tbuckley/cabot-search huggingface dataset:
Tendon injury and repair after core biopsies in chronic Achilles tendinosis evaluated by serial magnetic resonance imaging
Authors: A Shalabi, L Svensson, M Kristoffersen-Wiberg, P Aspelin, T Movin
Journal: British Journal of Sports Medicine (2004)

To evaluate the morphological response and healing process after transverse ultrasound guided core biopsies in chronic Achilles tendinosis using serial magnetic resonance imaging (MRI) over a period of one year.The study included 10 patients. Six had five transverse core biopsies and were longitudinally evaluated by MRI before the biopsies and then after one week, three months, seven months, and one year. These patients started a three month eccentric training programme one to two weeks after the biopsy. Four "non-biopsied" and untreated patients were used for comparison. The clinical outcome was categorised according to the level of pain and performance.The MRI one week after the biopsies showed an increase in tendon volume (T1-WI) and mean signal intensity (PD-WI) of 29% and 30% (p = 0.04). During follow up, tendon volume and mean signal intensity gradually decreased. One year after the biopsy, the tendon volume had decreased by 20% and the intratendinous signal by 28% compared with the index MRI (p = 0.04). The untreated patients showed an increase in both tendon volume (39%, p = 0.06) and intratendinous signal (37%, p = 0.14) at the one year follow up. After one year, pain and performance had improved in the treated patients but not the untreated patients.Five transverse ultrasound guided core biopsies induced a lesion in the diseased Achilles tendon. Alterations during healing such as tendon size and intratendinous signal intensity could be evaluated by MRI. The tendon alterations had decreased one year after the core biopsies.
Regression of Columnar Esophageal (Barrett's) Epithelium after Anti-Reflux Surgery
Authors: Douglas L. Brand, J. Thomas Ylvisaker, Martin Gelfand, Charles E. Pope
Journal: New England Journal of Medicine (1980)

Columnar esophageal (Barrett's) epithelium is thought to be a reparative or metaplastic response to gastroesophageal reflux.1 2 3 This epithelium has been associated with dysplasia and adenocarcinoma in situ4 , 5 and with frank adenocarcinoma.6 , 7 There is evidence in individual patients that prolonged severe reflux leads to orad progression of the columnar epithelium,1 , 8 but the effect of surgical correction of reflux on the epithelium is less certain. Two studies suggest that columnar epithelium tends to persist after anti-reflux surgery.9 , 10 We obtained multiple localized suction-biopsy specimens from 10 patients in whom reflux had been surgically treated and preoperative studies had revealed columnar epithelium. The reflux . . .
Nitric oxide synthase expression in AT2 receptor–deficient mice after DOCA-salt
Authors: Michael Obst, Volkmar Gross, Anton Bonartsev, Jürgen Janke, Dominik N. Müller, Joon-Keun Park, Eva Kärgel, Friedrich C. Luft
Journal: Kidney International (2004)

Nitric oxide synthase expression in AT<sub>2</sub> receptor–deficient mice after DOCA-salt. <h3>Background</h3> Angiotensin II type 2 receptor–deficient mice (AT<sub>2</sub>-/y) provide an opportunity to study the relationship between the angiotensin II type 1 receptor (AT<sub>1</sub>) and nitric oxide synthase (NOS) isoforms without concomitant AT<sub>2</sub> receptor–related effects. To test this relationship, the expression of renal NOS isoforms (neural, inducible, and endothelial) in AT<sub>2</sub>-/y and AT<sub>2</sub>+/y mice was examined. The mice were challenged with deoxycorticosterone acetate (DOCA)-salt to stimulate NO generation. <h3>Methods</h3> Gene expression analyses by real-time polymerase chain reaction (PCR) (TaqMan) were performed in kidneys to characterize neuronal nitric oxide synthase (nNOS), epithelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and the AT<sub>1</sub> receptor. Pressure-natriuresis experiments were done to determine the physiologic background. <h3>Results</h3> AT<sub>2</sub>-/y mice showed nNOS and iNOS up-regulation. DOCA-salt increased iNOS expression more in AT<sub>2</sub>-/y mice than in AT<sub>2</sub>+/y mice. Immunohistochemistry localized the iNOS expression with DOCA-salt mainly in the glomeruli. eNOS was not different between the groups, and was not affected by DOCA-salt. DOCA-salt increased mean arterial pressure more in AT<sub>2</sub>-/y mice than in AT<sub>2</sub>+/y mice. Concomitantly, the pressure-natriuresis relationship was shifted to the right in AT<sub>2</sub>-/y and AT<sub>2</sub>+/y mice after DOCA-salt. DOCA-salt decreased renal blood flow (RBF) and glomerular filtration rate (GFR) in both groups. iNOS blockade did not lower blood pressure. <h3>Conclusion</h3> We conclude that AT<sub>2</sub> receptor deletion and concomitant up-regulation of the AT<sub>1</sub> receptor is associated with up-regulation of nNOS and iNOS. Under DOCA-salt, renal iNOS expression was further increased. Because iNOS inhibition did not change blood pressure, iNOS may not be involved in the hemodynamics, but may contribute to organ damage.
Thrombotic thrombocytopenic purpura associated with HIV and visceral Kaposi's sarcoma treated with plasmapheresis and chemotherapy
Authors: Robert A. Avery, Troy M. Denunzio, Daniel B. Craig
Journal: American Journal of Hematology (1998)

We present a case of a patient who is HIV positive and developed both thrombotic thrombocytopenia purpura and visceral Kaposi's sarcoma (KS) with hemorrhage. This case presents a difficult management problem in that the patient's bleeding originated from KS lesions and did not quickly abate with plasmapheresis therapy despite both clinical and laboratory improvement after 2–4 days. Chemotherapy was initiated on day 13 and the patient's condition improved markedly afterward. We believe the addition of chemotherapy to plasmapheresis hastened the improvement of our patient's thrombotic thrombocytopenic purpura (TTP) and KS-related bleeding. Therefore, under similar conditions, we recommend combining plasmapheresis and chemotherapy at the onset of therapy. Am. J. Hematol. 58:148–149, 1998. Published 1998 Wiley-Liss, Inc.1 This article is a U.S. Government work and, as such, is in the public domain in the United States of America.
Resistance of clinical isolates of Haemophilus influenzae in United Kingdom 1986.
Authors: M Powell, C Koutsia-Carouzou, D Voutsinas, A Seymour, J D Williams
Journal: BMJ (1987)

Between 1 January and 31 March 1986, 2434 strains of Haemophilus influenzae collected from 23 laboratories in the United Kingdom were examined. With the same criteria as previous studies in 1977 and 1981 the prevalence of resistance was: ampicillin 7.8% (6.2% beta-lactamase producers and 1.6% non-producers), tetracycline 2.7%, chloramphenicol 1.7%, trimethoprim 4.2%, and sulphamethoxazole 3.5%. of the 87 capsulated strains, 15 produced beta-lactamase, nine were resistant to ampicillin but did not produce beta-lactamase, and two strains, one of which produced beta-lactamase, were resistant to chloramphenicol and tetracycline. Since 1977 the prevalence of resistance to ampicillin, chloramphenicol, and trimethoprim has increased significantly. During 1981-6 strains resistant to ampicillin but not producing beta-lactamase and strains resistant to trimethoprim have significantly increased.
The Supply of Rural Physicians-Reply
Authors: R. A. Rosenblatt, L. G. Hart, T. J. Cullen, D. M. Lishner, M. E. Whitcomb
Journal: JAMA (1993)

<h3>In Reply.</h3> —Drs Evans and Loge raise the important question of what constitutes the optimal mix of physician specialties in rural areas. Our study demonstrates that family physicians are much more likely than graduates of other disciplines to choose to practice in rural counties—particularly in small isolated rural counties—but the fact remains that the majority of physicians in rural America belong to other specialties. Rural communities need a balanced supply of physicians from a spectrum of disciplines, and general surgeons and general internists have a vital contribution to make to rural America. To the extent, however, that individual academic medical centers wish to increase the total supply of rural physicians within their service areas, investment in family medicine training is likely to produce the largest and most immediate dividends. We doubt that misclassifications account for the decline in the number and proportion of recent medical school graduates that identify themselves as general
Prevalence of Obesity in Children in Alabama and Texas Participating in Social Programs
Authors: Michelle Feese, Frank Franklin, Marianne Murdock, Kathy Harrington, Maria Brown-Binns, Theresa Nicklas, Sheryl Hughes, Miriam Morales
Journal: JAMA (2003)

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Role of Fourth-Generation Troponin in Predicting Mortality in Noncardiac Surgery
Authors: Christopher L. Wolfgang
Journal: JAMA Surgery (2013)

Of the 200 million adults worldwide who undergo noncardiac surgery each year, more than 1 million will die within 30 days.To determine the relationship between the peak fourth-generation troponin T (TnT) measurement in the first 3 days after noncardiac surgery and 30-day mortality. A prospective, international cohort study that enrolled patients from August 6, 2007, to January 11, 2011. Eligible patients were aged 45 years and older and required at least an overnight hospital admission after having noncardiac surgery. Patients' TnT levels were measured 6 to 12 hours after surgery and on days 1, 2, and 3 after surgery. We undertook Cox regression analysis in which the dependent variable was mortality until 30 days after surgery, and the independent variables included 24 preoperative variables. We repeated this analysis, adding the peak TnT measurement during the first 3 postoperative days as an independent variable and used a minimum P value approach to determine if there were TnT thresholds that independently altered patients' risk of death. A total of 15 133 patients were included in this study. The 30-day mortality rate was 1.9% (95% CI, 1.7%-2.1%). Multivariable analysis demonstrated that peak TnT values of at least 0.02 ng/mL, occurring in 11.6% of patients, were associated with higher 30-day mortality compared with the reference group (peak TnT≤0.01 ng/mL): peak TnT of 0.02 ng/mL (adjusted hazard ratio [aHR], 2.41; 95% CI, 1.33-3.77); 0.03 to 0.29 ng/mL (aHR, 5.00; 95% CI, 3.72-6.76); and 0.30 ng/mL or greater (aHR, 10.48; 95% CI, 6.25-16.62). Patients with a peak TnT value of 0.01 ng/mL or less, 0.02, 0.03-0.29, and 0.30 or greater had 30-day mortality rates of 1.0%, 4.0%, 9.3%, and 16.9%, respectively. Peak TnT measurement added incremental prognostic value to discriminate those likely to die within 30 days for the model with peak TnT measurement vs without (C index = 0.85 vs 0.81; difference, 0.4; 95% CI, 0.2-0.5; P < .001 for difference between C index values). The net reclassification improvement with TnT was 25.0% (P < .001).Among patients undergoing noncardiac surgery, the peak postoperative TnT measurement during the first 3 days after surgery was significantly associated with 30-day mortality.
Ectodomain shedding of EGFR ligands and TNFR1 dictates hepatocyte apoptosis during fulminant hepatitis in mice
Authors: Aditya Murthy, Virginie Defamie, David S. Smookler, Marco A. Di Grappa, Keisuke Horiuchi, Massimo Federici, Maria Sibilia, Carl P. Blobel, Rama Khokha
Journal: Journal of Clinical Investigation (2010)

The cell death receptor Fas plays a role in the establishment of fulminant hepatitis, a major cause of drug-induced liver failure. Fas activation elicits extrinsic apoptotic and hepatoprotective signals; however, the mechanisms by which these signals are integrated during disease are unknown. Tissue inhibitor of metalloproteinases 3 (TIMP3) controls the critical sheddase a disintegrin and metalloproteinase 17 (ADAM17) and may dictate stress signaling. Using mice and cells lacking TIMP3, ADAM17, and ADAM17-regulated cell surface molecules, we have found that ADAM17-mediated ectodomain shedding of TNF receptors and EGF family ligands controls activation of multiple signaling cascades in Fas-induced hepatitis. We demonstrated that TNF signaling promoted hepatotoxicity, while excessive TNF receptor 1 (TNFR1) shedding in Timp3-/- mice was protective. Compound Timp3-/-Tnf-/- and Timp3-/-Tnfr1-/- knockout conferred complete resistance to Fas-induced toxicity. Loss of Timp3 enhanced metalloproteinase-dependent EGFR signaling due to increased release of the EGFR ligands TGF-alpha, amphiregulin, and HB-EGF, while depletion of shed amphiregulin resensitized Timp3-/- hepatocytes to apoptosis. Finally, adenoviral delivery of Adam17 prevented acetaminophen-induced liver failure in a clinically relevant model of Fas-dependent fulminant hepatitis. These findings demonstrate that TIMP3 and ADAM17 cooperatively dictate cytokine signaling during death receptor activation and indicate that regulated metalloproteinase activity integrates survival and death signals during acute hepatotoxic stress.
POIKILODERMA-LIKE DEHMATOSES: REPORT OF A CASE WITH UNUSUAL LOCALIZATION AND ATYPICAL FEATURES.
Authors: FRANK E. CORMIA
Journal: British Journal of Dermatology (1937)

Journal Article POIKILODERMA‐LIKE DEHMATOSES: REPORT OF A CASE WITH UNUSUAL LOCALIZATION AND ATYPICAL FEATURES. Get access FRANK E. CORMIA, M.D. FRANK E. CORMIA, M.D. Montreal Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 49, Issue 1, 1 January 1937, Pages 13–21, https://doi.org/10.1111/j.1365-2133.1937.tb11144.x Published: 01 January 1937
Ozone inhalation induces exacerbation of eosinophilic airway inflammation and hyperresponsiveness in allergen‐sensitized mice
Authors: S. Kierstein, K. Krytska, S. Sharma, Y. Amrani, M. Salmon, R. A. Panettieri, J. Zangrilli, A. Haczku
Journal: Allergy (2008)

Background: Ozone (O 3 ) exposure evokes asthma exacerbations by mechanisms that are poorly understood. We used a murine model to characterize the effects of O 3 on allergic airway inflammation and hyperresponsiveness and to identify factors that might contribute to the O 3 ‐induced exacerbation of asthma. Methods: BALB/c mice were sensitized and challenged with Aspergillus fumigatus ( Af ). A group of sensitized and challenged mice was exposed to 3.0 ppm of O 3 for 2 h and studied 12 h later (96 h after Af challenge). Naive mice and mice exposed to O 3 alone were used as controls. Bronchoalveolar lavage (BAL) cellular and cytokine content, lung function [enhanced pause (P enh )], isometric force generation by tracheal rings and gene and protein expression of Fas and FasL were assessed. Apoptosis of eosinophils was quantified by FACS. Results: In sensitized mice allergen challenge induced a significant increase of P enh and contractile force in tracheal rings that peaked 24 h after challenge and resolved by 96 h. O 3 inhalation induced an exacerbation of airway hyperresponsiveness accompanied by recurrence of neutrophils and enhancement of eosinophils 96 h after allergen challenge. The combination of allergen and O 3 exposure inhibited Fas and FasL gene and protein expression and eosinophil apoptosis and increased interleukin‐5 (IL‐5), granulocyte‐macrophage‐colony stimulating factor (GM‐CSF) and G‐CSF protein levels. Conclusions: O 3 affects airway responsiveness of allergen‐primed airways indirectly by increasing viability of eosinophils and eosinophil‐mediated pathological changes.
Cimetidine suppression of CFU‐C in males
Authors: Samuel Gross, Diana A. Worthington‐White
Journal: American Journal of Hematology (1984)

Abstract A presumed cimetidine‐induced granulocytopenia in a 6‐year‐old male with acute lymphocytic leukemia (ALL) prompted an investigation of the effects of cimetidine on in vitro bone marrow granulocyte colony growth (CFU‐C) in normal individuals and ALL patients either on maintenance chemotherapy or off all therapy for at least 1 year. The addition of cimetidine resulted in a significant reduction of colony numbers as compared to untreated controls beginning at 1 × 10 −6 M (P &lt; 0.05) and increasing in significance as the concentration of cimetidine increased. Analysis of sex differences showed that CFU‐C derived from females were not adversely affected by the addition of cimetidine (except at levels far in excess of recommended dosages) whereas CFU‐C in males declined significantly from controls beginning at 1 × 10 −7 M (P &lt; 0.05) and became of greater significance as the concentration of cimetidine increased. These findings were identical for both normal individuals and ALL patients either receiving maintenance chemotherapy or off all therapy.
MYC, MAX, and Small Cell Lung Cancer
Authors: Charles M. Rudin, J.T. Poirier
Journal: Cancer Discovery (2014)

Abstract Summary: In this issue of Cancer Discovery, Romero and colleagues identify somatic mutations and deletions of MAX, and also define what seem to be mutually exclusive alterations in MYC family members and other MYC-associated factors in small cell lung cancer. Taken together, these data highlight the importance of MYC signaling in small cell lung cancer and suggest possible avenues for therapeutic intervention. Cancer Discov; 4(3); 273–4. ©2014 AACR. See related article by Romero et al., p. 292
A NEW ADENOID CURETTE.
Authors: W. STANLEY SAMSON
Journal: JAMA (1901)

The accompanying illustration shows a new adenoid curette, constructed on different principles from other sharp or dull curettes used in adenectomy. The main shaft of the instrument is 14 centimeters long, attached to a pistol grip. Upon the shaft rests a slide with two rings for the index and second fingers. To the slide is attached a second shaft, by means of which the blade can be moved 45 degrees forward and backward when traction is made upon the rings. The blades, two in number, resemble the Gottstein blade in general conformation. The dull blade has no cutting edge; the horizontal portion is round and the size of a No. 16 piano wire. The knife blade resembles the blade of the Gottstein curette very closely, excepting the knife, which is only 2 millimeters wide. The fenestra of each blade is 16 millimeters transversely and 20 millimeters longitudinally. The dull blade
Abstract 1324: Unraveling novel functions of the oncogene Astrocyte elevated gene-1 (AEG-1) contributing to hepatocarcinogenesis employing a transgenic mouse model
Authors: Jyoti Srivastava, Ayesha Siddiq, Luni Emdad, Prasanna Kumar Santhekadur, Dong Chen, Rachel Gredler, Xue-Ning Shen, Chadia L. Robertson, Jillian Stafflinger, Mark A. Subler, Catherine I. Dumur, Phillip B. Hylemon, Jolene J. Windle, Paul B. Fisher, Devanand Sarkar
Journal: Cancer Research (2012)

Abstract In vitro tissue culture and nude mice xenograft models have firmly established the role of Astrocyte elevated gene-1 (AEG-1) as a positive regulator of tumorigenesis, including hepatocarcinogenesis. To better appreciate the role of AEG-1 in hepatocarcinogenesis and to dissect the underlying molecular mechanism, we have created a transgenic mouse with hepatocyte-specific expression of AEG-1 (Alb/AEG1). Wild-type (WT) and Alb/AEG-1 mice were challenged with a hepatocarcinogen, N-nitrosodiethylamine (DEN), at 2 weeks of age. At 28 weeks of age, Alb/AEG-1 mice, but not WT mice, developed multinodular HCC with steatotic features and highly elevated serum liver enzymes. Affymetrix microarray analyses identified modulation of expression of genes associated with invasion, metastasis, angiogenesis and fatty acid synthesis in DEN-treated Alb/AEG-1 mice versus their WT counterparts. Hepatocytes isolated from Alb/AEG-1 mice demonstrated profound chemoresistance and dramatically evaded reduction in cell viability upon growth factor deprivation, which was associated with activation of multiple pro-survival signaling pathways. Compared to the WT hepatocytes, Alb/AEG-1 hepatocytes demonstrated marked resistance towards senescence, which was associated with abrogation of activation of a DNA damage response. Conditioned media (CM) from Alb/AEG-1 hepatocytes, but not form WT hepatocytes, induced marked angiogenesis. Mass spectrometric analysis of CM revealed noticeable increases in coagulation factors by AEG-1, which are known to play a significant role in regulating tumor invasion, angiogenesis and metastasis. siRNA-mediated knockdown of coagulation factor XII resulted in profound inhibition of AEG-1-induced angiogenesis. Our studies reveal novel aspects of AEG-1 functions, such as induction of steatosis, inhibition of senescence, a known anti-cancer mechanism, and activation of coagulation pathway to augment an aggressive hepatocarcinogenic phenotype. The Alb/AEG-1 mouse will be a useful model to decipher AEG-1 function in the context of hepatocarcinogenesis and to evaluate the efficacy of novel therapeutic strategies directed towards HCC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1324. doi:1538-7445.AM2012-1324
Trans-mesenteric neural crest cells are the principal source of the colonic enteric nervous system
Authors: Chihiro Nishiyama, Toshihiro Uesaka, Takayuki Manabe, Yohei Yonekura, Takashi Nagasawa, Donald F Newgreen, Heather M Young, Hideki Enomoto
Journal: Nature Neuroscience (2012)
Radiation Oncology Investigations: Clinical and Basic Research
Authors: Josephine L. Dorsch
Journal: JAMA (1994)

<i>Radiation Oncology Investigations</i>is a well-conceived journal, providing the oncology community with a focus on current concepts and developments in applying ionizing radiation in cellular and molecular biology as well as in the clinic. It is the promise of this journal to integrate emerging scientific concepts with technological developments in the rational approach to solving clinical dilemmas, which the reader will find exciting. The 41-member editorial board is international in composition, but the American oncologist will recognize all these reputable experts. If the first four issues are indicative, the reader can be assured that the authors selected will be well worth reading, and might otherwise be overlooked by readers of strictly scientific or clinical journals. <i>Radiation Oncology Investigations</i>is a bimonthly publication printed on acid-free paper. Tables and figures, generally in black-and-white, are not remarkable but are used effectively and contribute to easy reading. Abstracts are informative and summarize research
Prospective study of aetiological factors in burning mouth syndrome
Authors: P-J Lamey, A B Lamb
Journal: BMJ (1988)

A prospective study of 150 consecutive patients with burning mouth syndrome and with a minimum follow up period of 18 months is reported. Factors related to dentures, to vitamin B complex deficiency, and to psychological abnormalities were found to be important, and undiagnosed diabetes mellitus, reduced salivary gland function, haematological deficiencies, candidal infection, parafunctional habits, and allergy might also play a part. Given a protocol for management which takes all these factors into account, some two thirds of patients can be cured or have their symptoms improved.