tbuckley/cabot-search huggingface dataset:
Abstract 319: Mild Hypothermia Preserves Cerebral Cortex Microcirculation After Resuscitation in a Rat Model of Cardiac Arrest
Authors: Ping Gong, Shen Zhao, Jiangang Wang, Jie Qian, Zhengfei Yang, Xiaobo Wu, Jena Cahoon, Neil Duggal, Wanchun Tang
Journal: Circulation (2014)

Introduction: Mild hypothermia is one of the effective treatments in comatose patients after cardiac arrest. However, its neuroprotective mechanism is not fully clear. In the present study, we investigated the effect of mild hypothermia on cerebral cortex microcirculation and cerebral oxygen extraction ratio (CERO2). Hypothesis: Mild hypothermia is associated with an improved cerebral cortex microcirculation and a decreased CERO2. Methods: Twenty-five male Sprague-Dawley rats were randomized into 3 groups: hypothermic (HT, n=10), normothermic (NT, n=10) or sham control group (SC, n=5). Ventricular fibrillation was electrically induced and untreated for 8 mins, followed by 8 mins of precordial compressions and mechanical ventilations. Core temperature was reduced to 33±0.5°C at 14 mins after return of spontaneous circulation (ROSC) with a combination of ice packs, an electrical fan and a cooling blanket. The temperature was maintained at 33°C for 8 hrs. Hemodynamics, jugular venous and aortic blood gas, and cerebral cortex microcirculation were measured at baseline, 2, 4 and 8 hrs after ROSC. Results: Of the 20 experimental rats, 15 were successfully resuscitated. There was no significant difference in the rate of ROSC in the NT and HT groups (7/10 vs. 8/10; p&gt;0.05). Microvascular flow index was significantly reduced at 2, 4 and 8 hrs after ROSC but was significantly improved by mild hypothermia (Figure 1). Mild hypothermia significantly reduced the CERO2 after ROSC (Figure 2). Conclusions: Mild hypothermia improves the cerebral cortex microcirculatory blood supply/oxygen uptake mismatching after ROSC, which may provide one additional mechanism of cerebral protection.
Plant cysteine proteases that evoke itch activate protease-activated receptors
Authors: V.B. Reddy, E.A. Lerner
Journal: British Journal of Dermatology (2010)

Background Bromelain, ficin and papain are cysteine proteases from plants that produce itch upon injection into skin. Their mechanism of action has not been considered previously. Objectives To determine the mechanism by which these proteases function. Methods The ability of these proteases to activate protease-activated receptors was determined by ratiometric calcium imaging. Results We show here that bromelain, ficin and papain activate protease-activated receptors 2 and 4. Conclusions Bromelain, ficin and papain function as signalling molecules and activate protease-activated receptors. Activation of these receptors is the likely mechanism by which these proteases evoke itch.
ANOREXIA NERVOSA: THE DIAGNOSIS AND TREATMENT OF INANITION RESULTING FROM FUNCTIONAL DISORDERS
Authors: John M. Berkman
Journal: Annals of Internal Medicine (1945)

Article1 May 1945ANOREXIA NERVOSA: THE DIAGNOSIS AND TREATMENT OF INANITION RESULTING FROM FUNCTIONAL DISORDERSJOHN M. BERKMAN, M.D.JOHN M. BERKMAN, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-22-5-679 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIt is interesting that Gull, who first recognized anorexia nervosa as being a condition resulting from starvation, should have also discovered the cause of myxedema, a disease which bears his name. He has been appraised by the English as being one of the most brilliant clinicians of all times. His diagnostic acumen, ability of keen observation and unquestioned curiosity must have been enviable, particularly at a time when laboratory assistance and other aids to diagnosis were far inferior to those which we have at our disposal at the present time. The study of anorexia nervosa has in certain respects been...Bibliography1. BERKMAN JM: Anorexia nervosa, anorexia, inanition, and low basal metabolic rate, Am. Jr. Med. Sci., 1930, clxxx, 411-424. CrossrefGoogle Scholar2. SHEEHANMURDOCH HLR: Post-partum necrosis of the anterior pituitary; pathological and clinical aspects, Jr. Obst. and Gynaec. Brit. Emp., 1938, xlv, 456-489. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Rochester, Minnesota*Received for publication November 25, 1944. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySevere and Enduring Anorexia Nervosa: Enduring Wrong Assumptions?Psychological, nutritional, and energy expenditure differences in college females with anorexia nervosa vs. comparable-mass controlsLong-term Fracture Risk Among Women With Anorexia Nervosa: A Population-Based Cohort StudyThe Medical Complications of Anorexia NervosaDietary treatment of anorexia nervosaPsychological Elements of Gastrointestinal DisordersThe Diet Composition and Nutritional Knowledge of Patients with Anorexia NervosaPerception of hunger and satiety in anorexia nervosaREFERENCESClinical and metabolic features of anorexia nervosaMenstruation and fertility in anorexia nervosaDas Anorexia-nervosa-Problem unter besonderer Berücksichtigung der Pubertätsmagersucht und ihrer klinischen BedeutungPregnancy Associated with Anorexia Nervosa: Report of a CaseAnorexia nervosa: Fact and theoryPhysiologic Aspects of Anorexia NervosaAnorexia Nervosa, Anterior-Pituitary Insufficiency, Simmonds' Cachexia, and Sheehan's DiseaseThe treatment of amenorrhea in young women 1 May 1945Volume 22, Issue 5Page: 679-691KeywordsAnorexia nervosaResearch laboratoriesStarvation Issue Published: 1 May 1945 PDF downloadLoading ...
Abstract 1673: Alternative NF-κB signaling promotes inflammatory cell recruitment and lung tumor formation
Authors: Jamie Alicyn Ausborn, Dong-Sheng Cheng, Vasiliy Polosukhin, Wei Han, Fiona Yull, Timothy Blackwell
Journal: Cancer Research (2014)

Abstract Nuclear factor-κB (NF-κB) is a transcription factor that can be activated through either the classical or alternative signaling pathways. In lung tumors, high levels of classical and alternative pathway components have been observed. While many studies have demonstrated that classical NF-κB signaling is a central pathway regulating inflammation and tumorigenesis, the role of alternative NF-κB signaling remains undefined. We hypothesize that alternative NF-κB signaling in the lung epithelium plays a key role in inflammation and lung tumor formation through paracrine signaling to the inflammatory microenvironment. To investigate alternative NF-κB signaling in the lung epithelium, we generated a transgenic mouse model with doxycycline (dox)-inducible expression of the alternative pathway component p52 in airway epithelial cells (designated ALTA for alternative pathway trans-activated). When placed on dox, nuclear p52 is increased in the lungs of ALTA mice with no effect on activation of other NF-κB components. Surprisingly, alternative pathway activation alone did not cause a significant increase in inflammatory cell recruitment. However, in conjunction with the inflammatory stimulus lipopolysaccharide (LPS), alternative pathway activation caused increased mortality, which was associated with a significant increase in inflammation and increased lung permeability. To determine the effect of alternative pathway activation on lung tumor formation, mice were injected with the lung carcinogen urethane. Six weeks after urethane administration, ALTA mice demonstrated an increased number of bronchoalveolar lavage neutrophils, and by 6 months post-urethane, ALTA mice had an increased number of tumors, increased tumor size, and more advanced lesions. Together, these data suggest that alternative NF-κB signaling plays an important role in stimulus-induced inflammatory cell recruitment and that alternative pathway activation can promote lung tumor formation and progression. By defining the role of alternative NF-κB signaling in tumor formation, we hope to gain insight into the role of inflammation in lung carcinogenesis and to identify novel pathways and signaling targets that could potentially serve as therapeutic targets. Citation Format: Jamie Alicyn Ausborn, Dong-Sheng Cheng, Vasiliy Polosukhin, Wei Han, Fiona Yull, Timothy Blackwell. Alternative NF-κB signaling promotes inflammatory cell recruitment and lung tumor formation. [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 1673. doi:10.1158/1538-7445.AM2014-1673
Multiple eruptive dermatofibromas occurring in a patient with acute myeloid leukaemia
Authors: S-E. Chang, J-H. Choi, K-J. Sung, K-C. Moon, J-K. Koh
Journal: British Journal of Dermatology (2000)

Journal Article Multiple eruptive dermatofibromas occurring in a patient with acute myeloid leukaemia Get access S‐E. Chang, S‐E. Chang Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388–1 Poongnap‐dong, Songpa‐gu, Seoul 138–040, Korea E‐mail: derm@http://www.amc.seoul.kr Search for other works by this author on: Oxford Academic Google Scholar J‐H. Choi, J‐H. Choi Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388–1 Poongnap‐dong, Songpa‐gu, Seoul 138–040, Korea E‐mail: derm@http://www.amc.seoul.kr Search for other works by this author on: Oxford Academic Google Scholar K‐J. Sung, K‐J. Sung Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388–1 Poongnap‐dong, Songpa‐gu, Seoul 138–040, Korea E‐mail: derm@http://www.amc.seoul.kr Search for other works by this author on: Oxford Academic Google Scholar K‐C. Moon, K‐C. Moon Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388–1 Poongnap‐dong, Songpa‐gu, Seoul 138–040, Korea E‐mail: derm@http://www.amc.seoul.kr Search for other works by this author on: Oxford Academic Google Scholar J‐K. Koh J‐K. Koh Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388–1 Poongnap‐dong, Songpa‐gu, Seoul 138–040, Korea E‐mail: derm@http://www.amc.seoul.kr Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 142, Issue 5, 1 May 2000, Pages 1062–1063, https://doi.org/10.1046/j.1365-2133.2000.03508.x Published: 01 May 2000
The Role of Bioinformatics in Genomic Medicine
Authors: A. H. C. van Kampen, A. J. G. Horrevoets
Journal: Cardiovascular Research (2006)

For more than a century vast progress has been made in genetics and molecular biology. During the last decade newhigh-throughput experimental techniques have rapidly emerged. The automation of DNA sequencing has set the stage for the Human Genome Project in 1990 (Collins et al., 1998), which has led to genomics (the branch of genetics that studies organisms in terms of their full DNA sequences) and a range of related disciplines such as transcriptomics (the study of the complete gene expression state), proteomics (the study of the full set of proteins encoded by a genome), and metabolomics (the study of comprehensive metabolite profiles). In the remainder of this chapter these domains will all be referred to as genomics. Genomics has greatly accelerated fundamental research in molecular biology as it enables the measurement of molecular processes globally and from different points of view. This led to a range of applications in the biomedical sector and increasingly affects patient care (Collins et al., 2003; Subramanian et al., 2001; van Ommen, 2002).
Abstract 8952: Results of the Pediatric Lead Extractability and Survival Evaluation (PLEASE) Study
Authors: Charles I Berul, Vicki Freedenberg, Joseph Atallah, Seshadri Balaji, Yaniv Bar-Cohen, Anjan S Batra, Bryan C Cannon, Scott Ceresnak, Terrence U Chun, Mitchell I Cohen, Kathryn K Collins, Anne M Dubin, Christopher C Erickson, Wayne H Franklin, Naomi J Kertesz, Martin J LaPage, Ian H Law, Jeffrey P Moak, John Papagiannis, Thomas Paul, Ronn E Tanel, Svetlana Tisma-Dupanovic, Bruce L Wilkoff, Frank Zimmerman, Frank Cecchin
Journal: Circulation (2011)

Implantable cardioverter-defibrillator (ICD) therapy in children and congenital heart disease (CHD) patients is hampered by poor long-term lead survival. Lead extraction is technically difficult and carries substantial morbidity. Manufacturers developed distinct strategies for this issue: thinner lead bodies or a Gore ePTFE coil coating. Both design changes were thought to improve ease of lead removal, but have not been directly compared in children or adults. The purpose of this study was to assess thin and ePTFE-coated ICD lead survival in pediatric and CHD pts. Methods: The Pediatric Lead Extractability and Survival Evaluation (PLEASE) Study began as a Phase IV multicenter open-label prospective study [ NCT00335036 ], facilitated by the Pediatric &amp; Congenital EP Society. Initially designed as a randomized study, it changed to a parallel assignment registry when 1 lead had an advisory due to high incidence of failure, prompting concern about continued clinical equipoise. Pediatric and CHD pts who underwent ICD lead implant from 2005-2010 were eligible. The end date was NCDR ICD Registry v2.0 release (includes pediatric &amp; lead data). 23 centers participated; each site obtained IRB approval. De-identified data was sent to the PI center for verification and statistical analyses. Results: A total of 982 ICD pts (357 VVI, 558 DDD, 67 CRT-D) entered the PLEASE study, incl. 423 pts (43%) with CHD. Mean age at implant = 18.3 ± 9.9 yrs. Thin (&lt; 7Fr) ICD leads accounted for 51%, 23% were ePTFE-coated, 26% neither thin nor coated. There were 113 ICD lead failures (11.5%) at a mean lead-age of 2.2 ± 1.7 yrs, causing shocks in 55 pts. Failure occurred in 21% of thin leads vs 3.5% of ePTFE leads (p&lt;0.01). Extraction was performed on 142 (14.5%) leads overall; 21% of thin leads (incl. extraction of 29 functioning leads due to recall) vs. 4.4% of ePTFE leads (p&lt;0.01). There were 7 major extraction complications (4.9%), but no procedural mortality. Among thin leads, 90/270 (33.3%) of recalled leads failed vs 15/229 (6.6%) non-recalled thin leads. Conclusions: This Phase IV study demonstrates that ICD leads in children and CHD pts have suboptimal performance overall. Thinner leads were much more likely to fail and/or be extracted compared with ePTFE leads, chiefly driven by one lead type.
Macrophages Regulate the Systemic Response to DNA Damage by a Cell Nonautonomous Mechanism
Authors: Anat Geiger-Maor, Avital Guedj, Sharona Even-Ram, Yoav Smith, Eithan Galun, Jacob Rachmilewitz
Journal: Cancer Research (2015)

The DNA damage response (DDR) is a comprehensive and complex network of phosphorylation-mediated signaling pathways that originates endogenously from the DNA lesion and activates intrinsic DNA repair mechanisms. Here we describe a macrophage-dependent mechanism that regulates the response to DNA damage. We demonstrate that human monocytes, by releasing macrophage-derived HB-EGF, enhance DDR in neighboring cells suffering from DNA damage. Consequently, HB-EGF-treated cells exhibit higher double-strand break (DSB) rejoining and display lower levels of residual DSBs. Diethylnitrosamine (DEN) injection induce DSBs along with elevation in the number of macrophages and HB-EGF expression. Significantly, macrophage depletion or blocking HB-EGF activity results in higher levels of nonrepairable DSBs, suggesting that macrophages play a role in the resolution of DNA damage via HB-EGF. This study establishes that macrophages, acting through the activation of the EGFR cascade, constitute an important cell nonautonomous physiologic component of the DDR and points to a unique role played by immune cells in maintaining genome integrity.
Physiology of Alimentation.
Authors: Martin H. Fischer
Journal: JAMA (1907)

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
Risk of acute childhood leukaemia in Sweden after the Chernobyl reactor accident
Authors: U Hjalmars, M Kulldorff, G Gustafsson
Journal: BMJ (1994)

To evaluate the risk of acute childhood leukaemia in areas of Sweden contaminated after the Chernobyl reactor accident in April 1986.Population based study of childhood leukaemia diagnosed during 1980-92.Coordinates for places of residence of all 1.6 million children aged 0-15 years; aerial mapped areas of Sweden heavily contaminated after the Chernobyl accident.888 children aged 0-15 years with acute leukaemia diagnosed in Sweden during 1980-92, identified with place of birth and residence at diagnosis.Risk of leukaemia in areas contaminated after the Chernobyl accident compared with the rest of Sweden and in the same areas before the accident.During six and a half years of follow up after the accident the odds ratio for acute leukaemia was 0.9 (95% confidence interval 0.6 to 1.4) in highly contaminated areas (> or = 10 kBq/m2) compared with the same areas before the accident. For the subgroup acute lymphoblastic leukaemia in children aged under 5 years at diagnosis the odds ratio was 1.5 (0.8 to 2.6). For all cases diagnosed after May 1986 in highly contaminated areas compared with areas of low contamination the odds ratio was 0.9 (0.7 to 1.3). For acute lymphoblastic leukaemia in children aged under 5 years at diagnosis the odds ratio was 1.2 (0.8 to 1.9) in highly contaminated areas compared with areas of low contamination. Dose-response analysis showed no correlation between the degree of contamination and the incidence of childhood leukaemia.There has been no significant increase in the incidence of acute childhood leukaemia in areas of Sweden contaminated after the Chernobyl reactor accident.
Abstract 2213: Characteristics of Aspirin Non-Responders: Results from the Aspirin Resistance Testing and Initial Strategy for Treatment (ARTIST) Multicenter Trial
Authors: Lori B Daniels, Paul Clopton, W. F Peacock, Richard Nowak, Alex Harrison, Alan Wu, J. D Kirk, Alan S Maisel
Journal: Circulation (2007)

Introduction: Aspirin (ASA) therapy reduces the risk of thrombotic events by inhibiting platelet aggregation, however some individuals have a diminished response to ASA. The ability to predict ASA non-responsiveness has important therapeutic implications. We studied patients with suspected acute coronary syndrome (ACS) to determine the characteristics of patients with ASA non-responsiveness. Methods: We enrolled 1010 patients with suspected ACS in the emergency departments (ED’s) of 5 sites. All subjects were on outpatient ASA therapy or received ASA in the ED, and were excluded if on clopidogrel. Blood was tested for ASA non-responsiveness (defined as ASA reactive units ≥ 550) on a VerifyNow® (Accumetrics) device. Results: Overall prevalence of ASA non-responsiveness was 10.3% (95% C.I. 8.6–12.3%). Responsiveness to ASA did not differ by age or sex, but varied significantly by race. Hispanics had a higher prevalence of ASA non-responsiveness, while whites and Asians had a lower prevalence ( Figure ). Other factors associated with increased prevalence of ASA resistance included outpatient ASA therapy (p&lt;0.001), a history of alcohol (p=0.045) or drug abuse (p=0.02), a history of heart failure (p=0.01), and renal insufficiency (p=0.003). Patients with ASA non-responsiveness had lower BMI (p=0.006) and hemoglobin (p&lt;0.001), and higher BNP levels (p&lt;0.001), prothrombin time (p=0.01), and partial thromboplastin time (p&lt;0.001). Conclusions: Among suspected ACS patients, the prevalence of ASA non-responsiveness varies by race and is highest in Hispanics. ASA resistance is also more prevalent in patients with clinical characteristics consistent with poorer health. Prevalence of ASA Non-Responsiveness by Race
BILATERAL SUBDURAL HEMATOMA—AN UNUSUAL COMPLICATION OF MENINGOCOCCUS MENINGITIS
Authors: J NELSON, R M CLYNE, J G SHARNOFF
Journal: Annals of Internal Medicine (1946)

Case Reports1 November 1946BILATERAL SUBDURAL HEMATOMA—AN UNUSUAL COMPLICATION OF MENINGOCOCCUS MENINGITISJACK NELSON, M.D., ROBERT M. CLYNE, M.D., J. GEORGE SHARNOFF, M.D.JACK NELSON, M.D.Search for more papers by this author, ROBERT M. CLYNE, M.D.Search for more papers by this author, J. GEORGE SHARNOFF, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-25-5-862 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptCASE REPORTHistory: C. O., a 41 year old male, was admitted to Lincoln Hospital on November 14, 1944 with a five day history of chills and fever together with "red-colored" urine. Two days subsequently he began to have generalized aches and pains. On the day of admission he became increasingly weak, fell to his knees, and was brought to the hospital.Physical Examination:The patient appeared acutely ill but alert and oriented. The temperature was 104.4° F.; the pulse was 120. The respirations were 40 per minute, and the blood pressure was 102 mm. Hg systolic and 70 mm....Bibliography1. VOELKER AF: Item in Path. Reports Middlesex Hospital, 1894, p. 246. Google Scholar2. DENEHY WJ: Epidemic cerebrospinal meningitis, Brit. Med. Jr., 1916, ii, 684. CrossrefGoogle Scholar3. GORDON : 1922 (Quoted from Briton—reference below). Google Scholar4. BANKSMCCARTNEY HSJE: Meningococcal encephalitis, Lancet, 1942, i, 219. CrossrefGoogle Scholar5. BRITON D: Cerebrospinal fever, 1941, London, 152 pp. Google Scholar6. NETTERDÉBRÉ AR (a) : La méningite cérébrospinale, 1911, Paris. (b) BANKS, H. S., and MCCARTNEY, J. E.: Meningococcal adrenal syndromes and lesions, Lancet, 1943, i, 711. (c) Reference 4, above. Google Scholar7. MURRAY EG: The Meningococcus Medical Research Council Special Report Series, No. 124, H. M. Stationery Office, London, 1929. Google Scholar8. WORSTER-DROUGHTKENNEDY CAM: Cerebrospinal fever, 1919, A. and C. Black, London. Google Scholar9. APPELBAUMNELSON EJ: Sulfadiazine and its sodium compound in the treatment of meningococcic meningitis and meningococcemia, Am. Jr. Med. Sci., 1944, ccvii, 492. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication September 10, 1945.From the Medical Service of Dr. Kenneth Taylor, Lincoln Hospital, New York City, N. Y.Dr. Robert O. Kellog, Jr. participated in the clinical management of this case. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySubdural Lesions in Childhood, with Special Reference to Infectious Processes 1 November 1946Volume 25, Issue 5Page: 862-867KeywordsFeversHeart rateKneesMedical servicesMeningitisNeisseria meningitidisPainRespirationTemperatureUrine ePublished: 1 December 2008 Issue Published: 1 November 1946 PDF downloadLoading ...