tbuckley/cabot-search huggingface dataset:
The relationship of cardiac output and arterial pressure control.
Authors: A C Guyton
Journal: Circulation (1981)

Many basic concepts of cardiac output and arterial pressure control have changed considerably in the past few years. In general, each tissue controls its own local resistance and blood flow regardless of the level of arterial pressure; the sum of the local flows then determines the venous return and cardiac output. However, the arterial pressure is normally controlled by separate mechanisms that do not significantly alter the cardiac output. During acute circulatory stresses, such as exercise, the arterial pressure is controlled almost entirely by nervous reflex mechanisms; but over long periods, there reflex mechanisms fade away because they adapt. The arterial pressure is then controlled mainly by a renal-volume-endocrine pressure control system, in which the blood volume and total peripheral resistance are manipulated slowly to adjust the pressure.
A patient who changed my practice?: The new Holy Grail
Authors: M. Gradwell
Journal: BMJ (1998)

E was an 87 year old man with chronic bronchitis and some deafness. He presented yet again with increasing dyspnoea. I listened to his chest for the expected wheeze. “Haven't really got much better Doc, started the steroids like you said and doubled my inhalers.” Then I noted in the background the irregular, rapid pulse. I congratulated myself for my clinical acumen in spotting his atrial fibrillation.

For some time I had considered with unease the emerging evidence in favour of anticoagulation for older patients with atrial fibrillation. Audit within the practice showed only 60% of patients on any form of antithrombotic medication and most of these on aspirin.

I attend a typically didactic lecture from a group of teaching hospital cardiologists presenting the case for anticoagulation with impressive statistics and apparent scientific rigour. At the end …
Evidence for a Major Quantitative Trait Locus on Chromosome 17q21 Affecting Low-Density Lipoprotein Peak Particle Diameter
Authors: Yohan Bossé, Louis Pérusse, Jean-Pierre Després, Benoît Lamarche, Yvon C. Chagnon, Treva Rice, D.C. Rao, Claude Bouchard, Marie-Claude Vohl
Journal: Circulation (2003)

Several lines of evidence suggest that small dense LDL particles are associated with the risk of coronary heart disease. Heritability and segregation studies suggest that LDL particle size is characterized by a large genetic contribution and the presence of a putative major genetic locus. However, association and linkage analyses have thus far been inconclusive in identifying the underlying gene(s).An autosomal genome-wide scan for LDL peak particle diameter (LDL-PPD) was performed in the Québec Family Study. A total of 442 markers were genotyped, with an average intermarker distance of 7.2 cM. LDL-PPD was measured by gradient gel electrophoresis in 681 subjects from 236 nuclear families. Linkage was tested by both sib-pair-based and variance components-based linkage methods. The strongest evidence of linkage was found on chromosome 17q21.33 at marker D17S1301, with an LOD score of 6.76 by the variance-components method for the phenotype adjusted for age, body mass index, and triglyceride levels. Similar results were obtained with the sib-pair method (P<0.0001). Other chromosomal regions harboring markers with highly suggestive evidence of linkage (P< or =0.0023; LOD > or =1.75) include 1p31, 2q33.2, 4p15.2, 5q12.3, and 14q31. Several candidate genes are localized under the peak linkages, including apolipoprotein H on chromosome 17q, the apolipoprotein E receptor 2, and members of the phospholipase A2 family on chromosome 1p as well as HMG-CoA reductase on chromosome 5q.This genome-wide scan for LDL-PPD indicates the presence of a major quantitative trait locus located on chromosome 17q and others interesting loci influencing the phenotype.
Abstract 1810: Mechanistic studies of the dual Akt and JNK inhibitor Chaetoglobosin K: Effect on downstream pathways and AP-1 proteins in tumorigenic cells
Authors: Amna Ali, Diane F. Matesic
Journal: Cancer Research (2012)

Abstract We have previously shown that the anti-tumorigenic indolylcytochalasin Chaetoglobosin K (ChK) concomitantly down-regulates Akt and JNK activation in ras-transformed cells. This dual inhibition was found not be regulated by Rac1, a Rho protein that is involved in both signaling pathways, or MKK4, an upstream kinase of JNK. The purpose of this study was to determine: 1) the effect of ChK on the activation of downstream mediators of the PI3K/Akt (including mdm2), and JNK (including the activator protein-1 (AP-1) proteins and stat3) signaling pathways; 2) whether the upstream mitogen-activated protein kinase kinase 7 (MKK7) is involved in ChK's effect on JNK. The AP-1 transcription factor complex, composed of proteins of the JUN, FOS, and ATF families, has become a promising therapeutic target due to the proposed role of AP-1 activation in tumorigenesis. In these studies, ras-transformed rat liver epithelial cells were grown to confluence and treated with either ChK (5μM or 10μM) or vehicle (DMSO) for 24 hours. Cell proteins were extracted and separated using SDS-PAGE. Western blot analysis was performed using phosphorylation site-specific antibodies to monitor changes in MKK7, c-JUN, ATF-2, mdm2, and stat3 protein activation levels. The results of these studies indicate that ChK treatment decreased c-JUN and ATF-2 phosphorylation, but had no effect on stat3 phosphorylation. Additionally, ChK treatment decreased mdm2 phosphorylation. ChK did not alter MKK7 activation levels and, taking into consideration its lack of effect on MKK4, suggest ChK does not inhibit JNK via its archetypical MAPK signaling pathway. These studies indicate ChK may serve as a small molecule inhibitor of the AP-1 pathway proteins, as well as the Akt/mdm2 pathway. This data further supports ChK's potential as a unique targeted tumor therapy. This project was funded by NIH grant 1R15CA135415 Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1810. doi:1538-7445.AM2012-1810
Anticachectic Effects of Formoterol
Authors: Sílvia Busquets, Maria T. Figueras, Gemma Fuster, Vanessa Almendro, Rodrigo Moore-Carrasco, Elisabet Ametller, Josep M. Argilés, Francisco J. López-Soriano
Journal: Cancer Research (2004)

Abstract In cancer cachexia both cardiac and skeletal muscle suffer an important protein mobilization as a result of increased proteolysis. Administration of the β2-agonist formoterol to both rats and mice bearing highly cachectic tumors resulted in an important reversal of the muscle-wasting process. The anti-wasting effects of the drug were based on both an activation of the rate of protein synthesis and an inhibition of the rate of muscle proteolysis. Northern blot analysis revealed that formoterol treatment resulted in a decrease in the mRNA content of ubiquitin and proteasome subunits in gastrocnemius muscles; this, together with the decreased proteasome activity observed, suggest that the main anti-proteolytic action of the drug may be based on an inhibition of the ATP-ubiquitin-dependent proteolytic system. Interestingly, the β2-agonist was also able to diminish the increased rate of muscle apoptosis (measured as DNA laddering as well as caspase-3 activity) present in tumor-bearing animals. The present results indicate that formoterol exerted a selective, powerful protective action on heart and skeletal muscle by antagonizing the enhanced protein degradation that characterizes cancer cachexia, and it could be revealed as a potential therapeutic tool in pathologic states wherein muscle protein hypercatabolism is a critical feature such as cancer cachexia or other wasting diseases.
Ikaros integrates endocrine and immune system development
Authors: Shereen Ezzat, Rene Mader, ShunJiang Yu, Terry Ning, Philippe Poussier, Sylvia L. Asa
Journal: Journal of Clinical Investigation (2005)

Ikaros transcription factors are essential regulators of lymphopoiesis and the development of the immune system. We now show that Ikaros is expressed in hormone-producing pituitary corticomelanotroph cells, where it binds the proopiomelanocortin promoter and regulates endogenous gene expression. Loss of Ikaros in vivo results in contraction of the pituitary corticomelanotroph population, reduced circulating adrenocorticotrophic hormone levels, and adrenal glucocorticoid insufficiency. While hemopoietic reconstitution failed to correct this hormonal deficit, the phenotype of reduced body weight and diminished survival was rescued by systemic glucocorticoid-hormone administration. Given the established immunomodulatory properties of glucocorticoid hormones, these findings reveal a novel role for Ikaros in orchestrating immune-endocrine development and function.
Somatic Gene Transfer of Human ApoA-I Inhibits Atherosclerosis Progression in Mouse Models
Authors: Patrick Benoit, Florence Emmanuel, Jean Michel Caillaud, Laurent Bassinet, Graciela Castro, Pierre Gallix, Jean Charles Fruchart, Didier Branellec, Patrice Denèfle, Nicolas Duverger
Journal: Circulation (1999)

Background —Apolipoprotein (apo) A-I is the major component of HDL, and it displays antiatherogenic properties. Methods and Results —The human apoA-I gene has been transferred into different mouse models by use of a recombinant adenovirus under the control of an RSV-LTR promoter (AV RSV apoA-I). Administration of AV RSV apoA-I to C57BL/6 mice resulted in moderate expression of human apoA-I for 3 weeks, leading to a transient elevation (40% at day 11 after injection) of HDL cholesterol concentration. In contrast, administration of AV RSV apoA-I to human apoA-I–transgenic mice induced a large increase of human apoA-I and HDL cholesterol concentrations (300% and 360%, respectively, at day 14 after injection) for 10 weeks, indicating that an immune response to the transgene was one major hurdle for long-term duration of expression. Recombinant adenovirus expressing human apolipoprotein A-I (AV RSV apoA-I) was also injected into human apoA-I–transgenic/apoE-deficient mice, which are prone to develop atherosclerosis. Over a 6-week period, overexpression of human apoA-I inhibited fatty streak lesion formation by 56% in comparison with control. Conclusions —Somatic gene transfer of human apoA-I prevents the development of atherosclerosis in the mouse model.
Points from Letters: Death by Hanging
Authors: R. Pakenham-Walsh
Journal: BMJ (1949)

<h3>Objective:</h3> We tested whether maternal hypertensive disorders in pregnancy predict age-related change in cognitive ability in the offspring up to old age. <h3>Methods:</h3> Using mothers’ blood pressure and urinary protein measurements from the maternity clinics and birth hospitals, we defined normotensive or hypertensive pregnancies in mothers of 398 men, who participated in the Helsinki Birth Cohort 1934–1944 Study. The men underwent the Finnish Defence Forces basic ability test twice: first during compulsory military service at age 20.1 (SD = 1.4) years and then in a retest at age 68.5 (SD = 2.9) years. The test yields a total score and subscores for tests measuring verbal, arithmetic, and visuospatial reasoning. <h3>Results:</h3> Men born after pregnancies complicated by a hypertensive disorder, compared with men born after normotensive pregnancies, scored 4.36 (95% confidence interval, 1.17–7.55) points lower on total cognitive ability at 68.5 years and displayed a greater decline in total cognitive ability (2.88; 95% confidence interval, 0.07–5.06) after 20.1 years. Of the subscores, associations were strongest for arithmetic reasoning. <h3>Conclusion:</h3> Maternal hypertensive disorders in pregnancy predict lower cognitive ability and greater cognitive decline up to old age. A propensity to lower cognitive ability and decline up to old age may have prenatal origins.
THE EXPERIMENTAL PRODUCTION OF EPITHELIAL PROLIFERATION.
Authors: GUTHRIE McCONNELL
Journal: JAMA (1907)

The artificial reproduction of conditions simulating those found in malignant growths has been attempted for a long time, but until very recently without any very definite results. Since Virchow elaborated the irritation theory of origin of tumors many experiments have been made along that line. Brosch<sup>1</sup>painted the skin with a solution of paraffin and xylol and obtained a slight thickening and lengthening of the epithelial papillæ. Ribbert,<sup>2</sup>by means of repeated scratchings of the epithelium of the lower lip of a rabbit, produced a papillomatous outgrowth. As is well known, there may be marked epithelial proliferation following in the course of chronic inflammation. Bernard Fischer<sup>3</sup>undertook to bring about this condition without causing any lesion in the overlying epidermis. Many substances were injected without result until agar was used. This caused some change in the connective tissue with the formation of giant cells. Olive oil was
Increase in AIDS-Associated Illnesses Focuses New Attention on an Old Nemesis
Authors: Chris Anne Raymond
Journal: JAMA (1986)

THIS YEAR, for the first time since such data have been collected, experts are predicting an increase in tuberculosis in the United States, attributable primarily to the disease's prevalence in patients with the acquired immunodeficiency syndrome (AIDS) (<i>MMWR</i>1986;35:74-76;<i>JAMA</i>1986;256:362-366). Recent studies have shown that tuberculosis occurs with a greater than expected frequency in patients with AIDS or those at risk of AIDS, particularly intravenous drug abusers (<i>Ann Intern Med</i>1984;101:641-645; Handwerger S, et al;<i>Chest</i>, in press). The upswing in cases in large cities, and the ripple effects of a 1985 conference on Future Research in Tuberculosis may be effecting a resurgent interest in the field that many say is long overdue. But the attention that AIDS is directing at tuberculosis is viewed as a mixed blessing. AIDS has had a "boot-leg effect" on tuberculosis research, because of the interest in understanding more about mycobacterial infections common in
Prostacyclin Prevents Pulmonary Endothelial Cell Apoptosis Induced by Cigarette Smoke
Authors: S. Patrick Nana-Sinkam, Jong Deog Lee, Sylk Sotto-Santiago, Robert S. Stearman, Robert L. Keith, Qamrul Choudhury, Carlyne Cool, Jane Parr, Mark D. Moore, Todd M. Bull, Norbert F. Voelkel, Mark W. Geraci
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Impaired endothelial cell-dependent vasodilation, inflammation, apoptosis, and proliferation are manifestations of endothelial dysfunction in chronic obstructive pulmonary disease (COPD). Prostacyclin (PGI(2)) is a major product of the cyclooxygenase pathway with potent vasodilatory and antimitogenic properties and may be relevant to endothelial dysfunction in COPD.To determine if PGI(2) expression is altered in smoking-related lung disease and if it may be protective in COPD-associated endothelial dysfunction.We evaluated, by immunohistochemistry, Western blotting, and polymerase chain reaction, human emphysema tissue compared with normal tissue for expression of prostacyclin synthase (PGI(2)S). We examined the effects of cigarette smoke extract (CSE) and aldehyde components on eicosanoid expression in primary human pulmonary microvascular endothelial cells. Finally, we used a murine model of lung-specific PGI(2)S overexpression and in vitro studies to determine if PGI(2) expression has protective effects on cigarette smoke-induced endothelial apoptosis.Human emphysema lung tissue exhibited lower PGI(2)S expression within the pulmonary endothelium than in normal lung. In vitro studies demonstrated that CSE, and in particular the alpha,beta unsaturated aldehyde acrolein, suppressed PGI(2)S gene expression, whereas CSE significantly induced the upstream mediators COX-2 and cytosolic phospholipase A2 in human pulmonary microvascular endothelial cells. Mice with lung-specific PGI(2)S overexpression exhibited less endothelial apoptosis after chronic smoke exposure. In vitro, iloprost exhibited protective effects on CSE-induced apoptosis.PGI(2) has protective effects in the pulmonary vasculature after acute and chronic cigarette smoke exposure. An imbalance in eicosanoid expression may be important to COPD-associated endothelial dysfunction.
Administration after Reorganization
Authors: R. V. Stone, E. J. Hargadon
Journal: BMJ (1975)

Serum a-Fetoprotein in Cystic Fibrosis SIR,-Professor R. K. Chandra and others (29 March, p. 714), found raised serum levels of a-fetoprotein (AFP) in a heterozygote carrier of the gene for cystic fibrosis and in patientr with the disease and some of the siblings.Dr. J. C. Wallwork and others and Dr
THE TREATMENT OF "SPANISH INFLUENZA"
Authors: H. A. Klein
Journal: JAMA (1918)

To the Editor:  —In a number of cases of influenza and influenzal pneumonia, seen both in my private practice and at the Alexian Brothers' Hospital, I have used a treatment from which my results have been most satisfactory.  The clinical course of the condition may be divided for convenience into three stages. The first lasts from three to four days, and is characterized by chills, fever, muscular pain, etc. The second is of rather uncertain duration, and is characterized by involvement of the respiratory system varying in degree from a slight catarrhal condition to the involvement of a large area of one or both lungs. The third is characterized by disturbances of the circulatory system, dyspnea and cyanosis.  In the treatment, the patient receives as soon as possible from 10 to 20 c.c. of a saturated solution of quinin hydrochlorid. This is given intravenously and is repeated once or twice
Benefits of family mealtimes for nursing home residents: Protecting mealtimes may similarly benefit elderly inpatients
Authors: Abhay K Das, Tina McDougall, Jacqueline A J Smithson, Robert M West
Journal: BMJ (2006)

EDITOR—The study by Nijs et al of Dutch elderly nursing home residents showed that improving the ambience at mealtimes prevents a decline in body weight.1 A decline in nutritional status during hospital stay may be the result not only of illness but also of problems with feeding and catering policies, such as poor environment, lack …
Sex and Cyberspace—Virtual Networks Leading to High-Risk Sex
Authors: Kathleen E. Toomey
Journal: JAMA (2000)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Structural heterogeneity of hepatocyte “tight” junctions: A quantitative analysis
Authors: Suzanne Lagarde, Elwyn Elias, James B. Wade, James L. Boyer
Journal: Hepatology (1981)

Freeze fracture analyses of hepatocyte tight junctions reveal interconnecting strands which represent a semipermeable blood-bile barrier. In epithelia, strand number can be correlated with transepithelial resistance and junctional permeability, but a functional relationship is not always seen. We have devised an analytical method to measure accurately strand number as well as junction depth over a large area of junction. Measurements were obtained in five bile fistula rats and two marine elasmobranchs (little skates). In addition, choleretic infusions of 120 μmoles of taurodehydrocholate were administered to four additional rats over 1 hr to determine if functional changes in ion and fluid movement are associated with alternations in junctional structure. Using a microcomputer with a sonic digitizer, strand number and junction depth were obtained at intervals of 0.1 to 0.2 μ from transmission electron micrographs of fractures of rat and skate liver. Strand number averaged 4.1 ± 1.1 in control rats (798 measurements) and 4.1 ± 1.3 in the taurodehydrocholate-stimulated animals (296 measurements). Junction depths averaged 0.148 ± 0.092 μm in controls and increased to 0.167 ± 0.121 μm in taurodehydrocholate-stimulated rats, a difference which reached significance at the p &lt; 0.06 level. Similarly, values were obtained in skate livers where central zone pigment granules facilitated dissection of portal and central portions of lobule. Central zone strand number and junction depth averaged 5.1 ± 1.6 and 0.178 ± 0.100 μm, respectively (439 measurements), and were indistinguishable from values obtained from portal regions −5.0 ± 1.9 and 0.182 ± 0.099 μm, respectively (217 measurements). Although no quantitative differences in junction structure was observed in these studies, considerable variation was noted in junction depth (0.013 to 0.670 μm in the rat and 0.008 to 0.600 μm in skates) and number. We conclude that the anatomical barrier which forms the normal hepatocyte tight junction is a highly varied structure. If junctional structure as revealed by freeze fracture analysis correlates with changes in permeability, then permeability should vary considerably at multiple points along the surface of individual hepatocytes and would not be detected by present quantitative approaches which average junctional strand number and depth. Alternatively, regulation of junctional permeability may be more dependent on structural elements which are beyond the resolution provided by freeze fracture technique.
CHRONIC INTESTINAL STASIS IN CHILDREN
Authors: G. Taunton
Journal: BMJ (1919)

CHRONIC intestiual stasis is apt to be regarded as a con- dition affecting maturity because it -is generally after this stage of life has been reached that patients present them- selves for treatment.but only a few, if carefully ques- tioned, fail to give a history whicih leads to the suspicion that their condition started in clhildlhood or early infancy.Chlronic intestinal stasis in children produces ill effects in several ways.In the first place, from autointoxica- tion-thie introduction of poisons into the blood stream thlrough the intestinal muLcous mnembrane affecting harm- fully all the tissues of the body.These toxins are pro- duced normally during .digestionby the micro-organisms naturally present in the lumen of tlle bowel, and often in addition by other micro-organisms whiclh are able to estab- lish tle-mselves only in tlhe presence of stasis.The mucous