tbuckley/cabot-search huggingface dataset:
Protective Effect of 3-Aminobenzamide, an Inhibitor of Poly (ADP-Ribose) Synthetase, against Laryngeal Injury in Rats
Authors: YORAM STERN, ANDREW SALZMAN, ROBIN T. COTTON, BASILIA ZINGARELLI
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

The effect of 3-aminobenzamide, an inhibitor of poly (ADP-ribose) synthetase activity, was evaluated in a rat model of laryngeal injury induced by endotracheal intubation for 1 h. At 1 h after extubation, the laryngeal damage was characterized by areas of mucosal necrosis, submucosal edema, swelling of subglottic glands, and submucosal infiltration of inflammatory cells. Activity of myeloperoxidase, a marker of neutrophil infiltration, was also markedly increased into the damaged tissue. Immunohistochemistry for nitrotyrosine, an index of nitrosative stress, showed an intense staining in the inflamed larynx. Treatment with 3-aminobenzamide (10 mg/kg intraperitoneally) significantly reduced the appearance of mucosal damage and was associated with a significant reduction of tissue myeloperoxidase activity and nitrotyrosine immunoreactivity in the larynx. The results of this study suggest that poly (ADP-ribose) synthetase may play a role in the inflammatory process after laryngeal intubation and extubation, and administration of 3-aminobenzamide may be a beneficial therapeutic approach.
Urinary Perchlorate and Thyroid Hormone Levels in Adolescent and Adult Men and Women Living in the United States
Authors: Benjamin C. Blount, James L. Pirkle, John D. Osterloh, Liza Valentin-Blasini, Kathleen L. Caldwell
Journal: Environmental Health Perspectives (2006)

Perchlorate is commonly found in the environment and known to inhibit thyroid function at high doses. Assessing the potential effect of low-level exposure to perchlorate on thyroid function is an area of ongoing research.We evaluated the potential relationship between urinary levels of perchlorate and serum levels of thyroid stimulating hormone (TSH) and total thyroxine (T4) in 2,299 men and women, > or = 12 years of age, participating in the National Health and Nutrition Examination Survey (NHANES) during 2001-2002.We used multiple regression models of T4 and TSH that included perchlorate and covariates known to be or likely to be associated with T4 or TSH levels: age, race/ethnicity, body mass index, estrogen use, menopausal status, pregnancy status, premenarche status, serum C-reactive protein, serum albumin, serum cotinine, hours of fasting, urinary thiocyanate, urinary nitrate, and selected medication groups.Perchlorate was not a significant predictor of T4 or TSH levels in men. For women overall, perchlorate was a significant predictor of both T4 and TSH. For women with urinary iodine < 100 microg/L, perchlorate was a significant negative predictor of T4 (p < 0.0001) and a positive predictor of TSH (p = 0.001). For women with urinary iodine > or = 100 microg/L, perchlorate was a significant positive predictor of TSH (p = 0.025) but not T4 (p = 0.550).These associations of perchlorate with T4 and TSH are coherent in direction and independent of other variables known to affect thyroid function, but are present at perchlorate exposure levels that were unanticipated based on previous studies.
Conventional DCs reduce liver ischemia/reperfusion injury in mice via IL-10 secretion
Authors: Zubin M. Bamboat, Lee M. Ocuin, Vinod P. Balachandran, Hebroon Obaid, George Plitas, Ronald P. DeMatteo
Journal: Journal of Clinical Investigation (2010)

TLRs are recognized as promoters of tissue damage, even in the absence of pathogens. TLR binding to damage-associated molecular patterns (DAMPs) released by injured host cells unleashes an inflammatory cascade that amplifies tissue destruction. However, whether TLRs possess the reciprocal ability to curtail the extent of sterile inflammation is uncertain. Here, we investigated this possibility in mice by studying the role of conventional DCs (cDCs) in liver ischemia/reperfusion (I/R) injury, a model of sterile inflammation. Targeted depletion of mouse cDCs increased liver injury after I/R, as assessed by serum alanine aminotransferase and histologic analysis. In vitro, we identified hepatocyte DNA as an endogenous ligand to TLR9 that promoted cDCs to secrete IL-10. In vivo, cDC production of IL-10 required TLR9 and reduced liver injury. In addition, we found that inflammatory monocytes recruited to the liver via chemokine receptor 2 were downstream targets of cDC IL-10. IL-10 from cDCs reduced production of TNF, IL-6, and ROS by inflammatory monocytes. Our results implicate inflammatory monocytes as mediators of liver I/R injury and reveal that cDCs respond to DAMPS during sterile inflammation, providing the host with protection from progressive tissue damage.
Ineffectiveness of Chicken Anti-ulcer Factors in Treatment of Gastric and Duodenal Ulcer in Man
Authors: K. Brochner-Mortensen, N. B. Krarup, E. Meulengracht, Aa. Videbaek
Journal: BMJ (1955)

PENTOLINIUM TARTRATE AND RAUWOLFIA 1 patients who are already stabilized on pentolinium tartrate alone, the dose on adding rauwolfia has usually been reduced to one-third and final adjustments made from that level.A patient who has had no previous treatment is given rauwolfia for some weeks, as suggested by Smirk et al. (1954).Then pentolinium tartrate is added, starting with 20-mg.doses and increasing by increments of 20 mg. until satis- factory levels are obtained.We have found that a better control is achieved when the drug is given three times rather than twice daily.The reduction in dosage reduces or abolishes the undesir- able effects of the ganglionic blockade.Where formerly postural hypotension was a problem, this has been less evident on the combination.Rauwolfia has been shown to stimulate the intestine, and this, in addition to the smaller dose of pentolinium tartrate required, makes the control of the bowels easier.There is therefore less risk of cumulative effect through retention and subsequent absorption of pento- linium tartrate in the bowel.
Recent Trends in Cardiovascular and Thoracic Surgery
Authors: Alan T. Marty
Journal: JAMA (1976)

By collecting 27 original publications, most of which discuss a significant advance in thoracic and cardiovascular surgery, the editor has assembled an excellent anthology. The volume is dedicated to Hanoch Milwidsky, a pioneer thoracic surgeon from the Middle East who was killed by Arab terrorists in 1970. On the positive side, the text contains many essays by noted authorities. Bjork, Brock, Cooley, Ionescu, Ross, Senning, and Starr all discuss valve surgery. Effler, Favaloro, Kay, Matloff, and Vineberg illuminate myocardial revascularization. Bernard, Kirklin, and McGoon update selected aspects of congenital heart surgery. And Shumway summarizes cardiac transplantation. In addition, surgeons from many countries cover other topics like deep hypothermia, vena-caval interruption, and intractable peptic stricture of the esophagus. On the negative side, the book does not read like a book. There are no editorial overviews putting the many unrelated, short articles into some kind of perspective, and all the papers were
Inhibition of Neutral Endopeptidase Causes Vasoconstriction of Human Resistance Vessels In Vivo
Authors: Charles J. Ferro, James C. Spratt, William G. Haynes, David J. Webb
Journal: Circulation (1998)

Background —Neutral endopeptidase (NEP) degrades vasoactive peptides, including the natriuretic peptides, angiotensin II, and endothelin-1. Systemic inhibition of NEP does not consistently lower blood pressure, even though it increases natriuretic peptide concentrations and causes natriuresis and diuresis. We therefore investigated the direct effects of local inhibition of NEP on forearm resistance vessel tone. Methods and Results —Four separate studies were performed, each with 90-minute drug infusions. In the first study, 10 healthy subjects received a brachial artery infusion of the NEP inhibitor candoxatrilat (125 nmol/min), which caused a slowly progressive forearm vasoconstriction (12±2%; P =0.001). In a second two-phase study, 6 healthy subjects received, 4 hours after enalapril (20 mg) or placebo, an intra-arterial infusion of the NEP inhibitor thiorphan (30 nmol/min). Thiorphan caused similar degrees of local forearm vasoconstriction ( P =0.6) after pretreatment with both placebo (13±1%, P =0.006) and enalapril (17±6%, P =0.05). In a third three-phase study, 8 healthy subjects received intra-arterial thiorphan (30 nmol/min), the endothelin ET A antagonist BQ-123 (100 nmol/min), and both combined. Thiorphan caused local forearm vasoconstriction (13±1%, P =0.0001); BQ-123 caused local vasodilatation (33±3%, P =0.0001). Combined thiorphan and BQ-123 caused vasodilatation (32±1%, P =0.0001) similar to BQ-123 alone ( P =0.98). In a fourth study, 6 hypertensive patients (blood pressure &gt;160/100 mm Hg) received intra-arterial thiorphan (30 nmol/min). Thiorphan caused a slowly progressive forearm vasoconstriction (10±2%, P =0.0001). Conclusions —Inhibition of local NEP causes vasoconstriction in forearm resistance vessels of both healthy volunteers and patients with hypertension. The lack of effect of ACE inhibition on the vasoconstriction produced by thiorphan and its absence during concomitant ET A receptor blockade suggest that it is mediated by endothelin-1 and not angiotensin II. These findings may help to explain the failure of systemic NEP inhibition to lower blood pressure.
EARLY INDUCTION OF HYPOTHERMIA THERAPY PRIOR TO REVASCULARIZATION THERAPY IMPROVED NEUROLOGIC OUTCOMES IN CARDIAC ARREST CAUSED BY ACUTE CORONARY SYNDROME: J-PULSE- HYPO REGISTRY.
Authors: Shinichi Shirai, Kenji Ando, Yoshimitsu Soga, Kyohei Yamaji, Tatsuki Doijiri, Masahiko Goya, Masashi Iwabuchi, Hiroyoshi Yokoi, Hideyuki Nosaka, Masakiyo Nobuyoshi, Naohiro Yonemoto, Hiroyuki Yokoyama, Hiroshi Nonogi, Ken Nagao
Journal: Journal of the American College of Cardiology (2010)
Hydroxyurea-Induced gangrene of the toes in a patient with chronic myelogenous leukemia
Authors: Norimasa Yasuda, Sei-ichi Ohmori, Tadao Usui
Journal: American Journal of Hematology (2000)

To the Editor: Semenzato et al. proposed new criteria for large granular lymphocyte (LGL) leukemia because patients with low levels of GL were similar to those with levels greater than 2,000 GL/l [1].LGL leukemia is a GL proliferative disease often accompanied by pure red cell aplasia (PRCA).T-cell LGL leukemia is a clonal disease, and the phenotype of leukemic cells is CD3 + 4 -8 + .PRCA with thymoma is often associated with peripheral T cell expansion.We previously reported a case of PRCA with thymoma in which the T-cell receptor ␤ of both the thymus and peripheral mononuclear cells was rearranged [2].Thymoma and PRCA may be caused by T-cell clonal expansion, leukemia.We examined four patients with PRCA and thymoma (Table I), one of which was previously reported.Three of the four showed CD3 + 4 -8 + lymphocytosis and two exhibited T-cell receptor ␤ rearrangement of peripheral mononuclear cells.Patient 2 showed low levels of lymphocytes and the mononuclear cell's CD4/8 ratio of patient 3 was greater than 1.Due to the low levels of abnormal cells and low sensitivity of Southern blot analysis, we could not confirm the clonality of these two cases.According to treatment of PRCA with thymoma, the response rate of thymectomy was 12% [3].This limited effectiveness of thymectomy indicated that thymoma did not play a causative role in PRCA.Loughran reported 129 patients with LGL leukemia [4] and Oshimi et al. examined 33 patients [5].Neither study noted a complication of thymoma.PRCA with thymoma had been considered a distinct clinical entity from LGL leukemia.The old diagnostic criteria for LGL leukemia was "greater than 2,000 GL/l."The normal value of GL is 223 ± 99 l [4].Three of the 4 patients with PRCA and thymoma demonstrated levels greater than the mean + 3 SD (Table I).However, it is unknown whether or not a distinction between 'PRCA with thymoma' and 'PRCA with LGL leukemia' exists.Patients with LGL leukemia showed an indolent clinical course, and immunosuppressive therapy with cyclosporin A or low-dose cyclophosphamide was effective for the clinical symptoms.In contrast, patients with PRCA with thymoma were treated with more aggressive therapy such as surgical resection, intensive chemotherapy, or radiation.As the effectiveness of surgical resection for PRCA with thymoma is limited, PRCA with thymoma should be initially treated with immunosuppressive therapy.
Conjugation of 1-naphthol in human gastric epithelial cells.
Authors: P Dechelotte, M Varrentrapp, H J Meyer, M Schwenk
Journal: Gut (1993)

The biotransformation of xenobiotics is essential to the maintenance of the body9s integrity. Mucosal biotransformation has been well documented in the small and large intestine of animals and humans but whether the gastric mucosa plays a role in detoxifying ingested compounds remains largely unknown. The conjugation of the model phenolic compounds, 1-naphthol, by human gastric epithelial cells was assessed in vitro. Freshly isolated and cultured epithelial cells were prepared from surgical specimens obtained from patients undergoing total gastrectomy for cancer. Cell preparations were incubated with 1- 14C-naphthol over 1 hour and the glucuronide and sulphate conjugates formed were separated by thin-layer chromatography. Conjugation of 1-naphthol was observed with both freshly isolated and cultured cells. In freshly isolated cells, the 1 hour turnover of 1 microM 1-naphthol to its glucuronide and sulphate conjugates averaged 19% and 10% respectively. At higher 1-naphthol concentrations, both types of conjugate were formed at about the same rate, up to saturation (apparent Vmax = 0.07 nmol/mg protein/minute, and apparent Km = 40 microM). In cultured cells, the 1 hour turnover of 1 microM 1-naphthol to its glucuronide and sulphate conjugates averaged 35% and 8% respectively. These results suggest that the human gastric mucosa is a detoxifying organ, and that its role with regard to chemical carcinogenesis and drug first pass metabolism deserves further assessment.
The plasminogen activator system modulates sympathetic nerve function
Authors: Ulrich Schaefer, Takuji Machida, Sandra Vorlova, Sidney Strickland, Roberto Levi
Journal: The Journal of Experimental Medicine (2006)

Sympathetic neurons synthesize and release tissue plasminogen activator (t-PA). We investigated whether t-PA modulates sympathetic activity. t-PA inhibition markedly reduced contraction of the guinea pig vas deferens to electrical field stimulation (EFS) and norepinephrine (NE) exocytosis from cardiac synaptosomes. Recombinant t-PA (rt-PA) induced exocytotic and carrier-mediated NE release from cardiac synaptosomes and cultured neuroblastoma cells; this was a plasmin-independent effect but was potentiated by a fibrinogen cleavage product. Notably, hearts from t-PA–null mice released much less NE upon EFS than their wild-type (WT) controls (i.e., a 76.5% decrease; P &amp;lt; 0.01), whereas hearts from plasminogen activator inhibitor-1 (PAI-1)–null mice released much more NE (i.e., a 275% increase; P &amp;lt; 0.05). Furthermore, vasa deferentia from t-PA–null mice were hyporesponsive to EFS (P &amp;lt; 0.0001) but were normalized by the addition of rt-PA. In contrast, vasa from PAI-1–null mice were much more responsive (P &amp;lt; 0.05). Coronary NE overflow from hearts subjected to ischemia/reperfusion was much smaller in t-PA–null than in WT control mice (P &amp;lt; 0.01). Furthermore, reperfusion arrhythmias were significantly reduced (P &amp;lt; 0.05) in t-PA–null hearts. Thus, t-PA enhances NE release from sympathetic nerves and contributes to cardiac arrhythmias in ischemia/reperfusion. Because the risk of arrhythmias and sudden cardiac death is increased in hyperadrenergic conditions, targeting the NE-releasing effect of t-PA may have valuable therapeutic potential.
Mechanisms of the biological effects of PCBs, polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans in experimental animals.
Authors: R A Neal
Journal: Environmental Health Perspectives (1985)

Polychlorinated biphenyls, certain polychlorinated dibenzo-p-dioxins and certain polychlorinated dibenzofurans cause a variety of biological effects in experimental animals. The mechanism of the induction of certain enzymes is perhaps best understood. That is, there is binding of certain chlorinated biphenyls, dibenzo-p-dioxins and dibenzofurans to a receptor, translocation of the compound-receptor complex into the nucleus followed by an increased activity of a number of enzymes in the cell. Although the concentration of this receptor in various tissues of some mouse strains correlates well with the intensity of some of the biological effects observed in the mouse strains exposed to these compounds, this correlation apparently does not extend across various species. The current evidence suggests that the acute toxic effects of TCDD in various species is in some way associated with binding of TCDD to the receptor. However, biological effects of TCDD in addition to those resulting from binding to the receptor may be required to produce acute toxicity and, perhaps, other effects. The acute toxic effects of TCDD are probably caused by the parent compound rather than metabolites; however, this conclusion must be viewed as tentative. Also, it cannot be excluded at this time that biological effects other than acute toxicity may be caused by metabolites of TCDD. Finally, the acute toxic effects of TCDD appear not to be related, at least not directly, to the rate of metabolism of TCDD in experimental animals nor to the half-life of excretion.
In vivo cell tracking by bioluminescence imaging after transplantation of bioengineered cell sheets to the knee joint
Authors: Yuko Takaku, Kunihiko Murai, Taku Ukai, Satoshi Ito, Mami Kokubo, Masaaki Satoh, Eiji Kobayashi, Masayuki Yamato, Teruo Okano, Mamoru Takeuchi, Joji Mochida, Masato Sato
Journal: Biomaterials (2013)
Creative Part-Time Faculty Arrangements
Authors: Deborah J. Ziring
Journal: Annals of Internal Medicine (1994)

Letters15 February 1994Creative Part-Time Faculty ArrangementsDeborah J. Ziring, MDDeborah J. Ziring, MDHahnemann University Hospital; Philadelphia, PA 19102Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-120-4-199402150-00024 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:I read with great interest the article on part-time faculty in academic medicine [1]. During the past 4 years, I have served as Director of the Medical Residents Clinic and Director of the Third Year Medicine Clerkship and have participated in inpatient rounds. Through these responsibilities, I have significant contact with residents and students as a teacher and role model. After the birth of my first child last year, I felt constantly sleep-deprived, frustrated, and overwhelmed by the demands on my time. I quickly realized that I was no longer a positive role model but rather a ...REFERENCE1. Levinson W, Kaufman K, Bickel J. Part-time faculty in academic medicine: present status and future challenges. Ann Intern Med. 1993; 119:220-5. Google Scholar Author, Article, and Disclosure InformationAffiliations: Hahnemann University Hospital; Philadelphia, PA 19102 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByDiscrimination and abuse experienced by general internists in Canada 15 February 1994Volume 120, Issue 4Page: 346-347KeywordsAcademic medicineBirthInpatientsPatients Issue Published: 15 February 1994 CopyrightCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Antibodies against the GB virus C envelope 2 protein before liver transplantation protect against GB virus Cde novo infection
Authors: Hans Ludger Tillmann, Stefan Heringlake, Christian Trautwein, Doerte Meissner, Bjoern Nashan, Hans-Juergen Schlitt, Jon Kratochvil, Jeffrey Hunt, Xiaoxing Qiu, Sheng Chang Lou, Rudolf Pichlmayr, Michael Peter Manns
Journal: Hepatology (1998)

GB virus C (GBV-C) is a newly discovered RNA virus related to the Flaviviridae family. Although GBV-C is not yet associated with any cause of liver disease, a humoral immune response against the GBV-C envelope 2 (E2) protein has been observed. Therefore, we studied the prevalence and clinical relevance of GBV-C RNA and anti-E2 antibodies in patients undergoing orthotopic liver transplantation (OLT). In addition, we tested whether the prevalence of anti-E2 antibodies may protect against GBV-C infection. Of the 182 liver recipients included in this study, 117 of these were evaluated for GBV-C recurrence or de novo infection. GBV-C RNA was detected in sera or plasma using single-tube, reverse-transcriptase polymerase chain reaction, and anti-E2 antibody was detected by enzyme immunoassay (EIA). Cumulative patient and graft survival was tested by using Kaplan-Meier analysis. The independence of prognostic values was assessed by using Cox regression analysis. Before OLT, GBV-C RNA and anti-E2 were detected in 4.0% to 28.6% and 10.0% to 68.8%, respectively, of patients suffering from different forms of chronic liver diseases. GBV-C reinfection after OLT was determined in 85.7%. Of the patients without evidence of exposure to GBV-C before OLT, 30 of 65 (46.2%) became GBV-C RNA positive after OLT. None of the 38 patients who were anti-E2 antibody positive before OLT became GBV-C RNA positive after OLT. Neither patient nor graft survival was significantly affected by the presence of either GBV-C RNA or anti-E2 antibody before OLT. Our data indicate that 1) GBV-C RNA positive patients have a high risk of reinfection after OLT, and 2) the presence of anti-E2 antibodies before OLT is associated with an absence of GBV-C infection after OLT, which may indicate a protective role of anti-E2 antibodies.
Screening for mutations of the cationic trypsinogen gene: are they of relevance in chronic alcoholic pancreatitis?
Authors: N Teich, J Mössner, V Keim
Journal: Gut (1999)

BACKGROUND In hereditary pancreatitis mutations of exons 2 (N21I) and 3 (R117H) of the cationic trypsinogen gene have been described. AIMS To investigate whether the same mutations can also be found in patients with chronic alcoholic pancreatitis. METHODS Leucocyte DNA was prepared from 23 patients with chronic alcoholic pancreatitis, 21 with alcoholic liver cirrhosis, 34 individuals from seven independent families with hereditary pancreatitis, and 15 healthy controls. DNA was also obtained from pancreatic tissue (n=7) and from pancreatic juice (n=5) of patients suffering from chronic alcoholic pancreatitis. R117H was detected by restriction digestion with Afl III. N21I was identified by an allele specific polymerase chain reaction (PCR). RESULTS R117H was detected in four families with hereditary pancreatitis. The N21I mutation was identified in three families. All mutations were confirmed by sequencing of the corresponding DNAs. In patients with chronic alcoholic pancreatitis neither the exon 2 nor exon 3 mutations were present in blood leucocytes, pancreatic juice, or pancreatic tissue. DNA of the patients with alcoholic liver cirrhosis as well as all controls was of wild type. CONCLUSIONS The allele specific PCR may be used to screen for the N21I mutation of cationic trypsinogen. Both trypsinogen mutations were found in hereditary pancreatitis but do not seem to be major pathogenic factors in chronic alcoholic pancreatitis.
Irinotecan (CPT-11) in the treatment of mycosis fungoides
Authors: T. Yokote, T. Akioka, S. Oka, T. Yamano, S. Hara, K. Higashi, U. Enomoto, H. Kusakabe, K. Kiyokane, M. Tsuji, T. Hanafusa
Journal: British Journal of Dermatology (2005)