tbuckley/cabot-search huggingface dataset:
Cellular and molecular mechanisms of repair in acute and chronic wound healing
Authors: P. Martin, R. Nunan
Journal: British Journal of Dermatology (2015)

A considerable understanding of the fundamental cellular and molecular mechanisms underpinning healthy acute wound healing has been gleaned from studying various animal models, and we are now unravelling the mechanisms that lead to chronic wounds and pathological healing including fibrosis. A small cut will normally heal in days through tight orchestration of cell migration and appropriate levels of inflammation, innervation and angiogenesis. Major surgeries may take several weeks to heal and leave behind a noticeable scar. At the extreme end, chronic wounds - defined as a barrier defect that has not healed in 3 months - have become a major therapeutic challenge throughout the Western world and will only increase as our populations advance in age, and with the increasing incidence of diabetes, obesity and vascular disorders. Here we describe the clinical problems and how, through better dialogue between basic researchers and clinicians, we may extend our current knowledge to enable the development of novel potential therapeutic treatments.
Interactive case report: A 66 year old woman with a rash: case outcome * Commentary: Patient's perspective * Commentary: Vascular surgeon * Commentary: Dermatology * Commentary: View from primary care * Commentary: Learning from interactive case reports
Authors: J Bligh
Journal: BMJ (2003)

# A 66 year old woman with a rash: case outcome {#article-title-2} Three weeks ago ( BMJ 2003;326:588) we published the case of Ruth, who presented to her general practitioner with a rash after feeling unwell for some time. She had dermatomyositis diagnosed and, during investigation for possible underlying causes, was found to have an aneurysm of the splenic artery ( BMJ 2003;326:640). Ruth's case was discussed at a multidisciplinary meeting and a decision was made to treat her aneurysm with a covered stent placed under fluoroscopic guidance by a radiologist. A theatre space was booked for the same time as the procedure in case of complications. She had a repeat angiogram and a wire was passed across the aneurysm. Two covered stents were placed across the neck of the aneurysm and a repeat contrast injection showed that there was no communication between the splenic artery and the aneurysm sac (figure). Ultrasonography the next day showed the aneurysm filled with thrombus with no flow on colour Doppler. The following day contrast enhanced computed tomography showed no evidence of a leak. Follow up computed tomography continued to show no leak and no flow in the aneurysm sac. Ruth was given pneumococcal and haemophilus influenza vaccines as a prophylactic measure in case of future hyposplenism caused by migration or occlusion of the stent. As it was envisaged that Ruth would be taking steroids long term, she was referred for bone densitometry (dual x ray absorptiometry), which showed no evidence of osteoporosis. Ruth was reassured but advised that it would be sensible to increase her calcium intake to 1500 mg a day. She found this difficult to achieve and so was started on an oral calcium and vitamin D supplement. She was also advised … Correspondence to: N Kapur
Abstract 3762: Downregulation of TRPC3 enhances sensitivity to cisplatin and inhibits motility in epithelial ovarian cancer
Authors: Xiang Tao, Hongyan Jin, Zhenbo Zhang, Robert C. Bast, Youji Feng, Yinhua Yu
Journal: Cancer Research (2014)

Abstract Epithelial ovarian cancer (EOC) remains the most lethel gynecological malignancy. In the absence of an effective screening strategy, two thirds of patients are diagnosed in advanced clinical stage. Despite chemotherapy with cisplatin and paclitxel, primary or acquired chemoresistance faciltates survival of cancer cells, resulting in disease recurrence and death. Our previous studies indicate that ovarian cancer patients whose tumors overexpress transient receptor potential channel C3 (TRPC3) protein tend to relapse early and have shorter overall survival. In vitro studies indicated that follicle-stimulating hormone (FSH) induced resistance to cisplatin-induced apoptosis could be partially reversed by blocking expression of TRPC3 in EOC cell lines. To enhance sensitivity to platinum compounds, we have investigated the relationship between resistance to cisplatin and TRPC3. We have now found that expression of TRPC3 in recurrent cancer following chemotherapy is higher than in specimens from primary cytoreductive surgery. The expression of TRPC3 in the cisplatin-resistant EOC line A2780cp is higher than in the sensitive parental cell line A2780. An in vitro study showed that transient treatment of the EOC cell line HEY with cisplatin upregulated TRPC3 mRNA and membrane localized protein. Induced cisplatin-resistant cell line HEYcp augmented the expression of TRPC3 and enhanced invasive capacity in cell migration assays. Knockdown of TRPC3 expression in EOC cell lines with specific siRNA or miRNA decreased cell migratory ability and enhanced cisplatin-induced apoptosis when compared to EOC cells treated with scrambled control RNA. Our data indicate that TRPC3 may play an important role in cisplatin-resistance of EOC and could serve as a therapeutic target to resensitize cancer cells to cisplatin in culture and in xenografts. Citation Format: Xiang Tao, Hongyan Jin, Zhenbo Zhang, Robert C. Bast, Youji Feng, Yinhua Yu. Downregulation of TRPC3 enhances sensitivity to cisplatin and inhibits motility in epithelial ovarian cancer. [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 3762. doi:10.1158/1538-7445.AM2014-3762
Abstract 1972: The sodium channel auxiliary subunit SCN1B promotes breast tumor growth and metastasis
Authors: Michaela Nelson, Rebecca Millican-Slater, Lorna C. Forrest, William J. Brackenbury
Journal: Cancer Research (2014)

Abstract Voltage-gated Na+ channels (VGSCs) are heteromeric proteins composed of pore-forming α subunits and smaller β subunits. The β subunits are multifunctional channel modulators and are members of the immunoglobulin superfamily of cell adhesion molecules (CAMs). β1, encoded by SCN1B, is best characterized in the central nervous system (CNS), where it plays a critical role in regulating electrical excitability, neurite outgrowth and migration during development. β1 is also expressed in breast cancer cell lines, where it regulates adhesion and migration in vitro. Using the Oncomine database, we found that SCN1B mRNA was up-regulated in breast cancer, compared with normal breast. Similarly, β1 protein was up-regulated in a cohort of breast cancer tissue specimens compared with surrounding normal tissue. Over-expression of β1 in MDA-MB-231 cells substantially increased tumor growth and metastasis from orthotopic xenografts in immune-deficient mice. β1 had no effect on the density of Ki67-positive cycling cells in the primary tumors. However, β1 increased the density of CD31-positive vessel structures and reduced the density of apoptotic cells expressing activated caspase-3. β1-expressing MDA-MB-231 cells had an elongate morphology in tumors in vivo and in 2D culture in vitro. β1 potentiated the outgrowth of processes from MDA-MB-231 cells and MCF-7 cells co-cultured with fibroblasts, via trans-homophilic adhesion. Both the src family tyrosine kinase inhibitor PP2 and siRNA targeting fyn kinase blocked β1-mediated process extension in breast cancer cells. Thus, β1-mediated process outgrowth in breast cancer cells requires the presence and activity of fyn kinase. This recapitulates the mechanism by which β1 regulates neurite outgrowth in CNS neurons. We conclude that when present in breast tumors, β1 drives pathological growth and cellular dissemination by recapitulating its well-defined role in CNS ontogeny. This study is the first demonstration of a functional role for β1 as a CAM in tumor growth and metastasis. We propose that targeting β1-mediated adhesion interactions may have potential as a novel anti-cancer therapy. Citation Format: Michaela Nelson, Rebecca Millican-Slater, Lorna C. Forrest, William J. Brackenbury. The sodium channel auxiliary subunit SCN1B promotes breast tumor growth and metastasis. [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 1972. doi:10.1158/1538-7445.AM2014-1972
SARS Without Pneumonia?
Authors: Joan Stephenson
Journal: JAMA (2004)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Truncating mutations in CCM1, encoding KRIT1, cause hereditary cavernous angiomas
Authors: Sophie Laberge-le Couteulx, Hans H. Jung, Pierre Labauge, Jean-Pierre Houtteville, Christelle Lescoat, Michaelle Cecillon, Emmanuelle Marechal, Anne Joutel, Jean-François Bach, Elisabeth Tournier-Lasserve
Journal: Nature Genetics (1999)
Abstract 1688: Overcoming drug resistance to gemcitabine in pancreas cancer cells by targeting activated PI3K/mTOR pathway
Authors: Yuichi Murakami, Ai Shinoda, Kosuke Watari, Hiroshi Nabeshima, Akihiko Kawahara, Daisuke Nagayama, Yoshiki Naito, Koichi Higaki, Masako Inoue, Michihiko Kuwano, Mayumi Ono
Journal: Cancer Research (2014)

Abstract Pancreas cancer is one of the most difficult neoplasms to treat curatively and 5-year survival rate is only 5%. Gemcitabine, a difluorinated deoxycitidine, has been first reported to improve pancreas cancer both response rate and median overall survival of patients with pancreas cancer. Treatment with combination of gemcitabine and erlotinib was reported to prolong survival compared with gemcitabine alone against pancreas ductal adenocarcinoma, but its benefit is modest. Further development of potent combination therapeutics with gemcitabine should be very useful for treatment of pancreas cancer. In our present study, we examined whether the cytotoxic effect of gemcitabine could be potentiated when combined with other anticancer drugs including molecular targeted drugs and cytotoxic anticancer agents, and also whether such combination could overcome drug resistance to gemcitabine. We observed following findings [1]We first screened various anticancer agents that could synergistically potentiate cytotoxic effect of gemcitabine against pancreas cancer cell lines in culture, and observed that mTOR inhibitors, such as rapamycin, everolimus and AZD8055, synergistically enhanced the anti-proliferative effect of gemcitabine. [2] PI3K/mTOR/S6K-driven signaling pathway for de novo pyrimidine biosynthesis was markedly blocked when combined with gemcitabine and mTOR inhibitors. [3] We also observed that mTOR/S6K-driven de novo pyrimidine synthetic pathway was markedly activated in drug-resistant cancer cells as compared to their parental cell line. [4] Immunohistochemical analysis of clinical samples derived from resected pancreas tumors showed that mTOR was highly expressed in progressive pancreas cancer. Combination of gemcitabine and drugs targeting mTOR-driven signaling pathway will further provide potent therapeutics against both gemcitabine-sensitive and -resistant pancreas cancer. Furthermore, personalized therapeutics against pancreas cancer patients by this combination will be discussed based on expression levels of activated PI3K/mTOR/S6K in tumors. Citation Format: Yuichi Murakami, Ai Shinoda, Kosuke Watari, Hiroshi Nabeshima, Akihiko Kawahara, Daisuke Nagayama, Yoshiki Naito, Koichi Higaki, Masako Inoue, Michihiko Kuwano, Mayumi Ono. Overcoming drug resistance to gemcitabine in pancreas cancer cells by targeting activated PI3K/mTOR pathway. [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 1688. doi:10.1158/1538-7445.AM2014-1688
DRUG REACTIONS XVIII.
Authors: Ashley Levantine, John Almeyda
Journal: British Journal of Dermatology (1972)

Journal Article DRUG REACTIONS XVIII: Cutaneous Reactions to Antituberculous Drugs Get access Ashley Levantine, Ashley Levantine The London Hospital London, E.1 Search for other works by this author on: Oxford Academic Google Scholar John Almeyda John Almeyda The London Hospital London, E.1 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 86, Issue 6, 1 June 1972, Pages 651–655, https://doi.org/10.1111/j.1365-2133.1972.tb05087.x Published: 01 June 1972
Consensus recommendations for improvement of unmet clinical needs—the example of chronic graft-versus-host disease: a systematic review and meta-analysis
Authors: Jacopo Olivieri, Lucia Manfredi, Laura Postacchini, Silvia Tedesco, Pietro Leoni, Armando Gabrielli, Alessandro Rambaldi, Andrea Bacigalupo, Attilio Olivieri, Giovanni Pomponio
Journal: The Lancet Haematology (2015)
Vitamin D receptor polymorphisms and exacerbation frequency in COPD
Authors: Jennifer Quint, Gavin Donaldson, Nancy Wassef, John Hurst, Michael Thomas, Jadwiga Wedzicha
Journal: European Respiratory Journal (2011)

Background: Genetic variants in the vitamin D (vitD) pathway have been associated with COPD. FokI and BsmI polymorphisms in the vitD receptor (VDR) gene have been associated with muscle strength in COPD. These polymorphisms and the Taq1α VDR polymorphism have been associated with respiratory infection but they have not been investigated in COPD.  Methods: We studied 97 COPD patients (61 male, 28 frequent exacerbators (FE)); mean age 71.8 years (SD8.8) FEV1% predicted 50.3 (19.7), smoking history 50.7 (34.2) pack years. All patients were sampled in the winter (Jan/Feb/March) and summer (June/July/August) at baseline for vitD levels. Serum samples were tested for VitD(25-OH) by chemiluminescence based immunoassay. All polymorphisms were genotyped by forced RFLP (restriction fragment length polymorphism) using DNA extracted from blood. FEwere defined a priori as having ≥3 symptom based exacerbations per year, and infrequent (IE)  Results: All genotypes were within Hardy Weinberg equilibrium. The FokI polymorphism was not related to TaqI or BsmI. The BsmI and TaqI polymorphisms were linked. There was no relationship with genotyping and exacerbation frequency for any of the polymorphisms.  There was a seasonal difference in vitD levels but this was the same for all polymorphisms; all p>0.05.  Conclusions: FokI, BsmI and TaqI VDR polymorphisms are not associated with exacerbation frequency and do not affect vitD levels in COPD.
Dental Histology and Embryology.
Authors: Balint J. Orban
Journal: JAMA (1929)

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
ST-Segment Elevation Myocardial Infarction Treated by Radial or Femoral Approach in a Multicenter Randomized Clinical Trial
Authors: Ivo Bernat, David Horak, Josef Stasek, Martin Mates, Jan Pesek, Petr Ostadal, Vlado Hrabos, Jaroslav Dusek, Jiri Koza, Zdenek Sembera, Miroslav Brtko, Ondrej Aschermann, Michal Smid, Pavel Polansky, Abdul Al Mawiri, Jan Vojacek, Josef Bis, Olivier Costerousse, Olivier F Bertrand, Richard Rokyta
Journal: Journal of the American College of Cardiology (2013)
Abstract P195: Dietary Diversity and Quality, Change in Waist Circumference and Risk of Diabetes in the Multi-Ethnic Study of Atherosclerosis
Authors: Marcia C de Oliveira Otto, Nikhil S Padhye, Alain Bertoni, David R Jacobs, Dariush Mozaffarian
Journal: Circulation (2014)

Background: Diet guidelines recommend dietary diversity, but metrics for dietary diversity have not been well defined nor evaluated for impact on metabolic health. Also, whether diversity has effects independent of diet quality is unknown. Aims: To characterize metrics of dietary diversity and prospectively assess change in waist circumference (WC) and incident diabetes (DM) in a multi-ethnic population; and whether associations were independent of diet quality. Methods: Among 5,215 Whites, Hispanic, Blacks, and Chinese age 45-84 y and free of DM at baseline (2000-02), diet was assessed using a validated questionnaire, WC was directly measured, and incident DM defined from fasting glucose and medications. Three separate aspects of diet diversity were characterized: count (different food items eaten &gt;once/week), evenness (Berry index) and dissimilarity (Jaccard distance). Diet quality was characterized using DASH, AHEI, and a priori patterns. Diversity metrics were also separately defined based only on generally healthier or less healthy foods. We evaluated associations with 5 y change in WC using linear regression; and incident DM using Cox models. Results: After multivariable adjustment, neither count nor evenness was associated with WC or DM (Table). Higher dissimilarity was associated with gain in WC in Hispanic, Blacks and Chinese, but not Whites; and higher risk of DM in Chinese and Blacks. Most associations were independent of diet quality. No associations were found for diversity metrics defined on strata of only healthier or less healthy foods. Higher diet quality was associated with less WC gain in Hispanics only, and lower risk of DM in Whites and Chinese only. Conclusion: Our findings provide little evidence for benefits of dietary diversity for either WC or DM. Greater dissimilarity was actually positively associated with change in WC in most ethnicities. These results support need for greater investigation of role and relevance of diet diversity for metabolic health in diverse populations.
Triallelic and epigenetic-like inheritance in human disorders of telomerase
Authors: Laura C. Collopy, Amanda J. Walne, Shirleny Cardoso, Josu de la Fuente, Mahfuzah Mohamed, Helga Toriello, Hannah Tamary, Adam J. Y. V. Ling, Timothy Lloyd, Rebecca Kassam, Hemanth Tummala, Thomas J. Vulliamy, Inderjeet Dokal
Journal: Blood (2015)
LYMPHATIC LEUKEMIA OF TWENTY-FIVE YEARS' DURATION
Authors: Charles W. Mcgavran
Journal: Annals of Internal Medicine (1938)

Case Reports1 September 1938LYMPHATIC LEUKEMIA OF TWENTY-FIVE YEARS' DURATIONCHARLES W. MCGAVRAN, B.S., M.S., M.D., F.A.C.P.CHARLES W. MCGAVRAN, B.S., M.S., M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-12-3-396 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe following is a report of a case of chronic lymphatic leukemia and associated with it, a mild diabetes and a progressive cardiovascular disease. It is of unusual interest because of the duration of life after the discovery of the leukemia. Data concerning the duration of life after the onset of chronic lymphatic leukemia are quite meagre. Minot and Isaacs4in 1924 report on the duration of life in 87 cases the longest of which was under observation 22 years. The case here reported was observed 25 years and all this time the patient was under the personal observation of...References1. SABINCUNNINGHAMDOANKINDWALL : Normal rhythm of the white blood cells, Bull. John Hopkins Hosp., 1925, xxxvii, 14. Google Scholar2. WISEMAN BK: Personal communication. Google Scholar3. JOSLIN EP: Treatment of diabetes mellitus, 5th ed., 1935, Lea and Febiger, Philadelphia, page 408. Google Scholar4. MINOTISAACS GBR: Lymphatic leukemia; age, duration, and benefit derived from irradiation, Boston Med. and Surg. Jr., 1924, cxci, 1. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Columbus, Ohio*Received for publication September 23, 1937. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRegeneration, Hyperplasie und Onkogenese der lymphoretikulären OrganeSpontaneous Remission in Chronic Lymphocytic LeukemiaP. A. CHERVENICK, M.D., DANE R. BOGGS, M.D., M. M. WINTROBE, M.D., PH.D., F.A.C.P.HOST-TUMOR ANTAGONISM. III. PROLONGED SURVIVAL OF CERTAIN PATIENTS WITH CANCER. FORTUITOUS OCCURRENCE OR IMMUNITY MECHANISM?THE EARLY DIAGNOSIS AND NATURAL HISTORY OF CHRONIC LYMPHATIC LEUKEMIA*C. HOUGIE, M.B., B.S., L.R.C.P., M.R.C.S. (Eng.)The Use of Myleran and Similar Agents in Chronic LeukemiasLYMPHOCYTIC LEUKEMIA: AN ANALYSIS OF FREQUENCY, DISTRIBUTION AND MORTALITY AT THE UNIVERSITY OF CALIFORNIA HOSPITAL, 1913-1947*M. B. SHIMKIN, E. L. LUCIA, K. C. OPPERMANN, S. R. METTIER, F.A.C.P.Lymphosarcoma 1 September 1938Volume 12, Issue 3Page: 396-402KeywordsCardiovascular diseases ePublished: 1 December 2008 Issue Published: 1 September 1938 PDF downloadLoading ...