tbuckley/cabot-search huggingface dataset:
In vitro DNA synthesis by megaloblastic bone marrow: Effect of folates and cobalamins on thymidine incorporation and de novo thymidylate synthesis
Authors: Kshitish C. Das, Victor Herbert
Journal: American Journal of Hematology (1989)

Abstract The de novo pathway of thymidylate synthesis (i.e., methylation of dUMP to dTMP) is directly folate dependent and indirectly vitamin B 12 (cobalamins) dependent. In deficiency of these vitamins, this pathway is impaired, and exogenous deoxyuridine (dU) fails to suppress adequately in vitro incorporation of [ 3 H]thymidine ( 3 H‐TdR) into DNA via the salvage pathway (i.e., abnormal dU suppression). This abnormality is corrected by the addition of folate compounds (analogues) and/or vitamin B 12 depending on the nature of the underlying deficiency. We studied the effects of addition of PteGlu, 5‐methyl THF (5‐CH3‐FH4), 5‐formyl‐THF (5‐CHO‐FH4), and hydroxy‐cobalamin (OH‐cbl) on 3 H‐TdR incorporation into DNA and thymidine kinase activity (salvage pathway), and on [ 3 H]deoxyuridine ( 3 H‐dU) incorporation and dU suppression values (de novo pathway) in cultures of normal and megaloblastic bone marrows. The results showed that 3 H‐TdR incorporation into DNA and the salvage enzyme, thymidine kinase, activity were greater and 3 H‐dU incorporation into DNA less in megaloblastic cells as compared with normal cells. The addition of folates significantly reduced 3 H‐TdR incorporation and thymidine kinase activity and enhanced 3 H‐dU incorporation in folate and vitamin B 12 ‐deficient cells except that 5‐CH3‐FH4 had no effect on vitamin B 12 ‐deficient cells. None of these additives had any significant effect on normal cells. This study also showed that the addition of the deficient vitamin(s) to the “control tubes” in the dU suppression test is inappropriate, as these vitamins may at least partially correct the defect in cellular DNA synthesis caused by the deficiences of these vitamins and may mask these deficiencies in the results of the in vitro correction of the dU suppression abnormalities in mild cases of megaloblastic anemia.
A novel protein-repellent dental composite containing 2-methacryloyloxyethyl phosphorylcholine
Authors: Ning Zhang, Chen Chen, Mary AS Melo, Yu-Xing Bai, Lei Cheng, Hockin HK Xu
Journal: International Journal of Oral Science (2015)

Secondary caries due to biofilm acids is a primary cause of dental composite restoration failure. To date, there have been no reports of dental composites that can repel protein adsorption and inhibit bacteria attachment. The objectives of this study were to develop a protein-repellent dental composite by incorporating 2-methacryloyloxyethyl phosphorylcholine (MPC) and to investigate for the first time the effects of MPC mass fraction on protein adsorption, bacteria attachment, biofilm growth, and mechanical properties. Composites were synthesized with 0 (control), 0.75%, 1.5%, 2.25%, 3%, 4.5% and 6% of MPC by mass. A commercial composite was also tested as a control. Mechanical properties were measured in three-point flexure. Protein adsorption onto the composite was determined by the microbicinchoninic acid method. A human saliva microcosm biofilm model was used. Early attachment at 4 h, biofilm at 2 days, live/dead staining and colony-forming units (CFUs) of biofilms grown on the composites were investigated. Composites with MPC of up to 3% had mechanical properties similar to those without MPC and those of the commercial control, whereas 4.5% and 6% MPC decreased the mechanical properties (P<0.05). Increasing MPC from 0 to 3% reduced the protein adsorption on composites (P<0.05). The composite with 3% MPC had protein adsorption that was 1/12 that of the control (P<0.05). Oral bacteria early attachment and biofilm growth were also greatly reduced on the composite with 3% MPC, compared to the control (P<0.05). In conclusion, incorporation of MPC into composites at 3% greatly reduced protein adsorption, bacteria attachment and biofilm CFUs, without compromising mechanical properties. Protein-repellent composites could help to repel bacteria attachment and plaque build-up to reduce secondary caries. The protein-repellent method might be applicable to other dental materials. A new protein-repelling dental composite prevents bacterial attachment and plaque build-up while retaining its mechanical strength. Secondary tooth decay following tooth restoration is responsible for the replacement of almost half of all dental restorations within 10 years. An international team led by Hockin HK Xu at the University of Maryland now show that incorporating up to 3% 2-methacryloyloxyethyl phosphorylcholine (MPC) into a dental resin significantly repelled the deposit of salivary proteins that act as anchor points for bacterial attachment. After 48-h exposure to a solution that simulates the oral environment, the MPC resin had less bacterial coverage than controls, and its load-bearing capability was unaffected. MPC has already been incorporated successfully into several medical devices. This study suggests a promising new use in dental composites with the potential to prevent secondary tooth decay.
Reply to Dr. Froehlich
Authors: V. Terruzzi, F. Radaelli, G. Minoli
Journal: Endoscopy (2006)

We are grateful to Dr. Froehlich for his comments [1] and his interest in our article [2]. Dr. Froehlich considers that the left lateral patient position during endoscopic retrograde cholangiopancreatography (ERCP) is a valid alternative to the prone position, since it is probably more comfortable for the patient and carries a lower risk of aspiration. Unfortunately, we cannot provide any comments on this opinion, as we have no experience with the position (the local endoscopy suite is not equipped with a mobile radiology system, which is essential for working with the patient on the left side).
Cochrane at crossroads over drug company sponsorship
Authors: R. Moynihan
Journal: BMJ (2003)

Can independent scientific evaluation be sponsored by vested interests? The Cochrane Collaboration's decision on this question at its annual colloquium next week could have a big effect on its future 

As it turns 10 this month, the Cochrane Collaboration is at a crossroads, with its supporters deeply divided over whether to embrace drug company sponsorship. In just a decade the collaboration has fundamentally changed the way questions are asked and answered about what works and what doesn't in health care. Its rigorous methods for systematically reviewing and synthesising the best evidence have underpinned a collective move towards evidence based decision making among health professionals, policy makers, and consumers. Now, against a backdrop of growing global entanglement between doctors and drug companies, the collaboration must decide whether it can accept industry funding without compromising its reputation for integrity and independence.

Delegates to next week's annual Cochrane Colloquium in Barcelona will debate the thorny question of conflict of interest at the opening plenary session and in a series of high level meetings.

When the collaboration last got together in Melbourne in March, two senior professors of medicine ended up in a serious discussion about the issue, pre-empting the forthcoming conflict in Barcelona. One thought that the organisation might not be able to remain viable without industry support, whereas the other believed that the inevitable industry influence would destroy Cochrane's credibility.

Drummond Rennie, codirector of the Cochrane Center in San Francisco and a deputy editor of JAMA, thinks industry funding would be a catastrophe for Cochrane. “It would be far better that some reviews are not done than reviewers accept money from interested parties,” he said. In contrast, Peter Tugwell, a member of Cochrane's international steering committee and professor of medicine at the University of Ottawa, is comfortable with reviews being funded by …
PROGNOSTIC VALUE OF INCREMENTAL PACING MANEUVER FOR LONG-TERM RECURRENCES AFTER TYPICAL FLUTTER ABLATION
Authors: Ermengol Valles, Victor Bazan, Miguel Cainzos, Begoña Benito, Miguel Eduardo Jauregui, Jordi Bruguera, Julio Martí
Journal: Journal of the American College of Cardiology (2013)
Evolution of academic surgery.
Authors: A. P. Forrest
Journal: BMJ (1989)

Sitting by the River Dordogne on 14 July, I could not do other than think about the storming of the Bastille, which heralded the start of the French Revolution 200 years ago.Accounts in the English language concentrate on the years of terror rather than on t-he desperate need for change; for France was, in the words of Dickens, rolling "with exceeding smoothness downhill."'Many believe that in Britain clinical academic medicine also is doing just that.Britain abhors violent change, priding itself on evolution not revolution.This may produce the desired effect but only when those to be changed benefit, as in the remarkable social developments during my lifetime.Otherwise the process of evolution carries the risk of the "add on," much of the old, not necessarily the best, being maintained alongside the new, leading to waste, uncertainty, and, at times, chaos.What better example than our refusal to revolve our system ofmeasurement, so that whether buying petrol, food, or planning travel, we are unnecessarily troubling our minds with conver- sions between litres and gallons, kilograms and pounds, and kilometres and miles.Our European neighbours smile but cannot readily understand.Those who practise medicine use the most radical of invasive and extirpative procedures yet are funda- mentally conservative.Only too often the old is discarded only when those wishing to retain it have ceased to influence events.The process is expensive and in academic circles may cost more than the future permits.Such has been the case in medical education.For example, in surgery specialisation has changed the needs of postgraduate training.General surgery with its subspecialties is now but one of a series of major surgical specialties demanding specialist knowledge and skills.It no longer represents the core knowledge required by all surgeons.
India's consumer groups call for more rational prescribing
Authors: G. Mudur
Journal: BMJ (1996)

Consumer health groups in India have told doctors to prescribe drugs rationally or be prepared to be sued in consumer courts for medical negligence. The warning, issued through a press conference last month by a consortium of non-government consumer interest organisations, follows a survey of medical prescriptions that showed doctors to be writing irrational prescriptions.

The survey, conducted by the Voluntary Consumer Action Network, a consortium of around 20 consumer and health organisations, showed that many doctors prescribe tonics, vitamin formulations, and expensive drugs including third generation antibiotics when they are not indicated. General practitioners …
A critical role for transforming growth factor-beta in donor transfusion-induced allograft tolerance.
Authors: R Josien, P Douillard, C Guillot, M Müschen, I Anegon, J Chetritt, S Menoret, C Vignes, J P Soulillou, M C Cuturi
Journal: Journal of Clinical Investigation (1998)

Donor-specific (DST) or nonspecific blood transfusions administered before transplantation can enhance survival of vascularized allografts both in humans and animals but the immunological mechanisms of this effect remain unclear. We have analyzed the expression and the role of endogenous TGF-beta1 in a model of heart allograft tolerance, induced by pregraft DST in adult rats. We reported previously that this tolerance occurs despite a strong infiltration of leukocytes into the graft that are unable to produce both Th1- and Th2-related cytokines in vivo. Allografts from DST-treated rats express high levels of TGF-beta1 mRNA and active protein. This phenomenon is correlated with the rapid infiltration of leukocytes producing high amounts of TGF-beta1. TGF-beta1-producing cells are virtually absent among early infiltrating cells in rejected grafts but are found at a later time point. The induction of allograft tolerance in vivo is abrogated by administration of neutralizing anti-TGF-beta mAb. Moreover, overexpression of active TGF- beta1 in heart allografts using a recombinant adenovirus leads to prolonged graft survival in unmodified recipients. Taken together, our results identify TGF-beta as a critical cytokine involved in the suppression of allograft rejection induced by DST and suggest that TGF-beta-producing regulatory cells are also involved in allograft tolerance.
Alterations in the functional expression of receptors on cirrhotic rat hepatocytes
Authors: Carolyn N. d'Arville, Mysan Le, Thomas M. Kloppel, Francis R. Simon
Journal: Hepatology (1989)

Reduced hepatic uptake and clearance of macromolecules in liver cirrhosis is due to two major factors: increased diffusional barriers, resulting primarily from the deposition of excessive connective tissue in the space of Disse, and hepatocellular dysfunction, manifested by receptor and/or postreceptor defects. To probe the mechanisms underlying hepatocellular dysfunction in liver cirrhosis, we have investigated receptor-ligand interactions for asialoorosomucoid, insulin and epidermal growth factor in hepatocytes isolated from the livers of rats chronically exposed to phenobarbital and carbon tetrachloride for up to 12 weeks. Viable cells were allowed to attach at 37 degrees C and the high-affinity cell surface binding sites for each ligand were assessed at 4 degrees C in the presence of [125I]-ligand. In parallel incubations, digitonin (0.055%) was added to the binding medium to assess total cellular binding sites. Results demonstrated that chronic treatment of rats with phenobarbital increased hepatocyte asialoorosomucoid surface receptor affinity (p less than 0.05) but had no affect on the number of asialoglycoprotein binding sites. Treatment with CCl4 and phenobarbital significantly reduced the number of surface binding sites for asialoorosomucoid (p less than 0.05) and epidermal growth factor (p less than 0.02), although this treatment had no effect on either the binding affinity or the number of binding sites for insulin. The decrease in cell surface binding sites for asialoorosomucoid and epidermal growth factor was not due to a redistribution of the surface sites to intracellular locations, since the total number of cellular binding sites also was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
Abstract 2241: SHH pathway in uterine mesenchymal tumors
Authors: Natalia Garcia, Faila C. Souza, Nilo Bozzini, Glauco Baiocchi, Isabela W. Cunha, Fernando A. Soares, Edmund C. Baracat, Kátia C. Carvalho
Journal: Cancer Research (2014)

Abstract Background: Uterine leiomyoma (ULM) and leiomyosarcoma (ULMS) are smooth muscle tumors with distinct clinical behavior that can cause infertility and even lead to death. Little is known about the factors that influence these tumors biology. Identification of new molecular markers can help in the differential diagnosis between ULM from low grade ULMS. It was demonstrated that activation of the Sonic Hedgehog (SHH) signaling pathway is related to the development of several tumors, through its activity in the cell proliferation and differentiation. Here, we investigated the protein expression profile of SHH, PTCH1, SMO and GLI1 both ULM (including non-typical leiomyomas) and ULMS. Methods: We selected 57 samples of ULMS and 30 samples of ULM (10 samples non-typical - ULMA). All tissues were used in TMA construction. Immunohistochemistry reaction was performed using monoclonal antibody against SHH (1:50), PTCH (1:100), SMO (1:100) and GLI-1 (1:200) using sodium citrate pH 6,0 in pressure cooker. Results were evaluated by Aperio® automated method. Results: Our preliminary data showed similar protein profile between the leiomyosarcoma and non-typical leiomyoma. GLI 1 and PTCH showed higher expression compared to leiomyoma and myometrium (p&amp;lt;0.05). SMO, and SHH showed higher expression only in leiomyossarcomas (p&amp;lt;0.05). Conclusions: Ours preliminary results showed that expression of Sonic Hedgehog pathway members might play an important role in uterine smooth tumors, since ULMS showed higher levels of these proteins. However, the role of these proteins interactions must be clarified. Citation Format: Natalia Garcia, Faila C. Souza, Nilo Bozzini, Glauco Baiocchi, Isabela W. Cunha, Fernando A. Soares, Edmund C. Baracat, Kátia C. Carvalho. SHH pathway in uterine mesenchymal tumors. [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 2241. doi:10.1158/1538-7445.AM2014-2241
Garnering Support for Advance Care Planning
Authors: Terri R. Fried
Journal: JAMA (2010)

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
The lupus book
Authors: L. EULLER-ZIEGLER
Journal: Annals of the Rheumatic Diseases (2000)

The lupus book . Daniel J Wallace. (Pp 271; US$25.) Oxford: Oxford University Press, 2000. ISBN 0-19-513281-5.

Lupus is a common and complex disease. This book is written for patients, but physicians and health professionals dealing with systemic lupus erythematosus will also find it useful. The author's aim is to provide readers with all necessary information and practical advice.

The first part deals with the definition, a brief historical review, and the epidemiology of the disease (the prevalence is probably still underestimated). The second is devoted to the mechanisms …
Repeated arthralgia associated with granulocyte colony stimulating factor administration
Authors: A Tsukadaira
Journal: Annals of the Rheumatic Diseases (2002)

We report the case of a 69 year old man with non-small lung cancer, who developed arthralgia and myalgia twice during chemotherapy using 210 mg/day of paclitaxel and 110 mg/day of nedaplatine for every four week cycle. After starting chemotherapy, arthralgia and myalgia accompanied by rising fever suddenly occurred on the fifth consecutive day of subcutaneous administration of 100 μg/day of granulocyte colony stimulating factor (G-CSF; lenograstim). To determine the cause of the polyarthralgia we carried out arthroscopy in the most symptomatic joint. The left elbow and left hand joints were chosen for the biopsy. Microscopic findings of formalin fixed synovial tissue showed severe inflammatory infiltration accompanied by foreign body-type giant cell reaction, but no crystals or rheumatoid nodules (fig 1).



 Figure 1  
Microscopic findings …
Effect of rubella vaccination programme in schools on rubella immunity in a general practice population
Authors: S J Steele, F. Shenfield
Journal: BMJ (1982)

GPs in communities most affected by redun- dancies, nevertheless, the system of medical care survives intact.The wisdom of those who understood that service, free at the point of care, was the most important principle of medical care is never more evident than when another system without that guiding principle is subjected to similar stresses.I do not know which of my patients is delaying coming to see me because he is out of work.I am sure there are many who daily weigh their own long-term health and that of their family against immediate needs of transportation, housing, and food.Nearly every community- based physician in the US acknowledges this choice for patients.It is also a choice which in a Western and industrialised country in the late twentieth century should never need exist if the medical care system were indeed a humane one.
Hemophilia, Beaten on One Front, Is Beset on Others
Authors: Marsha F. Goldsmith
Journal: JAMA (1986)

"VISITS BY CLERGY in the middle of the night mending the feelings, visits by physicians in the middle of the night providing the morphine," recalls Donald S. Goldman, president of the National Hemophilia Foundation (NHF), concerning his childhood bouts with bleeding episodes. Speaking at a meeting in Washington, DC, commemorating the tenth anniversary of the Federal Hemophilia Treatment Centers Program, Goldman, an attorney from Livingston, NJ, said the program has so greatly improved the life of persons with hemophilia that "cold hard data don't reflect its significance." But the data do make clear the success of the 22 primary and 60 affiliate comprehensive care centers, in which about 70% of the 20 000 Americans with hemophilia are enrolled. A primary task of the centers is instruction and support of patients in carrying out home infusion of clotting factor, which means less time spent in hospitals and a major reduction in
Different Contributions of Endothelin-A and Endothelin-B Receptors in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Hearts
Authors: Satoshi Yamamoto, Noriko Matsumoto, Mitsuo Kanazawa, Marie Fujita, Masanori Takaoka, Cheryl E. Gariepy, Masashi Yanagisawa, Yasuo Matsumura
Journal: Circulation (2005)

Background— Endothelin (ET)-1 and norepinephrine (NE) are involved in myocardial ischemia/reperfusion injury. We investigated the role of ET-1 in ischemia/reperfusion–induced NE overflow and cardiac dysfunction using a selective ET A receptor antagonist (ABT-627), a selective ET B receptor antagonist (A-192621), and the spotting lethal ( sl ) rat, which carries a naturally occurring deletion in the ET B receptor gene. Methods and Results— According to the Langendorff technique, isolated hearts were subjected to 40-minute global ischemia followed by 30-minute reperfusion. In Sprague-Dawley rat hearts, ischemia/reperfusion–induced cardiac dysfunctions such as decreased left ventricular developed pressure and coronary flow and increased left ventricular end-diastolic pressure were worsened by treatment with A-192621. This agent enhanced excessive NE overflow in the coronary effluent from the postischemic heart. In contrast, treatment with ABT-627, in the absence or presence of A-192621, significantly improved postischemic cardiac dysfunction and markedly suppressed NE overflow to the same extent. Postischemic cardiac dysfunction and NE overflow in the heart of ET B receptor–deficient homozygous ( sl / sl ) rats were highly observed compared with cases in wild-type rats, and exaggerated responses to ischemia/reperfusion in sl / sl rats were abolished by ABT-627 treatment. Exogenously applied ET-1 produced severe cardiac dysfunction and a significant increase in NE overflow in a dose-dependent manner, but these responses were markedly suppressed in the presence of 5- N -ethyl- N -isopropyl-amiloride, an inhibitor of the Na + /H + exchanger (NHE). Conclusions— Pharmacological blockade or genetic deficiency of ET B receptors is detrimental to the postischemic heart, and exaggerated cardiac pathology under the above conditions is mediated by ET A receptor activation. ET A /NHE-mediated excessive NE overflow is contributive, at least in part, to postischemic cardiac dysfunction in rats.