tbuckley/cabot-search huggingface dataset:
LSD Use Among US High School Students
Authors: Keith Schuchard
Journal: JAMA (1994)

<h3>To the Editor.</h3> —We have recently presented data<sup>1</sup>from our annual survey of 522 328 junior and senior high school students from schools across the United States. This anonymous questionnaire on the prevalence of drug use was administered to all junior and senior students attending home rooms in these schools in 1993, and results were compared with 1992. Hallucinogen use increased significantly (<i>P</i>&lt;.01,<i>t</i>test), from 4.9% to 5.3%. Also, 83% of hallucinogen users reported most often getting "very high" or "bombed/stoned" when they used hallucinogens, as compared with 24% of beer drinkers, 66% of marijuana smokers, and 74% of cocaine users. Our experience suggests that many young people believe that cocaine is very dangerous. However, these same young students appear to believe that LSD is "spiritually uplifting." In our survey, 55% of high school seniors believed that trying LSD a few times is not harmful. These data
Health-Related Quality of Life Among Persons With Epilepsy--Texas, 1998
Journal: JAMA (2001)

Epilepsy is a central nervous system disorder characterized by unprovoked, recurrent seizures that may affect physical, mental, or behavioral functioning. In 1995, approximately 2.3 million persons residing in the United States had epilepsy. Approximately 181,000 new cases of epilepsy are diagnosed each year, with annual estimated costs of $12.5 billion in medical care and lost productivity. Because epilepsy has a substantial impact on health (e.g., physical and psychosocial difficulties, side effects of anticonvulsant therapy, lifestyle restrictions, and perceived stigmatization), self-reported physical and mental health-related quality of life (HRQOL) measures are useful in gauging the impact of epilepsy on persons with the disorder. Persons with chronic health disorders are at risk for impaired HRQOL. Few studies have examined the HRQOL of persons with epilepsy, and none has used a representative sample of adults residing in the United States. This report examines data from the 1998 Texas Behavioral Risk Factor Surveillance System (BRFSS) that included a question about epilepsy; findings indicate that persons with epilepsy reported substantially worse HRQOL than persons without epilepsy. Community-based interventions such as the Sepulveda Epilepsy Education Program that address medication self-management, psychosocial self-management, and other education interventions can improve the quality of life for persons with epilepsy.
VITAMIN D IN BLOOD AND IN MILK
Journal: JAMA (1934)

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
Changes in S-adenosylmethionine synthetase in human liver cancer: Molecular characterization and significance
Authors: J Cai
Journal: Hepatology (1996)

S-adenosylmethionine synthetase (SAMS) catalyzes the formation of S-adenosylmethionine (SAM) and is essential to normal cell function. There are two forms of SAMS, liver-specific and nonliver-specific (often referred to as "kidney"), which are products of two different genes. SAMS isoenzymes differ greatly in kinetic parameters and sensitivity to inhibition by methionine analogs. The current work studied changes in SAMS and their significance in liver cancer. Northern blot analysis showed that while normal liver expresses only liver-specific SAMS, both HepG2 and HuH-7 cells express only nonliver-specific SAMS. Absence of liver-specific SAMS messenger RNA (mRNA) was not because of gene deletion or rearrangement but complete lack of gene transcription. Reverse-transcription polymerase chain reaction (RT-PCR) with liver-and kidney-specific SAMS primers showed that liver-specific SAMS mRNA was absent with only kidney SAMS mRNA present in HepG2, HuH-7, Hep3B, and HuH-1 cells, and four consecutive hepatocellular carcinoma (HCC) specimens. Normal liver tissues from the same patients express both forms of SAMS mRNA. As a result of the change in SAMS expression, SAMS activity was higher in HepG2 and HuH-7 cells at physiologically relevant methionine concentrations but lower at high (mmol/L) methionine concentrations than rat hepatocytes. Treatment with ethionine and seleno-D,L-ethionine, two inhibitors known to have I50 values 50 to 60 times lower against SAMS purified from Novikoff hepatoma cells as compared with SAMS purified from normal rat liver, resulted in increased cell lysis in HepG2 and HuH-7 cells but not cultured rat hepatocytes. These agents did not affect cellular adenosine triphosphate (ATP) levels but inhibited SAMS activity in HepG2 and HuH-7 cells when added to their protein extracts. In summary, expression of SAMS is altered in human liver cancer. This occurrence may provide a potentially exploitable target for cancer chemotherapy.
Clinical significance of monitoring <i>KRAS</i> in tissue and serum of pancreatic cancer patients.
Authors: Fumiaki Watanabe, Koichi Suzuki, Hideki Ishikawa, Yuhei Endo, Kosuke Ichida, Yuji Takayama, Taro Fukui, Nao Kakizawa, Naoya Kasahara, Takaharu Kato, Hiroshi Noda, Toshiki Rikiyama
Journal: Journal of Clinical Oncology (2018)

286 Background: KRAS monitoring provides valuable information for early diagnosis and prediction of treatment outcome in colorectal cancer. KRAS mutation is observed in only half of colon cancer patients, whereas it is detected in 90% of pancreatic cancer patients. Therefore, investigating tumor DNA in serum by KRAS monitoring may be even more valuable in pancreatic cancer patients. In this study, we elucidated the clinical significance of KRAS monitoring in pancreatic cancer patients during treatment. Methods: KRAS in tumor tissues was analyzed for mutations by Scorpion ARMS or RASKET in 69 patients with pancreatic tumors. KRAS in serum was analyzed for mutations (G12D, G12V, G12C, G12A, G12S, G12R, G13D, Q61L, and Q61H) using droplet digital polymerase chain reaction in 58 patients who underwent the curative surgery (N = 39) or the chemotherapy (N = 19) and who had KRAS mutation in their tissues. Results: KRAS mutation in tumor tissues was detected in 62 of 69 patients (92.5%). These 62 patients showed significantly poorer prognosis (3years overall survival; 43.9%) than the seven patients without mutation (p = 0.03), who were all alive. Monitoring of KRAS in serum revealed KRAS mutation in 22 of 58 patients (37.9%). In patients who underwent the chemotherapy (N = 19), 2years OS of patients who detected KRAS mutation in serum (N = 9) was 0% and them which not detected it (N = 10) was 46.7% (p = 0.01). And in the curative resection group (N = 39), we detected KRAS mutations in serum among recurrent patients after surgery, but did not detect them among non-recurrent patients. Conclusions: KRAS mutation in serum could be a valuable predictive and prognostic biomarker in pancreatic cancer patients. Additionally, assessment of KRAS in tumor tissues may provide information about individual tumor biology. So, monitoring KRAS status of patients with pancreatic cancer may be useful of the treatment strategy.
Protecting boxers who won't quit
Authors: C. Marwick
Journal: JAMA (1993)

MOVES to regulate boxing, in the interest of boxers' health and safety, are growing more forceful—and proponents aren't pulling any punches. At the Seventh International Symposium on the Medical Aspects of Boxing, held in New York, NY, speakers called for the establishment of a national regulatory agency for the sport in the United States. This agency would enforce uniform medical standards to be followed in all states. Currently, the rules governing professional boxing and enforcement of these rules vary widely. Some states, such as New York, set high standards, including prefight physical examinations that are administered through the state's athletic commission. Other states, such as Oklahoma, have no regulatory body at all. Boxing officials say that a fighter who is denied a license to fight in New York will go to another state that has no medical standards, or that may not perform tests that are routine in New York.
Abstract 282: Vimentin serves as a signaling scaffold at focal adhesion sites to regulate lung cancer cell adhesion.
Authors: Lauren Havel, Adam I. Marcus
Journal: Cancer Research (2013)

Abstract Vimentin is a dynamic type III intermediate filament that is overexpressed in various cancers including non-small cell lung cancer (NSCLC). It is a classic biomarker for highly invasive tumors and is associated with increased likelihood of metastasis and poor survival. Vimentin filaments are dynamic and localize to focal adhesions, where they assemble and disassemble to promote cell migration. Our data show that vimentin depletion reduces cell adhesion and phosphorylated focal adhesion kinase (pFAK); therefore, we hypothesize that vimentin acts through FAK to regulate cell adhesion and metastasis. We show that vimentin filaments enter pFAK- and pSrc-positive focal adhesion sites, and upon vimentin depletion, pFAK, pSrc and total FAK levels decrease. To explore the mechanism behind this observation, we performed a phospho-proteomic screen for proteins whose phosphorylation is altered upon vimentin loss. One of the identified proteins was a guanine nucleotide exchange factor (GEF) that regulates rac1. We show that vimentin loss leads to GEF mis-localization and downstream rac1 inactivation. Furthermore, inactivation of the GEF itself resulted in aberrant cellular adhesion and loss of pFAK. Based upon this data, we propose that vimentin serves as a signaling scaffold to regulate FAK via a rac1-GEF interaction. This work provides insight into the mechanism by which vimentin affects cell adhesion and potentially NSCLC metastasis. Citation Format: Lauren Havel, Adam I. Marcus. Vimentin serves as a signaling scaffold at focal adhesion sites to regulate lung cancer cell adhesion. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 282. doi:10.1158/1538-7445.AM2013-282
Reply
Authors: Elliot B. Tapper, Anna S.‐F. Lok, Grace L. Su
Journal: Hepatology (2017)

Potential conflict of interest: Nothing to report. We thank Dr. Zheng and colleagues for their interest in our study on the risk of hepatic encephalopathy in a population‐based cohort of American veterans.1 Zheng et al. indicated that our study included few Asians. Given that our model was comprised of markers of liver function (albumin and bilirubin) and clinically significant portal hypertension (use of nonselective beta‐blockers) but not race, we have little reason to suspect that the performance of this model will be different in Asians. Zheng et al. questioned whether the impact of statins is linked to obesity, which they posit to be more prevalent in American patients with cirrhosis. Available data suggest that the beneficial effect of statins in patients with portal hypertension is related to improvements in vascular endothelial function and decreased inflammatory response to gut bacteria and not to cholesterol‐lowering.1 Indeed, there are data that statins prevent decompensation in Asian patients with hepatitis B–related cirrhosis.2 Zheng et al. posit that hepatitis B may be associated with cognitive changes (which may not have been captured in our data set).3 To our knowledge, evidence to support an effect of hepatitis C virus (more prevalent in our cohort) on cognition and brain function is more robust.4 However, and more importantly, there are no data linking the cerebral effects of either hepatitis B or C virus to development of hepatic encephalopathy in patients with no cirrhosis or increased risk of hepatic encephalopathy in those with cirrhosis.
Phenotypic and functional characterization of intrahepatic T lymphocytes during chronic hepatitis C
Authors: V Leroy
Journal: Hepatology (2003)

The pathogenesis of liver cell injury during chronic hepatitis C (CHC) is poorly understood. The cellular immune response is thought to play a key role in both inhibition of viral replication and liver pathology. However, little is currently known about which lymphocyte populations and which immune effectors contribute to or control liver damage. We investigated a panel of 15 phenotypic and functional markers of intrahepatic T-lymphocyte subsets irrespective of their antigen specificity in 48 hepatitis C virus (HCV)-infected patients and 8 healthy control subjects. Lymphocyte characteristics were evaluated from liver biopsy specimens both at gene expression level by real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR) and by immunochemistry, in relation with the degree of liver injury and with intrahepatic HCV-RNA levels. As compared with controls, we found major changes in T-lymphocyte subsets in HCV-infected patients, with a significant decrease of T-cell antigen receptor (TCR) δ and CD56 gene expression, associated with a concomitant increase of TCRα and CD8β that were correlated with cytotoxic factors, proinflammatory chemokines, and chemokine receptors including peforin, interferon gamma (IFN-γ), tumor necrosis factor α (TNF-α), RANTES, and CXCR3. The gene expression of CD8β, a specific marker for conventional TCRα+CD8+ lymphocytes, was correlated by multivariate analysis with both alanine aminotransferase (ALT) serum levels and histologic activity index. Furthermore, CD8 staining was observed by immunochemistry in the areas of lobular and piecemeal necrosis. In contrast, no lymphocyte marker was correlated with viral load, measured both in serum and in liver. In conclusion, these results strongly suggest key roles for CD8+ T cells as effectors of liver damage during chronic HCV infection and for their inability to control viral replication. (Hepatology 2003;38:829–841).
Manual of Medicine.
Journal: JAMA (1927)

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
News and Notices
Journal: British Journal of Dermatology (1983)

British Journal of DermatologyVolume 108, Issue 6 p. 741-741 News and Notices First published: June 1983 https://doi.org/10.1111/j.1365-2133.1983.tb01098.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume108, Issue6June 1983Pages 741-741 RelatedInformation
DNA Adduct Measurements and Tumor Incidence during Chronic Carcinogen Exposure in Rodents
Authors: Miriam C. Poirier, Frederick A. Beland
Journal: Environmental Health Perspectives (1994)

In an attempt to elucidate the relationship between DNA adduct formation and tumorigenesis, DNA adducts were measured in the livers and bladders of mice during chronic exposure to several different doses of 2-acetylaminofluorene (2-AAF) and 4-aminobiphenyl (4-ABP).Continuous oral adminis- tration of these compounds for 4 weeks produced an increase in DNA adduct formation during the first 2 weeks, followed by a plateau, which pre- sumably occurred because the rate of adduct removal offset the rate of adduct formation.The quantity of DNA adducts present at equilibrium correlated directly with the carcinogen concentration; therefore, when exposure was continued for 4 weeks, DNA adducts that reflected the plateau level at each dose could be expressed as a function of dose.Liver and bladder DNA adduct profiles thus obtained during administration of multiple doses of 2-AAF (to female mice) and 4-ABP (to male and female mice) were compared to profiles for tumor incidences obtained during lifetime exposures to the same doses.These experiments demonstrated similar profiles for DNA adduct formation and tumorigenesis in liver.In the bladder, DNA adducts were linear, but tumors only appeared at the higher doses in conjunction with cell proliferation.In addition to these aromatic amines, similar data are available for aflatoxin B1, diethylnitrosamine, and (methyinitrosamino)-1-(3-pyridyl)-1-butanone (also known as nicotine-derived nitrosoketone).Of the nine different biological situations (carcinogen/species/sex/organ) for which data are available, correlations between steadystate DNA adduct levels and tumorigenic response at the different doses were linear in five of the nine biological models.When the relationship between DNA adduct formation and tumor incidence was not linear, the profiles observed were considered to be the result of tissue-specific phe- nomena such as metabolic activation, cell proliferation, or cytotoxicity.-
Associations of Plasma Selenium with Arsenic and Genomic Methylation of Leukocyte DNA in Bangladesh
Authors: J. Richard Pilsner, Megan N. Hall, Xinhua Liu, Habibul Ahsan, Vesna Ilievski, Vesna Slavkovich, Diane Levy, Pam Factor-Litvak, Joseph H. Graziano, Mary V. Gamble
Journal: Environmental Health Perspectives (2010)

Background: Global hypomethylation of DNA is thought to constitute an early event in some cancers and occurs in response to arsenic (As) exposure and/or selenium (Se) deficiency in both in vitro and animal models.In addition, antagonism between As and Se, whereby each reduces toxicity of the other, has been well documented in animal models.Se status may therefore modify the health effects of As in As-exposed populations.oBjective: The primary objectives of our study were to test the hypothesis that Se deficiency is associated with genomic hypo methylation of lymphocyte DNA and to determine whether Se levels are associated with blood As (bAs) and urinary As (uAs) concentrations in adults exposed to As-contaminated ground water in Bangladesh.A secondary objective was to explore the relationships between plasma Se and As metabolites.design: We assessed plasma Se concentrations, As metabolite profiles in blood and urine, and genomic methylation of leukocyte DNA in a cross-sectional study of 287 adults.results: After adjustment for potential confounders, we observed an inverse association between Se (micrograms per liter) and genomic DNA methylation (disintegrations per minute per 1-µg/L increase in Se): β = 345.6;95% confidence interval (CI), 59-632.Se concentrations were inversely associated with total As concentrations (micrograms per liter) in blood (β = -0.04;95% CI, -0.08 to -0.01) and urine (β = -20.1;95% CI, -29.3 to -10.9).Se levels were negatively associated with the percentage of mono methyl arsinic acid (β = -0.59;95% CI, -1.04 to -0.13) and positively associated with the percentage of dimethyl arsinic acid (β = 0.53; 95% CI, 0.04 to 1.01) in blood.conclusions: Our results suggest that Se is inversely associated with genomic DNA methyla tion.The under lying mechanisms and implications of this observation are unclear and warrant further investigation.In addition, Se may influence bAs and uAs concentrations, as well as relative proportions of As metabolites in blood.
Comparison of Transtracheal Aspiration with Other Methods of Determining the Bacterial Flora of the Lower Respiratory Tract
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
HEPATIC COMA
Journal: JAMA (1961)

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