tbuckley/cabot-search huggingface dataset:
Three Transactions on the Cerebrum: A Posthumous Work
Journal: JAMA (1941)

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 epidemiology of disease expenses. The costs of caring for children with cancer
Authors: B. S. Bloom
Journal: JAMA (1985)

We determined medical costs and family out-of-pocket expenses over time for 569 children with malignant neoplasms. All medical charges (inpatient and outpatient), family out-of-pocket expenses, and wages lost were collected and annualized. The mean cost of cancer care and treatment per patient-year was $29,708, with variation by diagnosis, prognosis, and year since diagnosis. The mean annual hospital inpatient cost was $15,455; mean ambulatory care cost, $3,806; and family out-of-pocket disease-related expenses, $9,787. Family out-of-pocket expenses added about 50% to the total cost of disease-related care and consumed 38% of gross annual family income; wages lost accounted for nearly half. About 95% of all medical costs was paid by private, public, or charitable payers. Out-of-pocket medical expenses for which the family was responsible were about $1,000 each year. However, all nonmedical, disease-related expenses were borne by the family. (<i>JAMA</i>1985;253:2393-2397)
Dose equivalence of drugs for asthma.
Authors: J Lotvall, N Svedmyr
Journal: BMJ (1993)

which suggests that these tumours may be difficult to palpate.We were alarmed at the proportion of cases of pyloric stenosis in Macdessi and Oates's study in which clinical diagnosis was preceded by imaging (31% during 1988-91).Surely the practice in most paediatric units is to emphasise to students and juniors that pyloric stenosis should be diagnosed clinically, with imaging being reserved for difficult diagnoses.The number of barium examinations performed was just as alarming, and we question why these were performed.In our study no barium examinations were required to make the diagnosis.Finally, ultrasound imaging should be performed at the cotside immediately after the abdominal examination.Our policy is to perform both these assessments together to make a rapid diagnosis in the presence of the parents and hence alleviate parental anxieties.Over the years we have found that our juniors' ability to palpate pyloric tumours has improved as they are disappointed if the ultrasound scan proves them wrong.
NRG Oncology/NSABP B-51/RTOG 1304: Phase III trial to determine if chest wall and regional nodal radiotherapy (CWRNRT) post mastectomy (Mx) or the addition of RNRT to breast RT post breast-conserving surgery (BCS) reduces invasive breast cancer recurrence free interval (IBCRFI) in patients (pts) with positive axillary (PAx) nodes who are ypN0 after neoadjuvant chemotherapy (NC).
Authors: Eleftherios P. Mamounas, Hanna Bandos, Julia R. White, Thomas B. Julian, Atif J. Khan, Simona Flora Shaitelman, Mylin Ann Torres, Frank Vicini, Patricia A. Ganz, Susan Ann McCloskey, Soonmyung Paik, Nilendu Gupta, X. Allen Li, Dominic J. DiCostanzo, Joseph P. Costantino, Walter John Curran, Norman Wolmark
Journal: Journal of Clinical Oncology (2016)

TPS1097 Background: This phase III post-NC trial evaluates if CWRNRT post-Mx or whole breast irradiation (WBI) with RNRT after BCS significantly reduces the IBCR-FI rate in pts with PAx nodes that are negative after NC. Secondary aims are OS, LRR-FI, DRFI, DFS-DCIS, second primary cancer, and comparison of RT effect on cosmesis in reconstructed Mx pts. Correlative science examines RT effect by tumor subtype, molecular outcome predictors for residual disease pts, and predictors for the degree of reduction in loco-regional recurrence. Methods: Clinical T1-3, N1 IBC PAx nodes (FNA or core needle biopsy) pts complete ≥ 12 wks of NC (anthracycline and/or taxane). HER2+ pts receive anti-HER2 therapy (tx). Following NC BCS or Mx, sentinel node biopsy ( ≥ 3 nodes) and/or Ax dissection with histologically negative nodes is performed. ER/PR and HER-2neu status before NC required. Pts receive required systemic tx. Radiation credentialing with a facility questionnaire/case benchmark required. Randomization for Mx pts is to no CWRNRT or CWRNRT and for BCS pts to WBI or WBI RNRT. Statistics: 1636 pts to be enrolled over 5 yrs (definitive analysis at 7.5 yrs). Study is powered at 80% to test that RT reduces the annual hazard rate of events for IBCR-FI by 35% for an absolute risk reduction of 4.6% (5 yr cumulative rate). Intent-to-treat analysis with 3 interim analyses (43, 86, and 129 events) and a 4th/final analysis at 172 events. Pt-reported outcomes focusing on RT effect will be provided by 736 pts before randomization and at 3, 6, 12, and 24 mos. Accrual as of 1/29/16 is 266. (Drs. G Unzeitig, Doctor's Hospital of Laredo, J Stromberg, Beaumont Hospital, T Muanza, Jewish General Hospital, and W Warlick, Novant Health Presbyterian Medical Center, are acknowledged for high accrual.) Contacts: Questions: NRG Oncology Pgh Clin Coord Dpt: 1-800-477-7227 or ccd@nsabp.org. Support: U10 CA-2166; -180868, -180822; 189867; Elekta Clinical trial information: NCT01872975.
Therapeutics
Journal: JAMA (1918)

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
Norepinephrine induces apoptosis in neonatal rat cardiomyocytes through a reactive oxygen species?TNF$alpha;?caspase signaling pathway
Authors: Y FU
Journal: Cardiovascular Research (2004)

Objective: Norepinephrine (NE)-induced apoptosis in cardiomyocytes is an important cause of heart failure. Previous studies revealed that reactive oxygen species (ROS) are involved in apoptosis. Tumor necrosis factor-α (TNF), a well-known mediator that stimulates apoptosis, is not only produced by macrophages but also by cardiomyocytes. Until now, the role of TNF and its relationship to ROS in NE-induced apoptosis of cardiomyocytes have never been investigated. Methods: Neonatal rat cardiomyocytes were treated with various concentrations of NE. Apoptosis of cardiomyocytes was determined using the TUNEL assay. The level of secreted TNF was measured by ELISA and TNF mRNA expression was determined by semiquantitative reverse transcriptional polymerase chain reaction. Caspase activity was measured by a fluorogenic protease assay kit. Anti-TNF antibodies, caspase inhibitors and antioxidants (N-acetyl-l-cysteine or vitamin C) were added to determine if they could inhibit the apoptotic effect of NE. Results: NE induced apoptosis of cardiomyocytes in a dose- and time-dependent manner. NE up-regulated TNF mRNA expression and increased TNF secretion and caspase-2,-3,-6, and -9 activities. A neutralizing anti-TNF antibody and caspase-2 and -3 inhibitors significantly attenuated NE-induced apoptosis. Antioxidants completely abrogated NE-induced TNF secretion, caspase activation, and apoptotic death. Conclusion: NE induced apoptosis in neonatal rat cardiomyocytes through a ROS–TNF–caspase signaling pathway.
SOME DIFFICULTIES IN THE DIAGNOSIS OF OSTEOSARCOMA
Journal: JAMA (1920)

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
Risk of solid cancer after treatment for testicular germ cell cancer in the platinum era.
Authors: Michael Schaapveld, Harmke Groot, Sjoukje Lubberts, Ronald De Wit, Alfred Witjes, Jan M. Kerst, Igle Jan de Jong, Gerard Groenewegen, Alfonsus Johannes Maria van den Eertwegh, Philip Poortmans, Heinz Josef Klümpen, Hetty Berg, van de, Tineke Jacoba Smilde, Ben Vanneste, Maureen J.B. Aarts, Luca Incrocci, Alphonsus C.M. Van Den Bergh, Simon Horenblas, Jourik A. Gietema, Flora Van Leeuwen
Journal: Journal of Clinical Oncology (2018)

10069 Background: Testicular cancer (TC) treatment has been associated with increased risks of subsequent malignant neoplasms (SMNs). It is unknown whether changes in TC treatment over time have affected SMN risk. Methods: Solid SMN risk was evaluated in a multicenter cohort, comprising 5,848 one-year survivors treated for TC before age 50 years, between 1976-2007. SMN incidence was compared with cancer incidence in the general population. Cumulative incidences were estimated and treatment-specific risks were assessed using multivariable regression in a case-cohort design. Results: After a median follow-up of 14.1 years (interquartile range: 9.3-20.1 years) 350 solid SMNs were observed, translating into a 1.8-fold (95% Confidence Interval (95%CI):1.6-2.0) increased risk compared to the general population. Solid SMN risk was increased both in seminoma (180 SMNs) and non-seminoma (170 SMNs) patients (Standardized Incidence Ratios of 1.5, 95%CI:1.3-1.8 and 2.2, 95%CI:1.9-2.6, respectively). Non-seminoma patients experienced increased risk of SMNs of the thyroid, lung, stomach, pancreas, colon, bladder and of melanoma and soft tissue sarcoma, whereas seminoma patients experienced increased risk of SMNs of the small intestine, pancreas, and urinary bladder. Cumulative solid SMN incidence was 10.3% (95%CI:9.0%-11.6%) at 25 years of follow-up. In multivariable analysis, platinum-based chemotherapy was associated with increased risk of solid SMNs (Hazard ratio (HR) 2.40, 95%CI:1.58-3.62), colorectal SMNs (HR:3.85, 95%CI:1.67-8.92) and non-colorectal gastrointestinal SMNs (HR:5.00, 95%CI:2.28-10.95). With each additional cycle of platinum-containing chemotherapy, the HRs of solid SMNs and gastrointestinal SMNs increased with 22% (95%CI:16-48%) and 53% (95%CI:34-74%), respectively. The HR of infradiaphragmatic SMNs increased with 6% per Gray of radiation dose administered (95%CI: 5-7%, P < 0.001). Conclusions: Both radiotherapy and platinum-containing chemotherapy are associated with a dose-depended increased solid SMN risk, specifically with gastrointestinal SMNs.
Abstract 175: Methyltransferase protein A regulates colorectal cancer cell proliferation and metastasis through methylation of protein B
Authors: Songhwa Kang, Sang-Mo Kwon
Journal: Cancer Research (2019)

Abstract Post-translational modifications (PTMs) contribute to abnormal cell proliferation, adhesion, and morphology in cancer progression. Methylation is one such PTM that affects many of the protein properties and has a substantial role in tumorigenesis. Here, we identified that the methyltransferase protein A was upregulated in human colorectal cancer (CRC) and was associated with CRC proliferation, migration, and invasion in vitro. Our study showed that Protein B was a novel target of methyltransferase Protein A and that methylated Protein B was upregulated in human CRC. High expression of Protein A and B resulted in a poor prognosis of CRC; moreover, CRC proliferation, migration, and invasion were inhibited when protein A and B were unable to bind through specific residue, as predicted by in silico protein-protein docking analysis. Furthermore, our study showed that methylation of Protein B by methyltransferase protein A plays an important role in CRC proliferation and invasion via enhancement of HIF-1α stabilization. In conclusion, our data suggested that methylated Protein B may be a potentially valuable clinical prognostic marker of CRC and that interference with the binding of Protein B to methyltransferase Protein A may be a new anticancer target in CRC. Citation Format: Songhwa Kang, Sang-Mo Kwon. Methyltransferase protein A regulates colorectal cancer cell proliferation and metastasis through methylation of protein B [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 175.
Contributions to Resident Forum Encouraged
Journal: JAMA (1991)

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
Nebulised pentamidine as treatment for Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome.
Authors: R F Miller, P Godfrey-Faussett, S J Semple
Journal: Thorax (1989)

Nebulised pentamidine was used to treat 30 patients with Pneumocystis carinii pneumonia. Fourteen patients (group 1) received pentamidine isethionate 4 mg/kg (six patients) or 8 mg/kg (eight patients) via a standard jet nebuliser (Acorn, system 22) with a flow rate of 8 l/min. The aerosol droplets had a mass median aerodynamic diameter of 2.6 microns (geometric standard deviation (GSD) 2.9) and 46% of droplets were less than 3.9 microns. A further 16 patients (group 2) received 8 mg/kg pentamidine via a jet nebuliser with baffles to limit droplet size to below 4 microns (Respirgard II). This generated aerosol droplets with a mass median aerodynamic diameter of 0.8 micron (GSD 1.5) and 98% were less than 3.9 microns. Only three of the 14 patients in group 1 responded clinically to treatment, one after the lower dose of pentamidine. Treatment was discontinued in 10 patients and one patient died at bronchoscopy from haemorrhage. Thirteen of the 16 patients in group 2 responded. Side effects occurred infrequently; two patients from group 1 had a cough, six patients (four from group 2) had contact bleeding at bronchoscopy, and two further patients had haemoptysis. The differing response rate may be due to differences in the mean droplet size of the aerosols produced by the nebulisers. Nebulised pentamidine (8 mg/kg) when delivered by Respirgard II nebuliser appears to be as effective as conventional treatment for Pneumocystis carinii pneumonia of mild to moderate severity.
RESTING FROM LABOR (DAY)
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
Abstract 450: Phosphorylation Of Platelet αIIbβ3 Is Crucial For Arterial Thrombosis In Vivo And Microparticle Generation
Authors: Manojkumar Valiyaveettil, Weiyi Feng, Ganapati Mahabaleshwar, David Phillips, Tatiana Byzova, Eugene Podrez
Journal: Circulation (2007)

Functional activity of platelet fibrinogen receptor αIIbβ3 is crucial for hemostasis and thrombosis. The process of αIIbβ3 activation in platelet aggregation is tightly regulated. It has been previously shown that β3 subunit of the complex undergo tyrosine phosphorylation, which, in turn, is believed to control recruitment of several intracellular adaptors. Mutations of Tyr747/ Tyr759 within the cytoplasmic domain of αIIbβ3 (DiYF substitution) were found to result in reversible platelet aggregation. To assess whether αIIbβ3 tyrosine phosphorylation is critical for arterial thrombosis, we utilized intravital microscopy to monitor thrombus formation in vivo in WT and DiYF mice. Compared to WT, DiYF mice exhibited delayed platelet adhesion and reduced rate of thrombus formation at the initial stages of thrombosis. Likewise, isolated DiYF platelets exhibited reduced adhesion to collagen under in vitro sheer conditions compared to WT. The progression phase of thrombosis in vivo was similar in WT and DiYF mice. The most dramatic difference was observed at the final phase of thrombus formation since it took 3-times longer for blood vessels in DiYF mice to occlude compared to WT. To specifically address the role if β3 phosphorylation in platelet αIIbβ3 vs αvβ3 on leukocytes and vascular cells, we transfused labeled WT and DiYF platelets into irradiated WT mice with low blood cells and platelet counts. It was found that transfusion of DiYF but not WT platelets resulted in reversal of the thrombotic phenotype and significantly prolonged blood vessel occlusion time in vivo. Similar differences were observed in tail bleeding test. Importantly, we have found that the lack of β3 phosphorylation impaired an ability of platelets to generate microparticles in response to activation, an event believed to be critical for the final stages of thrombosis. When stimulated with thrombin and PMA, DiYF platelets shed ~50% less Annexin V-positive microparticles as compared to WT platelets. Thus, β3 tyrosine phosphorylation of αIIbβ3 in platelets is crucial for the microparticles generation by activated platelets and the overall process of arterial thrombosis in vivo.
Field Concentrations and Persistence of Polybrominated Biphenyls in Soils and Solubility of PBB in Natural Waters
Authors: L. W. Jacobs, S. F. Chou, J. M. Tiedje
Journal: Environmental Health Perspectives (1978)

Soil samples were collected from 28 fields which had received manure from Michigan's most highly contaminated dairy herds. The number of fields in each concentration range of PBB in soil were: 2, not detectable; 15, 0.0 to 8.0 ppb; 6, 14-102 ppb, and 5, 153 to 371 ppb. Plant tissue sampled from the 10 most highly contaminated fields contained no detectable PBB. No evidence of significant degradation of PBB was noted after 1 year incubation in soil. When 14C hexabromobiphenyl and heptabromobiphenyl isomers were incubated in soil less than 0.2% of the 14C was volatilized. Also gas chromatographic analysis of soil extracts showed no difference in recovery of the six major PBB isomers between sterilized and nonsterilized soil. Analysis of these extracts by thin layer chromatography and autoradiography showed no 14C-PBB intermediates. Photodegradation products of the major hexa- and heptabromobiphenyl isomers showed more but still minor (approximately 3%) biodegradation in soil. Much of the photodegradation products appeared bound to soil, since these products could not be extracted from soil. Photodegradation does not appear to be a significant fate of PBB in manures spread on fields since no change was noted in the relative concentrations of isomers in soil samples from our field survey. Studies with distilled, tap, river, and soil waters showed that PBB solubility was markedly influenced by water composition.
EHPnet: Painting a Healthier Picture
Journal: Environmental Health Perspectives (1997)

Committee will assess the impact on health of contaminants including radionuclides, persistent organic toxics, and toxic metals.The Conservation ofArctic Flora and Fauna Committee will compile lists of endangered species and environmentally protected areas.The Protection of the Arctic Marine Environment Committee will survey landbased sources of pollution and establish guidelines for environmentally sound devel- opment including that of offshore oil drilling.Finally, the Emergency Prevention, Preparedness, and Response Committee will assess emergency notification systems and compile a risk matrix that identifies environ- mental risk factors and their significance.According to Robert Senseney, polar affairs chief for the U.S. State Department, the Arctic Council is negotiating rules of procedure and guidelines for emergency pre- paredness and sustainable development.