tbuckley/cabot-search huggingface dataset:
An analysis of randomized trials evaluating the effect of cholesterol reduction on total mortality and coronary heart disease incidence.
Authors: I Holme
Journal: Circulation (1990)

The primary aim of this study was to estimate the relation between cholesterol reduction and total mortality and coronary heart disease (CHD) incidence. Secondarily, the clinical issues of whether the efficacy of cholesterol lowering is dependent on the treatment modality, presence of CHD at baseline, or the simultaneous introduction of other interventions was explored. All randomized clinical intervention trials of cholesterol reduction were used in an overview analysis of total mortality rate and CHD incidence; analysis was performed with weighted linear regression. The trials include those that used primary and secondary intervention, diet and drugs, and single or multifactor design. Nineteen trials were analyzed for total mortality, and of the 19, 16 were analyzed for CHD incidence rate. Net difference in cholesterol change between study groups was used as the independent variable, and the three previously mentioned dichotomous design characteristics were used as additional independent variables. For every 1% reduction in cholesterol, an estimated 2.5% reduction in CHD incidence is indicated (95% CL: 1.1, 3.9). With regard to CHD drug trials tended toward better efficiency in cholesterol lowering than did dietary trials. With regard to total mortality, this efficiency was higher in secondary than in primary preventive trials. The efficiency was also somewhat dependent on the baseline cholesterol level. This study shows that cholesterol reduction is effective in lowering CHD incidence, but cholesterol reduction must be at least 8-9% to be effective in lowering total mortality.
Books Received
Authors: B Sanders, M H Giolas
Journal: American Journal of Psychiatry (1991)

To test the hypothesis that dissociation in adolescence is positively correlated with stress or abuse experienced earlier, the authors assessed dissociation in a heterogeneous group of disturbed adolescents and examined the relationship between the degree of dissociation and the degree of reported childhood stress, abuse, or trauma.The subjects were 47 adolescents, 13-17 years old, who were institutionalized for periods of 1-13 weeks in a private mental hospital; 35 were girls and 12 were boys. Participants completed the Dissociative Experiences Scale and a child abuse and trauma questionnaire. The hospital records of 40 of the 47 adolescents were also available.Scores on the Dissociative Experiences Scale correlated significantly with self-reported physical abuse or punishment, sexual abuse, psychological abuse, neglect, and negative home atmosphere but not with abuse ratings made from hospital records.Together with the authors' previous work showing a relation between childhood stress and later dissociation in normal college students, these findings support the view that dissociation represents a reaction to early negative experience and places multiple personality disorder at the extreme end of a continuum of dissociative sequelae of childhood trauma. Researchers should continue to try to identify psychiatric patients with prominent dissociative characteristics or symptoms and attempt to correlate this phenomenology with negative earlier experiences.
Abstract 19072: Cardiac Autonomic Dysfunction in Mice Lacking Methyl CpG Binding Protein 2
Authors: Jose A Herrera, Christopher S Ward, Jeffrey L Neul
Journal: Circulation (2014)

Background: Rett Syndrome (RTT) is an X-linked dominant neurodevelopmental disorder primarily caused by mutations in Methyl-CpG-binding protein ( MECP2 ), a transcriptional regulator. Twenty-five percent of all deaths in RTT are sudden and unexpected, and autonomic nervous system (ANS) dysfunction is hypothesized to be the cause of sudden deaths in RTT. However, the role of MeCP2 in cardiac autonomic function has not been investigated in depth. Design/Methods: Male (2 months) and female (9 months) Mecp2 deficient and wildtype mice were implanted with ETA-F10 telemeters and 24h recordings were taken to calculate heart rate, heart rate variability, and incidence of arrhythmic events. Effects of pharmacological stimulants or inhibitors on heart rate were normalized to saline injection response. Results: Male Mecp2 deficient mice (NULL) have a decreased heart rate (WT = 634 ±3, NULL = 518 ±8, p&lt;0.001), while female deficient mice (NULL/+) do not present with a decreased heart rate. Interestingly, NULL and NULL/+ mice both have a high incidence of sinus pauses and AV block (WT 1/5, NULL 6/6, NULL /+ 4/4, p&lt;0.05). Additionally, both NULL and NULL/+ mice have increased bradycardia events defined as a heart rate below 200 bpm, (WT = 17 ±6, NULL = 307 ±94, NULL/+ = 198 ±67, p&lt;0.05) and an increased heart rate variability. The normalized heart rate response to atropine, a parasympathetic blocker, of NULL mice was above wildtype levels (p&lt;0.05) Chemical denervation by combined antagonism of parasympathetic (atropine) and sympathetic (propranolol) resulted in NULL mice having an increased normalized heart rate response compared to wildtype (p&lt;0.05). Finally, the incidence of AVB/sinus pauses counts per 30 minutes post-acute treatment with atropine and chemical denervation (NULL saline 49 ±10, NULL atropine 8 ±5, NULL atropine/propranolol 0.5 ±0.5 p&lt;0.05) decreased the severity of the cardiac phenotype in NULL mice. Conclusions: In summary, Mecp2 is required for a normal heart rhythm. Loss of Mecp2 causes bradycardia, sinus pauses, AV block, and increased heart rate variability that may be attributed by aberrant innervation. Acute atropine and chemical denervation was therapeutic and ameliorated the cardiac phenotype observed in Mecp2 deficient mice.
Role of Vitamin E in the Prevention of Cardiovascular Disease and Cancer
Authors: Sujeeth R Punnam
Journal: JAMA (2005)

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
Abstract 3964: Nanoparticle-Mediated Monocyte-Selective Transfection of Dominant-Negative Monocyte Chemoattractant Protein-1 (MCP-1) Gene Inhibits Plaque Rupture in ApoE-Deficient Mice
Authors: Jun-ichiro Koga, Kensuke Egashira, Tetsuya Matoba, Kaori Hara, Hiroyuki Tsujimoto, Kenji Sunagawa
Journal: Circulation (2008)

Preventing rupture of unstable plaque is the most effective strategy for acute coronary syndrome (ACS). Monocytes/macrophages play a key role in plaque destabilization and rupture. Monocyte chemoattractant protein-1 (MCP-1) and its receptor (CCR2) play an essential role in regulating monocyte recruitment and activation. Blockade of the MCP-1/CCR2 pathway by nanoparticle (NP)-mediated monocyte-selective transfection of dominant-negative MCP-1 (7ND) gene inhibits plaque rupture. We prepared bioabsorbable PLGA NP (mean diameter = 200 nm). Intravenous administration of NP incorporated with 7ND gene (5 mcg plasmid/1 mg PLGA) resulted in incorporation of NP via phagocytosis and gene transfer into CD11b + circulating monocytes, and suppressed monocyte function. We then examined the effect of 7ND-NP on plaque rupture of brachiocephalic arteries in apoE-deficient mice fed with high-fat diet and infused with angiotensin II (Figure A ). At 20 weeks, animals were divided into no treatment group and those treated weekly with intravenously 7ND-NP or FITC-NP (Figure B ). FITC-NP was detected in macrophages of destabilized brachiocephalic arterial plaques, but not in those of stable aortic plaques. 7ND-NP did not affect the size of atheroma, but did reduce the occurrence of plaque rupture (Figure C ), macrophage infiltration, and tissue factor expression. Blockade of MCP-1/CCR2 pathway by NP-mediated monocyte-targeting gene transfer stabilized atheroma and prevented plaque rupture. This nanotechnology platform may be a less invasive therapeutic strategy for stabilizing rupture-prone plaques and thus preventing ACS.
Abstract 3889: Modulation of breast cancer stem cell marker CD44 by all-trans-retinoic acid (ATRA)
Authors: Rui Kitadai, Robert Bednarczyk, Neha Tuli, Elyse Hanly, Ghada Benrahoma, Robert Suriano, Abraham Mittelman, Raj K. Tiwari
Journal: Cancer Research (2014)

Abstract Breast cancer stem cells (BCSCs), often characterized by cell surface marker expression as being CD44+/CD24- or CD44+/CD24low phenotypes, constitute a subpopulation of tumor cells that are highly tumorigenic. With respect to CD44, it has been reported that its expression is influenced by tumor microenvironment (TME) and that modulation of CD44 is detrimental to breast cancer stem cell self-renewal and differentiation. Interestingly, the factors that mitigate this effect are still unknown, which has led us to hypothesize that factors within the TME, comprising of differentiating agents, modulate the BCSC phenotype by regulating cell surface markers. MDA-MB 231 showed presence of BCSCs as CD44 positive cells were detected using immunofluorescence and Western blot analyses. The expression of CD44 on MDA-MB 231 was not responsive to the proinflammatory molecule IL-8 or estrogen. Both MDA-MB 231 and T47D were responsive to IL-8 and estrogen with respect to migration and invasion as examined in vitro using a Boyden Chamber assay suggesting that migration and invasion was independent of CD44 expression. Alternatively IL-8 responsiveness may be on a select clonal population of CD44- cells. The presence of differentiating agents within the TME has been explored. To examine the effect of differentiating agents, we used the classical all-trans-retinoic acid (ATRA) previously shown to promote tumor regression. CD44 expression was highly responsive to ATRA as it was down regulated following treatment. ATRA treatments also resulted in decreased migration and invasion of breast cancer cells. Our results led us to conclude that specific differentiating agents can affect breast cancer stem cell activity by directly down regulating key adhesion cell surface markers. Citation Format: Rui Kitadai, Robert Bednarczyk, Neha Tuli, Elyse Hanly, Ghada Benrahoma, Robert Suriano, Abraham Mittelman, Raj K. Tiwari. Modulation of breast cancer stem cell marker CD44 by all-trans-retinoic acid (ATRA). [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3889. doi:10.1158/1538-7445.AM2014-3889
The Year Book of Family Practice. 1977.
Authors: John Fry
Journal: Annals of Internal Medicine (1977)

REVIEWSdiscussed in two separate chapters.Neither of the two complete summaries of the US Dietary Goals is listed in the index.There is no listing for aging or geriatrics even though special issues pertaining to the nutritional status of the elderly are addressed in the chapter on drug-diet interactions and in the one on food assistance programs.These omissions prevent the use of this volume as a reference text.
Portrait of Dr Albert C. Getchell
Authors: M. Therese Southgate
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
Digital Computer Studies of Cell Multiplication by Monte Carlo Methods
Authors: Joseph G. Hoffman, Nicholas Metropolis, Verna Gardiner
Journal: JNCI Journal of the National Cancer Institute (1956)

Journal Article Digital Computer Studies of Cell Multiplication by Monte Carlo Methods Get access Joseph G. Hoffman, Joseph G. Hoffman Biophysics Division, Roswell Park Memorial Institute, Buffalo, New York Search for other works by this author on: Oxford Academic PubMed Google Scholar Nicholas Metropolis, Nicholas Metropolis Search for other works by this author on: Oxford Academic PubMed Google Scholar Verna Gardiner Verna Gardiner Theoretical Division, Los Alamos Scientific Laboratory, Los Alamos, New Mexico Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 17, Issue 2, August 1956, Pages 175–188, https://doi.org/10.1093/jnci/17.2.175 Published: 01 August 1956 Article history Received: 30 March 1956 Published: 01 August 1956
Optimization of oligonucleotide arrays and RNA amplification protocols for analysis of transcript structure and alternative splicing
Authors: John Castle, Phil Garrett-Engele, Christopher D Armour, Sven J Duenwald, Patrick M Loerch, Michael R Meyer, Eric E Schadt, Roland Stoughton, Mark L Parrish, Daniel D Shoemaker, Jason M Johnson
Journal: Genome biology (2003)

Microarrays offer a high-resolution means for monitoring pre-mRNA splicing on a genomic scale. We have developed a novel, unbiased amplification protocol that permits labeling of entire transcripts. Also, hybridization conditions, probe characteristics, and analysis algorithms were optimized for detection of exons, exon-intron edges, and exon junctions. These optimized protocols can be used to detect small variations and isoform mixtures, map the tissue specificity of known human alternative isoforms, and provide a robust, scalable platform for high-throughput discovery of alternative splicing.
Role of Toll-like Receptor 4 in Acute Myocardial Infarction and Longevity
Authors: Carmela Rita Balistreri, Giuseppina Candore, Giuseppina Colonna-Romano, Domenico Lio, Marco Caruso, Enrico Hoffmann, Claudio Franceschi, Calogero Caruso
Journal: JAMA (2004)

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
864. AAV-2-Mediated Expression of α-N-Acetyl-Glucosaminidase in Peripheral Tissues and the CNS in Mucopolysaccharidosis IIIB Mice by Combined Intravenous and Intracisternal Vector Delivery
Authors: Lu Kang, Jerillyn S. Jennings, Joseph Muenzer, Haiyan Fu
Journal: Molecular Therapy (2004)

Mucopolysaccharidosis (MPS) IIIB is an inherited lysosomal storage disease due to the deficiency of α-N-acetyl-glucosaminidase (NaGlu). MPS IIIB is characterized by multiple somatic disease and neurological dysfunction leading to premature death. No definite treatment is available for MPS IIIB patients. Two delivery strategies were combined to study the therapeutic effects of adeno-associated viral vector on both the somatic and central nervous system (CNS) in adult MPS IIIB mice, using an adeno-associated virus (AAV) serotype 2 vector (AAV2-CMV-hNaGlu) expressing human NaGlu and driven by a CMV promoter. The vector was injected into MPS IIIB mice (4–5 week old) by an intravenous (IV) injection (4-8 × 1011 viral particles) and an intracisternal (IC) injection of the vector (5 × 1010 viral particles), following pretreatment with an IV infusion of mannitol, to deliver the vector to both the somatic and CNS. The content of glycosaminoglycan (GAG) decreased to near normal levels in the liver of injected mice 6 months after injection (P < 0.01) and clearance of lysosomal storage was confirmed by transmission electron microscopy in hepactocytes, Kupfer cells and endothelial cells in liver. NaGlu enzyme activity was variable in liver in different injected animals, ranging from 10 to 100% of normal activity. A significant reduction of GAG storage was also observed in spleen and skeletal muscle (P < 0.05). No decrease of GAG was seen in lung, intestine, heart and kidney. NaGlu activity was only detected in liver, but not in any other peripheral tissues. In the CNS, there was a decrease of lysosmal storage in Purkinje cells, but no obvious correction of lysosomal storage in other brain areas, although significant levels of NaGlu activity (50–100% of normal) was observed in all injected mouse brains. Our results suggest that AAV2 vector can mediate the expression of enzyme in selective tissues with only partial correction of lysosomal storage in MPS IIIB mice.
Architectural Principles in Arthrodesis
Authors: Herbert Alfred Brittain, Platt, Harry, Sir
Journal: JAMA (1942)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 405: Mbd3 localizes at promoters, gene bodies and enhancers of active genes
Authors: Takashi Shimbo, Ying Du, Sara A. Grimm, Archana Dhasarathy, Deepak Mav, Ruchir R. Shah, Huidong Shi, Paul A. Wade
Journal: Cancer Research (2014)

Abstract The structure of chromatin is tightly regulated; its disregulation is causal for developmental abnormalities and for cancer. The nucleosome remodeling and deacetylase (NuRD) complex regulates chromatin structure and gene expression via its nucleosome remodeling and histone deacetylase activities. MBD3, a component of NuRD, has pleiotropic roles in embryonic stem (ES) cells and tumor biology. However, the results of recent studies are conflicting, resulting in an unclear model for NuRD function. Here, we investigated the localization of MBD3 in two human breast cancer cell lines (MCF-7 and MDA-MB-231) with two independent genomic technologies (DamID and ChIP-seq). DamID and ChIP-seq data were in an excellent agreement and led consistent conclusions in both cell lines. MBD3 localized not only at promoters and enhancers of active genes but also accumulated at gene bodies; this previously undescribed localization suggests an active role of MBD3 in transcription. MBD3 preferred hypomethylated, CpG rich promoters marked by H3K4me3. We also noted a subset of MBD3 that localized at silent promoters marked by H3K9me3 or H3K27me3, consistent with biochemical studies. Another subset of MBD3 co-localized with H3K27ac and was in physiological proximity with promoters, suggesting a role of MBD3 in the regulation of high-order structure of the genome. Functional analysis of chromatin demonstrated that MBD3 regulates nucleosome occupancy near promoters and in gene bodies. These data suggest multiple roles of MBD3/NuRD in the regulation of chromatin structure and gene expression for both active and silent genes. The findings serve as an important initial step in defining regulatory mechanism of MBD3/NuRD in ES cells and in tumor biology. Citation Format: Takashi Shimbo, Ying Du, Sara A. Grimm, Archana Dhasarathy, Deepak Mav, Ruchir R. Shah, Huidong Shi, Paul A. Wade. Mbd3 localizes at promoters, gene bodies and enhancers of active genes. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 405. doi:10.1158/1538-7445.AM2014-405