tbuckley/cabot-search huggingface dataset:
Direct percutaneous endoscopic jejunostomy using a transgastrostomic endoscope in patients with previous endoscopic gastrostomy
Authors: S. Nishiwaki, H. Araki, Y. Shirakami, J. Kawaguchi, T. Asano, M. Iwashita, A. Tagami, H. Hatakeyama, T. Hayashi, T. Maeda, S. Naganawa, K. Saitoh
Journal: Endoscopy (2009)

Direct percutaneous endoscopic jejunostomy (DPEJ) is an effective method for preventing aspiration following percutaneous endoscopic gastrostomy (PEG) [1]. Although DPEJ provides a stable access to maintain enteral feeding, it requires an endoscope of more than 160 cm long for tube placement [2].
German health ministry forum monitors quality of health information
Authors: A. Tuffs
Journal: BMJ (2002)

Three years ago the Federal Ministry of Health set up the Health Information System Action Forum (“afgis”) (http://www.afgis.de/) to ensure that health information in the electronic media was of the highest quality and to improve the use of electronic media in various fields of health care.

The forum is also is supposed to develop criteria and instruments for the judgment of health information quality and to point out risks and weaknesses of available …
Protein misfolding, congophilia, oligomerization, and defective amyloid processing in preeclampsia
Authors: Irina A. Buhimschi, Unzila A. Nayeri, Guomao Zhao, Lydia L. Shook, Anna Pensalfini, Edmund F. Funai, Ira M. Bernstein, Charles G. Glabe, Catalin S. Buhimschi
Journal: Science Translational Medicine (2014)

Preeclampsia is a pregnancy-specific disorder of unknown etiology and a leading contributor to maternal and perinatal morbidity and mortality worldwide. Because there is no cure other than delivery, preeclampsia is the leading cause of iatrogenic preterm birth. We show that preeclampsia shares pathophysiologic features with recognized protein misfolding disorders. These features include urine congophilia (affinity for the amyloidophilic dye Congo red), affinity for conformational state-dependent antibodies, and dysregulation of prototype proteolytic enzymes involved in amyloid precursor protein (APP) processing. Assessment of global protein misfolding load in pregnancy based on urine congophilia (Congo red dot test) carries diagnostic and prognostic potential for preeclampsia. We used conformational state-dependent antibodies to demonstrate the presence of generic supramolecular assemblies (prefibrillar oligomers and annular protofibrils), which vary in quantitative and qualitative representation with preeclampsia severity. In the first attempt to characterize the preeclampsia misfoldome, we report that the urine congophilic material includes proteoforms of ceruloplasmin, immunoglobulin free light chains, SERPINA1, albumin, interferon-inducible protein 6-16, and Alzheimer's β-amyloid. The human placenta abundantly expresses APP along with prototype APP-processing enzymes, of which the α-secretase ADAM10, the β-secretases BACE1 and BACE2, and the γ-secretase presenilin-1 were all up-regulated in preeclampsia. The presence of β-amyloid aggregates in placentas of women with preeclampsia and fetal growth restriction further supports the notion that this condition should join the growing list of protein conformational disorders. If these aggregates play a pathophysiologic role, our findings may lead to treatment for preeclampsia.
FOXO1 Inhibits Runx2 Transcriptional Activity and Prostate Cancer Cell Migration and Invasion
Authors: Haijun Zhang, Yunqian Pan, Li Zheng, Chungyoul Choe, Bruce Lindgren, Eric D. Jensen, Jennifer J. Westendorf, Liang Cheng, Haojie Huang
Journal: Cancer Research (2011)

Prostate cancer patients with regional lymph node involvement at radical prostatectomy often experience disease progression to other organs, with the bone as the predominant site. The transcription factor Runx2 plays an important role in bone formation and prostate cancer cell migration, invasion, and metastasis. Here we showed that the forkhead box O (FOXO1) protein, a key downstream effector of the tumor suppressor PTEN, inhibits the transcriptional activity of Runx2 in prostate cancer cells. This inhibition was enhanced by PTEN but diminished by active Akt. FOXO1 bound to Runx2 in vitro and in vivo and suppressed Runx2's activity independent of its transcriptional function. FOXO1 inhibited Runx2-promoted migration of prostate cancer cells, whereas silencing of endogenous FOXO1 enhanced prostate cancer cell migration in a Runx2-dependent manner. Forced expression of FOXO1 also inhibited Runx2-promoted prostate cancer cell invasion. Finally, we found that expression of PTEN and the level of FOXO1 in the nucleus is inversely correlated with expression of Runx2 in a cohort of prostate cancer specimens from patients with lymph node and bone metastasis. These data reveal FOXO1 as a critical negative regulator of Runx2 in prostate cancer cells. Inactivation of FOXO1 due to frequent loss of PTEN in prostate cancer cells may leave the oncogenic activities of Runx2 unchecked, thereby driving promiscuous expression of Runx2 target genes involved in cell migration and invasion and favoring prostate cancer progression.
Germ Cell Cancers
Authors: RONALD L. RICHARDSON
Journal: Annals of Internal Medicine (1981)

Letters and Corrections1 October 1981Germ Cell CancersRONALD L. RICHARDSON, M.D.RONALD L. RICHARDSON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-95-4-521_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The letters by Page (1) and Newcomer (2) in the May issue and the comments by other physicians in response to our article on unrecognized germ cell cancers (3) warrant a reply. Page (1) talks of killing a rhinoceros with an elephant gun, but we suspect that he has not only mistaken his quarry again but has also shot himself in the foot. Our article was not intended to be critical of pathologists' diagnostic acumen but was intended to point out the limitations of a diagnosis based on histologic findings alone in these patients and, more important,...References1. PAGE D. Undifferentiated malignant neoplasms. Ann Intern Med. 1981;94:710. Letter. LinkGoogle Scholar2. NEWCOMER L. Undifferentiated malignant neoplasms. Ann Intern Med. 1981;94:710-1. Letter. LinkGoogle Scholar3. RICHARDSONSCHOUMACHERFER RRM. The unrecognized extragonadal germ cell cancer syndrome. Ann Intern Med. 1981;94:181-6. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: RONALD L. RICHARDSON, M.D.Affiliations: Mayo Graduate School of Medicine Rochester, MN 55901 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1981Volume 95, Issue 4Page: 521-521KeywordsGerm cell cancerHomicidePathologists ePublished: 1 December 2008 Issue Published: 1 October 1981 PDF downloadLoading ...
LATENT VIRAL INFECTION OF CELLS IN TISSUE CULTURE
Authors: Herbert R. Morgan
Journal: The Journal of Experimental Medicine (1956)

Chick embryo tissues maintained for from 11 to 28 days in Hank's balanced salt solution lost their capacity to support the multiplication of psittacosis virus. The virus however infected such cells, as active multiplication of the virus occurred on the addition of beef embryo extract to this nutritionally poor medium at any period up to 28 days of cultivation in balanced salt solution. The virus remained in a state of latency for as long as 15 days in these starved cells in a non-infectious phase. These results obtained in this in vitro model system for the investigation of latent infections of cells with psittacosis virus suggest that cell nutrition as well as an alteration in the immunological defenses of the host may prove to be an important factor in the activation of latent viral infections.
P1132 PHARMACOKINETIC-RESPONSE ANALYSIS OF FALDAPREVIR IN PATIENTS WITH CHRONIC HCV GENOTYPE-1 INFECTION WITH PRIOR RELAPSE
Authors: T. Asselah, E. Zehnter, K. Agarwal, Y. Sakai, H. Yatsuhashi, B. Willems, D. Wright, F. Calinas, J.L. Calleja, F. Negro, J.O. Stern, A.-M. Quinson, N. Sha, N. Dorleacq, M. Schobelock, I.M. Jacobson
Journal: Journal of Hepatology (2014)
Regulation of insulin receptor substrate-1 in liver and muscle of animal models of insulin resistance.
Authors: M J Saad, E Araki, M Miralpeix, P L Rothenberg, M F White, C R Kahn
Journal: Journal of Clinical Investigation (1992)

Insulin rapidly stimulates tyrosine phosphorylation of a protein of approximately 185 kD in most cell types. This protein, termed insulin receptor substrate-1 (IRS-1), has been implicated in insulin signal transmission based on studies with insulin receptor mutants. In the present study we have examined the levels of IRS-1 and the phosphorylation state of insulin receptor and IRS-1 in liver and muscle after insulin stimulation in vivo in two rat models of insulin resistance, i.e., insulinopenic diabetes and fasting, and a mouse model of non-insulin-dependent diabetes mellitus (ob/ob) by immunoblotting with anti-peptide antibodies to IRS-1 and anti-phosphotyrosine antibodies. As previously described, there was an increase in insulin binding and a parallel increase in insulin-stimulated receptor phosphorylation in muscle of fasting and streptozotocin-induced (STZ) diabetic rats. There was also a modest increase in overall receptor phosphorylation in liver in these two models, but when normalized for the increase in binding, receptor phosphorylation was decreased, in liver and muscle of STZ diabetes and in liver of 72 h fasted rats. In the hyperinsulinemic ob/ob mouse there was a decrease in insulin binding and receptor phosphorylation in both liver and muscle. The tyrosyl phosphorylation of IRS-1 after insulin stimulation reflected an amplification of the receptor phosphorylation in liver and muscle of hypoinsulinemic animals (fasting and STZ diabetes) with a twofold increase, and showed a significant reduction (approximately 50%) in liver and muscle of ob/ob mouse. By contrast, the levels of IRS-1 protein showed a tissue specific regulation with a decreased level in muscle and an increased level in liver in hypoinsulinemic states of insulin resistance, and decreased levels in liver in the hyperinsulinemic ob/ob mouse. These data indicate that: (a) IRS-1 protein levels are differentially regulated in liver and muscle; (b) insulin levels may play a role in this differential regulation of IRS-1; (c) IRS-1 phosphorylation depends more on insulin receptor kinase activity than IRS-1 protein levels; and (d) reduced IRS-1 phosphorylation in liver and muscle may play a role in insulin-resistant states, especially of the ob/ob mice.
Eligibility criteria improve children's access to long term ventilation at home
Authors: S. Snelling
Journal: BMJ (1999)

EDITOR—Jardine et al comment that funding and home carers are common obstacles to discharge home for children on long term ventilation.1 Liverpool has a scheme which largely overcomes these obstacles.

Liverpool Health Authority and the local authority have agreed on eligibility criteria for joint funding for children with complex needs, which has removed the delay previously caused by funding negotiations. The eligibility criteria are based on a discussion document produced in …
The Role of Base Excision Repair in the Sensitivity and Resistance to Temozolomide-Mediated Cell Death
Authors: Ram N. Trivedi, Karen H. Almeida, Jamie L. Fornsaglio, Sandra Schamus, Robert W. Sobol
Journal: Cancer Research (2005)

Abstract DNA-alkylating agents have a central role in the curative therapy of many human tumors; yet, resistance to these agents limits their effectiveness. The efficacy of the alkylating agent temozolomide has been attributed to the induction of O6-MeG, a DNA lesion repaired by the protein O6-methylguanine-DNA methyltransferase (MGMT). Resistance to temozolomide has been ascribed to elevated levels of MGMT and/or reduced mismatch repair. However, &amp;gt;80% of the DNA lesions induced by temozolomide are N-methylated bases that are recognized by DNA glycosylases and not by MGMT, and so resistance to temozolomide may also be due, in part, to robust base excision repair (BER). We used isogenic cells deficient in the BER enzymes DNA polymerase-β (pol-β) and alkyladenine DNA glycosylase (Aag) to determine the role of BER in the cytotoxic effect of temozolomide. Pol-β–deficient cells were significantly more susceptible to killing by temozolomide than wild-type or Aag-deficient cells, a hypersensitivity likely caused by accumulation of BER intermediates. RNA interference–mediated pol-β suppression was sufficient to increase temozolomide efficacy, whereas a deficiency in pol-ι or pol-λ did not increase temozolomide-mediated cytotoxicity. Overexpression of Aag (the initiating BER enzyme) triggered a further increase in temozolomide-induced cytotoxicity. Enhanced Aag expression, coupled with pol-β knockdown, increased temozolomide efficacy up to 4-fold. Furthermore, loss of pol-β coupled with temozolomide treatment triggered the phosphorylation of H2AX, indicating the activation of the DNA damage response pathway as a result of unrepaired lesions. Thus, the BER pathway is a major contributor to cellular resistance to temozolomide and its efficacy depends on specific BER gene expression and activity.
Effect of ranitidine bismuth citrate on postprandial plasma gastrin and pepsinogens.
Authors: A G Fraser, W M Lam, Y W Luk, J Sercombe, A M Sawyerr, M Hudson, I M Samloff, R E Pounder
Journal: Gut (1993)

Ranitidine bismuth citrate was compared with an equipotent dose of ranitidine, to determine whether the former, by an anti-Helicobacter pylori activity, would counteract the rise of gastrin resulting from ranitidine9s gastric acid antisecretory activity. Twenty four men with duodenal ulcers were studied before and on the 8th day of dosing with either ranitidine bismuth citrate 800 mg twice daily or ranitidine 300 mg twice daily (double blind, randomised, parallel groups). Fasting and postprandial plasma gastrin and plasma pepsinogen I and II concentrations were measured, and a 13C-urea breath test was performed before and on the 8th day of dosing. The 13C-urea breath tests were positive in 21 patients before dosing and remained positive in nine of nine of the ranitidine dosed patients, whereas only two of 12 patients treated with ranitidine bismuth citrate remained positive. The expected rise in meal stimulated plasma gastrin with ranitidine was seen in the 12 patients who received ranitidine but, despite suppression of H pylori urease activity in 10 of 12 patients taking ranitidine bismuth citrate, there was no attenuation of the meal stimulated gastrin rise. There was no significant difference in the mean derived (4 hour) plasma pepsinogen I and II concentrations after dosing with ranitidine or ranitidine bismuth citrate.
End-stage liver disease candidates at the highest model for end-stage liver disease scores have higher wait-list mortality than status-1A candidates
Authors: Pratima Sharma, Douglas E. Schaubel, Qi Gong, Mary Guidinger, Robert M. Merion
Journal: Hepatology (2011)

Candidates with fulminant hepatic failure (Status–1A) receive the highest priority for liver transplantation (LT) in the United States. However, no studies have compared wait–list mortality risk among end–stage liver disease (ESLD) candidates with high Model for End–Stage Liver Disease (MELD) scores to those listed as Status–1A. We aimed to determine if there are MELD scores for ESLD candidates at which their wait–list mortality risk is higher than that of Status–1A, and to identify the factors predicting wait–list mortality among those who are Status–1A. Data were obtained from the Scientific Registry of Transplant Recipients for adult LT candidates (n = 52,459) listed between September 1, 2001, and December 31, 2007. Candidates listed for repeat LT as Status–1 A were excluded. Starting from the date of wait listing, candidates were followed for 14 days or until the earliest occurrence of death, transplant, or granting of an exception MELD score. ESLD candidates were categorized by MELD score, with a separate category for those with calculated MELD &gt; 40. We compared wait–list mortality between each MELD category and Status–1A (reference) using time–dependent Cox regression. ESLD candidates with MELD &gt; 40 had almost twice the wait–list mortality risk of Status–1A candidates, with a covariate–adjusted hazard ratio of HR = 1.96 ( P = 0.004). There was no difference in wait–list mortality risk for candidates with MELD 36–40 and Status–1A, whereas candidates with MELD &lt; 36 had significantly lower mortality risk than Status–1A candidates. MELD score did not significantly predict wait–list mortality among Status–1A candidates ( P = 0.18). Among Status–1A candidates with acetaminophen toxicity, MELD was a significant predictor of wait–list mortality ( P &lt; 0.0009). Posttransplant survival was similar for Status–1A and ESLD candidates with MELD &gt; 20 ( P = 0.6). Conclusion : Candidates with MELD &gt; 40 have significantly higher wait–list mortality and similar posttransplant survival as candidates who are Status–1A, and therefore, should be assigned higher priority than Status–1A for allocation. Because ESLD candidates with MELD 36–40 and Status–1A have similar wait–list mortality risk and posttransplant survival, these candidates should be assigned similar rather than sequential priority for deceased donor LT. (Hepatology 2012)
An in vitro assay for detection of glomerular binding IgG autoantibodies in patients with systemic lupus erythematosus.
Authors: L Budhai, K Oh, A Davidson
Journal: Journal of Clinical Investigation (1996)

The deposition of anti-dsDNA antibodies in the glomerulus is believed to play a critical role in the pathogenesis of nephritis in SLE. However, an absolute correlation between serum levels of anti-dsDNA antibodies and renal disease has not been found. Recently a glomerular binding assay (GBA) has been developed to detect IgG binding to isolated rat glomeruli. We have used the GBA to study sera from four groups of SLE patients: (A) + anti-dsDNA antibodies, active nephritis; (B) - anti-dsDNA antibodies, active nephritis; (C) + anti-dsDNA antibodies, no nephritis; and (D) - anti-dsDNA antibodies, no nephritis. The serum anti-dsDNA antibodies in group A and group C patients could not be distinguished on the basis of isotype, charge, or cross-reactivity with histones. Nevertheless, the mean intensity of glomerular immunofluorescence was significantly higher in group A than in the three other patient groups and distinguished between patients with serum anti-dsDNA antibodies who had nephritis and those without clinically apparent nephritis. GBA reactivity was unaffected by DNase treatment of sera, but was partially inhibited by preincubation with dsDNA. These findings are consistent with the hypothesis that some anti-dsDNA antibodies cross-react with glomerular components and that the presence of this cross-reactivity is associated with, and may be responsible for, the development of nephritis. In addition, we have identified a group of SLE patients with renal disease and typical renal histopathology and immune deposits who do not have serum anti-dsDNA antibodies or antibodies that directly bind to glomeruli in the GBA. The mechanism of renal immune deposition in these patients remains to be determined.
Diagnosis and Management of Adult Congenital Heart Disease
Authors: Gregory A. Crooke, Thierry H. Le Jemtel
Journal: Annals of Internal Medicine (2004)

Medical Writings: Book Notes2 March 2004Diagnosis and Management of Adult Congenital Heart DiseaseGregory A. Crooke, MD and Thierry H. Le Jemtel, MDGregory A. Crooke, MDFrom Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, New York.Search for more papers by this author and Thierry H. Le Jemtel, MDFrom Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, New York.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-140-5-200403020-00029 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Gatzoulis MA, Webb GD, Daubeney PE, eds. 517 pages. New York: Churchill Livingstone; 2003. $129.00. ISBN 0443071039. Order phone 800-545-2522.Field of medicine: Congenital heart disease and pediatric cardiology.Format: Hardcover book.Audience: Adult and pediatric cardiologists, especially those with limited exposure to large adult congenital centers. The book is designed as a resource for all members of health care teams caring for adult patients with congenital heart disease.Purpose: To review congenital heart disease in adults, covering anatomy, physiology, and medical and nonmedical issues, with emphasis on diagnosis and management of late sequelae.Content: The book is divided into ... Author, Article, and Disclosure InformationAffiliations: From Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, New York. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 2 March 2004Volume 140, Issue 5Page: 408KeywordsCongenital heart diseaseInfantsLesionsOutpatientsPediatric cardiologyPediatric surgeryPregnancySoftware toolsSurgeryYoung adults ePublished: 2 March 2004 Issue Published: 2 March 2004 Copyright & PermissionsCopyright © 2004 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Herpes Simplex Antigen in Immune Complexes of Patients With Erythema Multiforme
Authors: John A. Kazmierowski
Journal: JAMA (1982)

Serum samples from patients with erythema multiforme (EM) were examined for the presence of herpes simplex virus (HSV) antigen in immune complexes using the Raji cell radioimmunoassay. Raji-cell-bound immune complexes from eight of 12 patients with EM after HSV infection and four of four patients with EM of uncertain cause had increased anti-HSV binding, while patients with EM after drug exposure and patients with recurrent HSV infections without EM had binding in the same range as controls. Viral cultures for HSV of immune complexes eluted from Raji cells were negative. Sucrose density gradient ultracentrifugation studies of serum samples of patients with EM after HSV infection showed HSV antigen in large molecular weight fractions. The HLA typing of lymphocytes from 16 patients with EM after HSV infection was not different from that of controls. Immune complexes composed of antibody and HSV antigen are present in serum samples of patients with EM after HSV infection and some cases of EM of uncertain cause and may mediate the pathogenesis of these disorders.
Second cancers more common in people who receive donor stem cell transplants
Authors: Janice Hopkins Tanne
Journal: BMJ (2006)

Patients who received haematopoietic donor stem cell transplants to treat diseases such as leukaemia or myelodysplastic syndrome have almost double the risk of developing a second cancer in later years, compared with the general population. A study in the journal Cancer has found that the risk was almost four times higher for patients older than 40 years and for men patients receiving transplants from a female donor (2006 Nov 27, doi: 10.1002/cncr.22375). 

The study reviewed …