tbuckley/cabot-search huggingface dataset:
Abstract P324: Abdominal Visceral Adiposity and Liver Fat in Relation to Sex-Related Differences in Cardiometabolic Risk Profile: The INSPIRE ME IAA Study
Authors: Julie-Anne Nazare, Jessica Smith, Anne-Laure Borel, Steven M Haffner, Beverley Balkau, Robert Ross, Christine Massien, Natalie Alméras, Jean-Pierre Després
Journal: Circulation (2012)

Objectives: Sex differences in the cardiovascular risk profile are well established. The objectives of the present analyses were 1) to characterize sex differences in visceral adiposity (VA) and estimated liver fat content assessed by computed tomography (CT) and in the cardiometabolic risk (CMR) profile in a large international multiethnic cohort; 2) to determine whether differences between men and women in CMR factors remain after controlling for VA and/or liver fat. Methods: In the International Study of Prediction of Intra-abdominal adiposity and its Relationship with cardioMEtabolic risk/Intra-Abdominal Adiposity (INSPIRE ME IAA), 297 primary care physicians, cardiologists, endocrinologists/diabetologists recruited 4504 patients from 29 countries. VA and liver attenuation (inversely correlated to liver fat) were assessed by CT. Cardiometabolic risk factors (triglyceride (TG), HDL-C, Apolipoprotein B (ApoB), HOMA, 2h-glucose (OGTT), adiponectin, C-Reactive Protein (CRP)) were assessed using standardized methods. The present cross-sectional analyses were performed in 1193 men and 1214 women free of type 2 diabetes. Results: Whereas mean BMI was similar in women and men (27.5±0.1 vs 27.5±0.1 kg/m2), men had higher waist circumference (98.1±0.4 vs 89.6±0.4 cm), higher VA (165±2 vs 131±2 cm2) and lower liver attenuation (54.9±0.3 vs 57.4±0.3 HU) (p&lt;0.0001 for all) than women. Men displayed higher TG and HOMA but lower HDLc, CRP and adiponectin levels (p&lt;0.001 for all) than women. In both sexes, VA and liver fat were significantly correlated positively with CMR variables: TG, HOMA and CRP and negatively with HDLc and adiponectin (p&lt;0.05 simple regression analysis). In multiple regression analyses, VA and liver attenuation independently affected CMR variables. Sex differences in TG were eliminated after adjustment for VA or both variables simultaneously but HDLc remained higher in women even after such adjustment. HOMA was higher in women when adjusted for VA or for both variables and similar to men when adjusted for liver attenuation. Being not different between sexes before adjustment, 2h-glucose was higher in women when controlling for VA/liver fat. Adiponectin remained higher in women after all adjustments. Sex differences in CRP were magnified after adjustment for VA/liver fat and remained higher in women. Conclusion: In this large standardized international CT-imaging/cardiometabolic study, substantial sex differences in abdominal adiposity/liver fat and CMR factors were observed, with men presenting an overall more deteriorated CMR profile than women. Controlling for VA and liver fat was not sufficient to abolish sex differences in all inflammatory, insulin sensitivity or lipid factors.
The making of a myth
Authors: L. E. Arnold
Journal: JAMA (1973)

In 1967, Millichap and Fowler<sup>1</sup>published a valuable review of the available literature studying drug treatment of hyperkinetic children. They broke down the adequately controlled studies into several tables. They further digested the information by combining and averaging the results from many studies to get the average percentages improved with each drug. Using these percentages, they listed the drugs in the order of apparent efficacy as "the closest approximation possible with the evidence available." At the head of the list, with 83% improvement, was methylphenidate hydrochloride (Ritalin). Next came dextroamphetamine sulfate (Dexedrine) with 69% improvement. The casual reader might jump to the conclusion that methylphenidate's superiority to dextroamphetamine had been established. However, the rest of the article had already made it clear that these two percentages were based on separate studies of different drugs by different investigators on different population samples with different dosages and different criteria of improvement.
Abstract 1926: Ba/F3 NTRK cell panel, a powerful cell model for NTRK inhibitor discovery and development
Authors: Feng Hao, Zhaoshuai Bai, Guoqian Wang, Feng He, Changpeng Liu, Jinying Ning
Journal: Cancer Research (2019)

Abstract NTRK (Neurotrophic tyrosine kinase receptor)family, also named as TRK (Tropomyosin receptor kinase),is composedof three transmembrane protein receptors, TrkA, TrkB and TrkC,which play important rolesin neuronal differentiation and survival. Over-activation of NTRK1, NTRK2 and NTRK3 due to chromosomal rearrangement and mutations, was found in congenital fibrosarcoma, secretory breast carcinoma cancer and other types ofcancer. The identification of NTRK fusions as diver cancer genes has led to rapid development of anticancer therapeutic agents, including LOXO101, LOXO195 and TPX0005.Ba/F3 line is a popular system for studying both kinases and their inhibitors, because some protein kinases can render the Ba/F3 cells to be depended on the activation of the kinases instead of IL-3 supplement, while their inhibitors can antagonize the kinase-dependent growth effects. Our group used Ba/F3 cells togenerate a celllinepanel with 14 different NTRK fusion genes or mutations for NTRK inhibitor screening and development. Inaddition to use the cell lines for in vitro assays, thetransformed Ba/F3 linescan grow well in immune-deficient miceas in vivo models. LOXO101—a NTRK inhibitor—was used to test tumor growth inhibition, the results showedthat threewild-type fusion cell lineswere sensitive to LOXO101, but not other tumor models containing NTRK gatekeeper mutations. All the tumor models were sensitive to TPX0005, another NTRK inhibitor. Ourdata indicatethatthe celllinepanel of Ba/F3is apowerful cell model for new NTRK inhibitor discovery and development. Citation Format: Feng Hao, Zhaoshuai Bai, Guoqian Wang, Feng He, Changpeng Liu, Jinying Ning. Ba/F3 NTRK cell panel, a powerful cell model for NTRK inhibitor discovery and development [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 1926.
Antihypertensive Agents and Lipids
Authors: Bertram L. Kasiske
Journal: Annals of Internal Medicine (1995)

Letters15 October 1995Antihypertensive Agents and LipidsBertram L. Kasiske, MDBertram L. Kasiske, MDUniversity of Minnesota; Minneapolis, MN 55415Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-8-199510150-00018 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We appreciate Dr. Ernst's comments. His study of the effects of gallopamil [1] was unfortunately not included in our meta-analysis [2]. The report does not appear on MEDLINE, and it was apparently published too recently to have been mentioned in the bibliographies of the papers that we reviewed. However, the results of his study are not inconsistent with our conclusion that calcium antagonists had little effect on plasma lipids. Dr. Ernst noted apparent improvements in total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels during the uncontrolled, open-treatment phase of the study [1]. During the subsequent placebo-controlled phase, ...References1. Ernst E. Does gallopamil modify blood lipids? Drug Investigation. 1993; 6:42-7. Google Scholar2. Kasiske BL, Ma JZ, Kalil RS, Louis TA. Effects of antithypertensive therapy on serum lipids. Ann Intern Med. 1995; 122:133-41. Google Scholar Author, Article, and Disclosure InformationAuthors: Bertram L. Kasiske, MDAffiliations: University of Minnesota; Minneapolis, MN 55415 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 October 1995Volume 123, Issue 8Page: 634KeywordsBlood plasmaCalciumCholesterolClinical trialsHigh density lipoproteinLipidsLow density lipoprotein ePublished: 15 August 2000 Issue Published: 15 October 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Cancer drug sensitivity test has problems
Authors: Tom Hager
Journal: JAMA (1982)

A commercially available laboratory test for predicting the chemosensitivity of tumor cells is plagued by technical problems and appears to work effectively with only a few types of cancer, according to reports delivered at the 13th International Cancer Conference in Seattle. The Human Tumor Clonogenic Assay (HTCA)— also known as the human tumor stem cell assay—is an in vitro test designed to show whether a specific tumor is sensitive or resistant to a battery of anticancer drugs. In a manner analogous to bacterial sensitivity tests used for assigning antibiotics, HTCA results are now being used by some oncologists to tailor chemotherapy to the needs of individual patients. But a number of tumor types don't grow well—and leukemias and lymphomas don't grow at all—under the culture conditions used in the test. In addition, a National Cancer Institute (NCI) study has shown that HTCA is not sensitive to the effects of six
Evidence of preservation injury to bile ducts by bile salts in the pig and its prevention by infusions of hydrophilic bile salts
Authors: Martin Hertl, Robert P. C. Harvey, Paul E. Swanson, Delin D. West, Todd K. Howard, Surendra Shenoy, Steven M. Strasberg
Journal: Hepatology (1995)

Preservation injury to bile ducts is a serious problem in liver transplantation, especially when preservation exceeds 12 hours. The authors hypothesized that the injury was caused by contact of bile ducts with bile salts during cold preservation and might be preventable by infusion of more hydrophilic bile salts. Swine livers were harvested after intraportal infusions of saline (control), of the hydrophobic bile salt taurodeoxycholate, or of the hydrophilic bile salts tauroursodeoxycholate or dehydrocholate. The effect of infusing a combination of hydrophilic and hydrophobic bile acids was also studied. Bile samples were taken before and during the infusions. Then livers were perfused with UW solution, ducts were flushed retrograde with UW, and livers were stored at 0 to 1°C for 20 hours. Bile ducts were harvested after preservation, and coded microscopic slides of the specimens were examined by light microscopy. There was large variability in baseline bile salt concentration. Injury after preservation consisted of sloughing and pyknosis of surface and glandular epithelium. The histologic injury score determined after preservation was directly related to bile salt concentration in bile ducts at the time of flushing. During bile salt infusions, the infused bile salt replaced most or all of the other bile salts present in bile. Severe postpreservation injury of intrahepatic ducts occurred after taurodeoxycholate infusions, but injury was minimal when either of the two hydrophilic bile salts was infused. The mixture of bile acids produced intermediate results. Retrograde flushing with UW does not prevent injury to intrahepatic ducts. The authors conclude that the injury is caused by contact with bile salts, is dependent on bile salt concentration and composition, and is preventable. (Hepatology 1995; 21:1130-1137.)
European Perspectives
Journal: Circulation (2007)

P ercutaneous coronary intervention (PCI) and drug- eluting stents have rewritten the treatment of ischaemic heart disease, but chronic total occlusions (CTOs) still remain a major challenge for the interventional cardiologist.The crossing of such occlusions is well established, and failure to cross the lesion using conventional guidewire technology often prevents or impairs repair of the lesion in the catheter laboratory.Attention should now be focused on increasing the initial success rate, according to Dr Masahiko Ochiai, professor and cardiologist at the Division of Cardiology and Cardiovascular Medicine, Showa
Ophthalmology
Authors: F. C. Blodi
Journal: JAMA (1978)

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
Lumbar Puncture—Induced Meningitis
Authors: Robert H. K. Eng
Journal: JAMA (1981)

A retrospective study was done to evaluate the risk of lumbar puncture—induced meningitis. Fourteen percent (23/165) of patients with bacteremia caused by<i>Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitis</i>, and groups A and B streptococci had spontaneous meningitis (without a preceding lumbar puncture). In contrast, only 0.8% (7/924) of patients with blood culture containing other organisms had spontaneous meningitis and 2.1% (3/140) of these patients had clinical courses consistent with lumbar puncture—induced meningitis. However, the 2.1% incidence in the latter group is not significantly different from 0.8%, the expected incidence of spontaneous meningitis. It is suggested that if lumbar puncture—induced meningitis does occur, it is rare enough to be clinically insignificant. (<i>JAMA</i>1981;245:1456-1459)
INVESTIGATIONS OF THE TITANIC DISASTER—AMERICAN AND BRITISH
Journal: JAMA (2012)

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
Brain Death
Authors: Edward V. Spudis
Journal: JAMA (1978)

<h3>To the Editor.—</h3> The discussion of brain death by Veith et al (238:1651, 1977) was interesting. It is worrisome whenever bioscientists determine that any proposed criteria are infallible, especially with respect to such an ultimate decision as initiating a death certificate. The authors must be aware that the original EEG criteria for silence were modified to account for complete and incomplete recoveries in heavily sedated or hypothermic patients. Such patients may satisfy the electrical criteria for brain death. In the 1969 Harvard study such patients totaled three, or more than one in a thousand.<sup>1</sup>Are there no subtle environmental poisons that also dampen brain waves? Will there not be any synthetic reversible brain poisons discovered in 1982 or 1991? Which committee would add the new caveats? How would a new exception come to light in Kansas, for example, where the choiceless physician shall, under present law, pronounce death
Abstract 2347: NOD-like receptor NLRP12 suppresses hepatocellular carcinoma via regulation of JNK signaling
Authors: Hasan Zaki
Journal: Cancer Research (2019)

Abstract Hepatocellular carcinoma (HCC) is a deadly human cancer associated with chronic inflammation. The cytosolic pathogen sensor NLRP12, a member of NOD-like receptor, has emerged as a negative regulator of inflammation, but its role in HCC is unknown. Here we investigated the role of NLRP12 in HCC using mouse models of HCC induced by carcinogen diethylnitrosamine (DEN) or DEN plus hepatotoxin carbon tetrachloride (CCl4). Livers collected from wild-type and Nlrp12-/- mice at 10 and 5.5 months following DEN or DEN plus CCl4 treatment, respectively, were examined for tumor burden, histopathological changes, expression of inflammatory and tumor-promoting genes, and activation of signaling pathways. Primary hepatocytes from healthy mice were isolated, cultured, and used to assess cell signaling, apoptosis, and proliferation. Cancer genomics database analysis showed that NLRP12 expression is significantly reduced in human HCC and 2-3% HCC patients carry mutations in NLRP12. Nlrp12-/- mice were highly susceptible to DEN or DEN plus CCl4-induced HCC with increased inflammation, hepatocyte proliferation, and tumor burden. Consistently, Nlrp12-/- tumors showed higher expression of proto-oncogenes cJun and cMyc and downregulation of tumor suppressor p21. Interestingly, antibiotics treatment dramatically diminished tumorigenesis in Nlrp12-/- mouse livers. Signaling pathway analyses demonstrated higher JNK activation in Nlrp12-/- HCC and cultured hepatocytes during stimulation with microbial pattern molecules. Inhibition of JNK activation or NLRP12 overexpression reduced proliferative and inflammatory responses of Nlrp12-/- hepatocytes. In summary, this study demonstrated for the first time that NLRP12 negatively regulates HCC pathogenesis via downregulation of JNK-dependent inflammation and proliferation of hepatocytes. Citation Format: Hasan Zaki. NOD-like receptor NLRP12 suppresses hepatocellular carcinoma via regulation of JNK signaling [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 2347.
Lucent lesion in the femoral neck
Authors: J. T. Ferrucci
Journal: JAMA (1967)

Dr. Joseph T. Ferrucci, Jr.: This patient, a 30-year-old surgeon, noted the sudden onset of pain in his left hip while descending a staircase four months prior to admission. The pain persisted and was slightly aggravated by extremes of motion. Night pain occasionally occurred. A roentgenogram six weeks prior to this admission revealed a lesion in the left femoral neck. Aspirin was administered with considerable relief of symptoms. The physical examination and laboratory studies were not remarkable, and this examination of the hip was performed (Figure). <h3>Discussion</h3> Dr. Laurence L. Robbins: Dr. Dreyfuss, do you have any ideas about this? Dr. Jack R. Dreyfuss: There is an area of rarefaction in the intertrochanteric region somewhat nearer the lesser trochanter. There is no periosteal reaction or sclerosis, and I do not see any other lesions. Actually, this is a fairly large area of lucency, measuring over 4 cm in length. It
Tests and Standards for New and Nonofficial Remedies: Containing Tests and Standards for Nonofficial Drugs and Dosage Forms Which Stand Accepted by the Council on Pharmacy and Chemistry of the American Medical Association on January 1, 1953
Journal: JAMA (1953)

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
Author index
Authors: A1 Mardini, E Alstead, G Cambie, M Capelli, J-P Capron, Carneiro Chaves, Neiro Car, G Casalgrandi, R Cauda, G Chabrier, G Chatelain, ] Chircu, G Colucci, Copius Peereboom-Stegeman, Jhj Coppo, G Corungiu, F 37 Costa, 96 Cottalasso, A-M 98 Courouc~, G Cucchiaro, D Agostino, D Alessandro, Dall Amore, Da Pian, D Arienzo, De Bac, De Berardinis, De Caprio, De Cou~t, De Fazio, De Groot, De Jong, De Jonge, Del Olmo, De Nie, ] De Peyer, De Santis, G Deverbizier, J J8 Deviere, De Vos, De Wolf-Peeters, C Dhumeaux, G-J Diao, Di Donato, Di Giacomo, D Inca, A Gerolami, G Gerunda, G Giovine, J Gom~z-Moli, R Grijm, J Grimaud, G Groce, Raf Krom, G Laffi, La Rosa, La Villa, J I~4 Lepetit, G Lesage, Martinez Pardo, Martins Alves, G Masini, G Mazzacca, G Meani, ] Melot, Meyer Zum B~schenfelde, Mieli -Vergani
Journal: Journal of Hepatology (1985)
License in Germany.
Authors: B. Becker
Journal: JAMA (1898)

Toledo, Ohio, Jan. 3, 1898. <h3>To the Editor:</h3> —In Dr. Blech's reply in the last issue of theJournal, he says: An American graduate can matriculate at a German university. That has not been denied, but he is not admitted to the State examination unless fulfilling the requirements as stated in my explanation. He says: The gymnasium embraces a curriculum of seven years only. The classes are<i>Sexta, Quinta, Quarta, Tertia B, Tertia A, Secunda B, Secunda A, Prima B, Prima A</i>, with one year's course in each equals nine years if one is passed every year, which is not always the case. Age for admission to<i>Sexta</i>is 10 years. As to<i>Gewerbefreiheit</i>, those are<i>the quacks</i>, and have no sheepskin of any kind, while the question under consideration is the<i>full fledged license to practice</i>. These few remarks to show that Dr. Blech's corrections are incorrect, and that