tbuckley/cabot-search huggingface dataset:
Abstract 1317: Estradiol and progesterone promotes breast tumor growth through induction of AKT/mTOR pathway and inhibition of apoptosis
Authors: Arunkumar Arumugam, Thiyagarajan Boopalan, Alejandro Delgado, Pamela A. Agullo, Jacqueline Parada, Rajkumar Lakshmanaswamy
Journal: Cancer Research (2011)

Abstract Breast cancer development is accomplished by unbalanced regulation of several signaling pathways. Studies indentifying potential targets for mammary cancer treatment and prevention are vital. Copenhagen strain of rat is a well known animal model which is resistant to carcinogen-induced mammary carcinogenesis. In our laboratory, we were able to induce a very high incidence of mammary cancers in these rats using combination of carcinogen N-methyl-N-nitrosourea (MNU), followed by estradiol and progesterone treatment. We have demonstrated that the resistance to mammary carcinogenesis in these rats is not due to inhibition of initiation but due to reduced hormone promotional environment and we further extend our research to investigate the molecular mechanisms involved behind this hormone-induced promotion. In the present study, we exposed 7 week old female Copenhagen rats to N-methyl-N-nitrosourea (MNU; 50mg/kg body weight). Immediately after MNU treatment the rats were divided into the following groups: 1) Control 2) 17β-estradiol (30mg) 3) progesterone (30mg) and 4) 17β-estradiol (30mg) plus progesterone (30mg). All hormone treatments were administered via individual silastic pellets for a period of 9 months post carcinogen treatment. At the end of the treatment period rat mammary tumors were excised and used for molecular analysis. Quantitative RT-PCR and western blot analysis showed that ovarian hormones treatment triggered the AKT/mTOR pathway along with increased cell cycle progression. Intra cellular MAPK signaling was increased through activation of AKT/PI3K pathway. Hormone administration decreased the levels of caspase-3, caspase-8 and caspase-9. Together, our result indicates that hormone treatment induces mammary tumor growth through activation of AKT/PI3K/mTOR pathways and simultaneously inhibiting apoptosis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1317. doi:10.1158/1538-7445.AM2011-1317
Genes Within the Major Histocompatibility Complex Predict NIDDM in African-American Women in Alabama
Authors: Ronald T Acton, Jeffrey M Roseman, David S H Bell, Robert L Goldenberg, Mei-Ling Tseng, Chotip Vanichanan, Leigh A Harman, Rodney C P Go
Journal: Diabetes Care (1994)

OBJECTIVE To test the hypothesis that genes within the major histocompatibility complex (MHC) are associated with gestational diabetes mellitus (GDM) and, subsequently, non-insulin-dependent diabetes mellitus (NIDDM) in African-American women. RESEARCH DESIGN AND METHODS African-American women who presented with GDM were compared with pregnant African-American control subjects. Following pregnancy, GDM patients were assessed at various intervals of time (median = 6 years) to determine whether they had developed diabetes. RESULTS GDM patients who required insulin during pregnancy possessed a significantly higher frequency of A33, DR2, DR9, and BF-S phenotypes than control subjects. GDM patients who subsequently developed NIDDM had a significantly higher frequency of B41, DR2, and BF-S and a lower frequency of DR1 and DR6 phenotypes than control subjects. Even after controlling for age and body mass index, B41 and DR2 were independent predictors of developing insulin-requiring GDM and NIDDM in GDM subjects. CONCLUSIONS These results suggest that either one or more genes within the MHC are involved in the etiology of NIDDM.
Graduate Medical Education, 2009-2010
Authors: Sarah E. Brotherton, Sylvia I. Etzel
Journal: JAMA (2010)

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
Traumatic Paraplegia in Infancy
Authors: Franz E. Glasauer
Journal: JAMA (1972)

Two infants were rendered paraplegic in automobile accidents. The spinal cord injuries were at the levels customarily found in spinal injuries: the low cervical and upper thoracic areas. However, x-ray films of the spine failed to show any fracture-dislocation, and this lack of radiological evidence of injury is supported in the literature. Our findings here support the belief that the front seat of an automobile is the most dangerous location for an unrestrained child at any age. Infants who are improperly restrained or are unrestrained in the mother's lap are likely to be thrown forward at impact and suffer severe injuries or death. A proper restraining system allows for the infant's height and weight and offers maximum protection. These unfortunate injuries can be prevented by parental insistence on the proper restraints.
The Divine Banquet of the Brain — Medical Evidence — Edward Jenner's Homes
Authors: John Lister
Journal: New England Journal of Medicine (1966)

WHEN he rose to give the Harveian oration at the Royal College of Physicians Dr. Macdonald Critchley reminded those present that it was the two hundred and fifty-eighth time that fellows of the College had met in amity to commemmorate William Harvey.Explaining why he had chosen to speak on the "Divine Banquet of the Brain," he recalled that this was the topic of Harvey's third Lumleian Lecture given to the College three hundred and fifty years ago. Harvey was then thirty-seven years of age, and the College met in its second home at Amen Corner, which had been leased . . .
Wrongful Death: A medical tragedy
Authors: S. Goldbeck-Wood
Journal: BMJ (1996)

Sandra M Gilbert Norton, £15.95, pp 365 ISBN 0 393 03721 5

Elliot Gilbert, professor of English literature at the university of California, Davis, died on 11 February 1991 only hours after a radical prostatectomy for a large cancer. His death followed a series of medical mishaps ranging from a long and difficult resection of an adherent gland to mismanagement of a postoperative haemorrhage that was later deemed negligent. The circumstances were shrouded in evasions; communication with the family was bumblingly incompetent. Almost inevitably therefore, things ended in court. Wrongful Death is a final act of vengeance by his …
Pediatric Neurology: Principles and Practice, vols 1 &amp;amp; 2
Authors: Gerald F. Tremblay
Journal: JAMA (1994)

Child neurology is a young discipline. Doctors who specialized in the immature nervous system gained official recognition in 1968 by the American Board of Psychiatry and Neurology when it began certifying physicians qualified as having "special competence in child neurology." In 1971 a small group of child neurologists (Kenneth F. Swaiman, Francis S. Wright, Richard J. Allen, Paul R. Dyken, William S. Bell, Raymond W. M. Chun, George Wolcott, and Manuel R. Gomez) met to organize the Child Neurology Society (CNS). They elected Kenneth Swaiman its first president at the first national scientific meeting in 1972. The CNS membership directory listed about 50 members that year; the present directory lists well over 1000 members, most of whom practice in North America. Child neurologists typically treat headache, seizures, hyperactivity (attention deficit disorder), and developmental delay—all common conditions. But the theoretical scope of child neurology is vast. Cerebral dysgenesis, inborn errors of
Increased Expression of Visfatin in Macrophages of Human Unstable Carotid and Coronary Atherosclerosis
Authors: Tuva B. Dahl, Arne Yndestad, Mona Skjelland, Erik Øie, Arve Dahl, Annika Michelsen, Jan K. Damås, Siv H. Tunheim, Thor Ueland, Camilla Smith, Bjørn Bendz, Serena Tonstad, Lars Gullestad, Stig S. Frøland, Kirsten Krohg-Sørensen, David Russell, Pål Aukrust, Bente Halvorsen
Journal: Circulation (2007)

Although the participation of inflammation in atherogenesis is widely recognized, the identification of the different components has not been clarified. In particular, the role of inflammation in plaque destabilization is not fully understood.Our main findings were as follows: (1) In a microarray experiment, we identified visfatin, one of the most recently identified adipokines, as a gene that was markedly enhanced in carotid plaques from symptomatic compared with plaques from asymptomatic individuals. This finding was confirmed when carotid plaques from 7 patients with asymptomatic and 14 patients with symptomatic lesions were examined with real-time reverse transcription polymerase chain reaction. (2) Immunohistochemistry showed that visfatin was localized in areas that were rich in lipid-loaded macrophages. (3) The relationship between visfatin and unstable lesions was also found in patients with coronary artery disease, demonstrating a strong visfatin immunostaining in lipid-rich regions within the material obtained at the site of plaque rupture in patients with acute myocardial infarction. (4) Both oxidized low-density lipoprotein and tumor necrosis factor-alpha increased visfatin expression in THP-1 monocytes, with a particularly enhancing effect when these stimuli were combined. (5) Visfatin increased matrix metalloproteinase-9 activity in THP-1 monocytes and tumor necrosis factor-alpha and interleukin-8 levels in peripheral blood mononuclear cells. Both of these effects were abolished when insulin receptor signaling was blocked.Our findings suggest that visfatin should be regarded as an inflammatory mediator, localized to foam cell macrophages within unstable atherosclerotic lesions, that potentially plays a role in plaque destabilization.
Emboli in Infective Endocarditis: The Prognostic Value of Echocardiography
Authors: James M. Steckelberg, Joseph G. Murphy, David Ballard, Kent Bailey, A. Jamil Tajik, Charles P. Taliercio, Emilio R. Giuliani, Walter R. Wilson
Journal: Annals of Internal Medicine (1991)

Objective: To determine whether vegetations visualized on two-dimensional echocardiography are an independent risk factor for the development of subsequent emboli in patients with infective endocarditis and to assess the timing of emboli relative to the initiation of antimicrobial therapy. Design: Investigator-blinded, retrospective incidence cohort study. Setting: Tertiary referral center. Patients: Patients with left-sided native valve infective endocarditis who had two-dimensional echocardiography within 72 hours of beginning antimicrobial therapy. Measurements and Main Results: The crude incidence rate of first embolic events in patients receiving antimicrobial therapy was 6.2 per 1000 patient-days (95% CI, 4.2 to 9.2). The rates in patients with and without vegetations were 7.1 and 4.9 per 1000 patient-days, respectively (incidence rate ratio, 1.4; 95% CI, 0.6 to 3.3). The relation between vegetations and risk for emboli was microorganism-dependent: Stratified incidence rate ratios were 6.9 (95% CI, 1.1 to 42.5; P < 0.05) and 1.0 (95% CI, 0.2 to 3.9) for viridans streptococcal and Staphylococcus aureus endocarditis, respectively. The rate of first embolic events diminished over time (P < 0.001), falling from 13 per 1000 patient-days during the first week of therapy to less than 1.2 per 1000 patient-days after completion of the second week of therapy. Conclusions: Overall, the presence of vegetations on echocardiography was not associated with a significantly higher risk for embolus in patients with left-sided native valve infective endocarditis. The relative risk for embolic events associated with echocardiographically visualized vegetations may be microorganism-dependent, with a significantly increased risk seen only in patients with viridans streptococcal infection. The rate of embolic events declines with time after initiation of antimicrobial treatment.
Differential regulation of cyclins D1 and D3 in hepatocyte proliferation
Authors: David G. Rickheim, Christopher J. Nelsen, John T. Fassett, Nikolai A. Timchenko, Linda K. Hansen, Jeffrey H. Albrecht
Journal: Hepatology (2002)

Substantial evidence suggests that cyclin D1 plays a pivotal role in the control of the hepatocyte cell cycle in response to mitogenic stimuli, whereas the closely related protein cyclin D3 has not been extensively evaluated. In the current study, we examined the regulation of cyclins D1 and D3 during hepatocyte proliferation in vivo after 70% partial hepatectomy (PH) and in culture. In contrast to cyclin D1, which was nearly undetectable in quiescent liver and substantially up-regulated after PH, cyclin D3 was constitutively expressed and induced only modestly. In the regenerating liver, the concentration of cyclin D3 was only about 10% of that of cyclin D1. Cyclin D1 formed complexes primarily with cyclin-dependent kinase 4 (cdk4), which were markedly activated in the regenerating liver and readily sequestered the cell cycle inhibitory proteins, p21 and p27. Cyclin D3 bound to both cdk4 and cdk6. Cyclin D3/cdk6 activity was readily detectable in quiescent liver and changed little after PH, and this complex appeared to play a minor role in sequestering p21 and p27. In cultured hepatocytes, epidermal growth factor or insulin had little effect, but the combination of these agents substantially induced cyclin D1 and cell cycle progression. Inhibition of Mek1 or phosphoinositide 3-kinase markedly inhibited cyclin D1 expression and replication. In contrast, cyclin D3 was expressed in the absence of mitogens and was only modestly affected by these manipulations. In addition, growth-inhibitory extracellular matrix conditions inhibited cyclin D1 but not cyclin D3 expression. In conclusion, these results support the concept that cyclin D1 is critically regulated by extracellular stimuli that control proliferation, whereas cyclin D3 is regulated through different pathways and plays a distinct role in the liver.
Shaky-Leg Syndrome and Vitamin B<sub>12</sub>Deficiency
Authors: Julián Benito-León, Jesús Porta-Etessam
Journal: New England Journal of Medicine (2000)

To the Editor: A 68-year-old man presented with a three-year history of trembling of the legs. The tremor began immediately after he stood and subsided when he began walking. His medical history was irrelevant to this problem. Neurologic examination showed a fine, rapid tremor of the legs that began immediately after the patient rose to the standing position and that abated on walking. Sensation of pain and heat was impaired in a stocking distribution, and the Achilles tendon reflexes were absent. Results of the rest of the examination were normal. Results of laboratory tests were remarkable only for a serum . . .
IBD5 is associated with an extensive complicated Crohn's disease feature: implications from genotype-phenotype analysis
Authors: S Brescianini, T Trinh, M Stoll, S Schreiber, J D Rioux, M J Daly
Journal: Gut (2006)

Injection of amniotic fluid stem cells ameliorates the acute phase of acute tubular necrosis in animals by promoting proliferation of injured tubular cells and decreasing apoptosis, but whether these stem cells could be of benefit in CKD is unknown. Here, we used a mouse model of Alport syndrome, <i>Col4a5</i><sup>−/−</sup> mice, to determine whether amniotic fluid stem cells could modify the course of progressive renal fibrosis. Intracardiac administration of amniotic fluid stem cells before the onset of proteinuria delayed interstitial fibrosis and progression of glomerular sclerosis, prolonged animal survival, and ameliorated the decline in kidney function. Treated animals exhibited decreased recruitment and activation of M1-type macrophages and a higher proportion of M2-type macrophages, which promote tissue remodeling. Amniotic fluid stem cells did not differentiate into podocyte-like cells and did not stimulate production of the collagen IVa5 needed for normal formation and function of the glomerular basement membrane. Instead, the mechanism of renal protection was probably the paracrine/endocrine modulation of both profibrotic cytokine expression and recruitment of macrophages to the interstitial space. Furthermore, injected mice retained a normal number of podocytes and had better integrity of the glomerular basement membrane compared with untreated <i>Col4a5</i><sup>−/−</sup> mice. Inhibition of the renin-angiotensin system by amniotic fluid stem cells may contribute to these beneficial effects. In conclusion, treatment with amniotic fluid stem cells may be beneficial in kidney diseases characterized by progressive renal fibrosis.
Hydroxyl radical generation, levels of tumor necrosis factor-alpha, and progression to heart failure after acute myocardial infarction
Authors: Marco Valgimigli, Elisa Merli, Patrizia Malagutti, Olga Soukhomovskaia, Giordano Cicchitelli, Alessandra Antelli, Donatella Canistro, Gloria Francolini, Gaetano Macrì, Francesca Mastrorilli, Moreno Paolini, Roberto Ferrari
Journal: Journal of the American College of Cardiology (2004)
Association of Surgeons in Training Conference: Manchester 2013
Authors: J.E.F. Fitzgerald, A.J. Beamish, J. Shalhoub, P. Sinclair, J.R.L. Wild, S. Hornby
Journal: International Journal of Surgery (2013)

The Association of Surgeons in Training (ASiT) is a professional body and registered charity working to promote excellence in surgical training for the benefit of junior doctors and patients alike. With a membership of over 2000 surgical trainees from all ten surgical specialities, the association provides support at both regional and national levels throughout the United Kingdom and Republic of Ireland. Originally founded in 1976, ASiT is independent of the National Health Service (NHS), Surgical Royal Colleges, and specialty associations. The 2013 Annual Conference in Manchester brought together over 700 delegates for an educational weekend programme with expert guest speakers. Cutting edge clinical updates were complimented by debates on current training in surgery and focussed parallel sessions. The weekend started with 13 pre-conference courses covering a diverse range of topics including laparoscopic skills, ultrasound for surgeons, surgical drawing, core skills in neurosurgery and a masterclass in journal club. A record number of 1458 abstract submissions were received and those successful competed for 22 awards representing nearly £4000 in trainee prizes and bursaries. As the only national surgical trainee meeting for all specialties, ASiT continues to grow and we look forward to an even larger and more successful international conference next year.Download : Download high-res image (57KB)Download : Download full-size image
American Thyroid Association Guidelines for Use of Laboratory Tests in Thyroid Disorders
Authors: Martin I. Surks
Journal: JAMA (1990)

Selection of appropriate laboratory determinations will enable the clinician to diagnose thyroid dysfunction readily in the majority of patients. At the present time, estimation of free thyroxine and a "sensitive" thyrotropin assay are recommended as the principal laboratory tests for thyroid disease. A decrease in serum free thyroxine estimate and a raised level of serum thyrotropin confirm the diagnosis of hypothyroidism caused by thyroid gland failure. An increase in free thyroxine estimate combined with a serum sensitive thyrotropin level suppressed to less than 0.1 mU/L establishes the diagnosis of thyrotoxicosis. In sick patients, a normal or raised serum free thyroxine estimate together with a normal level of serum thyrotropin suggests that the patient has neither hypothyroidism nor thyrotoxicosis. Patients with severe illnesses, generally in the intensive care unit, and those treated with certain drugs, as well as individuals with unusual thyroid disorders, may present with confusing laboratory findings. An understanding of the regulation of the thyroid hormone system and/or judicious consultation with an endocrinologist should enable the clinician to diagnose thyroid disease, if present, in such patients. (<i>JAMA</i>. 1990;263:1529-1532)
Human platelet fraction arginine-vasopressin. Potential physiological role.
Authors: D G Bichet, M F Arthus, J N Barjon, M Lonergan, C Kortas
Journal: Journal of Clinical Investigation (1987)

Arginine-vasopressin (AVP) immunoreactivity (Ir) has been found to be elevated in platelet-rich plasma. PlatAVP was defined as platelet-rich plasma Ir minus platelet-poor plasma Ir (Pavp). PlatAVP, Pavp, and synthetic AVP were found to have identical retention time on high performance liquid chromatography analysis and similar mobility on thin-layer chromatography. During a standard osmotic suppression-stimulation test, Pavp increased with plasma osmolality (Posm, mosmol/kg H2O); Pavp (pg/ml) = 0.98 (Posm -274.4), r = 0.57, P less than 0.001, n = 65; but PlatAVP was not significantly correlated with Posm and remained at 5 pg/ml. This PlatAVP concentration was estimated to represent a true intraplatelet AVP concentration of 0.4 to 3.7 X 10(-9) M. Binding studies on intact human platelets demonstrated specific binding sites for [3H]AVP (n = 16; BMax = 98 +/- 30 binding sites/platelet; Kd = 0.72 +/- 0.24 nM). This in vitro affinity association constant (Kd) was close to the estimated in vivo intraplatelet AVP concentration. Measurement of PlatAVP could estimate vasopressin bound to a specific platelet receptor.
Diazemuls Versus Diazepam as Premedication in Upper Gastrointestinal Endoscopy: A Randomised Cross-Over Study
Authors: G. Bianchi Porro, M. Lazzaroni, F. Parente, M. Petrillo, O. Sangaletti, H. Zhu
Journal: Endoscopy (1991)

The efficacy and tolerability of Diazemuls versus conventional diazepam as endoscopic premedication was evaluated in a study with a cross-over design performed in 26 patients undergoing upper gastrointestinal tract endoscopy. No statistically significant differences were found between the two forms of premedication with regard to degree of sedation, patient compliance or recovery of psychomotor function. With respect to short-term amnesic effects, efficacy and tolerability Diazemuls was comparable to the conventional formulation of diazepam. Diazemuls may therefore be proposed as an alternative premedication for endoscopy.
INCREASED LEVELS OF SOLUBLE FMS-LIKE TYROSINE KINASE 1 (SFLT-1) ARE ASSOCIATED WITH WORSE OUTCOMES IN OUTPATIENTS WITH HEART FAILURE
Authors: Andreas P. Kalogeropoulos, Wai Hong Tang, Vasiliki Georgiopoulou, Anjan Deka, Ali Azeem, Catherine Norton, Vikas Bhalla, Stanley Hazen, Javed Butler
Journal: Journal of the American College of Cardiology (2012)