tbuckley/cabot-search huggingface dataset:
Geographic Miss
Authors: Manel Sabaté, Marco A. Costa, Ken Kozuma, I. Patrick Kay, Willem J. van der Giessen, Veronique L. M. A. Coen, Jurgen M. R. Ligthart, Pedro Serrano, Peter C. Levendag, Patrick W. Serruys
Journal: Circulation (2000)

A recognized limitation of endovascular beta-radiation therapy is the development of new stenosis at the edges of the irradiated area. The combination of injury and low-dose radiation may be the precursor of this phenomenon. We translated the radio-oncological concept of "geographic miss" to define cases in which the radiation source did not fully cover the injured area. The aims of the study were to determine the incidence and causes of geographic miss and evaluate the impact of this inadequate treatment on the outcome of patients treated with intracoronary beta-radiation.We analyzed 50 consecutive patients treated with beta-radiation after percutaneous coronary intervention. The prescribed dose ranged between 12 and 20 Gy at 2 mm from the source axis. By means of quantitative coronary angiography, the irradiated segment (IRS) and both edges were studied before and after intervention and at 6-month follow-up. Edges that were injured during the procedure constituted the geographic miss edges. Twenty-two edges were injured during the intervention, mainly because of procedural complications that extended the treatment beyond the margins of the IRS. Late loss was significantly higher in geographic miss edges than in IRSs and uninjured edges (0.84+/-0.6 versus 0.15+/-0.4 and 0.09+/-0.4 mm, respectively; P<0.0001). Similarly, restenosis rate was significantly higher in the injured edges (10% within IRS, 40.9% in geographic miss edges, and 1.9% in uninjured edges; P<0.001).These data support the hypothesis that the combination of injury and low-dose beta-radiation induces deleterious outcome.
Liver disease progression in hepatitis C virus carriers with normal alanine aminotransferase levels
Authors: Claudio Puoti, Lia Bellis, Olga Mitidieri Costanza, Maria Giuseppa Elmo
Journal: Hepatology (2014)

We read with great enthusiasm the article of Wiese et al.1 that, in our opinion, has a paramount relevance to understanding the natural history of hepatitis C virus (HCV) infection. In particular, this article does greatly in helping us to evaluate the progression to more severe liver damage of the so-called healthy HCV carriers (i.e., viremic persons with normal alanine aminotransferase [ALT] levels and liver histology). It is known that up to 30%-40% of patients with chronic HCV infection have persistently normal ALT levels,2 with many of them showing normal liver histology or minimal fibrosis. The natural course of HCV infection in these patients is not well known. Whereas some studies showed that HCV carriers with normal ALT have mild and stable disease, others reported a significant progression of fibrosis in approximately 20%-30% of such patients.3 In their first study4 describing the 20-year follow-up of over 1,000 women infected in East Germany in January 1979 by contaminated anti-D immune globulin, the researchers reported that 26 patients should be considered as true healthy carriers (i.e., normal liver, normal ALT, and persistent HCV viremia). At 25-year follow-up,5 only 11 women had remained in a healthy state, whereas the others had progressed to chronic hepatitis C (CHC). However, in this third evaluation after 35-year follow-up,1 no mention has been made about the histological and clinical status of these otherwise healthy, HCV-infected women. Thus, we wonder how many of these carriers had remained in a true healthy state 35 years after contamination and how many further carriers had progressed to CHC. Furthermore, the degree of liver damage was more or less severe in the carriers progressing to CHC with respect to other patients; were differences observed in virological response between the two groups of patients? Indeed, whether healthy HCV carriers should be offered antiviral treatment in clinical practice has been the subject of an ongoing debate.6 Introduction of the combination therapy of pegylated interferon plus ribavirin results in higher response rates,7 with a favorable risk/benefit ratio also in patients with mild or no fibrosis.8, 9 The important data of the East Germany HCV Study Group might give an answer to this unmet issue: What should we treat, the infection or the disease?10 Claudio Puoti, M.D.1 Lia Bellis, M.D.1 Olga Mitidieri Costanza, M.D.2 Maria Giuseppa Elmo, M.D.3 1Department of Internal Medicine and Liver Unit Marino General Hospital Rome, Italy 2Molecular Biology Unit Marino General Hospital Rome, Italy 3Department of Mental Health, Local Health Center Rome, Italy
Association between glioma susceptibility loci and tumour pathology defines specific molecular etiologies
Authors: Anna Luisa Di Stefano, Victor Enciso-Mora, Yannick Marie, Virginie Desestret, Marianne Labussière, Blandine Boisselier, Karima Mokhtari, Ahmed Idbaih, Khe Hoang-Xuan, Jean-Yves Delattre, Richard S. Houlston, Marc Sanson
Journal: Neuro-Oncology (2012)

Genome-wide association studies have identified single-nucleotide polymorphisms (SNPs) at 7 loci influencing glioma risk: rs2736100 (TERT), rs11979158 and rs2252586 (EGFR), rs4295627 (CCDC26), rs4977756 (CDKN2A/CDKN2B), rs498872 (PHLDB1), and rs6010620 (RTEL1). We studied the relationship among these 7 glioma-risk SNPs and characteristics of tumors from 1374 patients, including grade, IDH (ie IDH1 or IDH2) mutation, EGFR amplification, CDKN2A-p16-INK4a homozygous deletion, 9p and 10q loss, and 1p-19q codeletion. rs2736100 (TERT) and rs6010620 (RTEL1) risk alleles were associated with high-grade disease, EGFR amplification, CDKN2A-p16-INK4a homozygous deletion, and 9p and 10q deletion; rs4295627 (CCDC26) and rs498872 (PHLDB1) were associated with low-grade disease, IDH mutation, and 1p-19q codeletion. In contrast, rs4977756 (CDKN2A/B), rs11979158 (EGFR), and to a lesser extent, rs2252586 (EGFR) risk alleles were independent of tumor grade and genetic profile. Adjusting for tumor grade showed a significant association between rs2736100 and IDH status (P = .01), 10q loss (P = .02); rs4295627 and 1p-19q codeletion (P = .04), rs498872 and IDH (P = .02), 9p loss (P = .04), and 10q loss (P = .02). Case-control analyses stratified into 4 molecular classes (defined by 1p-19q status, IDH mutation, and EGFR amplification) showed an association of rs4295627 and rs498872 with IDH-mutated gliomas (P < 10−3) and rs2736100 and rs6010620 with IDH wild-type gliomas (P < 10−3 and P = .03). The frequency of EGFR and CDKN2A/B risk alleles were largely independent of tumor genetic profile, whereas TERT, RTEL1, CCDC26, and PHLDB1 variants were associated with different genetic profiles that annotate distinct molecular pathways. Our findings provide further insight into the biological basis of glioma etiology.
Debunking the July Phenomenon
Authors: Elizabeth A. Bailey, Karole Collier, Rachel R. Kelz
Journal: JAMA Surgery (2015)

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 Surgery HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Surgery journal
Prognostic Significance of the Epstein-Barr Virus, p53, Bcl-2, and Survivin in Nasopharyngeal Cancer
Authors: Kenneth W. Yip, Wei Shi, Melania Pintilie, Joseph D. Martin, Joseph D. Mocanu, Derek Wong, Christine MacMillan, Pat Gullane, Brian O'Sullivan, Carlo Bastianutto, Fei-Fei Liu
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Nasopharyngeal cancer (NPC) is a malignant epithelial carcinoma which is intimately associated with EBV. The latent presence of EBV affects the function of p53, Bcl-2, and survivin. We thus investigated the relationship between EBV status, p53, Bcl-2, and survivin in biopsy specimens from patients with primary NPC. Experimental Design: Archival formalin-fixed, paraffin-embedded NPC biopsies were evaluated in 80 patients treated with curative radiation from a single institution. The presence of EBV was determined using EBER in situ hybridization, whereas p53, Bcl-2, and survivin were assessed using immunohistochemistry. Results: The majority of NPC specimens in this patient cohort were EBER-positive (64 of 78, or 82%), which in turn, was significantly associated with ethnicity (P = 0.0007), and WHO subtype 2A/2B (P = 0.04). EBER-positive tumors were also associated with p53 (P = 0.002), Bcl-2 (P = 0.04), and nuclear survivin (P = 0.03) expression. Patients with EBER-positive NPC fared better, with a 10-year overall survival of 68% versus 48% for EBER-negative patients (P = 0.03). For nuclear survivin, patients with either low or high nuclear survivin fared worse than patients with intermediate survivin expression (P = 0.05), suggesting that there is an optimal proportion of survivin-expressing cells for best function and clinical outcome. Conclusions: With an extended median follow-up time of 11.4 years, EBV status remains a strong predictor for overall survival in NPC. EBV-positive NPC has strong molecular associations with p53, Bcl-2, and survivin expression. Furthermore, we provide clinical data revealing the potentially dual nature of survivin in predicting clinical outcome.
Intravenous ibandronate injections given every three months: a new treatment option to prevent bone loss in postmenopausal women
Authors: J A Stakkestad
Journal: Annals of the Rheumatic Diseases (2003)

To investigate the efficacy, safety, and dose response of three doses of ibandronate, given intermittently by intravenous (IV) injection every three months, in preventing postmenopausal osteoporosis.629 postmenopausal women, categorised according to time since menopause and baseline lumbar spine (L1-4) bone mineral density (BMD), were enrolled into a multicentre, double blind, placebo controlled trial. They were randomly allocated to receive IV ibandronate 0.5 mg, 1 mg or 2 mg, or placebo every three months. All women received daily calcium supplementation.One year's treatment with intermittent IV ibandronate injections produced a dose dependent gain in mean (SD) lumbar spine BMD from baseline of 2.5 (2.5)%, 1.8 (2.6)%, and 1.0 (2.8)% in the groups receiving 2 mg, 1 mg, and 0.5 mg ibandronate, respectively, compared with a loss of BMD of 0.4 (2.4)% in the women in the placebo group; p=0.0001 for each ibandronate dose v placebo. Highest BMD gains occurred in women with osteopenia receiving 2 mg ibandronate. Similarly, at the hip, all three doses of ibandronate produced significantly better gains in BMD than placebo (p<0.05), with the greatest gains in the women with osteopenia receiving the 2 mg dose. Ibandronate concomitantly and dose dependently suppressed markers of bone turnover in comparison with placebo, and injections were well tolerated.IV ibandronate injections, given every three months, may be an effective alternative to oral bisphosphonates and hormonal therapy in the prevention of bone loss in postmenopausal women.
MicroRNAs 29b, 133b, and 211 Regulate Vascular Smooth Muscle Calcification Mediated by High Phosphorus
Authors: Sara Panizo, Manuel Naves-Díaz, Natalia Carrillo-López, Laura Martínez-Arias, José Luis Fernández-Martín, María Piedad Ruiz-Torres, Jorge B. Cannata-Andía, Isabel Rodríguez
Journal: Journal of the American Society of Nephrology (2015)

Vascular calcification is a frequent cause of morbidity and mortality in patients with CKD and the general population. The common association between vascular calcification and osteoporosis suggests a link between bone and vascular disorders. Because microRNAs (miRs) are involved in the transdifferentiation of vascular smooth muscle cells into osteoblast-like cells, we investigated whether miRs implicated in osteoblast differentiation and bone formation are involved in vascular calcification. Different levels of uremia, hyperphosphatemia, and aortic calcification were induced by feeding nephrectomized rats a normal or high-phosphorus diet for 12 or 20 weeks, at which times the levels of eight miRs (miR-29b, miR-125, miR-133b, miR-135, miR-141, miR-200a, miR-204, and miR-211) in the aorta were analyzed. Compared with controls and uremic rats fed a normal diet, uremic rats fed a high-phosphorous diet had lower levels of miR-133b and miR-211 and higher levels of miR-29b that correlated respectively with greater expression of osteogenic RUNX2 and with lower expression of several inhibitors of osteoblastic differentiation. Uremia per se mildly reduced miR-133b levels only. Similar results were obtained in two in vitro models of vascular calcification (uremic serum and high–calcium and –phosphorus medium), and experiments using antagomirs and mimics to modify miR-29b, miR-133b, and miR-211 expression levels in these models confirmed that these miRs regulate the calcification process. We conclude that miR-29b, miR-133b, and miR-211 have direct roles in the vascular smooth muscle calcification induced by high phosphorus and may be new therapeutic targets in the management of vascular calcification.
Intradialytic Oral Nutrition Improves Protein Homeostasis in Chronic Hemodialysis Patients with Deranged Nutritional Status
Authors: Lara B. Pupim, Karen M. Majchrzak, Paul J. Flakoll, T. Alp Ikizler
Journal: Journal of the American Society of Nephrology (2006)

Decreased dietary protein intake and hemodialysis (HD)-associated protein catabolism predispose chronic HD (CHD) patients to deranged nutritional status, which is associated with poor clinical outcome in this population. Intradialytic parenteral nutrition (IDPN) reverses the net negative whole-body and skeletal muscle protein balance during HD. IDPN is costly and restricted by Medicare and other payers. Oral supplementation (PO) is a more promising, physiologic, and affordable intervention in CHD patients. Protein turnover studies were performed by primed-constant infusion of l-(1-13C) leucine and l-(ring-2H5) phenylalanine in eight CHD patients with deranged nutritional status before, during, and after HD on three separate occasions: (1) with IDPN infusion, (2) with PO administration, and (3) with no intervention (control). Results showed highly positive whole-body net balance during HD for both IDPN and PO (4.43 ± 0.7 and 5.71 ± 1.2 mg/kg fat-free mass per min, respectively), compared with a neutral balance with control (0.25 ± 0.5 mg/kg fat-free mass per min; P = 0.002 and <0.001 for IDPN versus control and PO versus control, respectively). Skeletal muscle protein homeostasis during HD also improved with both IDPN and PO (50 ± 19 and 42 ± 17 μg/100 ml per min) versus control (−27 ± 13 μg/100 ml per min; P = 0.005 and 0.009 for IDPN versus control and PO versus control, respectively). PO resulted in persistent anabolic benefits in the post-HD phase for muscle protein metabolism, when anabolic benefits of IDPN dissipated (−53 ± 25 μg/100 ml per min for control, 47 ± 41 μg/100 ml per min for PO [P = 0.039 versus control], and −53 ± 24 μg/100 ml per min for IDPN [P = 1.000 versus control and 0.039 versus PO]). Long-term studies using intradialytic oral supplementation are needed for CHD patients with deranged nutritional status.
Vascular Endothelial Growth Factor and Osteopontin in Stage I Lung Adenocarcinoma
Authors: NORIHARU SHIJUBO, TOSHIMITSU UEDE, SHIGEYUKI KON, MASAHIRO MAEDA, TATSUYA SEGAWA, AKIHIRO IMADA, MICHIO HIRASAWA, SHOSAKU ABE
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Tumor growth and metastasis are angiogenesis-dependent processes initiated and regulated by a number of cytokines. Vascular endothelial growth factor (VEGF) is a potent angiogenic protein with a selective mitogenic effect on vascular endothelial cells. Osteopontin (OPN) induces endothelial cell migration and upregulates endothelial cell migration induced by VEGF. To clarify the cooperative role of VEGF and OPN in tumor angiogenesis, we stained VEGF, OPN, and CD34 immunohistochemically in 87 cases of stage I non-small cell lung cancer (adenocarcinoma, 55, and squamous cell carcinoma, 32). Of the 87 patients studied, 27 patients had postoperative relapse and 60 patients did not. VEGF was found in 34 of 55 cases of adenocarcinomas and 14 of 32 squamous cell carcinomas, and OPN was found in 30 of 55 adenocarcinomas and 10 of 32 squamous cell carcinomas. In adenocarcinoma, microvessel counts of VEGF-positive and OPN-positive tumors were significantly higher than VEGF-negative and OPN-negative tumors, respectively, whereas in squamous cell carcinoma they were not. More importantly, patients with VEGF- and OPN-positive stage I lung adenocarcinoma had significantly worse prognosis as compared with other groups. Cooperation of OPN is important in VEGF-mediated tumor angiogenesis in stage I lung adenocarcinoma.
THE MANAGEMENT OF THE BREATH IN SINGING
Authors: W. A. Aikin
Journal: BMJ (1905)

any more likely to do so once a week to have an intramuscular injection."In reference to this, my opinion is that it is very easy indeed to see why a patient would prefer to go once a week to have an intramuscular injection rather than to go once a week or once a month to get medicine which he will have to take regularly until his next visit.In the case of the visit for the injection, he gets the injection and he has not to do anything until his next visit.In the case of the visit for medicine, it is only the beginning of his work; he has to take the medicine regularly, and every one knows the difficulty of getting patients to take medicine regularly unless they have symptoms present.Indeed, It seems to me that the intramuecular method does away with the dread of publicity; his friends cannot ask him why he is always taking "that medicine.'It minimizes the expense and provides a remedy for the innate carelessness of the individual-the three points on which Dr. Hall lays stress.-Iam, etc.,
Oral Bisphosphonate Use and Breast Cancer Incidence in Postmenopausal Women
Authors: Rowan T. Chlebowski, Zhao Chen, Jane A. Cauley, Garnet Anderson, Rebecca J. Rodabough, Anne McTiernan, Dorothy S. Lane, JoAnn E. Manson, Linda Snetselaar, Shagufta Yasmeen, Mary Jo O'Sullivan, Monika Safford, Susan L. Hendrix, Robert B. Wallace
Journal: Journal of Clinical Oncology (2010)

Purpose Emerging clinical evidence suggests intravenous bisphosphonates may inhibit breast cancer while oral bisphosphonates have received limited evaluation regarding breast cancer influence. Patients and Methods The association between oral bisphosphonate use and invasive breast cancer was examined in postmenopausal women enrolled onto the Women's Health Initiative (WHI). We compared a published hip fracture prediction model, which did not incorporate bone mineral density (BMD), with total hip BMD in 10,418 WHI participants who had both determinations. To adjust for potential BMD difference based on bisphosphonate use, the hip fracture prediction score was included in multivariant analyses as a BMD surrogate. Results Of the 154,768 participants, 2,816 were oral bisphosphonate users at entry (90% alendronate, 10% etidronate). As calculated hip fracture risk score was significantly associated with both BMD (regression line = 0.79 to 0.0478 log predicted fracture; P &lt; .001; r = 0.43) and breast cancer incidence (P = .03), this variable was incorporated into regression analyses to adjust for BMD difference between users and nonusers of bisphopshonate. After 7.8 mean years of follow-up (standard deviation, 1.7), invasive breast cancer incidence was lower in bisphosphonate users (hazard ratio [HR], 0.68; 95% CI, 0.52 to 0.88; P &lt; .01) as was incidence of estrogen receptor (ER) –positive invasive cancers (HR, 0.70; 95% CI, 0.52 to 0.94, P = .02). A similar but not significant trend was seen for ER-negative invasive cancers. The incidence of ductal carcinoma in situ was higher in bisphosphonate users (HR, 1.58; 95% CI, 1.08 to 2.31; P = .02). Conclusion Oral bisphosphonate use was associated with significantly lower invasive breast cancer incidence, suggesting bisphosphonates may have inhibiting effects on breast cancer.
EMT and Stem Cell–Like Properties Associated with miR-205 and miR-200 Epigenetic Silencing Are Early Manifestations during Carcinogen-Induced Transformation of Human Lung Epithelial Cells
Authors: Carmen S. Tellez, Daniel E. Juri, Kieu Do, Amanda M. Bernauer, Cindy L. Thomas, Leah A. Damiani, Mathewos Tessema, Shuguang Leng, Steven A. Belinsky
Journal: Cancer Research (2011)

Abstract Epithelial-to-mesenchymal transition (EMT) is strongly associated with cancer progression, but its potential role during premalignant development has not been studied. Here, we show that a 4-week exposure of immortalized human bronchial epithelial cells (HBEC) to tobacco carcinogens can induce a persistent, irreversible, and multifaceted dedifferentiation program marked by EMT and the emergence of stem cell–like properties. EMT induction was epigenetically driven, initially by chromatin remodeling through H3K27me3 enrichment and later by ensuing DNA methylation to sustain silencing of tumor-suppressive microRNAs (miRNA), miR-200b, miR-200c, and miR-205, which were implicated in the dedifferentiation program in HBECs and also in primary lung tumors. Carcinogen-treated HBECs acquired stem cell–like features characterized by their ability to form spheroids with branching tubules and enrichment of the CD44high/CD24low, CD133, and ALDH1 stem cell–like markers. miRNA overexpression studies indicated that regulation of the EMT, stem-like, and transformed phenotypes in HBECs were distinct events. Our findings extend present concepts of how EMT participates in cancer pathophysiology by showing that EMT induction can participate in cancer initiation to promote the clonal expansion of premalignant lung epithelial cells. Cancer Res; 71(8); 3087–97. ©2011 AACR.
OBSERVATIONS WITH THE ELECTRON MICROSCOPE ON CELLS OF THE CHICK CHORIO-ALLANTOIC MEMBRANE INFECTED WITH INFLUENZA VIRUS
Authors: J. S. Murphy, F. B. Bang
Journal: The Journal of Experimental Medicine (1952)

Preparations of influenza-infected chick chorio-allantoic membrane made by two types of tissue culture and by sectioning, have been studied in the electron microscope. Comparisons have been made of influenza A' (FM1), influenza A (PR8), and swine influenza (V15), three strains which produce different relative numbers of filaments. Normal surface projections which may be confused with influenza filaments are described. Extruded products of degenerating cells, usually bleb-shaped, may also be found both in uninfected allantoic fluid and tissue cultures. It appears that the filaments and spheres of influenza virus, concurrently projecting from the free cell surface, represent the only visible change in the cells until late in the infection,-how late the present work does not tell. No definite evidence of a generalized infection throughout the cytoplasm or of inclusions was found. Additional evidence is presented for the assumption that the filaments have a significant role in the final development of the free virus.