tbuckley/cabot-search huggingface dataset:
S15 Is Contrast-Enhanced Computed Tomography (CT) Scoring a Useful tool in Predicting Pleural Malignancy on Thoracoscopy?: Abstract S15 Table 1
Authors: B Buckley, M Haris, B Miller, S Leyakathali khan, S Diver, S Kearney, M Munavvar
Journal: Thorax (2012)

<h3>Background</h3> CT and Thoracoscopy are useful tools in the evaluation of patients with pleural diseases. Previous studies have shown that certain features on CT may help in differentiating malignant and benign pleura and these may correlate with thoracoscopic findings. We aimed to assess whether a simple scoring system based on CT appearance criteria could be used to predict the likelihood of pleural malignancy. <h3>Methods</h3> 104 patients who underwent semi-rigid thoracoscopy between January 2008 and April 2012 were studied. The scans were reviewed by the Chest Radiologist who was blinded to the thoracoscopic findings and pleural biopsy results. Five CT features were given a score of 1–3, where 3 suggested a feature was present, 1 not present and 2 if uncertain. An overall impression of likelihood of malignancy was then scored 1–3, 3 being malignant, 1 benign and 2 indeterminate. Data was analysed using chi-square and logistic regression. <h3>Results</h3> N=104, mean age 74 years (range 40–93); female 35(34%), male 69(66%). Pleural biopsy histology was available in 90 of which 57 (63%) were malignant and 33 (37%) benign; 7 did not have biopsy and 7 were either insufficient or non-diagnostic. In those with malignancy, pleural thickening was noted in 43 (sensitivity 88%, specificity 34%) and nodularity in 29 (sensitivity 52%, specificity 82%) on thoracoscopy. Using a score of 1 and 3, specificity and sensitivity for circumferential/diffuse pleural thickening was 39% and 65%, nodular pleural thickening 94% and 53%, parietal pleural thickening &gt;1cm 94% and 26%, mediastinal involvement 76% and 63%, smooth pleural thickening 33% and 81%, and overall impression score was 84% and 63%. Total score ≥8 for all 5 features and the overall impression (p&lt;0.0001) was significantly associated with malignancy. A score of 3 for nodular thickening (p&lt;0.0001), parietal thickening (p=0.03), mediastinal involvement (p=0.0011) and a combined score ≥ 4 for these 3 features (sensitivity 79%, specificity 73%, p=0.0001) was highly suggestive of malignancy. <h3>Conclusion</h3> These results suggest that a CT scoring system based on the above features can be reliably used to predict pleural malignancy prompting more intensive evaluation such as thoracoscopy, although this will require further validation.
Spatial Processing in the Brain: The Activity of Hippocampal Place Cells
Authors: Phillip J. Best, Aaron M. White, Ali Minai
Journal: Annual Review of Neuroscience (2001)

The startling discovery by O'Keefe & Dostrovsky (Brain Res. 1971; 34: 171-75) that hippocampal neurons fire selectively in different regions or "place fields" of an environment and the subsequent development of the comprehensive theory by O'Keefe & Nadel (The Hippocampus as a Cognitive Map. Oxford, UK: Clarendon, 1978) that the hippocampus serves as a cognitive map have stimulated a substantial body of literature on the characteristics of hippocampal "place cells" and their relevance for our understanding of the mechanisms by which the brain processes spatial information. This paper reviews the major dimensions of the empirical research on place-cell activity and the development of computational models to explain various characteristics of place fields.
CNS Metastases in Breast Cancer: Old Challenge, New Frontiers
Authors: Nancy U. Lin, Laleh Amiri-Kordestani, Diane Palmieri, David J. Liewehr, Patricia S. Steeg
Journal: Clinical Cancer Research (2013)

Abstract Despite major therapeutic advances in the management of patients with breast cancer, central nervous system (CNS) metastases remain an intractable problem, particularly in patients with metastatic HER2-positive and triple-negative breast cancer. As systemic therapies to treat extracranial disease improve, some patients are surviving longer, and the frequency of CNS involvement seems to be increasing. Furthermore, in the early-stage setting, the CNS remains a potential sanctuary site for relapse. This review highlights advances in the development of biologically relevant preclinical models, including the development of brain-tropic cell lines for testing of agents to prevent and treat brain metastases, and summarizes our current understanding of the biology of CNS relapse. From a clinical perspective, a variety of therapeutic approaches are discussed, including methods to improve drug delivery, novel cytotoxic agents, and targeted therapies. Challenges in current trial design and endpoints are reviewed. Finally, we discuss promising new directions, including novel trial designs, correlative imaging techniques, and enhanced translational opportunities. Clin Cancer Res; 19(23); 6404–18. ©2013 AACR.
Lasers, dermal fibroblasts and psoriasis
Authors: P. Saiag, B. Coulomb, C.M.E. Rowland-Payne, L. Dubertret, R. Touraine
Journal: British Journal of Dermatology (1986)

Journal Article Lasers, dermal fibroblasts and psoriasis Get access P. Saiag, P. Saiag Service de Dermatologie, Université Paris XII, Höpital Henri Mondor, 94010 Creteil, France Search for other works by this author on: Oxford Academic Google Scholar B. Coulomb, B. Coulomb Service de Dermatologie, Université Paris XII, Höpital Henri Mondor, 94010 Creteil, France Search for other works by this author on: Oxford Academic Google Scholar C.M.E. Rowland‐Payne, C.M.E. Rowland‐Payne Service de Dermatologie, Université Paris XII, Höpital Henri Mondor, 94010 Creteil, France Search for other works by this author on: Oxford Academic Google Scholar L. Dubertret, L. Dubertret Service de Dermatologie, Université Paris XII, Höpital Henri Mondor, 94010 Creteil, France Search for other works by this author on: Oxford Academic Google Scholar R. Touraine R. Touraine Service de Dermatologie, Université Paris XII, Höpital Henri Mondor, 94010 Creteil, France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 115, Issue 6, 1 December 1986, Pages 744–745, https://doi.org/10.1111/j.1365-2133.1986.tb06662.x Published: 01 December 1986
Sodium Orthovanadate Inhibits p53-Mediated Apoptosis
Authors: Akinori Morita, Shinichi Yamamoto, Bing Wang, Kaoru Tanaka, Norio Suzuki, Shin Aoki, Azusa Ito, Tomohisa Nanao, Soichiro Ohya, Minako Yoshino, Jin Zhu, Atsushi Enomoto, Yoshihisa Matsumoto, Osamu Funatsu, Yoshio Hosoi, Masahiko Ikekita
Journal: Cancer Research (2010)

Abstract Sodium orthovanadate (vanadate) inhibits the DNA-binding activity of p53, but its precise effects on p53 function have not been examined. Here, we show that vanadate exerts a potent antiapoptotic activity through both transcription-dependent and transcription-independent mechanisms relative to other p53 inhibitors, including pifithrin (PFT) α. We compared the effects of vanadate to PFTα and PFTμ, an inhibitor of transcription-independent apoptosis by p53. Vanadate suppressed p53-associated apoptotic events at the mitochondria, including the loss of mitochondrial membrane potential, the conformational change of Bax and Bak, the mitochondrial translocation of p53, and the interaction of p53 with Bcl-2. Similarly, vanadate suppressed the apoptosis-inducing activity of a mitochondrially targeted temperature-sensitive p53 in stable transfectants of SaOS-2 cells. In radioprotection assays, which rely on p53, vanadate completely protected mice from a sublethal dose of 8 Gy and partially from a lethal dose of 12 Gy. Together, our findings indicated that vanadate effectively suppresses p53-mediated apoptosis by both transcription-dependent and transcription-independent pathways, and suggested that both pathways must be inhibited to completely block p53-mediated apoptosis. Cancer Res; 70(1); 257–65
Is Relative Risk Reduction a Useful Measure for Patients or Families Who Must Choose a Method of Treatment?
Authors: H. Sam Wieand
Journal: Journal of Clinical Oncology (2003)

Article Tools EDITORIALS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2003.08.998 Journal of Clinical Oncology - published online before print November 1, 2016 PMID: 14581445 Is Relative Risk Reduction a Useful Measure for Patients or Families Who Must Choose a Method of Treatment? H. Sam WieandxH. Sam WieandSearch for articles by this author Show More University of Pittsburgh Cancer Institute Biostatistics Facility, Pittsburgh, PA https://doi.org/10.1200/JCO.2003.08.998 Full Text PDF Figures and Tables "Is Relative Risk Reduction a Useful Measure for Patients or Families Who Must Choose a Method of Treatment?." Journal of Clinical Oncology, 21(23), pp. 4263–4264© 2003 by American Society of Clinical Oncology
Councils could help new GP commissioning consortia with "back room" support
Authors: A. O'Dowd
Journal: BMJ (2010)

The new GP commissioning consortia that will control much of the NHS budget from 2013 may get some help from local authorities for joint “back room” support, MPs have been told.

Some services such as administration and human resources could be provided jointly for more than one GP consortium as well as for councils, as one possible example of closer joint working between health bodies and local authorities.

MPs on the parliamentary health select committee were quizzing NHS and local government witnesses as part of their ongoing inquiry into public expenditure.

Focusing on the implications of the government’s comprehensive spending review and plans to tighten public spending, the MPs …
Ghrelin controls hippocampal spine synapse density and memory performance
Authors: Sabrina Diano, Susan A Farr, Stephen C Benoit, Ewan C McNay, Ivaldo da Silva, Balazs Horvath, F Spencer Gaskin, Naoko Nonaka, Laura B Jaeger, William A Banks, John E Morley, Shirly Pinto, Robert S Sherwin, Lin Xu, Kelvin A Yamada, Mark W Sleeman, Matthias H Tschöp, Tamas L Horvath
Journal: Nature Neuroscience (2006)
Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn's disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density
Authors: M T Abreu
Journal: Gut (2004)

<b>Objectives:</b> Many patients with Crohn’s disease (CD) have low bone mineral density (BMD) that may not be solely attributable to glucocorticoid use. We hypothesised that low BMD in patients with CD is associated with elevated circulating levels of the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)<sub>2</sub>D). We further hypothesised that this was secondary to increased synthesis of 1,25(OH)<sub>2</sub>D by inflammatory cells in the intestine. The aim of this study was to examine the relationship between 1,25(OH)<sub>2</sub>D levels and BMD in patients with CD. <b>Methods:</b> An IRB approved retrospective review of medical records from patients with CD (n = 138) or ulcerative colitis (UC, n = 29). Measurements of vitamin D metabolites and immunoreactive parathyroid hormone (iPTH) were carried out. BMD results were available for 88 CD and 20 UC patients. Immunohistochemistry or real time reverse transcription-polymerase chain reaction (RT-PCR) for the enzyme 1α-hydroxylase was performed on colonic biopsies from patients with CD (14) or UC (12) and normal colons (4). <b>Results:</b> Inappropriately high levels of serum 1,25(OH)<sub>2</sub>D (&gt;60 pg/ml) were observed in 42% of patients with CD compared with only 7% in UC, despite no differences in mean iPTH. Serum 1,25(OH)<sub>2</sub>D levels were higher in CD (57 pg/ml) versus UC (41 pg/ml) (p = 0.0001). In patients with CD, there was a negative correlation between 1,25(OH)<sub>2</sub>D levels and lumbar BMD (<i>r</i> = −0.301, p = 0.005) independent of therapeutic glucocorticoid use. 1,25(OH)<sub>2</sub>D levels also correlated with CD activity. Lastly, immunohistochemistry and RT-PCR demonstrated increased expression of intestinal 1α-hydroxylase in patients with CD. <b>Conclusions:</b> These data demonstrate that elevated 1,25(OH)<sub>2</sub>D is more common in CD than previously appreciated and is independently associated with low bone mineral density. The source of the active vitamin D may be the inflamed intestine. Treatment of the underlying inflammation may improve metabolic bone disease in this subgroup of patients.
Mesenteric Fat Thickness Is an Independent Determinant of Metabolic Syndrome and Identifies Subjects With Increased Carotid Intima-Media Thickness
Authors: Kin Hung Liu, Yu Leung Chan, Wing Bun Chan, Juliana Chung Ngor Chan, Chiu Wing Winnie Chu
Journal: Diabetes Care (2006)

OBJECTIVE—Mesenteric fat, a reflection of visceral adiposity, may play an important role in the pathogenesis of metabolic syndrome and cardiovascular diseases (CVD). In this study, we examined the independent relationship between mesenteric fat thickness and metabolic syndrome and defined its optimal cutoff value to identify high-risk subjects for metabolic syndrome and CVD. RESEARCH DESIGN AND METHODS—A total of 290 Chinese subjects had an ultrasound examination for measurements of thickness of mesenteric, preperitoneal, and subcutaneous fat as well as carotid intima-media thickness (IMT). Anthropometric measurements and metabolic risk profile were assessed by physical examination and blood taking. RESULTS—Twenty (6.9%) subjects had metabolic syndrome according to the National Cholesterol Education Panel Adult Treatment Panel III criteria with Asian definitions for central obesity (waist circumference &amp;gt;80 cm in women and &amp;gt;90 cm in men). Mesenteric fat thickness had significant correlations (P &amp;lt; 0.05) with various metabolic variables. On multivariate regression, mesenteric fat thickness was an independent determinant of all components of metabolic syndrome after adjustment for age, sex, homeostasis model assessment of insulin resistance, and other fat deposits. The odds ratio of metabolic syndrome was increased by 1.35 (95% CI 1.10–1.66)-fold for every 1-mm increase in mesenteric fat thickness. On receiver-operating characteristic curve analysis, mesenteric fat thickness of ≥10 mm was the optimal cutoff value to identify metabolic syndrome, with sensitivity of 70% and specificity of 75%. Subjects with mesenteric fat thickness ≥10 mm had higher carotid IMT than those with thickness &amp;lt;10 mm (0.73 ± 0.19 vs. 0.64 ± 0.16 mm, P = 0.001). CONCLUSIONS—Mesenteric fat thickness was an independent determinant of metabolic syndrome and identified subjects with increased carotid IMT.
Epigenetic Silencing of <i>MicroRNA-34b/c</i> and <i>B-Cell Translocation Gene 4</i> Is Associated with CpG Island Methylation in Colorectal Cancer
Authors: Minoru Toyota, Hiromu Suzuki, Yasushi Sasaki, Reo Maruyama, Kohzoh Imai, Yasuhisa Shinomura, Takashi Tokino
Journal: Cancer Research (2008)

Abstract Altered expression of microRNA (miRNA) is strongly implicated in cancer, and recent studies have shown that, in cancer, expression of some miRNAs cells is silenced in association with CpG island hypermethylation. To identify epigenetically silenced miRNAs in colorectal cancer (CRC), we screened for miRNAs induced in CRC cells by 5-aza-2′-deoxycytidine (DAC) treatment or DNA methyltransferase knockout. We found that miRNA-34b (miR-34b) and miR-34c, two components of the p53 network, are epigenetically silenced in CRC; that this down-regulation of miR-34b/c is associated with hypermethylation of the neighboring CpG island; and that DAC treatment rapidly restores miR-34b/c expression. Methylation of the miR-34b/c CpG island was frequently observed in CRC cell lines (nine of nine, 100%) and in primary CRC tumors (101 of 111, 90%), but not in normal colonic mucosa. Transfection of precursor miR-34b or miR-34c into CRC cells induced dramatic changes in the gene expression profile, and there was significant overlap between the genes down-regulated by miR-34b/c and those down-regulated by DAC. We also found that the miR-34b/c CpG island is a bidirectional promoter which drives expression of both miR-34b/c and B-cell translocation gene 4 (BTG4); that methylation of the CpG island is also associated with transcriptional silencing of BTG4; and that ectopic expression of BTG4 suppresses colony formation by CRC cells. Our results suggest that miR-34b/c and BTG4 are novel tumor suppressors in CRC and that the miR-34b/c CpG island, which bidirectionally regulates miR-34b/c and BTG4, is a frequent target of epigenetic silencing in CRC. [Cancer Res 2008;68(11):4123–32]
Skin homing of Sézary cells involves SDF-1-CXCR4 signaling and down-regulation of CD26/dipeptidylpeptidase IV
Authors: Maria Grazia Narducci, Enrico Scala, Antonella Bresin, Elisabetta Caprini, Maria Cristina Picchio, Daniele Remotti, Gianluca Ragone, Francesca Nasorri, Marina Frontani, Diego Arcelli, Stefano Volinia, Giuseppe Alfonso Lombardo, Giannandrea Baliva, Monica Napolitano, Giandomenico Russo
Journal: Blood (2005)
A case of erythrokeratoderma variabilis without mutations in connexin 31
Authors: A. Ishida‐Yamamoto, D. Kelsell, J. Common, M.J. Houseman, M. Hashimoto, H. Shibaki, K. Asano, H. Takahashi, Y. Hashimoto, T. Senshu, I.M. Leigh, H. Iizuka
Journal: British Journal of Dermatology (2000)

Erythrokeratoderma (EK) variabilis is a heterogeneous group of diseases characterized by migratory erythematous patches and hyperkeratotic plaques. Mutations in connexin 31 have recently been found to underlie several cases of EK variabilis. We describe a Japanese girl with extensive lesions that appeared to be a form of EK variabilis, clinically resembling genodermatose en cocardes (Degos). Our patient had characteristic migratory rosette or target-like erythematous keratotic plaques with peripheral scaling in addition to relatively fixed keratotic plaques. Sequencing of the connexin 31 gene did not detect mutations. Skin biopsy showed parakeratotic hyperkeratosis with hypergranulosis. Immunohistochemically, suprabasal keratins, involucrin and profilaggrin were unequivocally expressed, while loricrin expression was greatly diminished and deiminated K1 was undetectable. Our results confirm aetiological heterogeneity in EK. The histological features suggest disruption of keratinocyte terminal differentiation at a very late stage.
Herpes Dating Services
Authors: Benjamin Raab
Journal: JAMA (1983)

To the Editor.—  We wish to comment on herpes dating services, a new social phenomenon that has recently emerged in many large cities (eg, New York, Chicago, Los Angeles). In our opinion, such services are not only unnecessary, but they actually may be detrimental from both medical and psychosocial points of view.  Recent surveys have shown that genital herpes simplex infections may be caused by either of the two major serotypes of herpes simplex virus (type 1 and type 2). 1 Type 2 genital first infections are followed by recurrent episodes in about 60% of cases as compared with the 14% recurrence rate after type 1 virus caused first genital infections. 2 By means of restriction endonuclease analysis, it further has been shown that within each of the two major serotypes, numerous genetically different strains exist. A person can become exogenously infected or reinfected in similar or different areas with
THE VIRAL ENVELOPE GLYCOPROTEIN OF MURINE LEUKEMIA VIRUS AND THE PATHOGENESIS OF IMMUNE COMPLEX GLOMERULONEPHRITIS OF NEW ZEALAND MICE
Authors: Takashi Yoshiki, Robert C. Mellors, Mette Strand, J. T. August
Journal: The Journal of Experimental Medicine (1974)

The use of monospecific antisera for the analysis by radioimmunoassay and immunofluorescence study of two major viral proteins, gp69/71 and p30 of murine leukemia virus, that could be of significance in the pathogenesis of immune complex glomerulonephritis of mice, particularly NZB and B/WF(1) hybrid mice, yielded the following conclusions. A remarkably high concentration of viral envelope glycoprotein, gp69/71, was detected in the spleen and serum of New Zealand mice (NZB, NZW, B/WF(1), and W/BF(1)); the concentration in the spleen was 10-fold greater than that found in AKR mice and 30-fold greater than that present in C57BL/6 mice. The gp69/71 was deposited along with bound immunoglobulins, apparently as an immune complex, in the diseased kidneys of mice, and the glomerular site and extent of deposition of gp69/71 was related to the severity of the glomerulonephritis. This study suggests that the pathogenesis of immune complex glomerulonephritis (and vasculitis) in mice is related to the expression of this specific viral envelope glycoprotein and to the host immune response to this protein.
Reticular dysgenesis–associated AK2 protects hematopoietic stem and progenitor cell development from oxidative stress
Authors: Alberto Rissone, Katja Gabriele Weinacht, Giancarlo la Marca, Kevin Bishop, Elisa Giocaliere, Jayashree Jagadeesh, Kerstin Felgentreff, Kerry Dobbs, Waleed Al-Herz, Marypat Jones, Settara Chandrasekharappa, Martha Kirby, Stephen Wincovitch, Karen Lyn Simon, Yuval Itan, Alex DeVine, Thorsten Schlaeger, Axel Schambach, Raman Sood, Luigi D. Notarangelo, Fabio Candotti
Journal: The Journal of Experimental Medicine (2015)

Adenylate kinases (AKs) are phosphotransferases that regulate the cellular adenine nucleotide composition and play a critical role in the energy homeostasis of all tissues. The AK2 isoenzyme is expressed in the mitochondrial intermembrane space and is mutated in reticular dysgenesis (RD), a rare form of severe combined immunodeficiency (SCID) in humans. RD is characterized by a maturation arrest in the myeloid and lymphoid lineages, leading to early onset, recurrent, and overwhelming infections. To gain insight into the pathophysiology of RD, we studied the effects of AK2 deficiency using the zebrafish model and induced pluripotent stem cells (iPSCs) derived from fibroblasts of an RD patient. In zebrafish, Ak2 deficiency affected hematopoietic stem and progenitor cell (HSPC) development with increased oxidative stress and apoptosis. AK2-deficient iPSCs recapitulated the characteristic myeloid maturation arrest at the promyelocyte stage and demonstrated an increased AMP/ADP ratio, indicative of an energy-depleted adenine nucleotide profile. Antioxidant treatment rescued the hematopoietic phenotypes in vivo in ak2 mutant zebrafish and restored differentiation of AK2-deficient iPSCs into mature granulocytes. Our results link hematopoietic cell fate in AK2 deficiency to cellular energy depletion and increased oxidative stress. This points to the potential use of antioxidants as a supportive therapeutic modality for patients with RD.
Hypercalcemia induced with an arotinoid in thyroparathyroidectomized rats. New model to study bone resorption in vivo.
Authors: U Trechsel, A Stutzer, H Fleisch
Journal: Journal of Clinical Investigation (1987)

A model of stimulated bone resorption was developed using a synthetic retinoid in thyroparathyroidectomized rats. The retinoid induced an increase in bone resorption and in the number of vertebral subperiosteal osteoclasts. The resulting increase in plasma Ca could be used as an easily measured index of bone resorption. Three bisphosphonates produced a dose-related prevention and reversal of retinoid-induced hypercalcemia. Their potencies were similar to those previously obtained by histomorphometry. Irradiation (600 rad) of the rats prevented hypercalcemia but failed to reverse it, showing that proliferation of osteoclast precursor cells was important in inducing, but not in maintaining, bone resorption. Calcitonin produced similar effects on calcemia and prevented the increase in osteoclast number but failed to reverse the increase, suggesting that it inhibited precursor proliferation. This model represents a new tool to study mechanisms of bone resorption and the action of inhibitors in vivo.