tbuckley/cabot-search huggingface dataset:
Abstract 437: Novel function of the BAP1 nuclear deubiquitinase in the non-homologous end joining (NHEJ) pathway of double strand DNA repair
Authors: Tatsuo Ito, Shigehisa Kitano, Hediye Erdjument-Bromage, Marc Ladanyi
Journal: Cancer Research (2014)

Abstract Background- The deubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of malignant pleural mesothelioma (MPM) and uveal melanoma and in subsets of sporadic cases of these cancers, as well as in clear cell renal carcinoma and intrahepatic cholangiocarcinoma. Methods and Results- We found that BAP1 knockdown is associated with increased DNA damage and that this effect of BAP1 knockdown is further enhanced by both X-irradiation and concomitant DNA-PKcs inhibitor II treatment in normal human mesenchymal stem cells and the MPM cell line H-Meso. A BAP1 mutant deficient in deubiquitinase activity is also associated with increased DNA damage in the H-Meso cells. Interactional total peptide (ITOP) analysis based on proteins identified by Liquid Chromatography coupled to tandem Mass Spectrometry (LC-MS/MS) of BAP1 protein complexes in H-Meso MPM cells and 293T cells identified known binding partners [HCF1, ASXL2, H2A] as well as possible novel interaction partners, notably PRKDC which encodes the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs) and functions with the Ku70/Ku80 heterodimer in the non-homologous end joining (NHEJ) pathway of DNA repair. Double stranded DNA damage resulted in prominent nuclear expression of BAP1 protein in H-Meso cells and phosphorylation of BAP1 at Serine 395. Overexpression of dominant negative BAP1 C91W mutant in MPM cells caused instability of DNA-PKcs. Although strong polyubiquitination of DNA-PKcs was observed upon DNA damage in MPM cells expressing BAP1 C91W, this polyubiquitination was not observed in the presence of wild type BAP1. A plasmid-based NHEJ assay also confirmed a significant effect of BAP1 on NHEJ activity. Conclusion- Functional complexes between BAP1 and the NHEJ family components point to a novel role in DNA repair and may shed light on BAP1's role as an important tumor suppressor Citation Format: Tatsuo Ito, Shigehisa Kitano, Hediye Erdjument-Bromage, Marc Ladanyi. Novel function of the BAP1 nuclear deubiquitinase in the non-homologous end joining (NHEJ) pathway of double strand DNA repair. [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 437. doi:10.1158/1538-7445.AM2014-437
Comparison Among Methods of Retinopathy Assessment (CAMRA) Study
Authors: Martha E. Ryan, Ramachandran Rajalakshmi, Vijayaraghavan Prathiba, Ranjit Mohan Anjana, Harish Ranjani, K.M. Venkat Narayan, Timothy W. Olsen, Viswanathan Mohan, Laura A. Ward, Michael J. Lynn, Andrew M. Hendrick
Journal: Ophthalmology (2015)
Comedonal and Cystic Fibrofolliculomas in Birt-Hogg-Dube Syndrome
Authors: Ohara Aivaz, Suzanne Berkman, Lindsay Middelton, W. Marston Linehan, John J. DiGiovanna, Edward W. Cowen
Journal: JAMA Dermatology (2015)

The differential diagnosis of extensive open comedones includes inherited genetic syndromes and several acquired conditions. Birt-Hogg-Dube syndrome (BHD) is not typically included in the differential diagnosis of syndromes with comedonal lesions. Given the potentially life-threatening systemic complications associated with BHD, early recognition and diagnosis of the condition is important.We describe comedonal or cystic fibrofolliculomas in 4 patients with BHD. Cutaneous lesions were identified on the face, neck, chest, and abdomen.Comedonal or cystic fibrofolliculomas are a variant of fibrofolliculomas that have not previously been well characterized in patients with BHD and represent a novel diagnostic clue to its early detection and diagnosis. Expanding the phenotypic features of BHD facilitates earlier diagnosis of the syndrome, which allows for early surveillance of renal cancer in affected patients as well as disease screening in their relatives.
Abstract 117: Effect of 'Early Defibrillation' on the Survival of Patients With Witnessed Cardiac Arrest From Ventricular Fibrillation in the Guideline 2005 Era in Japan
Authors: Tetsuya Matoba, Hiroshi Nonogi, Hiromi Seo, Hiroyuki Yokoyama, Naohiro Yonemoto, Ken Nagao, Takeshi Kimura
Journal: Circulation (2010)

Background: In the management of sudden cardiac arrest (SCA) from ventricular fibrillation (VF), early defibrillation is vital along with early CPR. Here we assess the relation between the time fro...
Susceptibility of Enterobacteriaceae to β-lactam agents and fluoroquinolones: a 3-year survey in France
Authors: J. Sirot, M.H. Nicolas-Chanoine, H. Chardon, J.L. Avril, C. Cattoen, J.C. Croix, H. Dabernat, T. Fosse, J.C. Ghnassia, E. Lecaillon, A. Marmonier, M. Roussel-Delvallez, C.J. Soussy, A. Trevoux, F. Vandenesch, C. Dib, N. Moniot-Ville, Y. Rezvani
Journal: Clinical Microbiology and Infection (2002)
Abstract 15766: Repolarization Parameters are Significantly Prolonged in Many Patients With Left Bundle Branch Block and Acute Myocardial Infarction
Authors: Kenneth W Dodd, Kendra D Elm, Erin M Dodd, Stephen W Smith
Journal: Circulation (2014)

Introduction: In patients with normal conduction, prolongation of repolarization parameters such as the QTc interval, JTc interval, and T-wave peak to end (Tpe) interval are associated with cardiac ischemia, ventricular tachydysrhythmias, and sudden cardiac death. These intervals are often considered “prolonged” at QTc &gt;450 ms, JTc &gt; 360 ms, and Tpe &gt; 120 ms. We are unable to find published manuscripts that report these parameters in LBBB. Furthermore, it has been proposed that the Bazett correction formula for QTc and JTc overestimates repolarization duration in patients with conduction disturbances. Aim: To report the QTc, JTc, and Tpe intervals in ED patients with LBBB with and without MI and to compare common correction formulas. Methods: Retrospectively, we identified ED patients with LBBB and ischemic symptoms: with no MI, with NSTEMI, and with angiographically-proven acute coronary occlusion (STEMI). The QT, JT, and Tpe intervals were measured manually in leads II, V3, and V5; the longest of each was used. QTc and JTc intervals were calculated by Bazett’s, Hodges’ and Framingham formulas. Statistics were by two-tailed Student’s t-test and Mann-Whitney U test. Results: The no-MI, NSTEMI, and STEMI groups consisted of 105, 24 and 33 patients. In the STEMI group, 24.3% of patients had Tpe &gt;= 120 ms compared to 4.8% of no-MI patients (p &lt; 0.001). By Hodges’ formula, 53.1% of patients with LBBB had QTc &gt;= 450 ms and 12.3% had JTc &gt;= 360 ms. Conclusion: Repolarizaton parameters are prolonged in many patients with LBBB. The Tpe interval, which has been proposed as a marker of transmural repolarization heterogeneity due to ischemia, is significantly prolonged in patients with STEMI and LBBB when compared to LBBB patients without MI. Between the STEMI, NSTEMI, and no-MI groups there was no significant difference in QTc or JTc by any formula (see Table 1). However, the overall mean QTc by Bazett’s was significantly longer than Hodge’s or Framingham (see Table 2).
Abstract 15843: PPARalpha/Sirt1 Heterodimer Suppresses Fatty Acid Oxidation Genes in the Heart Under Pressure Overload
Authors: Shinichi Oka, Peiyong Zhai, Takanobu Yamamoto, Yoshiyuki Ikeda, Junichi Sadoshima
Journal: Circulation (2014)

The healthy heart utilizes fatty acids as a primary source of energy, yet fatty acid oxidation (FAO) declines in the failing heart. The PPARα/RXR dimer transcribes genes involved in FAO through PPAR response element (PPRE). However, how PPARα targets are downregulated in the failing heart remains unknown. Here we report that the PPARα dimerization partner switches from RXR to Sirt1, a histone deacetylase that interacts with PPAR, thereby suppressing FAO gene expression during pressure overload (PO). The expression of Sirt1 was increased, whereas that of RXR was decreased in response to PO in mice. A consistent observation was made that demonstrated Sirt1 binding to PPARα increased, while RXR binding to PPARα decreased during PO (relative proteins bound to PPARα under PO conditions vs sham, Sirt1 3.7*, RXR 0.37*, p<0.05). Thus, the PPARα/RXR dimer switches to PPARα/Sirt1 in the failing heart. We observed similar expression changes of Sirt1 and RXR in the failing human heart, suggesting dimer conversion occ...
ANAPHYLAXIS TO THE INJECTION OF NICOTINIC ACID (NIACIN); SUCCESSFUL TREATMENT WITH EPINEPHRINE
Authors: L PELNER
Journal: Annals of Internal Medicine (1947)

Case Reports1 February 1947ANAPHYLAXIS TO THE INJECTION OF NICOTINIC ACID (NIACIN); SUCCESSFUL TREATMENT WITH EPINEPHRINELOUIS PELNER, M.D.LOUIS PELNER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-26-2-290 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAn anaphylactic reaction to nicotinic acid has not been previously reported in the literature, although sensitivity to the drug has been noted before. The present widespread use of nicotinic acid, both as a vitamin and as a drug, makesreports of these accidents mandatory, because they will undoubtedly be experienced by others. The morbidity can probably be avoided by a careful questioning of the patient before the injection of nicotinic acid is given. In our cases, the usual treatment for anaphylactic shock was sufficient to overcome the symptoms in these patients.Rachmilewitz and Glueck1described the occurrence of an urticarial dermatitis...Bibliography1. RACHMILEWITZGLUECK MHI: Treatment of pellagra with nicotinic acid, Brit. Med. Jr., 1938, ii, 346. CrossrefGoogle Scholar2. CHENROSEROBBINS KKCLEB: Toxicity of nicotinic acid, Proc. Soc. Exper. Biol. and Med., 1938, xxxviii, 241. CrossrefGoogle Scholar3. WATROUS RM Dermatitis from industrial contact with nicotinic acid, Jr. Am. Med. Assoc., 1939, cxii, 2132. CrossrefGoogle Scholar4. VAUGHAN WT: Practice of allergy, 1939, C. V. Mosby, St. Louis, p. 811. Google Scholar5. LAWS C: Sensitization to thiamin chloride, Jr. Am. Med. Assoc., 1941, cxvi, 176. SCHIFF, L.: Collapse following parenteral administration of a solution of thiamin hydrochloride, Jr. Am. Med. Assoc., 1941, c, 669. JOLLIFFE, N.: Treatment of neuropsychiatric disorders with vitamins, Jr. Am. Med. Assoc., 1941, cxvii, 1496. STERN, W. MORGENSTERN M.: Sensitization to thiamin hydrochloride. Report of another case, Ann. Int. Med., 1944, xx, 826. MISTRANI M. A.: Vitamin B, hypersensitivity with desensitization; report of a case, Jr. Allergy, 1944, xv, 150. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Brooklyn, N. Y.*Received for publication August 17, 1946. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byVitaminsLARYNGEAL SPASMREACTIONS AFTER VITAMIN-B INJECTIONToxic Labyrinthitis Following Oral Undecylenic Acid Treatment of PsoriasisVitamin Supplementation in Health and Disease 1 February 1947Volume 26, Issue 2Page: 290-294KeywordsAnaphylaxisDrugsEpinephrineMorbidityNiacinShock ePublished: 1 December 2008 Issue Published: 1 February 1947 PDF downloadLoading ...
Mechanisms of reduced susceptibility to amoxycillin-clavulanic acid in Escherichia coli strains from the health region of Tortosa (Catalonia, Spain)
Authors: M.O. Pérez-Moreno, O. Katargina, M. Pérez-Moreno, M. Carulla, C. Rubio, A.M. Jardí, J. Zaragoza
Journal: Clinical Microbiology and Infection (2004)
Lesson of the week: Treating hepatic hydrothorax
Authors: J. Borchardt
Journal: BMJ (2003)

Do not use a chest drain to treat hepatic hydrothorax 

When a patient presents with a large unilateral symptomatic pleural effusion many doctors will feel tempted to insert a chest drain. We caution against placement of a chest drain as a therapeutic reflex, particularly if the diagnosis is hepatic hydrothorax.

### Case 1

A 70 year old man was admitted to our department for shortness of breath. He was known to have cryptogenic liver cirrhosis. About two years before this admission he had developed ascites, and treatment with salt restriction, spironolactone, and frusemide (furosemide) was started. One year before admission his right kidney had been removed because of renal cancer. Subsequently he began to have recurrent right pleural effusion. Before he was admitted, weekly thoracenteses had become necessary as he continued to be short of breath.

On admission the patient seemed well except for mild tachypnea. We noted dullness to percussion above the right lung. The abdomen was mildly distended, but ascites was not evident. Jugular venous pressure was not raised, and the patient had no peripheral oedema. Blood count (except for platelets 65 000/mm3) and prothrombin time were normal; bilirubin was 30.8 μmol/l, and protein 71 g/l. The table shows additional results. Chest radiography confirmed a large right pleural effusion; abdominal ultrasonography showed only a small amount of ascitic fluid. Thoracentesis showed a transudate with protein 10 g/l and pH 7.49.

View this table:

Results of blood tests in a patient with hepatic hydrothorax and a chest drain



A chest drain was inserted and 2700 ml of fluid was drained. Subsequently the daily volume of drained fluid …
A Treatise on the Medical Jurisprudence of Insanity.
Authors: Isaac Ray
Journal: JAMA (1894)

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
Phosphorylation of cofilin by LIM-kinase is necessary for semaphorin 3A-induced growth cone collapse
Authors: Hiroyuki Aizawa, Shuji Wakatsuki, Ai Ishii, Kenji Moriyama, Yukio Sasaki, Kazumasa Ohashi, Yoko Sekine-Aizawa, Atsuko Sehara-Fujisawa, Kensaku Mizuno, Yoshio Goshima, Ichiro Yahara
Journal: Nature Neuroscience (2001)
245. Muscle-Derived Stem Cells Display an Extended, but Not Unlimited, Expansion Capability: Implication for Muscle Regeneration
Authors: Bridget M. Deasy, Burhan M. Gharaibeh, Michele Jones, Michael A. Lucas, Johnny Huard
Journal: Molecular Therapy (2004)

Stem cells are frequently considered the optimal cell type for regenerative cell-based therapies; however they generally represent a small fraction of cells isolated from a biopsy or other cell source. Ex vivo cell expansion is a necessary step to obtain clinically relevant numbers of cells. In addition, stem cells are often theorized as cells with unlimited long-term expansion potential. The purpose of this study is to test the long-term expansion capability of a population of muscle-derived stem cells. We first examined the proliferation kinetics of murine muscle-derived stem cells (MDSCs) to determine if they obey Hayflick's limit. We determined that these cells can be expanded for more than 300 population doublings (PDs) with no indications of replicative senescence. Next we examined how the molecular and behavioral stem cell phenotype, including the regenerative capacity, changes over time. We find that the MDSC population continues to maintain a relatively low level of desmin expression ( 65%) throughout the expansion. We observe that up to 200 PDs the MDSCs readily differentiate to form multinucleated myotubes, however expansion beyond 200 PDs leads to a decline in the number of cells entering the post-mitotic differentiated state. Remarkably, MDSC are capable of regenerating dystrophin expressing muscle fibers upon implantation in mdx muscular dystrophy model even after 200 population doublings. However, expansion beyond 200 PDs resulted in a subsequent decline in regeneration efficiency. Observed phenotypic changes highlight the inevitable aging of cells that results from cell expansion. Several findings including loss of contact inhibition, ability to grow on soft agar and an increase in numerical chromosomal abnormalities suggests that the MDSC may have become transformed. While the MDSC demonstrate a highly extended functional lifetime for muscle regeneration, we find that this potential is not unlimited.
Physicians and the Pharmaceutical Industry
Authors: Ashley Wazana
Journal: Annals of Internal Medicine (1990)

Context Controversy exists over the fact that physicians have regular contact with the pharmaceutical industry and its sales representatives, who spend a large sum of money each year promoting to them by way of gifts, free meals, travel subsidies, sponsored teachings, and symposia. Objective To identify the extent of and attitudes toward the relationship between physicians and the pharmaceutical industry and its representatives and its impact on the knowledge, attitudes, and behavior of physicians. Data Sources A MEDLINE search was conducted for English-language articles published from 1994 to present, with review of reference lists from retrieved articles; in addition, an Internet database was searched and 5 key informants were interviewed. Study Selection A total of 538 studies that provided data on any of the study questions were targeted for retrieval, 29 of which were included in the analysis. Data Extraction Data were extracted by 1 author. Articles using an analytic design were considered to be of higher methodological quality. Data Synthesis Physician interactions with pharmaceutical representatives were generally endorsed, began in medical school, and continued at a rate of about 4 times per month. Meetings with pharmaceutical representatives were associated with requests by physicians for adding the drugs to the hospital formulary and changes in prescribing practice. Drug company‐sponsored continuing medical education (CME) preferentially highlighted the sponsor’s drug(s) compared with other CME programs. Attending sponsored CME events and accepting funding for travel or lodging for educational symposia were associated with increased prescription rates of the sponsor’s medication. Attending presentations given by pharmaceutical representative speakers was also associated with nonrational prescribing.
A Case of Complete Carneyʼs Syndrome
Authors: CARMEN LANCHA, LUIS DIEZ, MERCEDES MITJAVILA, MaDOLORES RUEDA, ANGEL CRESPO
Journal: Clinical Nuclear Medicine (1994)

The triad of gastric leiomyoblastoma, paraganglioma, and pulmonary chondroma was first described by Carney in 1977. The authors report a case of a patient with gastric leiomyosarcoma, multiple pulmonary chondromata, and paraganglioma. This represents a complete form of Carney's triad. The paraganglioma was identified with I-123 MIBG.
NEUTROPHILS FROM PATIENTS WITH VENTILATOR-ASSOCIATED PNEUMONIA: PRO-INFLAMMATORY AND CYTOTOXIC INTERACTIONS WITH ALVEOLAR EPITHELIUM
Authors: H. Reid, A. Conway Morris, K. Kefala, T. Wilkinson, L. Farrell, T. S. Walsh, S. MacKenzie, J. M. Sallenave, K. Dhaliwal, C. Haslett, A. J. Simpson
Journal: Thorax (2008)
Expression and release of IL‐29 by mast cells and modulation of mast cell behavior by IL‐29
Authors: S. He, H. Zhang, H. Chen, H. Yang, T. Huang, Y. Chen, J. Lin, F. Wang, X. Chen, T.‐L. Li, P. Yang
Journal: Allergy (2010)

The role of interleukin (IL)-29 in innate immunity has been recognized recently, and it is regarded as a potent bioactive molecule. However, little is known about its role in the pathogenesis of allergy. Because mast cells are recognized as primary effector cells of allergy, we investigated the potential relationship between IL-29 and mast cells in this study.To examine the expression of IL-29 in mast cells and the influence of IL-29 on mast cell mediator release and accumulation.Expression of IL-29 in mast cells was determined by double-labeling immunohistochemistry and flow cytometry analysis. Mast cell cell-line was cultured to examine the mediator release, and mouse peritoneal model was employed to observe the mast cell accumulation.Large proportions of mast cells expressing IL-29 were localized in human tissue including the colon, tonsil and lung. Mast cells can release substantial quantity of IL-29 upon challenge with proteolytic allergens. Extrinsic IL-29 provoked IL-4 and IL-13 release from mast cell line P815 cells through PI3K/Akt and (JAK)/STAT3 signaling pathways, but failed to induce mast cell histamine release from human mast cells. Extrinsic IL-29 also induced mast cell infiltration in mouse peritoneum by a CD18- and ICAM1-dependent mechanism.Mast cell-derived IL-29 has the potential to be involved in the pathogenesis of allergic inflammation.