tbuckley/cabot-search huggingface dataset:
EXTH-36. PI3K INHIBITION IN CONJUNCTION WITH THE KETOGENIC DIET REDUCES GROWTH AND NEUROINFLAMMATION IN PEDIATRIC HIGH-GRADE GLIOMA
Authors: Evan Noch, Isaiah Yim, Lewis Cantley
Journal: Neuro-Oncology (2019)

Abstract Pediatric high-grade glioma remains a poorly treatable disease with high mortality. Targeted therapies have gained interest in this disease, but efficacy is limited by therapeutic resistance, often because of tumor heterogeneity. Phosphoinositide 3-kinase (PI3K) inhibitors represent a strong drug class for pediatric glioma, but their use is associated with insulin feedback that reactivates the PI3K pathway and drives therapeutic resistance. Here, we target insulin feedback that is the primary mechanism of PI3K inhibitor-related therapeutic resistance in pediatric high-grade glioma using the ketogenic diet. We treated patient-derived pediatric high-grade glioma stem cells with vehicle or the pan-PI3K inhibitor, BKM-120, in conjunction with phenformin to decrease glucose utilization. These cells exhibited 65% less proliferation when exposed to BKM-120 and phenformin. We treated NOD scid gamma (NSG) mice containing patient-derived pediatric high-grade glioma xenografts with vehicle or BKM-120 on a regular or ketogenic diet to determine whether reducing insulin feedback increases BKM-120 efficacy. Mice with intracranial glioma xenografts survived longer when treated with BKM-120 on the ketogenic diet than with BKM-120 or the ketogenic diet alone. We measured pro-inflammatory cytokines in glioma cells treated with BKM-120 and phenformin in comparison to vehicle-treated cells to determine their effect on neuro-inflammation. We also applied conditioned medium from glioma cells treated with BKM-120 and phenformin to cortical neurons to measure oxidative stress. We found that phenformin reduced the production of pro-inflammatory cytokines, including TNF-alpha, IFN-gamma, IL-1beta, and IL-6, by BKM-120-treated glioma cells. Cortical neurons treated with conditioned medium from BKM-120- and phenformin-treated glioma cells exhibited less oxidative stress than those treated with BKM-120 alone. Our results demonstrate that lowering glucose utilization and insulin feedback increases efficacy of PI3K inhibition and decreases neuro-inflammation. By using the ketogenic diet to reduce systemic glucose levels, this strategy may enhance efficacy and reduce morbidity of PI3K inhibitors in this population.
Meeting US Hypertension Goal Is Possible, but More Work Needed
Journal: JAMA (2014)

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
Learning and Courtship in Drosophila: Two Stories with Mutants
Authors: W. Quinn
Journal: Annual Review of Neuroscience (1984)

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
Pain
Authors: John Breth, James P. Rathmell
Journal: JAMA (2006)

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
IDIOPATHIC CHOROIDITIS.
Authors: ADELINE E. PORTMAN
Journal: JAMA (1896)

Idiopathic choroiditis is a subject on which we find, in text-books, almost nothing to aid in diagnosis of the disease which has had so little investigation by the busy oculists of the present time. As you know, the choroid consists of the vascular parenchyma, an exterior coat of endothelium upon its scleral surface, and the<i>lamina vitrea</i>. Upon the latter lies the pigmented epithelium which is assigned to the retina, though it always suffers when the choroid is affected. The blood supply of the choroid is from two groups. The capillary vessels, which lie nearer the inner surface, and the venous to the outer. The chief blood supply is from the short, posterior ciliary arteries. After entering near the optic nerve and piercing the sclerotic they pass into the choroid, then branch, forming the capillary network of the choroid, ending in the indented margin of the<i>ora serrata</i>. Long posterior
Reply
Authors: A.H. Patk
Journal: British Journal of Dermatology (1995)

Journal Article Reply Get access A.H. Patk A.H. Patk 46 Shailesh Society, Karve Nagar, Pune 410052, India Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 133, Issue 6, 1 December 1995, Pages 1011–1012, https://doi.org/10.1111/j.1365-2133.1995.tb06947.x Published: 01 December 1995
Abstract B35: Vinyl sulfone analogues of lysophosphatidylcholine irreversibly inhibit autotaxin and prevent angiogenesis in melanoma
Authors: Mandi Murph, Guowei Jiang, Molly Altman, Jia Wei, Sterling Tran, Duy Nguyen, Ali Alshamrani, William Hardman, Jianxing Zhang, Glenn Prestwich
Journal: Cancer Research (2015)

Abstract Autotaxin is an enzyme discovered in the conditioned medium of cultured melanoma cells and identified as a protein that strongly stimulates motility. Autotaxin is a unique ectonucleotide pyrophosphatase and phosphodiesterase that facilitates the removal of a choline headgroup from lysophosphatidylcholine to yield lysophosphatidic acid, which is a potent lipid stimulator of tumorigenesis. Thus, autotaxin has received renewed attention because it has a prominent role in malignant progression and represents a promising area of research with significant translational potential. Specifically, we sought to develop active site-targeted irreversible inhibitors as anti-cancer agents. Our goal was to discover agents with therapeutic efficacy in melanoma. For this purpose, we synthesized a set of lysophosphatidylcholine analogs that function as irreversible inhibitors of autotaxin and inactivate the enzyme. The analogs were tested in cell viability assays using multiple cancer cell lines. The IC50 values ranged from 6.74 – 0.39 μM, consistent with a Ki of 3.50 μM for inhibition of autotaxin by the analog CVS-16 (10b). A control compound, GWJ-A-10, which is missing the critical moiety, had little effect on cell viability and did not inhibit autotaxin. In addition, CVS-16 (10b) significantly inhibited melanoma cell wound closure and pore migration (data not presented herein). Most importantly, CVS-16 (10b) significantly inhibited melanoma progression in an in vivo tumor model by preventing angiogenesis. Taken together, this suggests that CVS-16 (10b) is a potent autotaxin inhibitor with significant biological activity, both in vitro and in vivo. Citation Format: Mandi Murph, Guowei Jiang, Molly Altman, Jia Wei, Sterling Tran, Duy Nguyen, Ali Alshamrani, William Hardman, Jianxing Zhang, Glenn Prestwich. Vinyl sulfone analogues of lysophosphatidylcholine irreversibly inhibit autotaxin and prevent angiogenesis in melanoma. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Melanoma: From Biology to Therapy; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(14 Suppl):Abstract nr B35.
Application of Log-Linear Model in Inference on Karyotypic Evolution in Chronic Myelocytic Leukemia
Authors: Tetsuo Hashimoto, Megu Ohtaki, Nanao Kamada, Hisashi Yamamoto, Masaki Munaka
Journal: Environmental Health Perspectives (1990)

Relationships among additional chromosome abnormalities in chronic myelocytic leukemia (CML) with translocation 9;22 [Philadelphia chromosome (Ph1)-positive CML] were analyzed by log-linear models on 709 karyotypes reported in the literature. Additional abnormalities, such as the gain of chromosome 8 (+8), gain of Philadelphia chromosome (+Ph1), isochromosome of the long arm (q) of chromosome 17 [i(17q)], and the gain of chromosome 19 (+19), were frequently observed. A four-way 2 x 2 x 2 x 2 contingency table was considered with respect to the appearance of these four abnormalities, then the hierarchical log-linear models having at least four main effects were fitted to the observed contingency table. Akaike's information criteria of the models reflected the fitness of the model very well. Parameter estimates of the interaction terms indicated that the combinations of two abnormalities, '+8 and +19', '+Ph1 and +19', and '+8 and i(17q)' were positively associated, while '+Ph1 and i(17q)', and '+19 and i(17q)' were negatively associated. Based on the results of the data analysis, an inference was made on the route of karyotypic evolution in Ph1-positive CML; it statistically supports the hypothesis presented by Heim and Mitelman.
High-dose cyclophosphamide, carmustine, and etoposide followed by autologous bone marrow transplantation in patients with lymphoid malignancies who have received dose-limiting radiation therapy.
Authors: C H Weaver, F R Appelbaum, F B Petersen, R Clift, J Singer, O Press, W Bensinger, J Bianco, P Martin, C Anasetti
Journal: Journal of Clinical Oncology (1993)

PURPOSE To evaluate high-dose chemotherapy followed by autologous bone marrow transplantation (ABMT) in patients with lymphoid malignancy who had received prior radiation therapy. PATIENTS AND METHODS Fifty-seven patients with non-Hodgkin's lymphoma (NHL; n = 23), Hodgkin's disease (HD, n = 32), or acute lymphoblastic leukemia (ALL; n = 2) with a history of previous radiation therapy were treated with cyclophosphamide (Cy; 7.2 g/m2), carmustine (300 mg/m2 or 600 mg/m2), and etoposide (2,400 mg/m2) (CBV) followed by ABMT. RESULTS The projected 2-year probabilities of survival, event-free survival (EFS), and relapse were .31, .24, and .76, respectively. For patients with intermediate- and high-grade lymphoma and HD the probabilities were .27, .10, and .14 for EFS and .57, .90, and .77 for relapse. The probability of nonrelapse mortality in the first 100 days post-ABMT was 33%. Idiopathic pneumonia syndrome (IPS) was observed in no patients who received carmustine 300 mg/m2 and 23% of patients who received carmustine 600 mg/m2 (P = .05). Eight-three percent of patients who received mediastinal radiation therapy less than 3 months before transplant developed IPS, compared with 13% who received radiation therapy more than 3 months before transplant (P = .001). CONCLUSION ABMT following high-dose CBV resulted in long-term disease-free survival in 25% of patients with lymphoid malignancies who had previously received dose-limiting radiation therapy. Fatal IPS and a high relapse rate were major factors limiting successful outcome following ABMT. The morbidity and mortality rates associated with the administration of carmustine 600 mg/m2 were prohibitively high, especially in patients who received mediastinal radiation immediately before ABMT, and were not associated with a decrease in post-ABMT relapse.
The Diseases of Children.
Journal: JAMA (1884)

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
Idiopathic Haemochromatosis
Authors: W. H. Crosby
Journal: BMJ (1967)

of a needle pick it out.It is the simplest of procedures: the mite clings to the point of the needle, it can be placed on a slide, and its lively antics watched with great amuse- ment under the microscope.This technique takes no more than a few minutes to master and yet I rarely see it practised.It is most impressive to teacher, student, nurse, and patient, and serves good purpose.The problem is quite different for the management of that very rare variety called Norwegian, or crusted, scabies of course.-I am, etc.,
CBTRUS Statistical Report: Primary brain and other central nervous system tumors diagnosed in the United States in 2010–2014
Authors: Quinn T Ostrom, Haley Gittleman, Peter Liao, Toni Vecchione-Koval, Yingli Wolinsky, Carol Kruchko, Jill S Barnholtz-Sloan
Journal: Neuro-Oncology (2017)
Glutethimide Intoxication
Authors: Eric G. Comstock
Journal: JAMA (1971)

<h3>To the Editor.—</h3> Wright and Roscoe deserve congratulations for their initiative in helping to dispell the misconception that dialysis of some form is the treatment of choice for the patient who has received an overdose of glutethimide. Their communication, "Acute Glutethimide Poisoning: Conservative Management of 31 Patients" (<b>214</b>:1704, 1970), illustrated that intensive supportive therapy alone yields satisfactory clinical results. The one death which occurred among the 31 cases reported was a patient who was grossly mismanaged in another hospital and died two hours after transfer to the Poisoning Treatment Center. Inclusion of this patient in the series of cases illustrating the results of treatment by intensive supportive care seems unjustified. It is suggested that this patient should be deleted from the series to be used as an example of the complications of mismanagement. With this modification their communication can be considered a report demonstrating 100% survival of a series
How Will Humans Act As Science Fiction Becomes Fact?
Journal: JAMA (1986)

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
ACCESSION TO THE NEWBERRY LIBRARY.
Journal: JAMA (1897)

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
Doctors must not accept inducements for referrals, GMC says
Journal: BMJ (2015)

we said that a BMJ investigation published in January accused the GMC of taking no action after a leading healthcare insurer gave it a dossier of evidence showing that some consultants were taking inducements to refer patients to private facilities.We should like to point out that after our investigation the GMC refuted these accusations.A spokesperson said that because the accusation related to "general concerns about incentives and referrals in private healthcare [and] did not include any allegations of wrongdoing relating to individual doctors," it had been unable to act.The GMC has no powers to carry out speculative industry wide inquiries to see what evidence of impaired fitness to practise it might find, the spokesperson explained.
EXAMINATIONS AND LICENSURE
Journal: JAMA (1962)

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
Genetics Education
Journal: JAMA (2000)

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
Ocular Phototoxicity
Authors: Sidney Lerman
Journal: New England Journal of Medicine (1988)

IN this issue of the Journal, Taylor et al. evaluate the effect of ultraviolet radiation on the ocular lens and its role as a risk factor in the development of cataracts.1 This important article emphasizes a growing concern over the effects of non-ionizing radiation (ultraviolet, visible, and infrared) on the eye. During the past two decades, there has been renewed interest in the photochemical changes in specific ocular tissues induced by ultraviolet and visible radiation.2 3 4 The eye is the only organ or tissue in the body (aside from the skin) that is particularly sensitive to the non-ionizing wavelengths of . . .
Pulmonary Medicine
Authors: Thomas L. Petty
Journal: JAMA (1990)

Chronic obstructive pulmonary disease (COPD) has been previously described as a major challenge both to basic scientists, who try to elucidate the disease mechanisms, and clinicians, who aim to alter the course and prognosis of the fifth leading cause of death in the United States.<sup>1-3</sup>There were an estimated 75 000 deaths from COPD in 1988, but certainly COPD contributed to the cause of death in many others, perhaps as many as 150 000. Chronic obstructive pulmonary disease will remain a challenge in the future because 51 million Americans continue to smoke. The prevalence of COPD, a degenerative disease, will continue to increase in our aging population. Although long-term oxygen therapy is now established as a treatment that improves survival in patients with advanced COPD and hypoxemia, two national consensus conferences have emphasized the problems inherent in prescribing and supplying oxygen for Medicare patients and in overall recommendations for