tbuckley/cabot-search huggingface dataset:
THE INANIMATE OBSERVER
Journal: JAMA (1967)

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
Interleukin 1 stimulates platelet-activating factor production in cultured human endothelial cells.
Authors: F Bussolino, F Breviario, C Tetta, M Aglietta, A Mantovani, E Dejana
Journal: Journal of Clinical Investigation (1986)

Monocyte-derived interleukin 1 (IL-1) was found to be a potent inducer of platelet-activating factor (PAF) in cultured human vascular endothelial cells (HEC). The product was identified as PAF by its behavior in chromatographic systems, its recovery of biological activity, and its physico-chemical properties and susceptibility to lipases. The response of HEC to IL-1 was concentration-dependent, took more than 2 h to become apparent, and decreased after 18 h of incubation. Most of the PAF produced was cell-associated and only a small amount (about 25% of the total) was released in the culture medium. To study the mechanism of IL-1-induced HEC-PAF production we tested the activity of 1-O-alkyl-sn-glycero-3-phosphocholine:acetyl/coenzyme A acetyltransferase in HEC. Acetyltransferase activity measured in IL-1-stimulated HEC lysates showed a three to five times greater maximum velocity, but the same Michaelis constant, as untreated cells. The regulation of PAF generation in HEC by IL-1 may be an important aspect of the two-way interaction between immunocompetent cells and vascular tissue.
Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis
Authors: Eric D. Berglund, Chen Liu, Jong-Woo Sohn, Tiemin Liu, Mi Hwa Kim, Charlotte E. Lee, Claudia R. Vianna, Kevin W. Williams, Yong Xu, Joel K. Elmquist
Journal: Journal of Clinical Investigation (2014)

The y axes for Figure 2, upper left panel, and Figure 5C were incorrect.
Antacids.
Journal: BMJ (1970)

been established.Treatment is principally that of the under- lying condition and has often been instituted before the neural complication makes its appearance.Surgical decompression or, in appropriate cases, irradiation alone is urgent in any of these conditions in which spinal cord compression occurs.Even in the case of secondary carcinomatous deposits these measures may provide rewarding palliation if instituted early enough.The spectre of the potentially treatable solitary intracerebral secondary remains, despite the well-recognized fact that its occurrence in post-mortem material declines in proportion to the thickness of the brain slices examined.The removal of a bronchial carcinoma has not been shown to result in improvement in the non-infiltrative polyneuropathies, but has been followed by regression of cerebellar degeneration.Oral steroids have been reported to relieve the distressing paraesthesiae and even the motor and sensory deficits in a very small number of these cases. TODAY'S DRUGS AntacidsWith the help of expert contributors we print in this section notes on drugs in current use.Antacids are drugs which neutralize or reduce the acidity of the gastric contents.The digestive properties of gastric juice are mainly due to pepsin.The function of gastric acid is considered to be the maintenance of an optimal pH for the action of pepsin (1-5-3-5).Pepsin has very little activity at pH 4-0 and none at pH 5-0.Acid and pepsin are secreted in response to stimuli from the parasympathetic nervous system and from the hormone gastrin, which is released from the gastric antrum in response to a number of stimuli, including a fall in gastric acidity.Our knowledge of the aetiology of peptic ulceration is still very incomplete.Modern opinion accepts the importance of acid secretion, but a number of other factors contribute to the susceptibility of the gastric and duodenal mucosa to the irri- tative and erosive effect of gastric juice.In fact, acid secretion may be normal or low in some patients with peptic ulceration-which emphasizes the importance of mucosal resistance.Aspirin, alcohol, and bile acids can all alter the physiological properties of the gastric mucosa and may predispose to erosion or ulceration.Relatively little is known, however, of the factors which affect mucosal resistance, and so treatment has mainly been directed at reducing gastric acidity.There is no doubt that antacids relieve the pain of peptic ulceration.
BG02: Muir‐Torre syndrome: a case of unusual coexisting genetic mutations
Authors: Z Haider, A Jackson, G Ryan, S Banka, C Moss
Journal: British Journal of Dermatology (2021)

Ectodermal dysplasias (EDs) are a highly heterogeneous group of genetic disorders associated with mutations in > 15 genes.However, the genetic basis of > 50% of ED conditions remains unknown (Wright JT, Fete M, Schneider H et al.Ectodermal dysplasias: classification and organization by phenotype, genotype and molecular pathway.Am J Med Genet A 2019; 179: 442-7).We report a boy with subtle features of ED for whom the recent discovery of a new ED gene led to a genetic diagnosis 9 years after his initial presentation.This now 13year-old white boy was diagnosed at 4 years of age with ED on the basis of missing and conical-shaped teeth and dry, wiry, slow-growing hair.He was minimally dysmorphic with slightly protuberant ears but entirely normal skin, nails and sweating.There was early speech delay but normal hearing, no relevant family history and his parents were nonconsanguineous.Initial genetic testing revealed no pathogenic variants in the EDA or EDAR.In 2017 he was recruited, as a trio with both unaffected parents, to the 100,000 Genome Project.Initial analysis using PanelApp panel 'ED without a known gene mutation v1.15', revealed no pathogenic variants.Subsequent panel-agnostic reanalysis of whole-genome data revealed pathogenic compound heterozygous TSPEAR (p.Leu191-Valfs*65 and p.Gly475Ser) variants.TSPEAR encodes the thrombospondin-type laminin G domain and EAR repeats (TSPEAR) protein, which is thought to regulate the Notch signalling pathway, important for the embryonic development of a stratified multilayer epidermis.Biallelic TSPEAR variants were recently identified to cause autosomal recessive ED (OMIM 618180, ED 14, hair/tooth type with or without hypohidrosis) characterized by hypodontia, conical teeth and abnormal hair texture.So far, TSPEAR-related ED has been reported in only five cases worldwide (Peled A, Sarig O, Samuelov L et at.Mutations in TSPEAR, encoding a regulator of Notch signalling, affect tooth and hair follicle morphogenesis.PLOS Genet 2016; 12: e1006369).The clinical features of this condition are subtle and there may be many other undiagnosed patients.Our patient now has an affected sister aged 2Á5 years, and knowledge of her genetic diagnosis will aid management and counselling.TSPEAR was not present in ED gene panel v1.15 but is included in the latest version (v1.19).It is important to note that, with the discovery of new genes, earlier negative results should be revisited.
Site-Specific Cell Proliferation in Renal Tubular Cells by the Renal Tubular Carcinogen tris(2,3-Dibromopropyl)phosphate
Authors: Michael L. Cunningham, Michael R. Elwell, H. B. Matthews
Journal: Environmental Health Perspectives (1993)

Our laboratory has been examining the mechanisms whereby chemicals are mutagenic in short-term in-vitro assays yet are not carcinogenic in 2-year rodent bioassays.Previous studies indicated that mutagenic carcinogens increased the amount of cell turnover in the target organ, but that mutagenic noncarcinogens failed to do so.The present study compares the inci- dence of cell proliferation in specific regions of the kidney, which is the site of carcinogenicity, with cell proliferation induced in a nontarget tissue, the liver, by the mutagenic renal tubular carcinogen tris(2,3-dibromopropyl)phosphate (TRIS).Renal tubular adenocarcinoma induced by TRIS was the only tumor type identified in male F344 rats, and it was localized in the outer medulla.Male F344 rats were fed a diet containing 0, 50, or 100 ppm TRIS for 14 days.These doses were identical to the doses given in the National Toxicology Program cancer bioassay.Replicating cells were labeled with bromodeoxyuridine administered by an osmotic minipump and identified in tissue sections from liver and kidney using immunohistochemical techniques.Examination of liver sections showed no chemically related increases in cell proliferation above control for either dose group.However, in the kidney, TRIS induced significant cell prolifera- tion that was localized in the renal outer medulla region, the target area for carcinogenesis.The labeling index (number of labeled cells/total number of cells counted) in the kidneys of TRIS-exposed rats was increased approximately 4-fold in the outer medulla and was not increased in the cortex or inner medulla.The results of this study suggest an association between the chemically-induced renal cell proliferation and the renal carcinogenicity of TRIS.
Increase in Epilepsy Cases
Journal: JAMA (2017)

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
NCCN Guidelines® Updates
Journal: Journal of the National Comprehensive Cancer Network (2013)

include:Adult Low-Grade Infiltrative Supratentorial Astrocytoma/Oligodendroglioma (Excluding Pilocytic Astrocytoma) ASTR-1• After "Maximal safe resection," the adjuvant treatment options for low-risk and high-risk patients were combined.Previously, low-risk patients were only "Observed" after maximal safe resection.• Footnote "h" was revised as follows: "High-risk features: 3 or more of:Astrocytoma, age >40 y, KPS <70, tumor dimension >6 cm, tumor crossing midline, preoperative neurological deficit of more than minor degree.One or no deletions on 1p and 19q, IDH1 or 2 not mutated, increased perfusion on imaging are also adverse factors that may be considered."ASTR-2• No prior fractionated external-beam pathway: the term "progression" was removed.
The Foot and Ankle: Their Injuries, Diseases, Deformities and Disabilities with Special Application to Military Practice
Journal: JAMA (1942)

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
Exploiting Defective DNA Repair in <i>IDH</i>-Mutant Cancers
Journal: Cancer Discovery (2017)

Abstract Data from a preclinical study suggest rethinking the “oncometabolite hypothesis,” which calls for blocking the product of neomorphic IDH1/2 mutations to halt tumor progression. Instead, exploiting the vulnerability of IDH1/2-mutant tumor cells to PARP inhibition, as a result of defective DNA repair, appears to be a more effective strategy that will soon be tested in the clinic.
Control and direction of allied health education. Education for teamwork and independent work
Authors: M. L. Moore
Journal: JAMA (1971)

When I was asked to discuss<i>control</i>and<i>direction</i>of allied health education programs—especially with regard to teamwork as well as independent work—I was saddened. To discuss<i>control</i>and<i>direction</i>does not suggest teamwork, and our major need is to<i>plan</i>for services to the public by preparing a sufficient quantity and quality of personnel—personnel who should be working cooperatively to meet the needs of the public. Perhaps we have a hidden agenda and actually are discussing control in a diverse way. We must determine for whom, by whom, and for what purpose control is instituted and for whom and for what purpose education is needed. Control may be exercised by forces—tangible and intangible—and is related to fear, status, and power. Basically, management and direction of a curriculum come through the budget. Four primary areas are involved in the regulatory process: (1) the selection, recognition, rank, and salary of the
Phase II trial of bevacizumab in persistent or recurrent epithelial ovarian cancer (EOC) or primary peritoneal cancer (PPC): A Gynecologic Oncology Group (GOG) study
Authors: R. A. Burger, M. Sill, B. J. Monk, B. Greer, J. Sorosky
Journal: Journal of Clinical Oncology (2005)

5009 Background: Development of targeted therapeutics is considered critical to improve outcomes for patients with EOC/PPC. Vascular Endothelial Growth Factor (VEGF) appears to be a promoter of tumor progression via induction of angiogenesis. Bevacizumab is a recombinant humanized anti-human VEGF monoclonal antibody recently FDA-approved to treat metastatic colorectal cancer. Methods: Eligible patients had persistent or recurrent EOC/PPC after receiving 1–2 prior cytotoxic regimens, measurable disease, and GOG performance status ≤ 2. Treatment consisted of bevacizumab 15 mg/kg IV Q 3 weeks until disease progression or prohibitive toxicity. Primary endpoints were progression-free survival (PFS) at 6 months, objective response rate, and toxicity by NCI criteria. The single-stage design limits the probability of declaring the agent active to 10% when inactive according to both tumor response and PFS at 6 months but is capable of detecting activity on either scale with 90% power. Results: From 4/02 to 8/04, 64 patients were enrolled. Two were excluded for wrong primary and borderline histology; thus, the sample included 62 patients. Median age was 57 (range 18–79) years, and prior treatment consisted of 1 or 2 regimens in 23 and 39 patients, respectively. The median disease free interval from completion of primary cytotoxic chemotherapy to first recurrence was 6.5 months. Early results showed some patients had confirmed objective responses and PFS in some was at least 6 months. The following grade 3 or 4 toxicities were observed: allergy (1 grade 3), cardiovascular (4 grade 3; 1 grade 4), gastrointestinal (3 grade 3), hepatic (1 grade 3), pain (2 grade 3), and pulmonary (1 grade 4). As of 11/15/04, 36 patients were off study, including 29 for disease progression and 1 for toxicity in 33 cases reported. Conclusions: Preliminary evidence exists for objective responses to bevacizumab, presumably a cytostatic agent. Efficacy and toxicity data for this study is expected to reach maturity and be analyzed in March, 2005, and comprehensive results will be presented. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Genentech BioOncology
Psychiatry
Journal: JAMA (1999)

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
Introduction
Authors: P.-P. Tak
Journal: Annals of the Rheumatic Diseases (2011)

It is a great privilege to host the 31st European Workshop for Rheumatology Research in Amsterdam, the Netherlands from 3 -6 March 2011.According to its unique tradition mastered through more than 30 years, EWRR 2011 will provide the opportunity for young and established researchers to present their recent work and meet colleagues from Europe and other parts of the world.The target audience for this meeting includes young scientists active in European rheumatology.In addition, key opinion leaders in (experimental) rheumatology as well as their counterparts from basic science attend this meeting.As such it represents an important networking event, and it is considered one of the most infl uential meetings in rheumatology worldwide.Many new insights into pathogenesis and treatment of infl ammatory disease will be discussed during the meeting.Presentations of posters and oral abstract presentations by young scientists are at the heart of the workshop.Selected lectures by world leaders in the fi eld of immune-mediated infl ammatory disease will provide a broad perspective and serve as an introduction to these presentations.This format traditionally facilitates optimal interactions.The congress centre and hotel are just a short walk from Central Station and situated in the historic city centre of charming Amsterdam.Thus, besides the scientifi c program, you will have the chance to enjoy Amsterdam's lively atmosphere.We hope that EWRR 2011 will be an interesting meeting for you and that you will enjoy your stay.
Circumferential fingernail
Authors: G F Alves, E Poon, J John, P R Salomao, W A D Griffiths
Journal: British Journal of Dermatology (1999)

We describe a Brazilian girl with a congenital circumferential nail on her left ring finger associated with other bony and soft tissue abnormalities of the affected limb. The tubular nail plate resembling a punch biopsy has been described as a circumferential nail, an extremely rare congenital malformation that can be associated with other congenital anomalies. In our review of the literature, there have only been two previous reports of this unusual condition affecting the fingernails.
A MODIFICATION OF THE BALDY-WEBSTER OPERATION
Journal: JAMA (1921)

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
Münchener Medizinische Wochenschrift
Journal: JAMA (1967)

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