tbuckley/cabot-search huggingface dataset:
Football Brain Injuries Draw Increased Scrutiny
Authors: Brian Vastag
Journal: JAMA (2002)

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
Targeted inhibition of the novel gene EG-1 blocks tumor proliferation.
Authors: Ming Lu, Liping Zhang, Maryam R. Sartippour, Mai N. Brooks
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

5517 

We recently discovered a novel gene and named it EG-1 (endothelial derived gene-1). Previously, we have demonstrated that the expression of EG-1 is significantly elevated in the epithelial cells of breast cancer, colorectal cancer, and prostate cancer. We have also shown that EG-1 stimulates cellular proliferation both in vitro and in vivo. Here, we report that inhibition of EG-1 blocks cellular proliferation in vitro and in vivo. As endogenous EG-1 expression was knocked down by specific siRNA's, human breast tumor cellular proliferation was significantly inhibited. A subcutaneous xenograft assay was carried out in a nude mouse model. We found that mice injected with MCF-7 human breast cancer cells infected with siRNA lentivirus had significantly smaller tumors, in comparison with those injected with cells infected by control lentivirus carrying an empty vector alone. Furthermore, rabbit polyclonal antibodies against EG-1 resulted in significantly decreased in vitro proliferation of MCF-7, T47-D, MDA-MB-231, and MDA-MB-361 human breast cancer cells, in comparison to treatment with pre-immune rabbit serum. These observations suggest that the novel gene EG-1 may be a potential target for successful cancer therapy.
119. Studies on the Targeting of Adenoviral Vectors Carrying a Tumor-Cell Specific Peptide
Authors: Karola Rittner, Valerie Schreiber, Klaus Schughart, Nicolas Futin, Catherine Ledoux, Monika Lusky
Journal: Molecular Therapy (2004)

Previously, we have described the identification of a tumor cell-specific peptide HEW (full sequence: HEWSYLAPYPWF) by panning of phage display libraries on the human colorectal cancer cell line WiDr (Rasmussen et al. 2002, Cancer Gene Therapy, 9:606). This peptide sequence was inserted into the HI loop of the wt fiber knob and of the CAR° fiber knob S408E of Ad5E1° vectors containing the b-galactosidase reporter gene. The in vitro infectivity of these viruses on various cell lines was tested. The HEW containing viruses showed a significantly increased infectivity on WiDr cells, as well as on the human breast cancer cell line MDA-MB435, but not on SW480, LoVo, CaCo2, HeLa and 293 indicating that the molecular target of the HEW peptide is not an ubiquitous receptor. Moreover, while the S408E mutation induced a 100-fold decrease of infectivity on CAR-positive cells (e.g. 293 and WiDr cells) the simultaneous insertion of the HEW peptide restored tumor cell-specific high infectivity on WiDr but not on 293 cells. Competion assays confirmed that the HEW receptor was an alternative entry pathway for HEW viruses (Schreiber V, PhD thesis 2003). With these studies we have obtained proof of concept for a de-and re-targeted Ad vector platform in vitro
Abstract 19192: Utility of Cardiac Computed Tomography in Detecting Malposition of Left Ventricular Assist Devices Associated With Pump Thrombosis
Authors: Mahwash Kassi, Su-Yeon Choi, Andrea M Cordero-Reyes, Arvind Bhimaraj, Barry H Trachtenberg, Guha Ashrith, Matthias Loebe, Jerry D Estep, Su Min Chang
Journal: Circulation (2014)

Introduction: Pump thrombosis is a potentially life-threatening event that currently presents a diagnostic challenge. We therefore sought to explore the diagnostic utility and the association of measured cardiac computed tomography (CT) parameters in patients with LVAD malfunction due to pump thrombosis. Methods: From 2009 to 2013, 150 patients underwent placement of Heart Mate II continuous flow pump at our institution. Of these 52 patients, underwent cardiac CT with contrast either as part of a prospective protocol or for suspected malfunction. 14 patients had pump thrombosis per the INTERMACS criteria and the remaining were used as controls. Rigorous linear and area measurements for the inflow and outflow tracts of LVADs were performed. Results: The mean age of the population was 55 ± 11, 36 were male, and 28 had ischemic cardiomyopathy. Results are shown in table 1. For inflow cannula, measurement of axial area shown in figure 1, was significantly higher in the pump thrombosis group compared to the control group 31±16 cm2 vs 20 ± 12 cm2 (p=.02). Although, the difference in the acute angle for the inflow cannula relative to the perpendicular axis between the midpoint of the mitral annulus and tip of inflow cannulas was not significantly different between the two groups, there was a trend towards greater angulation in the pump thrombosis group (60 ± 6 vs 53 ± 15) and there was a positive correlation between both measurements r=0.513, p-value= 0.003. Conclusions: Area in the axial view of the ventricle at the site of the inflow cannula tip may be a surrogate for off axis placement of the cannula. This area may be helpful in predicting pump thrombosis in patients.
Initial clinical phenotype of COPD: Correlation with the natuaral history of the disease
Authors: Luca Fasano, A.M. Grazia Pacilli, Paolo Carbonara, Valerio Di Scioscio, Ilaria Valentini, Giacomo Mistè, Angela Montanari, Mario Fabbri, Maurizio Zompatori, Stefano Nava
Journal: European Respiratory Journal (2011)

The chronic airflow limitation characteristic of COPD is caused by a mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), the relative contributions of which vary from person to person.  Aim of this study was to evaluate, at the time of the first specialist evaluation, the differences in lung and cardiac function and HRCT extent of emphysema in patients with a spirometric diagnosis of COPD but different initial clinical presentation (chronic bronchitis [CB] versus dyspnea [Dy]). 45 consecutive patients referred to our outpatients service by their GP were divided according to their main first symptom (chronic bronchitis or dyspnea).Patients with Dy had an obviously higher dyspnea score vs those with CB (MRC 2.9±0.9 vs 2.3±0.6, p=0.02) and produced much less sputum (p 29 mm (a surrogate sign of pulmonary hypertension) 18/24 vs 8/21 pts, p=0.02). Dy group had larger CT emphysema extension score (35±16 vs 27±13%, even if this difference did not reach statistical significance, p=0.06). In conclusion we have shown differences between the two COPD phenothypes with similar airflow limitation, with CB patients showing worst ABGS and indirect signs of pulmonary hypertension, while Dy group was characterized by a higher degree of emphysema.
Inactivation of p16INK4 in hepatocellular carcinoma
Authors: A Hui
Journal: Hepatology (1996)

We analyzed the p16INK4 status of 6 hepatocellular carcinoma (HCC) cell lines and 32 primary HCC tumors, including 9 early-stage tumors, to determine whether p16INK4 tumor-suppressor gene inactivation participates in hepatocarcinogenesis. p16INK4 was studied at its protein level through Western blotting, at its messenger RNA (mRNA) level through reverse-transcriptase polymerase chain reaction analysis (RT-PCR) and Northern blotting, and at its genomic level through Southern blotting and PCR-single-strand conformation polymorphism analysis. The p16 protein was absent from 3 of 6 cell lines (50%) and 11 of 32 primary tumors (34%), but present in noncancerous tissues, indicating that p16INK4 is involved in hepatocarcinogenesis. Furthermore, we suggest that the p16 protein loss may contribute to the following: (1) early-stage hepatocarcinogenesis, because it was observed in 22% of early stage tumors; and (2) tumor progression, because it occurred approximately twice as often in advanced rather than in early stage tumors (40%). It was striking that neither p16INK4 homozygous deletion and mutation nor loss of p16INK4 mRNA expression were observed in HCC cell lines and primary tumors, including those specimens from which the p16 protein was absent except the Li7HM cell line, in which p16INK4 mRNA was not detected. These results suggest that p16INK4 in HCC is inactivated predominantly by posttranscriptional regulation rather than by genomic aberrations and lack of transcription.
Fluids and Electrolytes.
Authors: Margaret Aurelia McEntee, Grace M. Gil
Journal: Annals of Internal Medicine (1991)

This book is designed to provide nursing students with everything they need to actively review fluids and electrolytes course content, to thoroughly prepare for classroom tests, and effectively practice for the NCLEX examination for RNs. Illustrations help synthesize main concepts of fluids and electrolytes into an easy-to-understand format.
Salt Intake and Sympathetic Activity
Authors: Feng J. He, Graham A. MacGregor
Journal: Circulation (2003)

Grassi et al 1 studied the effect of modest salt reduction on sympathetic activity in 27 hypertensive patients and concluded that this triggered a sympathetic activation and baroreflex impairment.These results need to be interpreted with caution.Firstly, the study was not randomized or double-blinded.Furthermore, 60% of patients (16 out of 27) originally recruited into the study were excluded from the analysis, a few because of unsatisfactory muscle sympathetic nerve traffic recording, but most because of poor compliance.However, no information was given about these patients.How far were they compliant?Was this based on urinary sodium?Additionally, no information whatsoever was given on how the reduction in salt intake was carried out.The decrease in body weight (2.3 kg) is much more than would be seen with a modest salt reduction.Therefore, there must have been other dietary changes, presumably calorie restriction.In addition, no account is taken of the adequacy of urine collections eg, 24-hour creatinine excretion, an essential component of a study on salt restriction.What is needed is a properly controlled, double-blinded randomized study of modest salt reduction looking at sympathetic tone.Even if there was an increase in sympathetic tone, this may be part of the normal physiological response, as is the increase in plasma renin activity.The authors' lack of scientific rigor is also evident in their quoting of Alderman's review on salt intake and cardiovascular disease.His studies have been severely criticized. 2 Grassi et al 1 do not seem to be aware of a more in-depth analysis of the data from the first National Health and Nutrition Examination Survey showing that a high salt intake was significantly associated with an increased risk of cardiovascular disease and all-cause mortality in overweight persons, and more recently, of heart failure. 3A study using a random sample of the Finnish adult population showed that a high salt intake was directly related to increased cardiovascular and total mortality. 4he authors do not quote any other papers showing that a long-term modest salt reduction does not have adverse effects.For instance, Beckmann et al 5 demonstrated that a modest reduction in salt intake, along with a reduction in body weight and saturated fat for 1 year, significantly reduced arterial plasma noradrenaline and adrenaline in hypertensive subjects.Furthermore, salt reduction lowers blood pressure in a similar mechanism to that of thiazide diuretics.Both stimulate the reninangiotensin system and in the short-term the sympathetic nervous system.However, outcome trials have repeatedly demonstrated that long-term treatment with thiazide diuretics significantly reduces cardiovascular morbidity and mortality in hypertensive patients.
A Top-Down Cortical Circuit for Accurate Sensory Perception
Authors: Satoshi Manita, Takayuki Suzuki, Chihiro Homma, Takashi Matsumoto, Maya Odagawa, Kazuyuki Yamada, Keisuke Ota, Chie Matsubara, Ayumu Inutsuka, Masaaki Sato, Masamichi Ohkura, Akihiro Yamanaka, Yuchio Yanagawa, Junichi Nakai, Yasunori Hayashi, Matthew E. Larkum, Masanori Murayama
Journal: Neuron (2015)
Diet in Infancy and Later Signs of Beta-Cell Autoimmunity
Authors: Peter Vuillermin, Katrina J Allen
Journal: New England Journal of Medicine (2011)

To the Editor: The analysis by Knip et al (Nov. 11 issue), 1 which suggests that dietary intervention through infant weaning to hydrolyzed formula has a long-lasting effect on markers of betacell autoimmunity, is flawed in that it has overestimated the evidence of benefit because of failure to adequately use the intention-to-treat principle. 2 First, children from whom follow-up samples were not obtained were excluded from the primary analysis of seroconversion to autoantibody positivity. Of the children who were excluded, diabetes (and presumably autoantibody positivity before clinical disease) developed in three in the treatment group versus none in the control group. Correct inclusion of these 3 children in an intention-to-treat protocol would minimize evidence of treatment effect, with the development of beta-cell autoimmunity in 11 of 113 infants randomly assigned to hydrolyzed formula (9.7%) and in 17 of 109 infants assigned to standard formula (15.6%). A second breach of the principle occurred by adjusting for the duration of exposure to the study formula. In so doing, the authors were able to invalidly “improve” the P value regarding the hazard of development of two or more markers of beta-cell autoimmunity between treatment groups from 0.12 to 0.07.
Abstract 19564: Cardiomyocyte Overexpression of the Mitochondrial Sodium/Calcium Exchanger Increases Matrix Calcium Efflux and Preserves Cardiac Function in Mouse Models of Heart Failure
Authors: Timothy S Luongo, Mary M Nwokedi, Erhe Gao, April C Carpenter, Anita Mehta, Jonathan P Lambert, Muniswamy Madesh, Jeffery D Molkentin, John W Elrod
Journal: Circulation (2014)

Objective:  The mitochondrial calcium ( mito Ca 2+ ) microdomain has been under intense investigation due to its significant influence on both energy production and cell death, both of which are suggested to contribute to the development of heart failure (HF). To examine the contribution of  mito Ca 2+  signaling in HF pathology, we developed mice with conditional overexpression of the  mito NCX candidate gene ( Slc8b1 , also known as NCLX), using the tetracycline-controlled cardiomyocyte-restricted expression system (αMHC-tTA, dox-off). Mice were maintained on doxycycline-containing chow until weaning after which time removal allowed expression of the transgene.   Results:  αMHC-tTA x TRE- mito NCX mice ( mito NCX-Tg) displayed a 3-fold increase in  mito NCX protein expression as compared to tTA littermate controls with no compensatory changes in the expression of other mitochondrial calcium channels. Examination of  mito Ca 2+  dynamics using multiple experimental systems revealed that overexpression of  mito NCX increased the rate of  mito Ca 2+  efflux from the matrix. Next, we subjected mice to two different surgical models of heart failure; myocardial infarction (permanent ligation of the left coronary artery, MI) and pressure-overload induced failure (transverse aortic constriction, TAC). Following the surgical induction of HF mice underwent weekly echocardiographic measurements of left ventricular (LV) function, dimensions and strain analysis. At baseline,  mito NCX-Tg mice displayed similar LV function and structure as tTA controls. However, following both TAC and MI  mito NCX-Tg mice exhibited significantly greater LV function (shown below as percent fractional shortening, %FS) and a preservation of LV structure as compared to tTA controls.   Conclusions:  These findings suggest that enhancing  mito Ca 2+  efflux during the development of HF is advantageous and represents a novel therapeutic approach.
Transplantation of Human Cancers to Nude Mice and Effects of Thymus Grafts2
Authors: Moshe Schmidt, Robert A. Good
Journal: JNCI Journal of the National Cancer Institute (1975)

Human cancers were transplanted to nude mice; a cell line originating in the foregut (distal stomach or first portion of the duodenum) produced exponential nonmetastasizing growth, preventable by prior thymus implantation. implantation of thymuses into mice with established tumors resulted in increased animal survival and in four instances in complete regression of the neoplasm. Cell lines of pancreatic carcinoma and melanoma and surgical specimens of melanoma and of neoplasms from the pancreas and colon showed variable growth patterns in this system. Repeated attempts to transplant gastric adenocarcinoma were unsuccessful.
Abstract 360: Ca/Calmodulin Kinase II (CaMKII) Overexpression Increases Effects of Reactive Oxygen Species to Enhance Late INa and Raise [Na 3]i and [Ca 2+]i
Authors: Stefan Wagner, Hanna M Ruff, Sarah L Weber, Luiz Belardinelli, Lars S Maier
Journal: Circulation (2007)

In heart failure (HF), CaMKII expression and reactive oxygen species (ROS) production are increased. We have shown that CaMKII increases late INa and [Na+]i. ROS enhance late INa leading to Na and ...
Abstract 16342: Rage Dependent Macropinocytosis Mediates Endocytosis of Enzyme Modified Non Oxidized LDL and Foam Cell Formation in Mouse Aortic Smooth Muscle Cells
Authors: Bijoy Chellan, Ling Yan, Catherine A Reardon, Marion H Bowman
Journal: Circulation (2014)

Background:  Vascular smooth muscle cell (SMC) derived foam cells contribute to human atherosclerosis. Enzymatically modified LDL (E LDL) induces SMC foam cells. Mechanism of E LDL uptake and the relative contribution of E LDL compared with other modified forms of LDL such as oxidized LDL in SMC foam cell formation are unknown.   Methods and Results:  Electrophoresis and FPLC analysis suggests E LDL (trypsin,cholesterol esterase modified) consists of fused LDL particles. Incubation of murine aortic SMCs with 10 μg/ml E LDL results in significant foam cell formation (analyzed by Oil Red O, lipid measurement) compared to SMCs incubated with acetylated LDL (500 μg/ml; -50%, p   Conclusions:  E LDL is highly potent in inducing foam cells in mouse aortic SMCs. This is mediated by Src, PI3K and RAGE regulated endocytosis of E LDL into SMCs. Inhibitors for macropinocytosis together with genetic ablation of RAGE completely prevents uptake of E LDL and foam cell formation in murine SMC.
Global Alliance on Vaccines and Immunizations
Authors: G. Walt
Journal: BMJ (2002)

EDITOR-We would like to dissociate ourselves from the views reported in Fleck's news item about the global initiative that seeks to save millions of children's lives by immunisation.1We were involved in the design and analysis of a study that was facilitated, funded, and published jointly with Save the Children UK.The report looked at four countries' experience with the application process to the Global Alliance on Vaccines and Immunizations (GAVI) and their perceptions about funding for systems support.Save
Abstract 13262: A Potent and Selective Covalent Inhibitor of JNK Protects Heart from both Ischemia/Reperfusion- and Hypertension-induced Heart Failure
Authors: Jinli Wang, Wanqing Sun, Yina Ma, George Techiryan, Tinghu Zhang, Jianming Zhang, Ji Li
Journal: Circulation (2014)

Introduction: c-Jun NH 2 -terminal kinases (JNKs) are critical mediators of a variety of detrimental stimuli including ischemia-reperfusion (I/R) and mechanical stress induced by pressure overload. Recently, we reported that a novel synthesized highly selective JNK inhibitor, JNK-IN-8, can form an ATP site-directed covalent bond with a conserved cysteine residual in all JNKs. Therefore, JNK-IN-8 may be broadly useful as a pharmacological tool for inhibiting JNK-dependent signal transduction that is involved in various pathological conditions. Hypothesis: The potent JNK inhibitor, JNK-IN-8, could act as a cardioprotectant against ischemia/reperfusion (I/R)- or hypertension-induced heart failure. Methods: The effects of JNK-IN-8 were monitored in a mouse I/R models with the left anterior descending coronary artery (LAD) occluded and subsequently released, and a mouse model of trans-aortic constriction (TAC), in which pressure overload hypertrophy was induced in 2 weeks. Results: JNK-IN-8 significantly reduced myocardial infarct area by 40% in I/R model relative to the vehicle group (p&lt;0.01). Interestingly, the immunohistochemistry data showed that JNK-IN-8 treatment attenuated macrophage infiltration and caspase-3 executed apoptosis in TAC mice (p&lt;0.01 vs. vehicle group). Moreover, the staining of wheat germ agglutinin (WGA) and Masson trichrome revealed a decrease in hypertrophy and fibrosis in the TAC hearts of JNK-IN-8 treated group (p&lt;0.05 vs. vehicle group). The immunoblotting data demonstrated that JNK-IN-8 selectively attenuated both I/R- and pressure overload-induced cardiac JNK and downstream p-p66 shc signaling pathways, while the levels of other family signals (p-p38 and p-ERK) remained unchanged, further indicating the specificity of JNK-IN-8 on JNK signaling in the heart. Conclusions: JNK-IN-8 can reduce I/R-injury induced myocardial infarction size, and attenuate pressure overload induced inflammation, apoptosis, hypertrophy and fibrosis. Thus JNK-IN-8 is a potential therapeutic drug for both I/R injury and pressure overload induced hypertrophy.
The History of Prostitution, its Extent, Causes and Effects Throughout the World.
Authors: William W. Sanger
Journal: JAMA (1895)

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