tbuckley/cabot-search huggingface dataset:
UK: the best place in the world to die
Authors: John Hughes
Journal: BMJ (2015)

But could still be better 

The 2015 Quality Of Death Index from the Economist Intelligence Unit once again ranks the United Kingdom as providing the best “quality of death” and “quality of palliative care” in a comparison of 80 countries.1 The exemplary features of the highest scoring health economies include a national policy framework for palliative care, relatively high levels of healthcare expenditure, good training in specialist and generalist palliative care, financial subsidies (from the charitable sector in the case of the UK), availability of opioids, and public awareness of palliative care.

However, even within the UK, there are notable failings. The report highlights examples of poor symptom control at the end of life, poor communications with patients and families, and inadequate generalist and specialist out of hours services. It cites this year’s …
Human IFNAR2 deficiency: Lessons for antiviral immunity
Authors: Christopher J. A. Duncan, Siti M. B. Mohamad, Dan F. Young, Andrew J. Skelton, T. Ronan Leahy, Diane C. Munday, Karina M. Butler, Sofia Morfopoulou, Julianne R. Brown, Mike Hubank, Jeff Connell, Patrick J. Gavin, Cathy McMahon, Eugene Dempsey, Niamh E. Lynch, Thomas S. Jacques, Manoj Valappil, Andrew J. Cant, Judith Breuer, Karin R. Engelhardt, Richard E. Randall, Sophie Hambleton
Journal: Science Translational Medicine (2015)

Human IFNAR2 deficiency causes fatal susceptibility to live viral vaccines.
Significance of AKT and ERK activation in clonogenic survival after Cr6+ exposure and protein tyrosine phosphatase (PTP) inhibition
Authors: Dongsoon Bae, Susan Ceryak
Journal: Cancer Research (2007)

AACR Annual Meeting-- Apr 14-18, 2007; Los Angeles, CA

286 

Increasing numbers of studies reveal that occupational and environmental exposures to certain hexavalent chromium compounds are associated with upper respiratory tract and pulmonary carcinogenesis through poorly defined mechanism(s) of action. Inappropriate activation/inactivation of key signals that control cell survival after genotoxic insult can contribute to autonomous cell growth and carcinogenesis. The PI3K/AKT signaling cascades are important integrators of growth and survival signals in lung carcinogenesis. Our previous studies showed that maintenance of protein tyrosine phosphorylation by PTP inhibition, which is coincident with AKT activation, overrides Cr6+-induced growth arrest and enhances clonogenic survival in human lung fibroblasts (HLFs). To test the hypothesis that AKT activation is a key determinant of cellular survival response after Cr6+ genotoxic insult, we examined the effect of AKT1 knockdown on cell survival after Cr6+exposure and PTP inhibition. HLFs were transiently transfected with akt1 siRNA or d/n akt1 plasmid via nucleofector. Transfected cells were treated with 0-2μM Cr6+ in the presence and absence of PTP inhibition with sodium orthovanadate, for 24h, then washed and replated to examine clonogenic survival. Expression level of akt1 mRNA and AKT1 proteins was determined by quantitative PCR and Western blot, respectively. PTP inhibition decreased Cr6+-induced clonogenic lethality even after AKT1 silencing although AKT1 activity was sufficient to override Cr6+-induced G1/S arrest. This finding prompted us to examine other survival pathway(s) that may contribute in the maintenance of cellular survival after abrogation of AKT signaling. ERK was hyperactivated after AKT1 silencing in the presence of PTP inhibition. Moreover, phosphotyrosine profiling array showed that PTP inhibition following Cr6+ treatment increased phosphorylation status of adaptor phosphotyrosine proteins, FGR and ABL, which are upstream of both AKT and ERK pathways. These findings suggest that the balance between AKT and ERK pathways under control of upstream regulatory phosphotyrosine kinases may be a molecular mechanism to govern cell survival in the face of genotoxic insult with or without PTP inhibition in HLFs. In conclusion, AKT activation may not be solely necessary by itself to enhance clonogenic survival after Cr6+ insult and PTP inhibition, and the balance between AKT and ERK activation after PTP inhibition may be critical for overriding Cr6+-induced growth arrest/death signaling. Studies on the roles of AKT/ERK crosstalk in genotoxin-induced clonogenic death are currently being examined and will add new insights to the understanding of Cr6+-mediated lung carcinogenesis. Supported by NIH grant CA 107972
Protein Metabolism and Injury
Authors: J. M. Kinney, D. H. Elwyn
Journal: Annual Review of Nutrition (1983)

INTRODUCTION . . . . . . . . . . . . . . . . . . ........ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433 BODY COMPOSITION AND PROTEIN LOSS . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . ... . . 434 PROTEIN-ENERGY INTERRELATIONS . . . . . . . . . . . . . . . . . . . . ... .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 436 PROTEIN METABOLISM IN STARVATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 437 PROTEIN METABOLISM IN INJURY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 439 PLASMA AMINO ACIDS IN INJURy .... . .       442 MUSCLE AND PLASMA AMINO ACIDS IN INJURy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444 PROTEIN SYNTHESIS AND DEGRADATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 445 Whole Body Protein Turnover . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 446 Norlfl(ll Values . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . .. . . . . . . . . .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . 447 Effects of Nutrition and Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447 Effects of Injury on Whole Body Protein Turnover . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 448 RATES OF PROTEIN SYNTHESIS AND DEGRADATION IN INDIVIDUAL ORGANS OR TISSUES . . . . . . . . . . . . . . . . . . . . . . . . . . . . ......... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 450 Liver. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . .. . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . . . . . . . . . . . . . 45 1 Muscle ..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 1 Effects of Injury on Protein Turnover in Individual Organs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 452 Factors Mediating the Effect of Injury on Muscle Protein Degradation . . . . . . . . . . . . . . . . 453 THE INFLUENCE OF NUTRITION ON PROTEIN METABOLISM . . . . . . . . . . . . . . . . . . . . . . 453 FUTURE STUDIES OF THE EFFECTS OF INJURY ON PROTEIN METABOLISM 458
Production of spike and nucleocapsid recombinant proteins of porcine epidemic diarrhea virus for antibody detection by ELISA
Authors: Anchalee Srijangwad, Dachrit Nilubol, Wanchai Chongcharoen, Waranyoo Phoolcharoen, Taksina Chuanasa, Angkana Tantituvanon
Journal: Asian Journal of Pharmaceutical Sciences (2015)
Triple Combination of Antibiotics Effective Against MRSA
Authors: Julie A. Jacob
Journal: JAMA (2015)

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
Screening for High Blood Pressure in Adults: U.S. Preventive Services Task Force Recommendation Statement
Authors: Albert L. Siu
Journal: Annals of Internal Medicine (2015)

Update of the 2007 U.S. Preventive Services Task Force (USPSTF) reaffirmation recommendation statement on screening for high blood pressure in adults.The USPSTF reviewed the evidence on the diagnostic accuracy of different methods for confirming a diagnosis of hypertension after initial screening and the optimal rescreening interval for diagnosing hypertension.This recommendation applies to adults aged 18 years or older without known hypertension.The USPSTF recommends screening for high blood pressure in adults aged 18 years or older. (A recommendation) The USPSTF recommends obtaining measurements outside of the clinical setting for diagnostic confirmation before starting treatment.
Management of Nephrolithiasis: New Approaches to "Surgical" Kidney Stones
Authors: A G Mulley
Journal: Annual Review of Medicine (1988)

CD40 is a cell-surface member of the TNF (tumor necrosis factor) receptor superfamily. Upon activation, CD40 can license dendritic cells to promote antitumor T cell activation and re-educate macrophages to destroy tumor stroma. Numerous agonist CD40 ...Read More
Prognosis in Chronic Lymphocytic Leukemia
Authors: Leonid L. Yavorkovsky
Journal: JAMA Oncology (2015)

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 Oncology HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Oncology journal
Predicted vs Observed Clinical Event Risk for Cardiovascular Disease
Authors: Andrew P. DeFilippis, Michael J. Blaha
Journal: JAMA (2015)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Transcriptional repressor ZEB2 promotes terminal differentiation of CD8+ effector and memory T cell populations during infection
Authors: Kyla D. Omilusik, J. Adam Best, Bingfei Yu, Steven Goossens, Alexander Weidemann, Jessica V. Nguyen, Eve Seuntjens, Agata Stryjewska, Christiane Zweier, Rahul Roychoudhuri, Luca Gattinoni, Lynne M. Bird, Yujiro Higashi, Hisato Kondoh, Danny Huylebroeck, Jody Haigh, Ananda W. Goldrath
Journal: The Journal of Experimental Medicine (2015)

ZEB2 is a multi-zinc-finger transcription factor known to play a significant role in early neurogenesis and in epithelial-mesenchymal transition–dependent tumor metastasis. Although the function of ZEB2 in T lymphocytes is unknown, activity of the closely related family member ZEB1 has been implicated in lymphocyte development. Here, we find that ZEB2 expression is up-regulated by activated T cells, specifically in the KLRG1hi effector CD8+ T cell subset. Loss of ZEB2 expression results in a significant loss of antigen-specific CD8+ T cells after primary and secondary infection with a severe impairment in the generation of the KLRG1hi effector memory cell population. We show that ZEB2, which can bind DNA at tandem, consensus E-box sites, regulates gene expression of several E-protein targets and may directly repress Il7r and Il2 in CD8+ T cells responding to infection. Furthermore, we find that T-bet binds to highly conserved T-box sites in the Zeb2 gene and that T-bet and ZEB2 regulate similar gene expression programs in effector T cells, suggesting that T-bet acts upstream and through regulation of ZEB2. Collectively, we place ZEB2 in a larger transcriptional network that is responsible for the balance between terminal differentiation and formation of memory CD8+ T cells.
Phase I clinical and pharmacologic study of weekly cisplatin combined with weekly irinotecan in patients with advanced solid tumors.
Authors: L B Saltz, D Spriggs, L J Schaaf, G K Schwartz, D Ilson, N Kemeny, J Kanowitz, C Steger, M Eng, P Albanese, D Semple, C K Hanover, G L Elfring, L L Miller, D Kelsen
Journal: Journal of Clinical Oncology (1998)

PURPOSE In vitro synergy between cisplatin and irinotecan (CPT-11) has been reported. We designed a combination schedule of these agents to maximize the potential for synergistic interaction. PATIENTS AND METHODS To maximize the opportunity for synergy, we divided the cisplatin into four consecutive weekly treatments, followed by a 2-week rest. Each dose of cisplatin was immediately followed by a dose of irinotecan. The dose of cisplatin was fixed at 30 mg/m2/wk. The initial irinotecan dose was 50 mg/m2/wk and this was escalated by 30% increments in successive cohorts of three to six patients to establish the maximum-tolerated dose (MTD). Pharmacokinetics of irinotecan and its metabolites, SN-38 and SN-38 glucuronide (SN-38G), were analyzed. RESULTS Of 35 patients with solid tumors enrolled onto this trial, 30 were assessable for toxicity and response. The MTD for this regimen was 30 mg/m2/wk of cisplatin plus 50 mg/m2/wk of irinotecan in previously treated patients and 30 mg/m2/wk of cisplatin plus 65 mg/m2/wk of irinotecan in chemotherapy-naive patients. Neutropenia was the dose-limiting toxicity (DLT) encountered in this trial. Diarrhea was infrequent and rarely dose-limiting. Seven of 30 assessable patients achieved a partial response. No alteration in irinotecan, SN-38, or SN-38G pharmacokinetics resulted from the administration of cisplatin with irinotecan. CONCLUSION The administration of cisplatin and irinotecan on this weekly schedule provides a practical and well-tolerated regimen that has the potential to maximize any clinical synergy between the two agents. Evidence of substantial clinical activity was seen in this phase I study.
Changes in criteria for tumor response.
Authors: D J Perry, L F Diehl
Journal: Journal of Clinical Oncology (1985)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1985.3.2.287 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 3968555 Changes in criteria for tumor response. D J PerryxD J PerrySearch for articles by this author , L F DiehlxL F DiehlSearch for articles by this author https://doi.org/10.1200/JCO.1985.3.2.287 PDF "Changes in criteria for tumor response.." Journal of Clinical Oncology, 3(2), p. 287© 1985 by American Society of Clinical Oncology
Racial Variation in the Uptake of Onco<i>type</i> DX Testing for Early-Stage Breast Cancer
Authors: Megan C. Roberts, Morris Weinberger, Stacie B. Dusetzina, Michaela A. Dinan, Katherine E. Reeder-Hayes, Lisa A. Carey, Melissa A. Troester, Stephanie B. Wheeler
Journal: Journal of Clinical Oncology (2015)

Oncotype DX (ODX) is a tumor gene-profiling test that aids in adjuvant chemotherapy decision-making. ODX has the potential to improve quality of care; however, if not equally accessible across racial groups, disparities in cancer care quality may persist or worsen. We examined racial disparities in ODX testing uptake.We used data from the Carolina Breast Cancer Study, phase III, a longitudinal, population-based study of 2,998 North Carolina women who received a diagnosis of breast cancer between 2008 and 2014. Our primary analysis used modified Poisson regression to determine the association between race and whether ODX testing was ordered among two strata: node-negative and node-positive breast cancer.A total of 1,468 women with estrogen receptor-positive, human epidermal growth factor receptor-2-negative, stage I or II breast cancer met inclusion criteria. Black patients had higher-grade and larger tumors, more comorbidities, younger age at diagnosis, and lower socioeconomic status than non-black women. Overall, 42% of women had ODX test results in their pathology reports. Compared with those who did not receive ODX testing, women who received ODX testing tended to be younger and have medium tumor size and grade. Our regression analyses indicated no racial disparities in ODX uptake among node-negative patients. However, racial differences were detected among node-positive patients, with black patients being 46% less likely to receive ODX testing than non-black women (adjusted relative risk, 0.54; 95% CI, 0.35 to 0.84; P = .006).We did not find racial disparities in ODX testing for node-negative patients for whom ODX testing is guideline recommended and widely covered by insurers. However, our findings suggest that a newer, non-guideline-concordant application of ODX testing for node-positive breast cancer was accessed less by black women than by non-black women, reflecting more guideline concordant care among black women.
Argyrophil Cell Microneoplasia in the Mastomys' Stomach-An Observation on Early Carcinoid Formation 2 3
Authors: Jun Soga, Tatsuro Kohro, Kenji Tazawa, Hideo Kanahara, Muneaki Sano, Takeshi Sakashita, Kenzo Tajima, Morooka Hisashi, Karaki Yoshiaki
Journal: JNCI Journal of the National Cancer Institute (1975)

To analyze the early stages of argyrophil cell carcinoid growth, complete serial sections were cut from the glandular portion of the stomachs of 22 Mastomys and submitted to Sevier-Munger's reaction. The 154 grossly invisible foci of argyrophil cell microproliferation thus detected were classified into three stages of microproliferations (I, II, and III), and the last stage was definitely a microcarcinoid. There was a gradual transition in cell proliferation among these three stages; the first stage (microproliferation I), in which the cells were morphologically indistinguishable from those of hyperplastic proliferation by general morphologic criteria, was where the initial change of argyrophil cell carcinoid formation was detectable by a light microscope. Whereas multiple occurrences of microcarcinoids accounted for the multiplicity of well-developed tumors in the stomachs of Mastomys, a well-developed carcinoid in this species was formed by the confluence of several microcarcinoids.
Effects of Anesthesia on Intermediary Metabolism
Authors: E A Brunner, S C Cheng, M L Berman
Journal: Annual Review of Medicine (1975)

Major inhalational anesthetics cause inhibition in the electron transport chain in the region of Complex I resulting in decreased oxygen utilization, inhibition of metabolism of NAD-linked substrates, but not of succinate, inhibition of mitochondrial calcium uptake, and depression of synaptic transmission because of postulated changes in ACh sensitivity or GABA inhibition. Many cellular metabolic effects in CNS and other tissues are secondary to the above. Many metabolic changes noted with anesthetics occur subsequent to activation of the sympathetic nervous system either directly by the anesthetic or by surgical stimulation in the presence of light anesthesia. Many important studies remain to be done.
Nutritional Management of Glycogen Storage Disease
Authors: P H Parker, M Ballew, H L Greene
Journal: Annual Review of Nutrition (1993)

INTRODUCTION   . TYPE I GLYCOGEN STORAGE DISEASE   . Blood Glucose Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lactic Acid Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hyperlipidemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . Hyperuricemia . . . . . . . . . . . . . . Hypophosphatemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Platelet Dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Growth Impairment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hepatic Adenoma and Carcinoma . . . . .. . . . . . . . . . .. . . . . . . . . . . . . . Renallnvolvemenl   . NUTRITIONAL MANAGEMENT OF GSD-   . Nocturnal Nutrient Infusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Daytime Feedings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Patient Education . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . TYPE II GLYCOGEN STORAGE DISEASE . . . . . . . . . . . . . . . . . . . . . . . . .