tbuckley/cabot-search huggingface dataset:
First European human gastric peroral endoscopic myotomy, for treatment of refractory gastroparesis
Authors: Jean-Michel Gonzalez, Geoffroy Vanbiervliet, Veronique Vitton, Alban Benezech, Valentin Lestelle, Jean-Charles Grimaud, Marc Barthet
Journal: Endoscopy (2015)

Gastroparesis is a chronic functional syndrome that affects 4 % of the population [1] with an impact on quality of life. The etiologies include diabetic, post gastric surgery, and idiopathic forms [2]. Diagnosis is based on symptoms related to gastric emptying and on endoscopy and scintigraphy. The therapeutic options, including drugs (metoclopramide, erythrocin), surgery (pyloroplasty, gastric electrical stimulation), or endoscopy (botulinum toxin injection) remain insufficiently effective [3] [4] [5] [6] [7]. However, the physiopathology of gastroparesis implies stomach motility disorders as well as pyloric hypertonicity [8], and a US team has recently described the first case of gastric peroral endoscopic myotomy (G-POEM) by submucosal tunnel creation, and has reported a good outcome [9] [10].
Generation of endoderm-derived human induced pluripotent stem cells from primary hepatocytes
Authors: Hua Liu, Zhaohui Ye, Yonghak Kim, Saul Sharkis, Yoon-Young Jang
Journal: Hepatology (2010)

Recent advances in induced pluripotent stem (iPS) cell research have significantly changed our perspective on regenerative medicine. Patient-specific iPS cells have been derived not only for disease modeling but also as sources for cell replacement therapy. However, there have been insufficient data to prove that iPS cells are functionally equivalent to human embryonic stem (hES) cells or are safer than hES cells. There are several important issues that need to be addressed, and foremost are the safety and efficacy of human iPS cells of different origins. Human iPS cells have been derived mostly from cells originating from mesoderm and in a few cases from ectoderm. So far, there has been no report of endoderm–derived human iPS cells, and this has prevented comprehensive comparative investigations of the quality of human iPS cells of different origins. Here we show for the first time reprogramming of human endoderm-derived cells (i.e., primary hepatocytes) to pluripotency. Hepatocyte-derived iPS cells appear indistinguishable from hES cells with respect to colony morphology, growth properties, expression of pluripotency-associated transcription factors and surface markers, and differentiation potential in embryoid body formation and teratoma assays. In addition, these cells are able to directly differentiate into definitive endoderm, hepatic progenitors, and mature hepatocytes. Conclusion : The technology to develop endoderm–derived human iPS cell lines, together with other established cell lines, will provide a foundation for elucidating the mechanisms of cellular reprogramming and for studying the safety and efficacy of differentially originated human iPS cells for cell therapy. For the study of liver disease pathogenesis, this technology also provides a potentially more amenable system for generating liver disease-specific iPS cells. (Hepatology 2010;51:1810–1819)
Variant Creutzfeldt-Jakob Disease With Extremely Low Lymphoreticular Deposition of Prion Protein
Authors: Simon Mead, Jonathan D. F. Wadsworth, Marie-Claire Porter, Jacqueline M. Linehan, Wojciech Pietkiewicz, Graham S. Jackson, Sebastian Brandner, John Collinge
Journal: JAMA Neurology (2014)

Human transmission of bovine spongiform encephalopathy causes the fatal neurodegenerative condition variant Creutzfeldt-Jakob disease (vCJD) and, based on recent human prevalence studies, significant subclinical prion infection of the UK population. To date, all clinical cases have been fatal, totaling 228 mostly young adults residing in the United Kingdom.Here we describe the investigation and case history of a patient recently diagnosed as having vCJD in the United Kingdom. Although his presentation, imaging findings, cerebrospinal fluid investigation results, and clinical progression were typical of other cases, tonsillar biopsy and subsequent examination of multiple tissues at autopsy showed minimal deposition of disease-associated prion protein in peripheral lymphoreticular tissue. The result of a blood test for vCJD, the Direct Detection Assay for vCJD, was negative.These findings suggest that some patients with vCJD have very low peripheral prion colonization and therefore may not have detectable prion deposition in diagnostic tonsillar biopsy or markers of prion infection in blood. These results have implications for accurate interpretation of diagnostic tests and prevalence studies based on lymphoreticular tissue or blood.
The prolonged survival of fibroblasts with forced lipid catabolism in visceral fat following encapsulation in alginate-poly-l-lysine
Authors: Fangping Yang, Xulang Zhang, Andrei Maiseyeu, Georgeta Mihai, Rumana Yasmeen, David DiSilvestro, Santosh K. Maurya, Muthu Periasamy, K. Valerie Bergdall, Gregg Duester, Chandan K. Sen, Sashwati Roy, L. James Lee, Sanjay Rajagopalan, Ouliana Ziouzenkova
Journal: Biomaterials (2012)
A controlled clinical trial to assess the effect of a calcium channel blocker on the progression of coronary atherosclerosis.
Authors: D Waters, J Lespérance, M Francetich, D Causey, P Théroux, Y K Chiang, G Hudon, L Lemarbre, M Reitman, M Joyal
Journal: Circulation (1990)

To determine whether calcium channel blockers influence the progression of coronary atherosclerosis, 383 patients age 65 years or less with 5-75% stenoses in at least four coronary artery segments were selected at random within 1 month of coronary arteriography to participate in double-blind therapy with a placebo or nicardipine 30 mg three times daily. Coronary events (5 deaths, 22 myocardial infarctions, and 28 unstable anginas) occurred in 28 of 192 nicardipine patients and 23 of 191 placebo patients (p = NS). At 24 months coronary arteriography was repeated in 335 patients. Progression, defined as a 10% or more worsening in diameter stenosis, measured quantitatively, was found in 147 of 1,153 lesions (12.7%) in 168 nicardipine patients and in 170 of 1,170 lesions (14.5%) in 167 placebo patients (p = NS). Ninety-two nicardipine patients (55%) and 95 placebo patients (57%) had progression at one or more sites (p = NS). Regression, that is, an improvement by 10% or more in diameter stenosis, was seen in 140 of 2,323 lesions (6.0%) overall, with no significant intergroup difference. Among the 217 patients with 411 stenoses of 20% or less in the first study, such minimal lesions progressed in only 15 of 99 nicardipine patients compared with 32 of 118 placebo patients (15% versus 27%, p = 0.046). In this subgroup, 16 of 178 minimal lesions in nicardipine patients and 38 of 233 minimal lesions in placebo patients progressed (p = 0.038). By stepwise logistic-regression analysis, baseline systolic blood pressure (p = 0.04) and the change in systolic blood pressure between baseline and 6 months (p = 0.002) correlated with progression of minimal lesions. This suggested blood pressure reduction may account for the beneficial action of nicardipine. These results suggested nicardipine has no effect on advanced coronary atherosclerosis but may retard the progression of minimal lesions.
Abstract 1648: MICA variation and soluble MICA are possible prognostic biomarkers for HBV-induced hepatocellular carcinoma
Authors: Koichi Matsuda, Vinod Kumar, Yusuke Nakamura
Journal: Cancer Research (2012)

Abstract Hepatitis B virus (HBV) infection still remains to be one of the dominant risk factor for hepatocellular carcinoma (HCC). Both genetic as well as environmental factors influence the progression of chronic hepatitis B (CHB) to HCC. MHC class I polypeptide-related chain A and B (MICA and MICB) molecules are induced in response to viral infection as well as various stresses. We have recently revealed that SNP in MICA promoter was significantly associated with HCV-induced HCC risk as well as lower sMICA level in serum. To investigate the possible involvement of MICA in hepatocellular carcinogenesis caused by HBV-infection, we analyzed MICA gene polymorphisms and the levels of soluble MICA (sMICA) in HBV-induced HCC patients. The genetic association analysis revealed a nominal association at rs2596542 in which G allele was associated with susceptibility to HBV-induced HCC (P=0.029 with odds ratio of 1.19). We also found a significant elevation of sMICA in HBV-induced HCC cases. Moreover, genotypes at SNP rs2596542 located in the upstream of MICA promoter, was significantly associated with sMICA levels (P = 0.009). Interestingly. HCC patients with high sMICA (&amp;gt; 5 pg/ml) exhibited poor prognosis compared with patients with low sMICA (P = 0.008). Thus, our results highlight the importance of MICA genetic variations and sMICA as predictive biomarkers for HBV-induced HCC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1648. doi:1538-7445.AM2012-1648
British study highlights stigma of sick doctors
Authors: C Court
Journal: BMJ (1994)

Doctors who are sick do not seek help because of the stigma of illness and because of peer pressure and professional loyalty, according to a new study. The study found that attitudes of denial learnt in medical training and lack of insight into personal illness also played their part (see editorial on page 557).

Eight health authority districts were studied by the department of public health medicine at the United Medical and Dental Schools at St Thomas's Hospital in London. The report, which was funded by the Nuffield Provincial Hospitals Trust, concludes that there …
CHRONIC CATARRHAL DEAFNESS.NOTES ON SOME VERY SIMPLE EXPERIMENTS AS TO THE INFLUENCE OF SOUND WAVES ON OSSICULAR RIGIDITY.
Authors: PHILIP D. KERRISON
Journal: JAMA (1906)

That most cases of chronic catarrhal deafness are due largely to rigidity of the ossicles depending on morbid changes within the tympanum is an etiologic truism. The correction of this condition by some form of passive exercise—exercise that will move, not segments of the drum membrane, but the drum membrane and ossicles together—is not yet within our grasp. It is a fascinating possibility, a problem the solution of which would be of more value to humanity than could possibly result from the most brilliant development of otology along any other lines. <h3>METHODS USUALLY EMPLOYED.</h3> I wish (1) to consider, briefly, the methods usually employed for exercising the drum membrane and ossicles, and (2) to speak of some very simple experiments as to the influence of sound waves on ossicular rigidity. Of the various measures employed, inflation and pneumatic massage are in most common use. Inflation of the tympanum either by
Impaired Assembly yet Normal Trafficking of MHC Class I Molecules in Tapasin Mutant Mice
Authors: Andres G Grandea, Tatiana N Golovina, Sara E Hamilton, Venkataraman Sriram, Thomas Spies, Randy R Brutkiewicz, John T Harty, Laurence C Eisenlohr, Luc Van Kaer
Journal: Immunity (2000)
The 2009 Breast Cancer Screening Recommendations of the US Preventive Services Task Force
Authors: Steven H. Woolf
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
In-flight Deaths-Reply
Authors: Richard O. Cummins
Journal: JAMA (1989)

<h3>In Reply.—</h3> Drs Davis and Schurict raise two important points about our article on in-flight deaths during commercial air travel: first, that the data reported by commercial air carriers on travel-related deaths and on in-flight medical emergencies are an inaccurate underestimate of the problem, and second, that a new definition of deaths related to air travel is necessary. I agree strongly with both points. Other articles<sup>1-3</sup>have discussed the problems of in-flight deaths and medical emergencies, and they concur that underreporting occurs. In a 6-month survey at Los Angeles (Calif) International Airport, Speizer and colleagues<sup>1</sup>observed 7 in-flight deaths out of 8.74 million passenger arrivals. This rate of 0.8 deaths per million passengers is significantly higher than the rate of 0.31 deaths per million passengers recorded in the voluntary airline reports to the International Air Travelers Association.<sup>4</sup> We recently reported on air traveler deaths in a 1-year
One-year Treatment of Morpholino Antisense Oligomer Improves Skeletal and Cardiac Muscle Functions in Dystrophic mdx Mice
Authors: Bo Wu, Bin Xiao, Caryn Cloer, Mona Shaban, Arpana Sali, Peijuan Lu, Juan Li, Kanneboyina Nagaraju, Xiao Xiao, Qi Long Lu
Journal: Molecular Therapy (2010)

Antisense therapy has been successful to skip targeted dystrophin exon with correction of frameshift and nonsense mutations of Duchenne muscular dystrophy (DMD). Systemic production of truncated but functional dystrophin proteins has been achieved in animal models. Furthermore, phase I/II clinical trials in United Kingdom and the Netherlands have demonstrated dystrophin induction by local and systemic administrations of antisense oligomers. However, long-term efficacy and potential toxicity remain to be determined. The present study examined 1-year systemic effect of phosphorodiamidate morpholino oligomers (PMO) treatment targeting mutated dystrophin exon 23 in mdx mice. PMO induced dystrophin expression dose-dependently and significantly improved skeletal muscle pathology and function with reduced creatine kinase (CK) levels by a regimen of 60 mg/kg biweekly administration. This regimen induced <2% dystrophin expression in the heart, but improved cardiac functions demonstrated by hemodynamics analysis. The results suggest that low levels of dystrophin induction may be able to provide detectable benefit to cardiac muscle with limited myopathy. Body weight, serum enzyme tests, and histology analysis showed no sign of toxicity in the mice treated with up to 1.5 g/kg PMO for 6 months. These results indicate that PMO could be used safely as effective drugs for long-term systemic treatment of DMD. Antisense therapy has been successful to skip targeted dystrophin exon with correction of frameshift and nonsense mutations of Duchenne muscular dystrophy (DMD). Systemic production of truncated but functional dystrophin proteins has been achieved in animal models. Furthermore, phase I/II clinical trials in United Kingdom and the Netherlands have demonstrated dystrophin induction by local and systemic administrations of antisense oligomers. However, long-term efficacy and potential toxicity remain to be determined. The present study examined 1-year systemic effect of phosphorodiamidate morpholino oligomers (PMO) treatment targeting mutated dystrophin exon 23 in mdx mice. PMO induced dystrophin expression dose-dependently and significantly improved skeletal muscle pathology and function with reduced creatine kinase (CK) levels by a regimen of 60 mg/kg biweekly administration. This regimen induced <2% dystrophin expression in the heart, but improved cardiac functions demonstrated by hemodynamics analysis. The results suggest that low levels of dystrophin induction may be able to provide detectable benefit to cardiac muscle with limited myopathy. Body weight, serum enzyme tests, and histology analysis showed no sign of toxicity in the mice treated with up to 1.5 g/kg PMO for 6 months. These results indicate that PMO could be used safely as effective drugs for long-term systemic treatment of DMD.
Impact of Non–Small-Cell Lung Cancer-Not Otherwise Specified Immunophenotyping on Treatment Outcome
Authors: Luisella Righi, Tiziana Vavalà, Ida Rapa, Simona Vatrano, Jessica Giorcelli, Giulio Rossi, Enrica Capelletto, Silvia Novello, Giorgio V. Scagliotti, Mauro Papotti
Journal: Journal of Thoracic Oncology (2014)
A Common Genetic Fingerprint in Leprosy and Crohn's Disease?
Authors: Erwin Schurr, Philippe Gros
Journal: New England Journal of Medicine (2009)

The cause-and-effect relationship between severe infections and death suggests that microbial pathogens are evolutionary sculptors of the genome. However, the genetic component of susceptibility to infections in the general population is complex and heterogeneous and is modulated by environmental factors such as determinants of microbial virulence. Thus, it is a challenge to identify specific genetic effects in human populations. Availability of the human genome sequence, combined with knowledge of genetic variation, has facilitated the genomewide association study, a powerful approach to detecting genetic associations. In this issue of the Journal, Zhang and colleagues1 describe a genomewide association study of leprosy, . . .
Interaction of acidosis and increased extracellular potassium on action potential characteristics and conduction in guinea pig ventricular muscle.
Authors: Y Kagiyama, J L Hill, L S Gettes
Journal: Circulation Research (1982)

We studied the individual and combined effects of extracellular acidosis and increases in extracellular potassium on action potential characteristics and conduction in order to gain a better understanding of the effects of acute ischemia. At each level of potassium between 2.7 and 17 mm, acidosis induced by increasing Pco2 (respiratory acidosis) and by decreasing HCO3- (metabolic acidosis) decreased resting membrane potential, the maximum rate of rise of the action potential upstroke (Vmax), and slowed conduction. Metabolic acidosis consistently and significantly lengthened the steady state action potential duration whereas respiratory acidosis did not. Respiratory acidosis caused changes in resting membrane potential, Vmax, and conduction velocity; which occurred more rapidly and were of greater magnitude than the changes induced by metabolic acidosis. The changes in Vmax induced both types of acidosis were due to a change in the resting membrane potential-Vmax relationship as well as to the changes in the resting membrane potential. The conduction slowing induced by acidosis was greater when potassium was 9 and 13 mM than when potassium was 5.4 mm. Our results suggest that acidosis causes important changes in the electrophysiological properties of ventricular fibers and that many of the known electrophysiological effects of acute ischemia can be mimicked by the combined effects of extracellular acidosis and an increase in extracellular potassium.
Abstract 2248: The implication of STAT3 degradation and its mitochondrial functions in cellular senescence
Authors: Sebastian Igelmann, Xavier Deschênes-Simard, Frédéric Lessard, Véronique Bourdeau, Gerardo Ferbeyre
Journal: Cancer Research (2014)

Abstract Cellular senescence is a stable growth arrest of the cell cycle considered to be a mechanism of tumor suppression. We have recently described a senescence associated protein degradation or SAPD process that targets many proteins required for tumor progression. The Signal transducer and activator of transcription 3 is one of the targets of SAPD and its downregualtion by RNAi is sufficient to trigger senescence. In the last decade several different functions of STAT3 have been described. Beyond its canonical role as a transcription factor, it has been shown that STAT3 is imported into mitochondria and regulate the activity of the respiratory chain. In this study we want to clarify which function of STAT3 is required to prevent senescence. To do that we have made several mutants of STAT3 affecting different domains of the protein and tested their ability to rescue the senescence response to an anti-Stat3 shRNA. We have found that phosphorylation on residue S727 of STAT3 is important to reestablish proliferation in shSTAT3 induced senescence. Further, transcriptional activity of STAT3 is not required to rescue senescence as a mutant unable to enter the nucleus or the transcriptionally death STAT3 K180A are both able to bypass shSTAT3-induced senescence. Moreover, phosphorylation on Y705 seems not to be important as Y705F STAT3 is also able to reestablish proliferation. All in all, it seems that mitochondrial function of STAT3 is required to prevent senescence since STAT3 S727 phosphorylation is linked to the mitochondrial import of STAT3. Citation Format: Sebastian Igelmann, Xavier Deschênes-Simard, Frédéric Lessard, Véronique Bourdeau, Gerardo Ferbeyre. The implication of STAT3 degradation and its mitochondrial functions in cellular senescence. [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 2248. doi:10.1158/1538-7445.AM2014-2248
Treatment of Bilateral Renal Cell Cancer and Multiple Lung Metastasis: Nephron-Sparing Surgery and Resection of Lung Tumors after Interleukin-2 Therapy
Authors: Yoshihiko Tomita, Tomoyuki Imai, Toshiki Tanikawa, Takaki Mizusawa, Toshio Kanai, Kota Takahashi
Journal: European Urology (1998)
Compensation for medical accidents.
Authors: R Barnes
Journal: BMJ (1991)

results comparable to and in some ways superior to more traditional forms of care (W D Savage and R M Cochrane, Nivel international conference on primary care obstetrics and perinatal health, s'Hertogenbosch, 1991).We accept that such a scheme, in which hospital specialists visit local surgeries during their antenatal clinics and in which women therefore need not attend hospital at all, would be inappropriate in some areas.Nevertheless, some may wish to emulate the idea for the benefits outlined above and for the fruitful interprofessional respect that such care engenders.