tbuckley/cabot-search huggingface dataset:
1150 Dynamics and early diagnosis of HBV resistance to lamivudine: a thorough quasispecies analysis
Authors: C PALLIER, L CASTERA, A SOULIER, B PELLEGRIN, R BRILLET, J METREAU, D DHUMEAUX, J PAWLOTSKY
Journal: Hepatology (2003)

The (-) enantiomer of 3'-thiacytidine (lamivudine) has been found to be a potent inhibitor of hepatitis B virus (HBV) and human immunodeficiency virus (HIV) replication. Mutation of methionine to valine or isoleucine at the YMDD (tyrosine, methionine, aspartate, aspartate) motif of the HIV reverse transcriptase has been shown to be responsible for lamivudine resistance in HIV. The hepadnaviruses also have the YMDD motif in their DNA polymerase. Therefore, it is possible that hepadnaviruses could develop lamivudine resistance by a similar mutation at this motif. We analyzed the HBV from a liver transplantation patient who developed recurrent HBV viremia during lamivudine treatment. The polymerase gene was amplified by polymerase chain reaction (PCR), and the region coding for the YMDD motif was sequenced. The pretreatment HBV sequence coded for YMDD, while the lamivudine-resistant mutant HBV coded for YIDD (tyrosine, isoleucine, aspartate, aspartate). With the documented changes in the YMDD motif of lamivudine-resistant HIV, it is likely that the methionine-to- isoleucine mutation in the YMDD motif of the HBV polymerase contributes significantly to the lamivudine-resistance of HBV isolated from this patient. (Hepatology 1996 Sep;24(3):714-7)
Hospitals reject proposed tariff cuts for 2015-16 over safety fears
Authors: G. Iacobucci
Journal: BMJ (2015)

NHS hospitals in England have taken the unprecedented step of rejecting the proposed national payment tariff for 2015-16 after concluding that they could “no longer guarantee sustainable and safe care” under the financial terms being offered.

NHS Providers, the organisation that represents hospital, community, ambulance, and mental health trusts, said that 75% of its more than 200 members had voted to reject the tariff for 2015-16, as the proposed settlement required “unachievable efficiency savings” and would put the care of patients at risk. It said that the veto was a “last resort” but that it was imperative that service providers were “fully and properly paid” for the care they provided. It pointed out that 80% of England’s hospitals were already in financial deficit and that the 2015-16 offer would lead to £1.7bn (€2.3bn; $2.6bn) being taken away from NHS providers, despite an expected 4% increase in demand. …
Antigen‐presenting cell function of epidermal cells activated by hapten application
Authors: None Nakano
Journal: British Journal of Dermatology (1998)

Exposure to haptens initiates a series of immune and inflammatory reactions that cause migration of epidermal Langerhans cells (LC) to draining lymph nodes, antigen processing, and presentation to T cells. In the present study, the antigen-presenting cell (APC) function of epidermal cells (EC) following hapten application was determined using a cell transfer system. This function of EC in inducing contact sensitivity (CS) in the recipient mice appeared as early as 6 h after hapten painting, and reached its maximum at 24 h. The amount of hapten on EC did not correlate with the function, i.e. the amount retained on the cells was greatest immediately after hapten painting and decreased over time. Several experiments were performed to identify the cell type responsible for the APC function. Through immunomagnetic bead separation, the APC function was detected in Ia- EC, as well as in unfractionated EC from hapten-painted mice. A purified population of Ia+ cells (LC) induced CS with much less efficiency than unseparated cells. Depletion of LC by anti-Ia monoclonal antibody (mAb) and complement-mediated lysis did not impair the APC function, whereas it was reduced by the depletion of Thy-1+ cells by anti-Thy-1 mAb and complement-mediated lysis. Moreover, adherent cells that were harvested from a 48-h culture of EC obtained from hapten-painted skin, and were free of contaminating LC and gamma omega T cells, had a strong capacity to induce CS. These findings indicate that keratinocytes (KC) acquire APC function as well as LC, with hapten application. Phenotypically increased expression of intercellular adhesion molecule-1 (ICAM-1) and Thy-1 on EC was observed following hapten application, whereas expression of Ia and B7/BB1 was unaltered. The APC function of EC from hapten-painted skin was dependent on ICAM-1 and Thy-1 expression, as the mAbs for these molecules reduced the capacity to induce CS. These results suggest that hapten application induces not only LC but also KC to mature functionally and become potent APCs, and that these KC exert the APC function complementarily at local sites following the migration of LC with potent APC function to the draining lymph node.
Hydroxyurea and Sickle Cell Disease
Authors: Debra L. Weiner, Carlo Brugnara
Journal: JAMA (2003)

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
Homozygous Type II Hyperlipoproteinemia Treatment
Authors: John F. Balfour
Journal: JAMA (1974)

Dietary treatment was minimally effective in two children with homozygous type II hyperlipoproteinemia who had no evidence of atherosclerosis. Neither patient could tolerate cholestyramine resin in therapeutic doses. A partial ileal bypass operation was performed on each child, aged 10 and 8 years old. Although plasma cholesterol levels were not reduced to accepted normal values, they were reduced by 42% and 33%, respectively, below the average preoperative postdietary levels. Three years after the operations, neither child shows adverse effects on health and growth, and there is still no evidence of atherosclerosis.
β-Blockade and Recurrent Myocardial Infarction
Authors: Richard J. Jones
Journal: JAMA (1982)

In a recent issue ofThe Journal,<sup>1</sup>there was presented a randomized controlled trial on a treatment for arteriosclerotic heart disease that is finally definitive: it is the final report of the National Heart, Lung, and Blood Institute's multicentered, randomized, double-blind trial of propranolol hydrochloride in patients who have recovered from an acute myocardial infarction. The results are favorable to propranolol use in such patients. One may be sure that the statistics were beyond challenge, because the trial was finished prematurely, nine months ahead of its anticipated date of termination. Previously, there were good reasons to think that β-blockade might be beneficial in patients who had coronary heart disease, but the benefits measured in terms of mortality were so clear-cut that one must accept the recommendation of the group: "The use of propranolol in patients with no contraindications to β-blockade who have had a recent myocardial infarction is recommended
A common alternative splicing signature is associated with SF3B1 mutations in malignancies from different cell lineages
Authors: D Gentien, O Kosmider, F Nguyen-Khac, B Albaud, A Rapinat, A G Dumont, F Damm, T Popova, R Marais, M Fontenay, S Roman-Roman, O A Bernard, M-H Stern
Journal: Leukemia (2014)
Detection of CBP rearrangements in acute myelogenous leukemia with t(8;16)
Authors: RH Giles, JG Dauwerse, C Higgins, F Petrij, JW Wessels, GC Beverstock, H Döhner, M Jotterand-Bellomo, JHF Falkenburg, RM Slater, G-J B van Ommen, A Hagemeijer, BA van der Reijden, MH Breuning
Journal: Leukemia (1997)
Preservation of myofilament calcium responsiveness underlies protection against myocardial stunning by ischemic preconditioning
Authors: N Pérez
Journal: Cardiovascular Research (1999)

Objective: Whereas diminution of infarct size by ischemic preconditioning (IP) is well-accepted, protection against stunning is controversial. Since stunning is characterized by decreased myofilament Ca2+ responsiveness, we investigated whether IP would preserve myofilament responsiveness in a model of stunning. Methods: Rat hearts were retrogradely perfused with Krebs–Henseleit (K–H) solution for 20 min and then subjected to 20 min of no-flow global ischemia, followed by 20 min of reperfusion in the absence (stunning) or in the presence (IP) of a previous 5-min period of ischemia followed by 15 min of reperfusion. A group of hearts perfused under non-ischemic conditions served as control. Thin ventricular trabeculae were dissected from each of the experimental groups and loaded with fura-2 to measure intracellular calcium concentration ([Ca2+]i) and developed force. Results: After 20 min of reperfusion, left ventricular developed pressure decreased in stunned hearts to 61±5% of control (P<0.01), whereas recovery was complete in the IP hearts (97±4%). Steady-state [Ca2+]i–force relationships revealed a decreased maximal Ca2+-activated force in stunned hearts relative to control, but no change in the IP group. The Ca2+ required for 50% activation increased in stunning but not in IP. Conclusions: These results show that the decrease in myofilament responsiveness that characterizes stunning is prevented by ischemic preconditioning.
PHYSICIANS IN RURAL COMMUNITIES
Authors: Willard C. Stoner
Journal: JAMA (1927)

<h3>To the Editor:</h3> —I am interested in the discussions that arise from time to time in reference to the present dearth of physicians in rural communities in comparison with the past, and in the suggestions for the solution of the problem. I refer particularly to the editorial of February 12 and Dr. Pusey's discussion of the survey which he made. We lose sight of the changing conditions and make erroneous comparisons. The country red school house where many of us once attended and taught is almost obsolete. The centralized school has replaced the country school, lessened the teaching personnel, established efficiency, and changed the educational problem of the rural community. Good roads and automobile transportation have made it possible. The development of hospitals in county seat towns and other towns of size to warrant hospitals is furnishing in medicine very largely that which the centralized school has furnished in education.
Source of raised serum estrogens in male rats with portal bypass.
Authors: G C Farrell, A Koltai, M Murray
Journal: Journal of Clinical Investigation (1988)

We sought to establish the mechanism for the raised serum estrogen levels that occur in male rats with portal hypertension and resultant portal bypass. Using the portal vein ligated (PVL) rat model, we evaluated plasma steroid hormone concentrations, metabolic clearance rate (MCR) of estradiol, and hepatic metabolism of androstenedione to estrogens and other products. In contrast to serum testosterone levels that were reduced, serum androstenedione levels were normal in the PVL rat. Estradiol MCR was measured by a constant intravenous infusion technique and was found to be similar in PVL and control animals. Androstenedione MCR was determined during constant intravenous infusion of [3H]androstenedione, and the resultant radiolabeled steroids present in plasma were separated by thin layer chromatography. The MCR of androstenedione was not diminished in PVL rats compared with controls. However, there was a sevenfold increase in the plasma estradiol derived from [3H]androstenedione in rats with portal bypass. Examination of radiolabel excreted in bile during infusion of [3H]androstenedione showed that 25-46% of this steroid was converted to estradiol in PVL rats compared with less than 3% in control male rats (P less than 0.001). Moreover, there was a selective reduction in the excretion of 16 alpha-hydroxyandrostenedione, a finding which suggested that the metabolism of androstenedione via this pathway was decreased. Androstenedione 16 alpha-hydroxylation is known to be catalyzed by a male-specific cytochrome P-450 isoform, P-450UT-A. We conclude that raised plasma estradiol levels after portal bypass in male rats are due to increased production rates, resulting in turn from enhanced aromatization of androstenedione to estradiol. On the basis of the observed specific changes in androstenedione hydroxylation pathways, it is proposed that alterations in levels of sex-specific forms of cytochrome P-450 occur in male rats with portal bypass and could account for the enhanced formation of estradiol.
Human Langerhans cells use an IL-15R-α/IL-15/pSTAT5-dependent mechanism to break T-cell tolerance against the self-differentiation tumor antigen WT1
Authors: Emanuela Romano, Jesse W. Cotari, Rosa Barreira da Silva, Brian C. Betts, David J. Chung, Francesca Avogadri, Mitsu J. Fink, Erin T. St Angelo, Babak Mehrara, Glenn Heller, Christian Münz, Gregoire Altan-Bonnet, James W. Young
Journal: Blood (2012)
Addiction to Sextromoramide
Authors: B. A. M. Thompson
Journal: BMJ (1964)

31 October 164Correspondence & MEDICALJOUNA deemed adequate, without definition of the circumstances, which might be, for all one can tell, during attendance as an out-patient.It does seem strange that, during such a " rigidly designed and strictly controlled " trial, one of the control group should have " died suddenly at home before completion of treat- ment " ; or that histological confirmation of the disease at biopsy has not been offered in either the control or treatment group.
Risk of venous thromboembolism from use of oral contraceptives containing different progestogens and oestrogen doses: Danish cohort study, 2001-9
Authors: O. Lidegaard, L. H. Nielsen, C. W. Skovlund, F. E. Skjeldestad, E. Lokkegaard
Journal: BMJ (2011)

To assess the risk of venous thromboembolism from use of combined oral contraceptives according to progestogen type and oestrogen dose.National historical registry based cohort study.Four registries in Denmark.Non-pregnant Danish women aged 15-49 with no history of thrombotic disease and followed from January 2001 to December 2009.Relative and absolute risks of first time venous thromboembolism.Within 8,010,290 women years of observation, 4307 first ever venous thromboembolic events were recorded and 4246 included, among which 2847 (67%) events were confirmed as certain. Compared with non-users of hormonal contraception, the relative risk of confirmed venous thromboembolism in users of oral contraceptives containing 30-40 µg ethinylestradiol with levonorgestrel was 2.9 (95% confidence interval 2.2 to 3.8), with desogestrel was 6.6 (5.6 to 7.8), with gestodene was 6.2 (5.6 to 7.0), and with drospirenone was 6.4 (5.4 to 7.5). With users of oral contraceptives with levonorgestrel as reference and after adjusting for length of use, the rate ratio of confirmed venous thromboembolism for users of oral contraceptives with desogestrel was 2.2 (1.7 to 3.0), with gestodene was 2.1 (1.6 to 2.8), and with drospirenone was 2.1 (1.6 to 2.8). The risk of confirmed venous thromboembolism was not increased with use of progestogen only pills or hormone releasing intrauterine devices. If oral contraceptives with desogestrel, gestodene, or drospirenone are anticipated to increase the risk of venous thromboembolism sixfold and those with levonorgestrel threefold, and the absolute risk of venous thromboembolism in current users of the former group is on average 10 per 10,000 women years, then 2000 women would need to shift from using oral contraceptives with desogestrel, gestodene, or drospirenone to those with levonorgestrel to prevent one event of venous thromboembolism in one year.After adjustment for length of use, users of oral contraceptives with desogestrel, gestodene, or drospirenone were at least at twice the risk of venous thromboembolism compared with users of oral contraceptives with levonorgestrel.
Lack of effect of acyclovir on postherpetic neuralgia.
Authors: M. W. McKendrick, J. I. McGill, M. J. Wood
Journal: BMJ (1989)

cytotoxic drugs, just when the risk of emesis is highest.Conversely, in the placebo group antiemetic drug concentrations would have been lower during the period of maximum risk of emesis and approaching a steady state only the next day.Other drugs likely to accumulate during pretreatment may also be suitable, and their pharmacokinetics should be studied.We thank Janssen Pharmaceutical Limited, who generouslv supplied the domperidone and dexamethasone with matched placebo.1
Corneal Angiography for Guiding and Evaluating Fine-Needle Diathermy Treatment of Corneal Neovascularization
Authors: Natasha Spiteri, Vito Romano, Yalin Zheng, Sohraab Yadav, Rahul Dwivedi, Jern Chen, Sajjad Ahmad, Colin E. Willoughby, Stephen B. Kaye
Journal: Ophthalmology (2015)
Control of Autophagic Cell Death by Caspase-10 in Multiple Myeloma
Authors: Laurence Lamy, Vu N. Ngo, N.C. Tolga Emre, Arthur L. Shaffer, Yandan Yang, Erming Tian, Vinod Nair, Michael J. Kruhlak, Adriana Zingone, Ola Landgren, Louis M. Staudt
Journal: Cancer Cell (2013)
MAFG Is a Transcriptional Repressor of Bile Acid Synthesis and Metabolism
Authors: Thomas Q. de Aguiar Vallim, Elizabeth J. Tarling, Hannah Ahn, Lee R. Hagey, Casey E. Romanoski, Richard G. Lee, Mark J. Graham, Hozumi Motohashi, Masayuki Yamamoto, Peter A. Edwards
Journal: Cell Metabolism (2015)
Treatment of medulloblastoma with postoperative chemotherapy alone: an SFOP prospective trial in young children
Authors: Jacques Grill, Christian Sainte-Rose, Anne Jouvet, Jean-Claude Gentet, Odile Lejars, Didier Frappaz, François Doz, Xavier Rialland, Fabienne Pichon, Anne-Isabelle Bertozzi, Pascal Chastagner, Dominique Couanet, Jean-Louis Habrand, Marie-Anne Raquin, Marie-Cécile Le Deley, Chantal Kalifa
Journal: The Lancet Oncology (2005)
Control of Medical Appliances
Authors: N. P. Henderson
Journal: BMJ (1945)

<h3>Abstract</h3> The endothelium responds to a multitude of chemical and mechanical factors in regulating vascular tone, angiogenesis, blood pressure and blood flow. The endothelial volume regulatory anion channel (VRAC) has been proposed to be mechano-sensitive, to activate in response to fluid flow/hydrostatic pressure and putatively regulate vascular reactivity and angiogenesis. Here, we show that the Leucine Rich Repeat Containing Protein 8a, LRRC8a (SWELL1) functionally encodes VRAC in human umbilical vein endothelial cells (HUVECs). Endothelial SWELL1 (SWELL1) expression positively regulates AKT-eNOS signaling while negatively regulating mTOR signaling, via a SWELL1-GRB2-Cav1-eNOS signaling complex. Endothelium-restricted SWELL1 KO (SWELL1 KO) mice exhibit enhanced tube formation from ex-vivo aortic ring explants in matrigel angiogenesis assays, develop hypertension in response to chronic angiotensin II infusion and have impaired retinal blood flow with both diffuse and focal blood vessel narrowing in the setting of Type 2 diabetes (T2D). These data demonstrate that SWELL1 antithetically regulates AKT-eNOS and mTOR signaling in endothelium and is required for maintaining vascular function, particularly in the setting of T2D.
337 Celecoxib, a selective cyclooxygenase-2 inhibitor, shows anti-proliferative, pro-apoptotic and anti-fibrotic effects in human hepatic stellate cells
Authors: Y.-H. Paik, K.-S. Lee, H.-J. Lee, S.-H. Kang, S.-H. Ahn, K.-H. Han, C.-Y. Chon, Y.-M. Moon
Journal: Journal of Hepatology (2006)
Specialised care for early psychosis
Authors: Tom K J Craig
Journal: BMJ (2005)

Monitoring global health Problems are primarily nationalEditor-Murray et al urge for improved global reporting of health data. 1 They also highlight the difficulty of showing national decision makers that good health data can strongly support decision making.Why is this?A reason may be that data are always subject to interpretation.The article by Murray et al is a case in point.They want to establish "an independent monitoring organisation," arguing that the World Health Organization is not fit to undertake the job because of tension between advocacy, monitoring, and evaluation.But evidence that it is this tension that leads to poor monitoring by WHO is weak, at best.In reality, the problems of global health reporting are primarily national (and subnational).The fact that the sum of deaths claimed by different programmes is greater than the actual number of deaths reflects epidemiological methods and the current limitations in global health reporting, more than any WHO failure.The global burden of disease project was limited by these issues, but it was undertaken as effectively in WHO as in any other organisation.Not only are there problems in capacity, understanding the value of surveillance, and coverage of health services.The reporting of health events can be politically sensitive or even economically damaging.It is therefore likely that political interference will continue (whoever collects the data) until governments can be shown that honesty pays.It is perhaps this failure that needs to be dealt with rather than setting up yet another organisation without a proper analysis of the reasons (and locus) for failures in global health reporting.
Tachycardia-induced failure alters contractile properties of canine ventricular myocytes
Authors: U. Ravens, K. Davia, C. H. Davies, P. O'Gara, A. J. Drake-Holland, J. W. Hynd, M. I.M. Noble, S. E. Harding
Journal: Cardiovascular Research (1996)

Rapid cardiac pacing has been used as a model for experimentally-induced cardiomyopathy. However, its relevance to human heart failure is not clear at present because little is known about changes in size and function of ventricular myocytes. We have therefore studied the responses to graded increases in frequency and calcium in canine ventricular myocytes from failing hearts. The aim of our study was to evaluate the resemblance between canine pacing-induced and human end-stage heart failure.Myocytes were isolated from the left ventricular wall of dogs that were in heart failure after 6 weeks of pacing at 250 beats/min. Cell shortening was measured by edge detection.Clinical signs of failure included dyspnea, ascites, and heart dilatation; the hemodynamic parameters were: LVdP/dtmax 1613 +/- 149 vs. 4713 +/- 304 mmHg/s in 6 control dogs; LVEDP 17.2 +/- 4.4 vs 5.6 +/- 1.1 mmHg; LV volume 60.5 +/- 6.2 vs. 30-35 ml. Myocytes from failing hearts were longer and thinner than those from controls (from factor: 0.40 +/- 0.01 vs. 0.47 +/- 0.01, P < 0.001, > 30 cells/heart). With 6 mM Ca2+ and at 0.5 Hz, contraction amplitude was significantly attenuated in myocytes from failing hearts: 6.6 +/- 0.9% cell shortening vs. 10.0 +/- 0.8% in controls (P < 0.05). This deficit was exacerbated at higher stimulation rates. Time-to-peak contraction and time-to-50% relaxation were not altered. There was no difference in sensitivity to thapsigargin.As with cells from human failing hearts, contraction amplitude showed rate-dependent depression in this animal model, whereas features like slowing of contraction and relaxation and reduced sensitivity to thapsigargin, were not reproduced.