tbuckley/cabot-search huggingface dataset:
Cell Biology Update
Authors: B Vastag
Journal: JAMA (2001)

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 641: Targeted inhibition of BRAF signaling in melanoma enhances the activity of a multivalent immunotherapeutic vaccine
Authors: Robert Suriano, Neha Tuli, Jan Geliebter, Raj K. Tiwari, Marc K. Wallack
Journal: Cancer Research (2014)

Abstract Development of a successful immunotherapeutic vaccine targeting melanoma requires the use of multiple melanoma associated antigens (MAA). Expression of several MAAs is regulated by the micropthalmia transcription factor (MITF), which in turn is regulated by members of the MAPK pathway, such as ERK. It is also known that 70% of melanomas express the genetic lesion BRAFV600E. Based on this knowledge, we hypothesize that the use of a specific BRAFV600E inhibitor would enhance MITF mediated MAA expression and thus serve as a viable target for immunotherapy. We have developed a vaccinia virus based melanoma vaccine using patient derived primary melanoma cells that are rich in MAAs such as gp100, tyrosinase, and TRP-1. Our results indicated that our cells were either homozygous or heterozygous for the mutated BRAF gene. In addition, our cells were responsive to treatment by PLX-4032, an FDA approved treatment for melanoma, as evidenced by inhibition of phosphorylation of MEK and ERK, two key players in the MAPK pathway. Phenotypically, the migratory and invasive properties of our cell lines were also altered by PLX-4032. Most interestingly was the observation that upon treatment with PLX-4032, the expression of various MAAs was altered. Specifically, the expression of gp100, MART-1, and tyrosinase increased both on the RNA level as well as on the protein level. Our results warrant further investigation into a combinatorial therapeutic approach to treat melanoma by which increasing the expression of various immunologically relevant MAAs, upon treatment with PLX-4032, followed by vaccination may lead to a more robust and targeted anti-melanoma immune response. Citation Format: Robert Suriano, Neha Tuli, Jan Geliebter, Raj K. Tiwari, Marc K. Wallack. Targeted inhibition of BRAF signaling in melanoma enhances the activity of a multivalent immunotherapeutic vaccine. [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 641. doi:10.1158/1538-7445.AM2014-641
SOME REFLECTIONS ON MEDICAL EDUCATION
Authors: W S MIDDLETON
Journal: Annals of Internal Medicine (1951)

Article1 June 1951SOME REFLECTIONS ON MEDICAL EDUCATIONWILLIAM S. MIDDLETON, M.D., F.A.C.P.WILLIAM S. MIDDLETON, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-34-6-1457 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMedical education had its origin in the priesthood of antiquity. For many generations the shaman, or priest, and the practitioner of the healing art were one and the same individual. Under the Hippocratic oath, the knowledge of the medical skills was imparted only to physicians and to the sons of physicians. Chomel termed this the traditional method of medical instruction. In the evolution of Greek culture, medicine was eventually separated from the priesthood. The first medical school at Alexandria was founded by Alexander of Macedonia. Notable medical figures, as Herophilus, Erasistratus and Galen, trained in this school. With the Roman...Bibliography1. Riesman D: Medicine in modern society, 1938, Princeton University Press, Princeton. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Madison, Wisconsin*Being in substance the address given at Regional Meetings in Trenton, New Jersey, and Chapel Hill, North Carolina. Received for publication March 28, 1951.From the Department of Medicine, University of Wisconsin Medical School. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byMedical Education for Tomorrow 1 June 1951Volume 34, Issue 6Page: 1457-1462KeywordsMedical education ePublished: 1 December 2008 Issue Published: 1 June 1951 PDF downloadLoading ...
Surgical Technique and Principles of Operative Surgery
Authors: A.V. Partipilo
Journal: JAMA (1949)

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 333: Poloxamer 188 Prevents the Impairment in Mitochondrial Respiration Induced by ST-Segment Elevation Myocardial Infarction
Authors: Jason A Bartos, Timothy R Matsuura, Guillaume Debaty, Scott H McKnite, Jennifer N Rees, Frank Bates, Joseph M Metzger, Demetris Yannopoulos
Journal: Circulation (2014)

Introduction: Poloxamer 188 (P188) is a nonionic copolymer shown to protect neurons, skeletal muscle, and potentially cardiac muscle from ischemia/reperfusion injury. P188 is proposed to seal stress-induced gaps in cell membranes, but its mechanism remains unproven. We hypothesized that P188 would improve mitochondrial function after ischemia and reperfusion in a porcine model of ST segment Elevation Myocardial Infarction (STEMI). Methods: Occlusion of the second obtuse marginal artery was performed in 12 pigs using an intracoronary balloon catheter. Animals were randomized to P188 or Control. After 45 minutes of ischemia, the balloon was removed. The P188 group received an intra-coronary bolus of P188 (250 mg/kg) into the left main coronary artery followed by a continuous intravenous P188 infusion (500 mg/kg) over 4 hours. Controls received equivalent volumes of normal saline. After 4 hours of reperfusion, heart tissue was harvested from the infarct zone and the non-ischemic anterior wall. Mitochondria w...
Bilateral congenital adipose plantar nodules
Authors: A. España, R.M. Pujol, M.A. Idoate, J. Vázquez-Doval, J. Romaní
Journal: British Journal of Dermatology (2000)

SIR, Plantar nodular lesions at birth secondary to the presence of subcutaneous fat tissue are an unusual finding.1 We describe three neonates with congenital symmetrical plantar nodular lesions made up of mature adipose tissue separated by thin fibrous septa Patient 1. A 4‐year‐old boy attended our clinic at the age of 6 weeks. Prenatal, postnatal and family history were unremarkable, and there was no maternal history of drug intake during pregnancy. At birth, solitary, symmetrical, skin‐coloured, non‐inflammatory, painless, 1‐cm diameter, soft nodular lesions, unattached to the underlying tissues, were observed on the medial aspect of both heels (Fig. 1a). Examination was otherwise unremarkable. X‐ray of the bones of the feet revealed no significant abnormalities. Surgical excision of one lesion was performed, and after a follow‐up period of 4 years, no clinical recurrence was noted. The growth of the lesion on the contralateral foot was proportionate to his development. The boy has had normal psychomotor development, and no associated systemic abnormalities have been detected.
Abstract 15573: Impact of Coronary Calcification on Different Culprit Lesion Morphology in Acute Coronary Syndrome
Authors: Katsuya Miura, Keigo Dote, Masaya Kato, Shota Sasaki, Noboru Oda, Eisuke Kagawa, Yoshinori Nakano
Journal: Circulation (2014)

Background: Previous studies have reported plaque rupture and erosion were the most common causes of acute coronary syndrome (ACS) and spotty calcifications was identified as a marker of plaque rupture. Optical coherence tomography (OCT) offers a high-resolution imaging to assess the plaque morphology and coronary calcification. Purpose: The aim of this study was to evaluate the relationship between the distribution of coronary calcification and the culprit lesion morphology in patients with ACS. Methods: We enrolled consecutive 183 patients with ACS (mean age: 68 ± 11 years, 148 males). Culprit lesion was assessed by OCT and patients were divided into the rupture and non-rupture group according to the OCT findings. Maximum radial thickness, cross-sectional area of calcification and radial depth from the lumen and longitudinal length of calcification were compared between 2 groups. Results: Plaque rupture was detected at culprit site in 105 patients and coronary calcification was identified in 58 patients. There were no significant differences in age and gender between 2 groups. Maximum thickness, area and longitudinal length of calcification were smaller in rupture group (457.4 ± 284.9 μm vs. 722.1 ± 384.1 μm, p &lt; 0.01, 0.7 ± 0.4 mm 2 vs. 1.8 ± 1.4 mm 2 , p &lt; 0.01, 2.2 ± 1.1 mm vs. 5.6 ± 5.3 mm, p[[Unsupported Character - Codename &amp;shy;]] &lt; 0.01, respectively). Radial depth of calcification from the lumen was significantly geater in rupture group (150.0 ± 65.3 μm vs. 83.1 ± 63.3 μm, p&lt;0.001). Conclusions: Distribution of coronary calcification could be associated with morphological etiology of ACS.
94. Targeting Endothelial Cells in Mice with Adeno-Associated Virus Serotype 1 Vector
Authors: Haiyan Fu, Joseph Muenzer, Richard J. Samulski, Kang Lu, Jerillyn S. Jennings, Douglas M. McCarty
Journal: Molecular Therapy (2004)

Top of pageAbstract
Adeno-associate virus (AAV) has a broad spectrum of tissue tropism, with different AAV serotypes displaying tissue affinities consistent with the presence of their receptor molecules. While the cellular receptor molecule(s) for AAV serotype 1 (AAV-1) is not known, we have found that endothelial cells of mice are a primary target of AAV-1. Self-complementary AAV vectors expressing green fluorescent protein (GFP) from a CMV promoter were delivered into adult mice by intravenous (IV) or intracisternal (IC) injection, 10 minutes after an IV infusion of mannitol. Multiple tissues, including brain, spinal cord, liver, spleen, kidney, heart and skeletal muscle, were examined for transgene expression by GFP immunofluorescence assay at 1 and 3 months postinjection. IV delivery of 1 1011 AAV-1 vector particles resulted in GFP expression in hepatocytes (>50%), cardiac myocytes (30%), skeletal muscle cells (50%), and a global distribution of GFP-positive neuronal and non-neuronal cells in brain and spinal cord. After IC injection (2 1010 particles), a broad dispersion of GFP expression was observed in neuronal and non-neuronal cells in cerebellum, brain stem, cerebral cortex, hippocampus, thalamus, olfactory and spinal cord, as well as in hepactocytes (5% with and 2–3% without mannitol pretreatment). Surprisingly, GFP was readily detected in endothelial cells of blood vessels in all tissues analyzed after IV delivery, and in brain and liver blood vessels after IC injection. The identity of endothelial cells was confirmed by immunofluorescence using an antibody against Von Willibrand factor. Transduction of endothelial cells was not observed using the same vector genome in an AAV-2 capsid. These results demonstrated that AAV-1 is very efficiently taken up by endothelial cells after IV or IC administration of vector. Our data also demonstrates that AAV vector when delivered into the cerebral spinal fluid enters the systematic circulation and can infect endothelial cells as well as other cells types in peripheral tissues. We speculate that AAV-1 vector may provide a valuable tool in therapeutic gene delivery for many diseases directly or indirectly involving endothelial cells.
Gamma/delta T cells regulate airways disease during rhinovirus-induced asthma exacerbations
Authors: Nicholas Glanville, Nathan Bartlett, Simon Message, Ross Walton, Sebastian Johnston
Journal: European Respiratory Journal (2011)

Human rhinovirus (RV) infections are associated with asthma exacerbations but the underlying mechanisms are poorly understood. In a human asthma exacerbation model we found increased γδT cell numbers in the airways of atopic asthmatics following RV infection and that greater bronchoalveolar lavage (BAL) γδT cell numbers were associated with greater airway hyperresponsiveness (AHR) and obstruction.

Aim: To define the role of γδT cells in RV-induced asthma exacerbations using a mouse model.

Methods: The mouse RV-induced asthma exacerbation model comprised sensitisation and challenge of BALB/c mice with ovalbumin and infection with RV1B (RV-OVA) or UV-inactivated RV1B control (UV-OVA) concomitant with final allergen challenge. γδT cells were depleted by intraperitoneal injection of anti-γδTCR antibody.

Results: RV infection increased total and activated lung γδT cell numbers in OVA sensitised and challenged mice. Anti-γδTCR vs isotype control antibody treatment in RV-OVA mice enhanced AHR and BAL neutrophilia at 48 hrs post-infection (p<0.05) and lung Th2 cell numbers on day 7 (p<0.001), with enhancements in BAL mucus protein and serum IgE levels reaching near significance. BAL IL-10 levels were conversely reduced by 50% (p<0.01) 24 hrs after infection. Intracellular cytokine staining showed lung γδT cells to be potent producers of IL-17a.

Conclusions: Consistent with the human model, RV infection in the mouse asthma exacerbation model enhances γδT cell numbers in the airways. Depletion studies support a disease suppressing function for γδT cells in RV-induced asthma exacerbations, possibly via production of Th2 regulating cytokines IL-10 and IL-17a.
Functional studies for the<i>TRAF6</i>mutation associated with hypohidrotic ectodermal dysplasia
Authors: H. Fujikawa, M. Farooq, A. Fujimoto, M. Ito, Y. Shimomura
Journal: British Journal of Dermatology (2012)

Background Hypohidrotic ectodermal dysplasia (HED) is a rare condition characterized by hypotrichosis, hypohidrosis and hypodontia. A de novo heterozygous mutation in the tumour necrosis factor receptor‐associated factor 6 gene (TRAF6) was recently identified in a patient with HED, while functional consequences resulting from the mutation remained unknown. Objectives To determine the mechanism by which the TRAF6 mutation results in HED. Methods We performed coimmunoprecipitation (co‐IP) studies to determine whether the mutation would affect the interaction of TRAF6 with transforming growth factor β‐activated kinase 1 (TAK1), TAK1‐binding protein 2 (TAB 2) and ectodysplasin‐A receptor‐associated death domain protein (EDARADD). We then performed co‐IP and glutathione S‐transferase‐pulldown assays to determine the TRAF6 binding sequences in EDARADD. In addition, we analysed the effect of the mutant TRAF6 protein on the affinity between wild‐type TRAF6 and EDARADD, as well as on EDARADD‐mediated nuclear factor (NF)‐κB activation. Results The mutant TRAF6 protein was capable of forming a complex with TAK1 and TAB 2 in a similar way to wild‐type TRAF6. However, the mutant TRAF6 protein completely lost the affinity to EDARADD, while the wild‐type TRAF6 bound to the N‐terminal domain of EDARADD. Furthermore, the mutant TRAF6 inhibited the interaction between the wild‐type TRAF6 and EDARADD, and also potentially reduced the EDARADD‐mediated NF‐κB activity. Conclusions We conclude that the mutant TRAF6 protein shows a dominant negative effect against the wild‐type TRAF6 protein, which is predicted to affect the EDARADD‐mediated activation of NF‐κB during the development of ectoderm‐derived organs, and to lead to the HED phenotype.
Lithium carbonate and L-tryptophan in the treatment of bipolar and schizoaffective disorders
Authors: T D Brewerton, V I Reus
Journal: American Journal of Psychiatry (1983)

The authors review theoretical and clinical data supporting the hypothesis that L-tryptophan may potentiate the effects of lithium carbonate and report on a double-blind clinical comparison of lithium plus L-tryptophan and lithium plus placebo in 9 bipolar and 7 schizoaffective patients. Overall the combination of lithium and L-tryptophan resulted in significantly greater improvement. However, the results may have been confounded by the greater, although nonsignificant, doses of neuroleptics administered to the group receiving L-tryptophan. The authors discuss the interactions of lithium and L-trypotophan with the serotonin system.
CUTANEOUS AMEBIASIS: REPORT OF TWO CASES WITH ONE AUTOPSY
Authors: Y S SONG
Journal: Annals of Internal Medicine (1956)

Case Reports1 June 1956CUTANEOUS AMEBIASIS: REPORT OF TWO CASES WITH ONE AUTOPSYYO SEUP SONG, M.D.YO SEUP SONG, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-44-6-1211 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONLesions of the skin produced by Endamoeba histolytica have been reported by various authors since 1892.1 Although cutaneous amebiasis is still recognized as a rare condition, its presence should be considered when one encounters extensive necrosis and ulceration of the skin and underlying tissues.Amebiasis cutis can be divided into the following three types, depending on the association with a primary visceral lesion.1. Those cases following either surgery, or developing secondarily to a spontaneous external rupture of an infected organ with subsequent involvement of the skin. The primary site is usually a colic or appendiceal ulceration or liver...Bibliography1. Craig CF: Amebic invasion of the skin. The etiology, diagnosis, and treatment of amebiasis, 1944, The Williams and Wilkins Co., Baltimore, p. 167. Google Scholar2. EngmanHeithaus MFAS: Cutaneous amebiasis. Report of a case, J. Cutan. Dis. 37: 716, 1919. Google Scholar3. Heimburger LE: Amebiasis cutis, Arch. Dermat. and Syph. 11: 49, 1925. CrossrefGoogle Scholar4. Van Hoff L: Abcès, fistules et ulcères d'origine Amibienne, Trop. Dis. Bull. 23: 656, 1926. Google Scholar5. ColeHeideman WHML: Amebic ulcer of the abdominal wall following appendectomy with drainage, J. A. M. A. 92: 537 (Feb. 18) 1929. CrossrefGoogle Scholar6. EngmanMeleney MH: Amebiasis cutis. Report of two cases, Surgery 13: 460, 1943. Google Scholar7. Kreutzer FL: Cutaneous amebiasis, Surgery 29: 149, 1951. MedlineGoogle Scholar8. McVaySprunt LVDH: A long term evaluation of Aureomycin in the treatment of amebiasis, South. M. J. 45: 183, 1952. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Memphis, Tennessee*Received for publication December 10, 1954.From the Division of Pathology and Microbiology, The University of Tennessee, and The City of Memphis Hospitals, Memphis, Tennessee. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byHyperthermia, Fever and Infectious DiseasesSPORADIC AMOEBIASIS IN VICTORIA 1 June 1956Volume 44, Issue 6Page: 1211-1218KeywordsAmebiasisEnterocolitisLesionsLiverMicrobiologyNecrosisSkin infectionsSurgeryUlcerative colitisUlcers ePublished: 1 December 2008 Issue Published: 1 June 1956 PDF downloadLoading ...
Interleukin 4 receptor α chain polymorphism Gln551Arg is associated with adult atopic dermatitis in Japan
Authors: N. Oiso, K. Fukai, M. Ishii
Journal: British Journal of Dermatology (2000)

Journal Article Interleukin 4 receptor α chain polymorphism Gln551Arg is associated with adult atopic dermatitis in Japan Get access N. Oiso, N. Oiso Department of Dermatology, Osaka City University Medical School, 1‐4‐3 Asahimachi, Abeno‐ku, Osaka 545‐8585, Japan Search for other works by this author on: Oxford Academic Google Scholar K. Fukai, K. Fukai Department of Dermatology, Osaka City University Medical School, 1‐4‐3 Asahimachi, Abeno‐ku, Osaka 545‐8585, Japan Kazuyoshi Fukai, M.D. E‐mail: fukai@msic.med.osaka‐cu.ac.jp Search for other works by this author on: Oxford Academic Google Scholar M. Ishii M. Ishii Department of Dermatology, Osaka City University Medical School, 1‐4‐3 Asahimachi, Abeno‐ku, Osaka 545‐8585, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 142, Issue 5, 1 May 2000, Pages 1003–1006, https://doi.org/10.1046/j.1365-2133.2000.03485.x Published: 01 May 2000