tbuckley/cabot-search huggingface dataset:
A Complete Outline of Fractures (Including Fractures of the Skull) for Students and Practitioners
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The Chemical Laboratory and the Council on Pharmacy and Chemistry
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Possible etiologic mechanisms in chemical carcinogenesis.
Authors: E Farber
Journal: Environmental Health Perspectives (1987)

Some highlights in the development of our knowledge about carcinogens as etiological agents for cancer are reviewed briefly. Advances during the past 20 years relating to metabolic activation with the genesis of reactive metabolites, molecular targets and their interactions with activated carcinogens, oncogenes as molecular targets and the dependence on cell proliferation, all relating to the initiation process, are reviewed. Critical to initiation is the new phenotype in the initiated cell, known only in one instance, the rat liver, in which the characteristic change is one of resistance to many xenobiotic influences. The need for clonal expansion of initiated cells as essential for carcinogenic effects is discussed. Differential inhibition has been shown as a dominant mechanistic pattern in the liver. In other systems, the manner in which clonal expansion is achieved is not evident. The need for studies of the processes involved in carcinogenesis, as well as the agents, is emphasized, in view of the continuing validity of the cell concept as the key to integrating the increasingly large volume of data from the molecular with the biological.
WHY EAT RAISINS?
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
Dietary Modulation of DNA Adduct Formation of the Food Mutagen 2-Amino-3-Methylimidazo-[4,5-f]quinoline in the Male Fischer 344 Rat
Authors: Herman A. J. Schut
Journal: Environmental Health Perspectives (1994)

In numerous in vivo systems it has been shown that diets high in menhaden oil (a fish oil high in .-3fatty acids) can inhibit the carcinogenic process.In the present study, we have assessed the effects of a diet containing menhaden oil on 2-amino-3-methylimidazo[4,5-f]quinoline (IQ)-DNA adduct formation in target tissues of the male Fischer 344 rat.Young adult male Fischer 344 rats were maintained on either a) an AIN-76A diet containing 5% corn oil, b) an isocaloric AIN-76A diet modified to contain 2% corn oil and 19% menhaden oil (MO diet), or c) a regular laboratory rodent diet (chow diet) for 6 weeks prior to receiving a single oral dose of 10 or 50 mg IQ/kg.Groups of four animals were killed 1 or 6 days after IQ administra- tion.Using 32P-postlabeling assays, IQ-DNA adducts were isolated and quantitated in the liver, small intestine, and large intestine.Adduct patterns were similar in all cases.Adduct levels, expressed as relative adduct labeling values (RAL x 107), were related to dose in all three tissues, with liver levels up to 1 0-fold higher than the large intestine and up to 20-fold higher than the small intestine.On day one, liver adduct levels in animals on the AIN-76A diet were similar to those in animals on the chow diet, but those in animals on the MO diet were approximately 2-fold lower.On day six, these differences were much lower, probably as a result of the more efficient removal of liver adducts in animals on AIN-76A or chow diets.In the intestines, removal of adducts in animals on either AIN-76A or MO diet was slower than that in the liver, while that in animals on the chow diet was similar to that in the liver.While dietary MO is generally thought to inhibit experimental tumorigenesis at the promotional stage, the present results show that MO diets may also inhibit the initiation process by inhibiting the initial rate of IQ-DNA adduct formation.It also appears, however, that MO diets may impair the process of adduct removal.
MAC
Journal: JAMA (1979)

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
Perforation of Heart During Cardiac Catheterization and Selective Angiocardiography
Journal: JAMA (1963)

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
Panobinostat (LBH589) in Combination with the β-Catenin Inhibitor Tegavivint (BC2059) Exerts Significant Anti-Myeloma Activity Both in Vitro and In Vivo
Authors: Ioanna Savvidou, Tiffany Khong, Sophie Whish, Tara Sepehrizadeh, Sridurga Mithraprabhu, Michael DeVeer, Andrew Spencer
Journal: Blood (2019)
The MILO (MEK inhibitor in low-grade serous ovarian cancer)/ENGOT-ov11 study: A multinational, randomized, open-label phase 3 study of binimetinib (MEK162) versus physician’s choice chemotherapy in patients with recurrent or persistent low-grade serous carcinomas of the ovary, fallopian tube, or primary peritoneum.
Authors: Bradley J. Monk, Rachel N. Grisham, Christian Marth, Susana N. Banerjee, Felix Hilpert, Robert L. Coleman, Eric Pujade-Lauraine, Sandro Pignata, Mansoor Raza Mirza, Amit M. Oza, Josep M. del Campo, Martin Klaus Oehler, Adam James, Janna Christy-Bittel, Emma Barrett, Adam P. Boyd, Ignace Vergote
Journal: Journal of Clinical Oncology (2015)

TPS5610 Background: Low-grade serous (LGS) carcinomas of the ovary, fallopian tube and primary peritoneum are a unique subset of serous carcinomas for which current therapies (chemotherapy, hormonal) have demonstrated limited efficacy. KRAS or BRAF mutations, which activate the RAS/RAF/MEK/ERK signaling pathway, are present in many LGS carcinomas. Binimetinib is a potent inhibitor of MEK1/2, a key component of the RAS/RAF/MEK/ERK pathway, and has demonstrated activity in other disease settings where dysregulation of this pathway is present. Methods: This is a 2-arm, open-label, 2:1 randomized Phase 3 study of binimetinib vs physician's choice chemotherapy (pegylated liposomal doxorubicin, paclitaxel or topotecan) in patients with LGS carcinomas. Eligible patients must have LGS carcinoma that is recurrent or persistent following at least 1 prior platinum-based chemotherapy and no more than 3 prior lines of chemotherapy, and must have RECIST v1.1-defined measurable disease confirmed by blinded independent central review (BICR). Prior to randomization, confirmation of LGS diagnosis is required. Patients are eligible regardless of RAS/RAF mutational status; however, tumor tissue will be retrospectively analyzed for mutations in RAS/RAF and other genes. Prior treatment with a MEK inhibitor or BRAF inhibitor is prohibited. Randomization is stratified by last platinum-free interval and number of prior systemic therapy regimens. The primary endpoint is progression-free survival as determined by the BICR; secondary endpoints include overall survival, overall response, duration of response, disease control rate, safety, quality of life and pharmacokinetics of binimetinib. Binimetinib is administered 45 mg BID orally. Patients receive therapy until disease progression or unacceptable toxicity. Crossover is permitted from physician's choice chemotherapy to binimetinib upon BICR-confirmed progression. This study will enroll 300 patients worldwide (NCT01849874). Clinical trial information: NCT01849874.
Non-Q-Wave Myocardial Infarction: Pathophysiology, Prognosis, And Therapeutic Strategy
Authors: R. Gibson
Journal: Annual Review of Medicine (1989)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Functional consequences of somatic mutations in cancer using protein pocket-based prioritization approach
Authors: Huy Vuong, Feixiong Cheng, Chen-Ching Lin, Zhongming Zhao
Journal: Genome Medicine (2014)

Recently, a number of large-scale cancer genome sequencing projects have generated a large volume of somatic mutations; however, identifying the functional consequences and roles of somatic mutations in tumorigenesis remains a major challenge. Researchers have identified that protein pocket regions play critical roles in the interaction of proteins with small molecules, enzymes, and nucleic acid. As such, investigating the features of somatic mutations in protein pocket regions provides a promising approach to identifying new genotype-phenotype relationships in cancer. In this study, we developed a protein pocket-based computational approach to uncover the functional consequences of somatic mutations in cancer. We mapped 1.2 million somatic mutations across 36 cancer types from the COSMIC database and The Cancer Genome Atlas (TCGA) onto the protein pocket regions of over 5,000 protein three-dimensional structures. We further integrated cancer cell line mutation profiles and drug pharmacological data from the Cancer Cell Line Encyclopedia (CCLE) onto protein pocket regions in order to identify putative biomarkers for anticancer drug responses. We found that genes harboring protein pocket somatic mutations were significantly enriched in cancer driver genes. Furthermore, genes harboring pocket somatic mutations tended to be highly co-expressed in a co-expressed protein interaction network. Using a statistical framework, we identified four putative cancer genes (RWDD1, NCF1, PLEK, and VAV3), whose expression profiles were associated with overall poor survival rates in melanoma, lung, or colorectal cancer patients. Finally, genes harboring protein pocket mutations were more likely to be drug-sensitive or drug-resistant. In a case study, we illustrated that the BAX gene was associated with the sensitivity of three anticancer drugs (midostaurin, vinorelbine, and tipifarnib). This study provides novel insights into the functional consequences of somatic mutations during tumorigenesis and for anticancer drug responses. The computational approach used might be beneficial to the study of somatic mutations in the era of cancer precision medicine.
Death Investigation — United States, 1987
Journal: JAMA (1989)

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
Insulin Pharmacokinetics
Authors: Christian Binder, Torsten Lauritzen, Ole Faber, Stig Pramming
Journal: Diabetes Care (1984)

Where adjustments of diet, physical activity, and dosage of insulin are well known to diabetologists and diabetic patients, present-day knowledge of factors of importance to the pharmacokinetics of insulin is frequently ignored. The pharmacokinetics of insulin comprise the absorption process, the distribution including binding to circulating insulin antibodies, if present, and to insulin receptors, and its ultimate degradation and excretion. The distribution and metabolism of absorbed insulin follow that of endogenous insulin. The distribution and metabolism cannot be actively changed, except in the case of circulating insulin antibodies, which in rare cases also may cause insulin resistance. The use of insulin preparation of low immunogeneity will avoid or reduce this course of variation in action. The absorption process, the detailed mechanisms of which are still unknown, is influenced by many variables where some can be controlled, thereby reducing the intrapatient variability in insulin absorption, which may reach 35%, causing a corresponding metabolic lability. Besides the known differences in timing among different preparations, the size of dose, the injected volume, and the insulin concentration are determinants of absorption role. Fortuitous injection technique contributes to variance, as do changes in blood flow of the injected tissue. This may be induced by changes in ambient temperature, exercise of injected limb, or local massage. Regional differences are also due to differences in blood flow. Serum insulin peaks may peak up to 1 h after injection of soluble insulin into the thigh versus into the abdominal wall. Local degradation of insulin seems of less importance but may, in rare cases, be the cause of high insulin “requirements.” Available evidence is reviewed and the importance of implementing the consequences in the daily care of the insulin-treated patient is emphasized.
PRMT1 Interacts with AML1-ETO to Promote Its Transcriptional Activation and Progenitor Cell Proliferative Potential
Authors: Wei-Jong Shia, Akiko J. Okumura, Ming Yan, Ali Sarkeshik, Miao-Chia Lo, Shinobu Matsuura, Yukiko Komeno, Xinyang Zhao, Stephen D. Nimer, John R. Yates, Dong-Er Zhang
Journal: Blood (2011)
Newer concepts in hypertrophic obstructive cardiomyopathy II
Authors: P. M. Shah
Journal: JAMA (1979)

THE SYMPTOMS, when present, are generally those of left ventricular outflow obstruction, namely, dyspnea, syncope, angina, and palpitations. It is not uncommon to see a patient for evaluation of a murmur detected during a routine examination. <h3>Clinical Features</h3><h3>Dyspnea.—</h3> Effort dyspnea and paroxysmal nocturnal dyspnea constitute the most common symptoms and represent evidence of pulmonary congestion. Because elevations in pulmonary venous and left atrial pressures occur in the face of a hyperdynamic, hypercontractile left ventricle, these must necessarily be attributed to reduced compliance of the ventricle. In some patients, especially those with volume overload, frank pulmonary edema may be noted. <h3>Syncope and Dizziness.—</h3> Frank syncope and dizziness short of loss of consciousness (presyncope) are common. These are generally effort related although not predictably so. The frequency of the episodes is highly variable. The exact mechanism is obscure; however, it is probably related to reflex vasodilation and hypotension induced by stretching
Daunorubicine in acute myelogenous leukemia in adults
Authors: R. S. Bornstein
Journal: JAMA (1969)

Daunorubicine (daunomycin, rubidomycin) is an antibiotic with antitumor activity in a wide variety of transplantable animal tumors. Its biologic mechanism of action is by inhibition of deoxyribonucleic acid synthesis with a lesser inhibition on ribonucleic acid synthesis. It is effective in certain solid tumors, and clinical investigations show a potent antileukemic activity. Twelve adult patients with acute myelogenous leukemia were given daunorubicine, 1 mg/kg of body weight, daily for five days. Three complete and two partial remissions were obtained. Bone marrow hypoplasia was the primary toxic reaction encountered. This drug appears to be an effective therapy for the induction of remissions in adults with acute myelogenous leukemia. Since cardiopulmonary toxic reactions have been reported with large total doses of daunorubicine, maintenance therapy with other chemotherapeutic agents has been employed.
Influenza vaccination
Authors: M. A. Riddiough
Journal: JAMA (1983)

Cost-effectiveness analysis was used to evaluate influenza vaccination. From 1971-1972 through 1977-1978, vaccination of an elderly person 65 years of age or older saved net medical care costs while improving health. Vaccination of younger high-risk adults aged 15 through 64 years also improved health for a low net cost per year of healthy life gained. By covering influenza vaccination during those years, the Medicare program would have incurred a net cost for each vaccination of $13 per year of healthy life gained for medical costs connected with influenza and $791 per year gained including costs of treating other illnesses in later life. The analysis indicates the need for epidemiologic research on the extent of influenza and the mechanism of its spread. The results also raise the issue of public policy to promote influenza vaccination among high-risk persons as a low-cost, preventive technology. (<i>JAMA</i>1983;249:3189-3195)
Incorrect Study Group.
Journal: JAMA (1988)

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