tbuckley/cabot-search huggingface dataset:
Radiofrequency ablation of very-early-stage hepatocellular carcinoma inconspicuous on fusion imaging with B-mode US: value of fusion imaging with contrast-enhanced US
Authors: Ji Hye Min, Hyo Keun Lim, Sanghyeok Lim, Tae Wook Kang, Kyoung Doo Song, Seo-youn Choi, Hyunchul Rhim, Min Woo Lee
Journal: Clinical and Molecular Hepatology (2014)

Background/Aims To determine the value of fusion imaging with contrast-enhanced ultrasonography (CEUS) and computed tomography (CT)/magnetic resonance (MR) images for percutaneous radiofrequency ablation (RFA) of very-early-stage hepatocellular carcinomas (HCCs) that are inconspicuous on fusion imaging with B-mode ultrasound (US) and CT/MR images. Methods This retrospective study was approved by our institutional review board and the requirement for informed consent was waived. Fusion imaging with CEUS using Sonazoid contrast agent and CT/MR imaging was performed on HCCs (<2 cm) that were inconspicuous on fusion imaging with B-mode US. We evaluated the number of cases that became conspicuous on fusion imaging with CEUS. Percutaneous RFA was performed under the guidance of fusion imaging with CEUS. Technical success and major complication rates were assessed. Results In total, 30 patients with 30 HCCs (mean, 1.2 cm; range, 0.6-1.7 cm) were included, among which 25 (83.3%) became conspicuous on fusion imaging with CEUS at the time of the planning US and/or RFA procedure. Of those 25 HCCs, RFA was considered feasible for 23 (92.0%), which were thus treated. The technical success and major complication rates were 91.3% (21/23) and 4.3% (1/23), respectively. Conclusions Fusion imaging with CEUS and CT/MR imaging is highly effective for percutaneous RFA of very-early-stage HCCs inconspicuous on fusion imaging with B-mode US and CT/MR imaging. Keywords: Hepatocellular carcinoma; Radiofrequency ablation; Contrast-enhanced ultrasonography; Sonazoid; Fusion imaging
Two Cases of Intractable Uterine Haemorrhage for which Vaginal Hysterectomy was Performed
Authors: C. E. Purslow
Journal: BMJ (1899)

There can be no doubt that the crotchet hook had penetrated the vaginal roof through the posterior fornix, (a) judging from this case alone, for two reasons: (i) the position the crochet hook occupied in the peritoneal cavity, and (2) the length of the crochet hook, 41 inches, (b) associating this case with the report of a similar case before the Royal Medical and Chirurgical Society' in May, I855, by Mr. Erichsen and
Mammary-Specific Ron Receptor Overexpression Induces Highly Metastatic Mammary Tumors Associated with β-Catenin Activation
Authors: Glendon M. Zinser, Mike A. Leonis, Kenya Toney, Peterson Pathrose, Megan Thobe, Sarah A. Kader, Belinda E. Peace, Shirelyn R. Beauman, Margaret H. Collins, Susan E. Waltz
Journal: Cancer Research (2006)

Abstract Activated growth factor receptor tyrosine kinases (RTK) play pivotal roles in a variety of human cancers, including breast cancer. Ron, a member of the Met RTK proto-oncogene family, is overexpressed or constitutively active in 50% of human breast cancers. To define the significance of Ron overexpression and activation in vivo, we generated transgenic mice that overexpress a wild-type or constitutively active Ron receptor in the mammary epithelium. In these animals, Ron expression is significantly elevated in mammary glands and leads to a hyperplastic phenotype by 12 weeks of age. Ron overexpression is sufficient to induce mammary transformation in all transgenic animals and is associated with a high degree of metastasis, with metastatic foci detected in liver and lungs of &amp;gt;86% of all transgenic animals. Furthermore, we show that Ron overexpression leads to receptor phosphorylation and is associated with elevated levels of tyrosine phosphorylated β-catenin and the up-regulation of genes, including cyclin D1 and c-myc, which are associated with poor prognosis in patients with human breast cancers. These studies suggest that Ron overexpression may be a causative factor in breast tumorigenesis and provides a model to dissect the mechanism by which the Ron induces transformation and metastasis. (Cancer Res 2006; 66(24): 11967-74)
Capture-recapture as a tool for programme evaluation
Authors: C. Watts, A. Zwi, D. Wilson, S. Mashababe, G. Foster
Journal: BMJ (1994)

vasodilatation induced by prostaglandin, just as readily as it fits with the use of trimethoprim.Once the patient was well again, non-steroidal antiinflammatory drugs would not be expected to cause problems, and thus rechallenge with the drug would be of no discriminatory value in this case.It seems unnecessary to propose an unusual effect of trimethoprim when the case is readily explained by the known and commonly observed effects ofnon-steroidal anti-inflammatory drugs, C A O'CALLAGHAN Renal Unit, Guy's Hospital, London SEl 9RT
Health department approves more than 100 private firms to run NHS services
Authors: G. Iacobucci
Journal: BMJ (2013)

More than 100 private firms have been given the green light to provide a host of NHS services in England under the government’s “any qualified provider” scheme.

Department of Health figures show that 105 private companies have been approved to run services such as physiotherapy, adult hearing services, and community diagnostics, alongside 140 NHS organisations.

Firms such as Care UK, Virgin Care, and BMI Healthcare are set to increase their share of NHS service provision through the new policy, which allows accredited private, NHS, and not for profit providers to operate a range of NHS community and mental health services without undergoing a …
Calmodulin-Androgen Receptor (AR) Interaction: Calcium-Dependent, Calpain-Mediated Breakdown of AR in LNCaP Prostate Cancer Cells
Authors: Ronald P. Pelley, Kannagi Chinnakannu, Shalini Murthy, Faith M. Strickland, Mani Menon, Q. Ping Dou, Evelyn R. Barrack, G. Prem-Veer Reddy
Journal: Cancer Research (2006)

Abstract Chemotherapy of prostate cancer targets androgen receptor (AR) by androgen ablation or antiandrogens, but unfortunately, it is not curative. Our attack on prostate cancer envisions the proteolytic elimination of AR, which requires a fuller understanding of AR turnover. We showed previously that calmodulin (CaM) binds to AR with important consequences for AR stability and function. To examine the involvement of Ca2+/CaM in the proteolytic breakdown of AR, we analyzed LNCaP cell extracts that bind to a CaM affinity column for the presence of low molecular weight forms of AR (intact AR size, ∼114 kDa). Using an antibody directed against the NH2-terminal domain (ATD) of AR on Western blots, we identified ∼76-kDa, ∼50-kDa, and 34/31-kDa polypeptides in eluates of CaM affinity columns, suggesting the presence of CaM-binding sites within the 31/34-kDa ATD of AR. Under cell-free conditions in the presence of phenylmethylsulfonyl fluoride, AR underwent Ca2+-dependent degradation. AR degradation was inhibited by N-acetyl-leu-leu-norleu, an inhibitor of thiol proteases, suggesting the involvement of calpain. In intact cells, AR breakdown was accelerated by raising intracellular Ca2+ using calcimycin, and increased AR breakdown was reversed with the cell-permeable Ca2+ chelator bis-(O-aminophenoxy)-ethane-N,N,N′,N′-tetraacetic acid tetra-(acetoxymethyl)-ester. In CaM affinity chromatography studies, the Ca2+-dependent protease calpain was bound to and eluted from the CaM-agarose column along with AR. Caspase-3, which plays a role in AR turnover under stress conditions, did not bind to the CaM column and was present in the proenzyme form. Similarly, AR immunoprecipitates prepared from whole-cell extracts of exponentially growing LNCaP cells contained both calpain and calpastatin. Nuclear levels of calpain and calpastatin (its endogenous inhibitor) changed in a reciprocal fashion as synchronized LNCaP cells progressed from G1 to S phase. These reciprocal changes correlated with changes in AR level, which increased in late G1 phase and decreased as S phase progressed. Taken together, these observations suggest potential involvement of AR-bound CaM in calcium-controlled, calpain-mediated breakdown of AR in prostate cancer cells. (Cancer Res 2006; 66(24): 11754-62)
Primary Care Interventions to Prevent Child Maltreatment: U.S. Preventive Services Task Force Recommendation Statement
Authors: Virginia A. Moyer
Journal: Annals of Internal Medicine (2013)

Chinese translationUpdate of the child abuse and neglect portion of the 2004 U.S. Preventive Services Task Force (USPSTF) recommendation statement on screening for family and intimate partner violence.The USPSTF commissioned a systematic review on interventions to prevent child maltreatment for children at risk, focusing on new studies and evidence gaps that were unresolved at the time of the 2004 recommendation. Beneficial outcomes considered include reduced exposure to maltreatment and reduced harms to physical or mental health or mortality.This recommendation applies to children in the general U.S. population from newborn to age 18 years who do not have signs or symptoms of maltreatment.The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of primary care interventions to prevent child maltreatment. (I statement).
Antibiotics Increase Incidence of Hepatitis
Authors: Murry M. Robinson
Journal: JAMA (1961)

<h3>To the Editor:—</h3> Cholestatic hepatitis due to intrahepatic disease but mimicking extrahepatic obstruction due to the use of chlorpromazine, proclorperazine, methyltestosterone, and other drugs has been reported. Hepatocellular hepatitis caused by iproniazide and cinchophen has also been observed, but, to the best of my knowledge, no critical reports of hepatic dysfunction, which does not completely fit either of the types above, and due to antibiotics have appeared. A variety of types of hepatotoxicity has occurred in approximately 12% of patients who have been treated in excess of 14 days with triacetyloleandomycin or erythromycin propionyl ester with lauryl sulfate. The hepatotoxicity may be discovered purely on a laboratory level where it is characterized by increased transaminase levels, hyperbilirubinemia, and increased peripheral eosinophilia, while flocculation tests and alkaline phosphatase levels remain within normal limits, or it may be accompanied by clinical symptoms which may be quite severe and which resemble those of
Prognostic value of deep sequencing method for minimal residual disease detection in multiple myeloma
Authors: Joaquin Martinez-Lopez, Juan J. Lahuerta, François Pepin, Marcos González, Santiago Barrio, Rosa Ayala, Noemí Puig, María A. Montalban, Bruno Paiva, Li Weng, Cristina Jiménez, María Sopena, Martin Moorhead, Teresa Cedena, Immaculada Rapado, María Victoria Mateos, Laura Rosiñol, Albert Oriol, María J. Blanchard, Rafael Martínez, Joan Bladé, Jesús San Miguel, Malek Faham, Ramón García-Sanz
Journal: Blood (2014)
Clazosentan for patients with subarachnoid haemorrhage: lessons learned – Authors' reply
Authors: R Loch Macdonald, Randall T Higashida, Emanuela Keller, Stephan A Mayer, Andy Molyneux, Andreas Raabe, Peter Vajkoczy, Isabel Wanke, Doris Bach, Aline Frey, Angelina Marr, Sébastien Roux, Neal Kassell
Journal: The Lancet Neurology (2011)
MicroRNA-519c Suppresses Hypoxia-Inducible Factor-1α Expression and Tumor Angiogenesis
Authors: Shih-Ting Cha, Pai-Sheng Chen, Gunnar Johansson, Chia-Yu Chu, Ming-Yang Wang, Yung-Ming Jeng, Sung-Liang Yu, Jin-Shing Chen, King-Jen Chang, Shiou-Hwa Jee, Ching-Ting Tan, Ming-Tsan Lin, Min-Liang Kuo
Journal: Cancer Research (2010)

Hypoxia-inducible factor-1alpha (HIF-1alpha) is widely considered to be one of the key regulators of tumor angiogenesis. The upstream regulation is complex and involves several growth factors, cytokines, and hypoxia. Herein, we have identified miR-519c as a hypoxia-independent regulator of HIF-1alpha, acting through direct binding to the HIF-1alpha 3' untranslated region and leading to reduced tumor angiogenesis. Overexpression of miR-519c resulted in a significant decrease of HIF-1alpha protein levels and reduced the tube formation of human umbilical vein endothelial cells; similarly, antagomir inhibition of miR-519c increased the level of HIF-1alpha protein and enhanced angiogenic activity, suggesting an important role of miR-519c in HIF-1alpha-mediated angiogenesis. Consistent with the overexpression of miR-519c in cancer patients with better prognosis, mice injected with miR-519c-overexpressing cells exhibited dramatically reduced HIF-1alpha levels, followed by suppressed tumor angiogenesis, growth, and metastasis. In addition, we found that hepatocyte growth factor (HGF), a known HIF-1alpha inducer, reduced the miR-519c levels through an Akt-dependent pathway. This regulation was posttranscriptional and may be mediated by suppression of miR-519c maturation. Taken together, our findings provide the first evidence that miR-519c is a pivotal regulator of tumor angiogenesis and that microenvironmental HGF contributes to regulating miR-519c biogenesis in cancer cells.
Portal Hypertension: A Multidisciplinary Approach to Current Clinical Management.
Authors: P C HAYES
Journal: Gut (1999)

Portal Hypertension: A Multidisciplinary Approach to Current Clinical Management. Edited by Knechtle SJ. (Pp 298; illustrated; $150.00/£93.75.) Futura Publishing Company, 1998. ISBN 0-87993-414-X.

I am sure most academics, from time to time, have considered writing a monograph about their favourite subject. Enthusiasm soon wanes however with the realisation of the amount of work and when publishers introduce market related factors such as cost (around £50), authorship (ideally international), usefulness to trainees, etc. The authors of this book however went ahead to write a 300 page monograph on portal hypertension costing $150 and written exclusively by American authors, half of whom are from the same institution.

The first thing that strikes me about this book is that it is surgically orientated, which is perhaps not surprising given the authors, but what is surprising is its concentration on transjugular intrahepatic portosystemic stent shunts (TIPSS). Most …
357 POSITRON EMISSION TOMOGRAPHY (PET/CT) USING FLUORO-CHOLINE ALLOWS TO DIFFERENTIATE ADENOMA FROM FOCAL NODULAR HYPERPLASIA
Authors: F. Bumsel, V. Huchet, L. Arrive, D. Wendum, F. Paye, R. Poupon, J.N. Talbot, O. Rosmorduc
Journal: Journal of Hepatology (2008)
A monoclonal antibody to the carboxyterminal domain of procollagen type I visualizes collagen-synthesizing fibroblasts. Detection of an altered fibroblast phenotype in lungs of patients with pulmonary fibrosis.
Authors: J A McDonald, T J Broekelmann, M L Matheke, E Crouch, M Koo, C Kuhn
Journal: Journal of Clinical Investigation (1986)

Excessive collagen deposition plays a critical role in the development of fibrosis, and early or active fibrosis may be more susceptible to therapeutic intervention than later stages of scarring. However, at present there is no simple method for assessing the collagen-synthesizing and secreting activity of fibroblasts in human tissues. Type I procollagen carboxyterminal domains are proteolytically removed during collagen secretion. Thus, antibodies to these domains should stain fibroblasts synthesizing type I collagen but not extracellular collagen fibrils which could mask the signal from the cells. We developed and characterized a monoclonal antibody (Anti-pC) specific for the carboxyterminal propeptide of type I procollagen. To determine the relationship between Anti-pC staining and collagen synthesis, we stained embryonic and adult chicken tendon. Embryonic chick tendon fibroblasts actively synthesizing type I collagen stained heavily with Anti-pC, while quiescent adult tendon fibroblasts did not stain with Anti-pC. Wounded adult tendons developed fibroblasts that stained with Anti-pC at the wound site. Thus, Anti-pC specifically visualized fibroblasts actively synthesizing collagen. Lung biopsies from patients with fibrotic lung disease were stained with Anti-pC. Interstitial and intraalveolar fibroblasts in biopsies from patients with active fibrosis stained intensely with Anti-pC, while normal human lung was unstained. The absence of staining in normal lung supports the hypothesis that fibrosis is associated with an altered collagen-synthesizing phenotype of tissue fibroblasts. Anti-pC may provide a useful clinical tool for assessing fibrogenic activity at sites of tissue injury.
Protein Kinase C α Is a Central Signaling Node and Therapeutic Target for Breast Cancer Stem Cells
Authors: Wai Leong Tam, Haihui Lu, Joyce Buikhuisen, Boon Seng Soh, Elgene Lim, Ferenc Reinhardt, Zhenhua Jeremy Wu, Jordan A. Krall, Brian Bierie, Wenjun Guo, Xi Chen, Xiaole Shirley Liu, Myles Brown, Bing Lim, Robert A. Weinberg
Journal: Cancer Cell (2013)
Correlation between the bronchial subepithelial layer and whole airway wall thickness in patients with asthma
Authors: K Kasahara
Journal: Thorax (2002)

The epithelial reticular basement membrane (Rbm) of the airway wall thickens in patients with asthma. However, whether the thickening parallels whole airway wall thickening, which limits airflow, is unknown. The aim of this study was to examine the correlation between the bronchial Rbm thickening and whole airway wall thickening in asthma. In addition, the association of Rbm and whole wall thickening with airflow obstruction was examined.Forty nine patients with asthma and 18 healthy control subjects took part in the study. The Rbm thickness was measured in bronchial biopsy specimens and whole airway wall thickness was assessed with high resolution computed tomographic (HRCT) scanning after pretreatment with oral steroids for 2 weeks and inhaled beta2 agonist to minimise reversible changes of the airway walls. The percentage airway wall area (WA%; defined as (wall area/total airway area) x 100) and percentage airway wall thickness (WT%; defined as [(ideal outer diameter - ideal luminal diameter)/ideal outer diameter] x 100) were determined from HRCT scans to assess whole airway wall thickness. Spirometric tests were also performed.WA% and WT% were higher in patients with asthma than in healthy subjects. Both WA% and WT% were strongly correlated with Rbm thickness. Moreover, these three indices of airway wall thickness were inversely correlated with the percentage of predicted forced expiratory volume in 1 second in patients with asthma.These findings indicate that Rbm thickening parallels whole airway wall thickening which can cause irreversible airflow obstruction in patients with asthma.
Report warns of continuing violations of code on breast milk substitute marketing
Authors: Susan Mayor
Journal: BMJ (2004)

Many manufacturers of breast milk substitutes continue to violate an international code on marketing, a new report published last week says.

The report analysed the promotional practices of 16 international baby food companies and 14 bottle and teat companies between January 2002 and April 2004. It was published by the International Baby Food Action Network, a coalition of public interest groups working to reduce infant morbidity and mortality, as …
1010. A β-hCG Expressing Trackable and Tumor Targeted Conditionally Replicating Adenovirus for Treatment of Prostate Cancer
Authors: Maria Rajecki, Anna Kanerva, Lotta Kangasniemi, Kah-Whye Peng, Merja Sarkioja, Ulf-Hakan Stenman, Henrik Alfthan, Akseli Hemminki
Journal: Molecular Therapy (2005)

Background: Prostate cancer is the most common cancer among males. Despite some recent advances in the treatment of advanced prostate cancer, disseminated hormone refractory disease remains incurable and causes significant mortality. The use of conditionally replicating adenoviruses (CRAds) in the treatment of cancer is intriguing because of their capability to replicate and cause oncolysis of tumor cells. Moreover, they can be used as vectors to deliver a gene of interest into cancer cells. However, the transduction efficacy of native Ad5 is often low due to variable expression of the coxsackie-adenovirus receptor (CAR) on advanced prostate tumor cells. Further, little data is available on the in vivo persistence or magnitude of virus replication. Such data might be obtainable by coupling virus replication to expression of a secretable marker, measurable in blood. One promising molecule in this regard is the human chorionic gonadotropin -chain (-hCG). Because men are unlikely to produce large amounts of this molecule (used routinely as a pregnancy test) and the baseline production in prostate tumor cells is low, the amount of -hCG in blood during treatment with a virus expressing -hCG could provide a non-invasive approach to evaluate the persistence and amplitude of virus replication.
Abstract 1377: Characterisation of mechanisms of resistance to sunitinib in a unique pre-clinical RCC model
Authors: Melissa Taylor, Amélie Barthélémy, Bernard Escudier, Françoise Farace
Journal: Cancer Research (2012)

Abstract Background: Resistance to sunitinib, a broad spectrum tyrosine kinase inhibitor considered as first-line therapy for advanced clear cell renal carcinoma (ccRCC), is almost inevitable in patients. However, understanding the mechanisms underlying resistance to sunitinib remains incomplete. In order to decipher underlying drug-induced resistance mechanisms and identify potential targets to overcome sunitinib resistance in ccRCC, we developed a unique ccRCC xenograft model that mimicked clinical resistance to sunitinib. Methods: Untreated and sunitinib-treated Balb/C mice xenografted with RENCA cells were monitored for tumor growth. Sunitinib (40 mg/kg/day) administered 5 days/7 initially inhibited growth of xenografts, but tumors escaped after 6 weeks of continuous therapy. These sunitinib-induced resistant tumors were then removed and re-implanted to naïve Balb/C mice where re-implanted tumors exhibited immediately an aggressive phenotype. Re-implanted sunitinib-resistant tumors remained refractory to further treatment with sunitinib but responded to treatment with sorafenib and rapamycine, mimicking a strategy and tumor response that is often observed in the clinical setting. Transcriptomic and proteomic analyses of untreated, sunitinib-responsive and sunitinib-resistant tumors were performed, as well as evaluations of microvessel densities and host circulating angiogenic cells. Results: The aggressive phenotype of re-implanted sunitinib-resistant tumors suggested that the drug-induced acquired resistance was of intrinsic nature. However, transcriptomic analyses showed no differences in gene expression levels between untreated, sunitinib-responsive and sunitinib-resistant tumors. Proteomic analyses of tumors and serum samples are ongoing, as well as thorough analyses of the different angiogenic cellular compartments underlying host microenvironment responses. Conclusion: We have established a unique xenograft ccRCC model that mimicks clinical resistance to sunitinib. Our results show that while sunitinib-induced resistance is apparently intrinsic, tumor and host microenvironment are most likely critical mediators of resistance. 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 1377. doi:1538-7445.AM2012-1377
Such data can benefit medicine as well as surgery
Authors: J. A. Snowden, D. Pamphilon, K. Kirkland, G. H. Jackson
Journal: BMJ (2011)

The BMJ has called for better outcome data to improve care after publication of the Society of Cardiothoracic Surgeons’ report.1 2 Both publications focus on surgery, but the situation is similar in medical specialties.

Blood and marrow transplantation has been subjected to evolving external review. Over the past decade a system of external accreditation has been rolled out throughout Europe (JACIE; …