra-terminal (BET) family proteins, epigenetic readers of acetylated lysine residues.This suggests that whatever chromatin remodeling is induced by ATRX-KD, it leads to increased activity of DNA enhancers of PD-L1 and specific immunosuppressive cytokines.These results dovetail with recent findings from our laboratory and others which show that ATRX loss in glioma, 6 Overall survival