tbuckley/cabot-search huggingface dataset:
Counter-regulatory phosphatases TNAP and NPP1 temporally regulate tooth root cementogenesis
Authors: Laura E Zweifler, Mudita K Patel, Francisco H Nociti, Helen F Wimer, Jose L Millán, Martha J Somerman, Brian L Foster
Journal: International Journal of Oral Science (2014)

Cementum is critical for anchoring the insertion of periodontal ligament fibers to the tooth root. Several aspects of cementogenesis remain unclear, including differences between acellular cementum and cellular cementum, and between cementum and bone. Biomineralization is regulated by the ratio of inorganic phosphate (Pi) to mineral inhibitor pyrophosphate (PPi), where local Pi and PPi concentrations are controlled by phosphatases including tissue-nonspecific alkaline phosphatase (TNAP) and ectonucleotide pyrophosphatase/phosphodiesterase 1 (NPP1). The focus of this study was to define the roles of these phosphatases in cementogenesis. TNAP was associated with earliest cementoblasts near forming acellular and cellular cementum. With loss of TNAP in the Alpl null mouse, acellular cementum was inhibited, while cellular cementum production increased, albeit as hypomineralized cementoid. In contrast, NPP1 was detected in cementoblasts after acellular cementum formation, and at low levels around cellular cementum. Loss of NPP1 in the Enpp1 null mouse increased acellular cementum, with little effect on cellular cementum. Developmental patterns were recapitulated in a mouse model for acellular cementum regeneration, with early TNAP expression and later NPP1 expression. In vitro, cementoblasts expressed Alpl gene/protein early, whereas Enpp1 gene/protein expression was significantly induced only under mineralization conditions. These patterns were confirmed in human teeth, including widespread TNAP, and NPP1 restricted to cementoblasts lining acellular cementum. These studies suggest that early TNAP expression creates a low PPi environment promoting acellular cementum initiation, while later NPP1 expression increases PPi, restricting acellular cementum apposition. Alterations in PPi have little effect on cellular cementum formation, though matrix mineralization is affected. The timing and site of action of two key enzymes help regulate the formation of cementum, one of the mineralized substances of teeth. An international team led by Brian Foster from the US National Institute of Arthritis and Musculoskeletal and Skin Diseases considered the roles of two enzymes — tissue non-specific phosphatase (TNAP) and ectonucleotide pyrophosphatase/phosphodiesterase 1 (NPP1) — in cementum development. They showed in mice that early TNAP expression created a particular environment in teeth with low levels of pyrophosphate, a mineral inhibitor. This promoted the creation of a type of cementum that does not incorporate cells into its structure. Later on in development, the expression of NPP1 boosted levels of pyrophosphate, which restricted this type of cementum. These enzymes had little effect on cementum containing cells. The researchers confirmed these patterns in extracted human teeth.
Dependence on ACTH
Authors: ULRICH EHRIG
Journal: Annals of Internal Medicine (1972)

Letters, Comments, and Corrections1 September 1972Dependence on ACTHULRICH EHRIG, M.D., JAMES G. RANKIN, M.D.ULRICH EHRIG, M.D.Search for more papers by this author, JAMES G. RANKIN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-77-3-482_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: After reading the recent article by Dr. Kimball (1), we had an opportunity to observe a 40-year-old physician who had been dependent on adrenocorticotrophin (ACTH) for 3 years.He had a 7-year history of alcoholism and simultaneously used large amounts of psychotropic drugs, including methylphenidate, amitriptyline, methaqualone, and a combination of dextroamphetamine and barbiturates (Dexedrine®). Lately, he had treated himself with propylthioracil, 100 mg three times daily for 5 months, for sweating, tachycardia, and nervousness, despite normal thyroid function tests. He also administered testosterone propionate to himself on one occasion. He first began using ACTH in 1969...References1. KIMBALL C: Psychological dependency on steroids? Ann Intern Med 75:111-113, 1971 LinkGoogle Scholar2. AMATRUDAHURSTD'ESOPO TMN: Certain endocrine and metabolic facets of the steroid withdrawal syndrome. J Clin Endocrinol Metab 25:1207-1217, 1965 CrossrefMedlineGoogle Scholar3. DOLE V: Narcotic addiction, physical dependence and relapse. N Engl J Med 286:988-992, 1972 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ULRICH EHRIG, M.D.; JAMES G. RANKIN, M.D.Affiliations: Addiction Research Foundation Toronto 4, Ontario Canada PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byGlucocorticoid TherapyOn the various forms of corticosteroid withdrawal syndrome 1 September 1972Volume 77, Issue 3Page: 482-482KeywordsAdrenocorticotropic hormoneAlcoholismAnxietyDrugsPropionatesTachycardiaTestosteroneThyroid ePublished: 1 December 2008 Issue Published: 1 September 1972 PDF downloadLoading ...
Pulmonary Imaging in Fat Embolism Syndrome
Authors: HEE-MYUNG PARK, REN?? P. DUCRET, DUNCAN C. BRINDLEY
Journal: Clinical Nuclear Medicine (1986)

Ventilation/perfusion lung scanning can be used to effectively detect fat embolism following skeletal trauma. Typical ventilation/perfusion findings may be present when the chest radiograph is normal, and clinical findings are equivocal.
Performance of ventilators for noninvasive positive-pressure ventilation in children
Authors: B. Fauroux, K. Leroux, G. Desmarais, D. Isabey, A. Clément, F. Lofaso, B. Louis
Journal: European Respiratory Journal (2008)

The aim of the present study was to evaluate the performance characteristics of all the ventilators proposed for home noninvasive positive-pressure ventilation in children in France. The ventilators (one volume-targeted, 12 pressure-targeted and four dual) were evaluated on a bench which simulated six different paediatric ventilatory patterns. For each ventilator, the quality of the inspiratory and expiratory trigger and the ability to reach and maintain the preset pressures and volumes were evaluated with the six patient profiles. The performance of the ventilators showed great variability, and depended upon the type of trigger (flow or pressure), type of circuit and patient profile. Differences were observed between the preset and measured airway pressure and between the tidal volume measured by the ventilator and on the bench. Leaks were associated with an inability to detect the patient’s inspiratory effort or autotriggering. No single ventilator was able to adequately ventilate the six paediatric profiles. Only a few ventilators were able to ventilate the profiles simulating the youngest patients. A systematic paediatric bench evaluation is recommended for every ventilator proposed for home ventilation, in order to detect any dysfunction and guide the choice of the appropriate ventilator for a specific patient.
Peripartum Diastasis of the Symphysis Pubis
Authors: Jason M Parker, Modushudan Bhattacharjee
Journal: New England Journal of Medicine (2009)

A 21-year-old primigravida at nearly 40 weeks' gestation presented with a spontaneous onset of pelvic pain and difficulty in walking. After a rapid delivery, the postpartum physical examination revealed pain only with weight bearing and abduction and adduction at both hips. Pelvic radiography showed a 23-mm diastasis of the symphysis pubis (arrow). The reported incidence of nontraumatic diastasis varies widely, from 1 in 300 pregnancies to 1 in 30,000 pregnancies. In a nonpregnant woman, the normal pubic symphysis gap ranges from 4 to 5 mm. With pregnancy, the gap increases by at least 2 to 3 mm, which is thought . . .
Interferon alfa treatment of HCV RNA carriers with persistently normal transaminase levels: A pilot randomized controlled study
Authors: Angelo Sangiovanni, Rino Morales, GianCarlo Spinzi, MariaGrazia Rumi, Antonietta Casiraghi, Roberto Ceriani, Enrico Colombo, Maurizio Fossati, Alberto Prada, Enrico Tavani, Giorgio Minoli
Journal: Hepatology (1998)

Most patients with serum hepatitis C virus (HCV) RNA and persistently normal alanine transaminase (ALT) levels show histological features of mild to moderately active chronic hepatitis. Some cirrhosis has also been reported. To assess whether interferon (IFN) treatment led to long-term HCV suppression in these patients, 31 previously untreated patients (15 men, 16 women; mean age, 44 years) with serum HCV RNA, persistently normal ALT levels on at least four consecutive occasions 2 months apart, and histological features of chronic hepatitis (21 mild activity, 10 moderate activity) were randomized to receive IFN-α-2a, 3 MU three times a week for 6 months (n = 16), or no treatment (n = 15). All patients were followed up for at least 6 months after treatment ended. HCV RNA was tested by nested reverse-transcription polymerase chain reaction (RT-PCR) using 5′-untranslated region complementary primers, quantified by branched-DNA assay, and typed by nested RT-PCR testing for the HCV core region. Treated and untreated patients had similar epidemiological, virological, and histological characteristics. At the end of treatment, serum HCV RNA was still detected in 15 patients (94%) and 14 controls (93%). ALT levels flared up in 10 patients receiving IFN (62%) and in 1 control (62% vs. 7%; P &lt; .005, χ 2 test). In conclusion, 6 months’ treatment with IFN-α-2a did not eradicate HCV RNA from serum in carriers with persistently normal ALT levels but caused ALT flare-ups in two thirds of them. Until more is known about the natural history of HCV RNA carriers with normal ALT levels, these patients should not be treated with IFN.
Abstract P6-08-13: Alteration of REDD-1 Mediated mTOR Pathway and HIF-1σ Regulation in Human Breast Cancer
Authors: S Lee, JS. Koo
Journal: Cancer Research (2010)

Abstract A hypoxia-related protein, REDD1 (regulated in development and DNA damage response 1), inhibits the mammalian target of rapamycin (mTOR) signaling pathway in normal cells under hypoxic condition, but a loss of REDD1 causes tumorigenesis in certain tumor cells. The purpose of this study is to investigate REDD 1 -mediated regulation of the mTOR pathway in breast cancer. Tissue microarray included samples from 224 patients with breast cancer, and 30 patients with papilloma were used as control group. The immunohistochemistry (IHC) such as estrogen receptor (ER), progesterone receptor (PR), HER-2, epithelial growth factor receptor (EGFR), cytokeratin (CK) 5/6, Glut-1, HIF-1α, REDD 1, AMPK ≥1, 14-3-3 σ, PTEN, phospho-Akt, phospho-mTOR, phospho-S6, and Ki-67 were performed. Phenotypic classification of breast cancer was performed based on the results of IHC for ER, PR, and HER-2 and fluorescent in Situ Hybridization (FISH) for HER-2: luminal A, luminal B, HER-2 overexpression, and triple negative breast cancer (TNBC). Glut-1and HIF-1 alpha were more highly expressed in TNBC, HER-2 overexpressiontype, and papilloma than luminal A and B (P = 0.000). REDD1 expression was higher in papilloma than breast cancer (P = 0.000), but no difference was found among the 4 breast cancer phenotypes (P = 0.307). HIF-1α expression was an important factor of decreased time to disease free survival and overall survival in univariate analysis (P = 0.003, and 0.000, respectively) and multivariate Cox analysis (P = 0.018, odd ratio: 7.6, and P = 0.002, odd ratio: 13.7, respectively). Among human breast cancer phenotypes, HER-2 overexpression and TNBC type demonstrated down-regulation of REDD1 under hypoxic tumor environment. In HER-2 overexpression and TNBC type, tumor cell proliferation and survival in hypoxic tumor environment could be possible due to dysinhibition of the mTOR pathway and HIF-1α stabilization through down-regulation of REDD1. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-08-13.
Activation of H-ras Oncogene in Rat Bladder Tumors Induced by N-Butyl-N-(4-hydroxybutyl)nitrosamine1
Authors: J. Fujita, N. Ohuchi, N. Ito, S. H. Reynolds, O. Yoshida, H. Nakayama, Y. Kitamura
Journal: JNCI Journal of the National Cancer Institute (1988)

Ras-oncogene activation was investigated in the bladder tumors of F344 male rats given N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in drinking water. DNA from one of the nine transitional cell carcinomas contained an H-ras oncogene detectable by the NIH/3T3 transfection assay. Analysis of p21 ras proteins suggested that the activating mutation resided within codon 61 of the H-ras gene and that such activating mutations were not present in other tumors. In contrast to mutational activation of ras genes, enhanced expression of p21 was observed in all tumors examined by immunohistochemical techniques with the use of Formalin-fixed paraffin-embedded tissue sections and an anti-ras p21 antibody, RAP-5. Further histochemical analysis of bladder tissues at various stages of the BBN-induced carcinogenic process indicated that the enhanced expression of p21 appeared early; the reactivity with RAP-5 was observed in diffuse hyperplastic epithelia after 5 weeks of exposure to BBN. The frequency of ras oncogenes, activated either by point mutations or overexpression of p21, in BBN-induced rat bladder carcinomas has thus been shown to be similar to that observed in human bladder carcinomas. [J Natl Cancer Inst 1988;80:37–43]
Suppression of MicroRNA-9 by Mutant EGFR Signaling Upregulates FOXP1 to Enhance Glioblastoma Tumorigenicity
Authors: German G. Gomez, Stefano Volinia, Carlo M. Croce, Ciro Zanca, Ming Li, Ryan Emnett, David H. Gutmann, Cameron W. Brennan, Frank B. Furnari, Webster K. Cavenee
Journal: Cancer Research (2014)

The EGF receptor (EGFR) is amplified and mutated in glioblastoma, in which its common mutation (ΔEGFR, also called EGFRvIII) has a variety of activities that promote growth and inhibit death, thereby conferring a strong tumor-enhancing effect. This range of activities suggested to us that ΔEGFR might exert its influence through pleiotropic effectors, and we hypothesized that microRNAs might serve such a function. Here, we report that ΔEGFR specifically suppresses one such microRNA, namely miR-9, through the Ras/PI3K/AKT axis that it is known to activate. Correspondingly, expression of miR-9 antagonizes the tumor growth advantage conferred by ΔEGFR. Silencing of FOXP1, a miR-9 target, inhibits ΔEGFR-dependent tumor growth and, conversely, de-repression of FOXP1, as a consequence of miR-9 inhibition, increases tumorigenicity. FOXP1 was sufficient to increase tumor growth in the absence of oncogenic ΔEGFR signaling. The significance of these findings is underscored by our finding that high FOXP1 expression predicts poor survival in a cohort of 131 patients with glioblastoma. Collectively, these data suggest a novel regulatory mechanism by which ΔEGFR suppression of miR-9 upregulates FOXP1 to increase tumorigenicity.
How protective is the working time directive?: Two doctors mull over personal horror stories
Authors: Farheena N Mecci, Akheel A Syed
Journal: BMJ (2004)

EDITOR—As junior doctors of many years' standing (and several more ahead of us), with experience of work and training in two different parts of the world, we empathise with Abbasi's experiences as the European Working Time Directive was conceived.1 2

The thrills of 56 hour continuous shifts are highly overrated. …
Effects of Potassium on Blood Pressure Control
Authors: RICHARD L. TANNEN
Journal: Annals of Internal Medicine (1983)

Potassium depletion causes hypotension in normotensive animals and can lower the blood pressure in hypertensive animals and humans. Potential mechanisms for this hypotensive effect include a decrease in aldosterone levels, a decrease in vasopressin, and decreased responsiveness to the pressor effects of angiotensin II. The decreased response to angiotensin II could result from increased prostaglandin production, receptor occupancy, or a decrease in angiotensin II receptor affinity. A high potassium intake has no effect on blood pressure in normotensive animals and humans, but lowers blood pressure in those with hypertension. Mechanisms for this antihypertensive effect include natriuresis with sodium depletion, a decrease in plasma renin activity, an alteration in the neurogenic components of blood pressure regulation, and effects on resistance vessels related either to a high potassium concentration or to a decrease in the number of angiotensin II receptors.
CHANGE IN MITRAL VALVE CONFIGURATION AFTER UNDERSIZED SADDLE SHAPED MITRAL VALVE ANNULOPLASTY IN FUNCTIONAL MITRAL REGURGITATION: QUANTITATIVE ANALYSIS WITH REAL TIME THREE-DIMENSIONAL ECHOCARDIOGRAPHY AND THE SOFTWARE SYSTEM
Authors: Yasuhiro Shudo, Taichi Sakaguchi, Sokichi Kamata, Shigeru Miyagawa, Hiroyuki Nishi, Yasushi Yoshikawa, Yasushi Yoshikawa, Satsuki Fukushima, Shunsuke Saito, Kazuhiro Taniguchi, Koji Takeda, Takafumi Masai, Yoshiki Sawa
Journal: Journal of the American College of Cardiology (2011)
What about male specific HPV related diseases?
Authors: C. Foresta, A. Ferlin, A. Garolla
Journal: BMJ (2009)

The paper by Kim and Goldie and the editorial by Castle and Scarinci on the cost effectiveness of routinely vaccinating preadolescent boys against human papillomavirus (HPV) ignored some important aspects.1 2 Firstly, by vaccinating girls only, males …
NATIONAL VARIATION IN PRENATAL DIAGNOSIS OF CONGENITAL HEART DISEASE BY STATE AND LESION TYPE: AN ANALYSIS OF THE SOCIETY OF THORACIC SURGEONS CONGENITAL HEART SURGERY (STS-CHS) DATABASE
Authors: Michael D. Quartermain, Sara Pasquali, Kevin Hill, David Goldberg, James Huhta, Jeffrey Jacobs, Marshall Jacobs, Sung Hee Kim, Ross Ungerleider
Journal: Journal of the American College of Cardiology (2014)
Effects of Cyclosporine Therapy on Plasma Lipoprotein Levels
Authors: Christie M. Ballantyne
Journal: JAMA (1989)

Accelerated atherosclerosis is a leading cause of death in long-term survivors of heart and renal transplantation and may be exacerbated by the frequent occurrence of posttransplant hyperlipidemia. Attempts to define the mechanism for hyperlipidemia in transplant recipients are confounded by dramatic changes in metabolism and nutritional status after transplantation, as well as by treatment with multiple immunosuppressive and antihypertensive drugs. To avoid these pitfalls and to determine if cyclosporine alone adversely affects lipid levels, we measured lipoprotein levels in a prospective, double-blind, randomized, placebo-controlled trial of cyclosporine in 36 men with amyotrophic lateral sclerosis. Plasma total cholesterol, triglyceride, high-density lipoprotein cholesterol, and apolipoprotein B levels were measured at baseline, 2 weeks, 1 month, and 2 months. Significant increases of 21% in total cholesterol, 31% in low-density lipoprotein cholesterol, and 12% in apolipoprotein B levels occurred only in the cyclosporine group. Cyclosporine therapy alone adversely affects plasma lipoprotein levels by increasing total cholesterol levels, primarily due to an increase in low-density lipoprotein cholesterol level. (<i>JAMA</i>. 1989;262:53-56)
Outcome of Asthma and Wheezing in the First 6 Years of Life
Authors: Wayne J. Morgan, Debra A. Stern, Duane L. Sherrill, Stefano Guerra, Catharine J. Holberg, Theresa W. Guilbert, Lynn M. Taussig, Anne L. Wright, Fernando D. Martinez
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

The effect of early life wheezing on respiratory function and continued symptoms through adolescence has not been fully described. Using data from a population-based birth cohort in Tucson, Arizona, we previously described four phenotypes based on the occurrence of wheezing lower respiratory illnesses before age 3 yr and active wheeze at age 6 yr: never wheezers (n = 425), transient early wheezers (n = 164), persistent wheezers (n = 113), and late-onset wheezers (n = 124).We sought to determine the prognosis for these phenotypes, with reference to lung function and symptoms, through adolescence.Current wheeze was assessed by questionnaire, lung function was measured by conventional spirometry, and atopy was determined by skin prick tests.The prevalence of atopy and wheeze by age 16 yr was similar for never and transient wheezers and for persistent and late-onset wheezers. Both transient early, and persistent wheezers had significantly lower FEF(25-75) (-259 ml/s, p < 0.001, and -260 ml/s, p = 0.001, respectively), FEV1 (-75 ml, p = 0.02, and -87 ml, p = 0.03, respectively), and FEV1:FVC ratio (-1.9%, p = 0.002, and -2.5%, p = 0.001, respectively) through age 16 yr compared with never wheezers. Late-onset wheezers had levels of lung function similar to those of never wheezers through age 16 yr. There was no significant change in lung function among subjects with any of the four phenotypes, relative to their peers, from age 6 to 16 yr.Patterns of wheezing prevalence and levels of lung function are established by age 6 yr and do not appear to change significantly by age 16 yr in children who start having asthma-like symptoms during the preschool years.
TCT-477 Clinical characteristics, procedural and clinical outcome of patients treated with PCI for definitive stent thrombosis: a 12 years single centre experience
Authors: Eduard Fernandez-Nofrerias, Oriol Rodriguez-Leor, Xavier Carrillo, Josepa Mauri, Carlos Labata, Carolina Oliete, Carmen Rivas, Antoni Bayes-Genis
Journal: Journal of the American College of Cardiology (2013)