tbuckley/cabot-search huggingface dataset:
Pulmonary function in adolescent idiopathic scoliosis: a 25 year follow up after surgery or start of brace treatment
Authors: K Pehrsson, A Danielsson, A Nachemson
Journal: Thorax (2001)

<h3>BACKGROUND</h3> Pulmonary function in patients with adolescent idiopathic scoliosis many years after posterior spinal surgery or brace treatment has not been documented. <h3>METHODS</h3> A consecutive group of patients treated by posterior fusion or a brace at least 20 years previously was investigated. 90% attended a clinical follow up. Lung volumes were determined before treatment in 251 patients, 1.4 years after surgery in 141 patients, and 25 years after surgery or start of brace treatment in 110 patients. Vital capacity (VC) was calculated as percentage predicted according to height and age and the results were corrected for loss of height due to scoliosis. Scoliosis angles were measured and smoking habits were recorded. An age and sex matched control group was also examined with the same questionnaire and pulmonary function tests. <h3>RESULTS</h3> VC increased from 67% predicted immediately before surgery to 73% (p&lt;0.001) after surgery and to 84% (p&lt;0.001) at the present follow up, mean change 10.8% (95% CI 9.5 to 12.1). In the brace treated patients VC increased from 77% predicted before treatment to 89% (p&lt;0.001) 25 years after start of treatment, mean change 12.3% (95% CI 10.5 to 14.1). The mean Cobb angle at the present follow up study was 40° in both surgically and brace treated patients. The present results of lung volumes did not correlate with pretreatment or post-treatment Cobb angles or smoking habits. <h3>CONCLUSIONS</h3> Patients treated by posterior fusion or a brace gradually increase their pulmonary function up to 25 years after treatment. Smoking and curve size are not risk factors for reduced pulmonary function.
Risk of adverse birth outcomes in populations living near landfill sites
Authors: P. Elliott
Journal: BMJ (2001)

<h3>Abstract</h3> <b>Objective:</b> To investigate the risk of adverse birth outcomes associated with residence near landfill sites in Great Britain. <b>Design:</b> Geographical study of risks of adverse birth outcomes in populations living within 2 km of 9565 landfill sites operational at some time between 1982 and 1997 (from a total of 19 196 sites) compared with those living further away. <b>Setting:</b> Great Britain. <b>Subjects:</b> Over 8.2 million live births, 43 471 stillbirths, and 124 597 congenital anomalies (including terminations). <b>Main outcome measures:</b> All congenital anomalies combined, some specific anomalies, and prevalence of low and very low birth weight (&lt;2500 g and &lt;1500 g). <b>Results:</b> For all anomalies combined, relative risk of residence near landfill sites (all waste types) was 0.92 (99% confidence interval 0.907 to 0.923) unadjusted, and 1.01 (1.005 to 1.023) adjusted for confounders. Adjusted risks were 1.05 (1.01 to 1.10) for neural tube defects, 0.96 (0.93 to 0.99) for cardiovascular defects, 1.07 (1.04 to 1.10) for hypospadias and epispadias (with no excess of surgical correction), 1.08 (1.01 to 1.15) for abdominal wall defects, 1.19 (1.05 to 1.34) for surgical correction of gastroschisis and exomphalos, and 1.05 (1.047 to 1.055) and 1.04 (1.03 to 1.05) for low and very low birth weight respectively. There was no excess risk of stillbirth. Findings for special (hazardous) waste sites did not differ systematically from those for non-special sites. For some specific anomalies, higher risks were found in the period before opening compared with after opening of a landfill site, especially hospital admissions for abdominal wall defects. <b>Conclusions:</b> We found small excess risks of congenital anomalies and low and very low birth weight in populations living near landfill sites. No causal mechanisms are available to explain these findings, and alternative explanations include data artefacts and residual confounding. Further studies are needed to help differentiate between the various possibilities. <h3>What is already known on this topic</h3> Various studies have found excess risks of certain congenital anomalies and low birth weight near landfill sites Risks up to two to three times higher have been reported These studies have been difficult to interpret because of problems of exposure classification, small sample size, confounding, and reporting bias <h3>What this study adds</h3> Some 80% of the British population lives within 2 km of known landfill sites in Great Britain By including all landfill sites in the country, we avoided the problem of selective reporting, and maximised statistical power Although we found excess risks of congenital anomalies and low birth weight near landfill sites in Great Britain, they were smaller than in some other studies Further work is needed to differentiate potential data artefacts and confounding effects from possible causal associations with landfill
Comparison of Francisella tularensis genomes reveals evolutionary events associated with the emergence of human pathogenic strains
Authors: Laurence Rohmer, Christine Fong, Simone Abmayr, Michael Wasnick, Theodore J Larson Freeman, Matthew Radey, Tina Guina, Kerstin Svensson, Hillary S Hayden, Michael Jacobs, Larry A Gallagher, Colin Manoil, Robert K Ernst, Becky Drees, Danielle Buckley, Eric Haugen, Donald Bovee, Yang Zhou, Jean Chang, Ruth Levy, Regina Lim, Will Gillett, Don Guenthener, Allison Kang, Scott A Shaffer, Greg Taylor, Jinzhi Chen, Byron Gallis, David A D'Argenio, Mats Forsman, Maynard V Olson, David R Goodlett, Rajinder Kaul, Samuel I Miller, Mitchell J Brittnacher
Journal: Genome biology (2007)

Abstract Background Francisella tularensis subspecies tularensis and holarctica are pathogenic to humans, whereas the two other subspecies, novicida and mediasiatica , rarely cause disease. To uncover the factors that allow subspecies tularensis and holarctica to be pathogenic to humans, we compared their genome sequences with the genome sequence of Francisella tularensis subspecies novicida U112, which is nonpathogenic to humans. Results Comparison of the genomes of human pathogenic Francisella strains with the genome of U112 identifies genes specific to the human pathogenic strains and reveals pseudogenes that previously were unidentified. In addition, this analysis provides a coarse chronology of the evolutionary events that took place during the emergence of the human pathogenic strains. Genomic rearrangements at the level of insertion sequences (IS elements), point mutations, and small indels took place in the human pathogenic strains during and after differentiation from the nonpathogenic strain, resulting in gene inactivation. Conclusion The chronology of events suggests a substantial role for genetic drift in the formation of pseudogenes in Francisella genomes. Mutations that occurred early in the evolution, however, might have been fixed in the population either because of evolutionary bottlenecks or because they were pathoadaptive (beneficial in the context of infection). Because the structure of Francisella genomes is similar to that of the genomes of other emerging or highly pathogenic bacteria, this evolutionary scenario may be shared by pathogens from other species.
Risk-Adapted, Combined-Modality Therapy With VAMP/COP and Response-Based, Involved-Field Radiation for Unfavorable Pediatric Hodgkin's Disease
Authors: Melissa M. Hudson, Matthew Krasin, Michael P. Link, Sarah S. Donaldson, Catherine Billups, Thomas E. Merchant, Larry Kun, Amy L. Billet, Sue Kaste, Nancy J. Tarbell, Scott Howard, Alison M. Friedmann, Craig A. Hurwitz, Jeffrey A. Young, Karen C. Marcus, Shesh Rai, Traci Cowan, Howard J. Weinstein
Journal: Journal of Clinical Oncology (2004)

To evaluate the efficacy of vinblastine, doxorubicin, methotrexate, and prednisone (VAMP) and cyclophosphamide, vincristine, and procarbazine (COP) chemotherapy and response-based, involved-field radiation, a combined-modality regimen that limits doses of alkylating agents, anthracyclines, and radiation, in children with advanced and unfavorable Hodgkin's disease.From 1993 to 2000, 159 children and adolescents with unfavorable Hodgkin's disease received three alternating cycles (total of six cycles) of VAMP/COP chemotherapy followed by response-based, involved-field radiation therapy: 15 Gy was administered to patients achieving a complete response, and 25.5 Gy was administered to those achieving a partial response after the first two cycles of chemotherapy and to all sites of bulky lymphadenopathy. Unfavorable disease was defined as clinical stage I and II with bulky peripheral nodal disease greater than 6 cm, initial bulky mediastinal mass 33% or more of the intrathoracic diameter, and/or "B" symptoms and all stage III and IV.Study enrollment was closed after an interim analysis estimated a 5-year event-free survival (EFS) rate below a predefined level. Disease presentation was localized (stage I/II) in 77 patients (48.4%) and advanced (stage III/IV) in 82 patients (51.6%). At a median follow-up of 5.8 years (range, 1.3 to 10.0 years), 38 patients had events, including relapse/progression (n = 35), second malignancy (n = 2), and accidental death (n = 1); nine relapses (25.7%) occurred greater than 4 years from diagnosis. Five-year survival and EFS estimates are 92.7% +/- 2.5% and 75.6% +/- 4.1%, respectively.Risk-adapted combined-modality therapy with VAMP/COP and response-based, involved-field radiation therapy results in an unsatisfactory outcome for pediatric patients with unfavorable presentations of Hodgkin's disease.
CXCR4 Regulates Growth of Both Primary and Metastatic Breast Cancer
Authors: Matthew C. P. Smith, Kathryn E. Luker, Joel R. Garbow, Julie L. Prior, Erin Jackson, David Piwnica-Worms, Gary D. Luker
Journal: Cancer Research (2004)

The chemokine receptor CXCR4 and its cognate ligand CXCL12 recently have been proposed to regulate the directional trafficking and invasion of breast cancer cells to sites of metastases. However, effects of CXCR4 on the growth of primary breast cancer tumors and established metastases and survival have not been determined. We used stable RNAi to reduce expression of CXCR4 in murine 4T1 cells, a highly metastatic mammary cancer cell line that is a model for stage IV human breast cancer. Using noninvasive bioluminescence and magnetic resonance imaging, we showed that knockdown of CXCR4 significantly limited the growth of orthotopically transplanted breast cancer cells. Mice in which parental 4T1 cells were implanted had progressively enlarging tumors that spontaneously metastasized, and these animals all died from metastatic disease. Remarkably, RNAi of CXCR4 prevented primary tumor formation in some mice, and all mice transplanted with CXCR RNAi cells survived without developing macroscopic metastases. To analyze effects of CXCR4 on metastases to the lung, an organ commonly affected by metastatic breast cancer, we injected tumor cells intravenously and monitored cell growth with bioluminescence imaging. Inhibiting CXCR4 with RNAi, or the specific antagonist AMD3100, substantially delayed the growth of 4T1 cells in the lung, although neither RNAi nor AMD3100 prolonged overall survival in mice with experimental lung metastases. These data indicate that CXCR4 is required to initiate proliferation and/or promote survival of breast cancer cells in vivo and suggest that CXCR4 inhibitors will improve treatment of patients with primary and metastatic breast cancer.
Tumour-like presentation of pulmonary sarcoidosis
Authors: MJ Abramowicz, V Ninane, M Depierreux, P de Francquen, JC Yernault
Journal: European Respiratory Journal (1992)

We report a case of pulmonary sarcoidosis, which initially presented as a left apical infiltrate. The later course mimicked a pulmonary neoplasm, with left upper lobe atelectasis secondary to bronchial stenosis, resulting from both endobronchial sarcoidosis and extrinsic compression by enlarged lymph nodes. Extrinsic pressure from sarcoid nodes on the left main pulmonary artery and recurrent laryngeal nerve, also caused a reduction in pulmonary parenchymal perfusion and left vocal cord paresis.
Human papillomavirus testing and liquid-based cytology in primary screening of women younger than 35 years: results at recruitment for a randomised controlled trial
Authors: Guglielmo Ronco, Paolo Giorgi-Rossi, Francesca Carozzi, Paolo Dalla Palma, Annarosa Del Mistro, Laura De Marco, Margherita De Lillo, Carlo Naldoni, Paola Pierotti, Raffaella Rizzolo, Nereo Segnan, Patrizia Schincaglia, Manuel Zorzi, Massimo Confortini, Jack Cuzick
Journal: The Lancet Oncology (2006)
Hypnotherapy in severe irritable bowel syndrome: further experience.
Authors: P J Whorwell, A Prior, S M Colgan
Journal: Gut (1987)

Fifteen patients with severe intractable irritable bowel syndrome previously reported as successfully treated with hypnotherapy, have now been followed up for a mean duration of 18 months. All patients remain in remission although two have experienced a single relapse overcome by an additional session of hypnotherapy. Experience with a further 35 patients is reported giving a total group of 50. This group was divided into classical cases, atypical cases and cases exhibiting significant psychopathology. The response rates were 95%, 43%, and 60% respectively. Patients over the age of 50 years responded very poorly (25%) whereas those below the age of 50 with classical irritable bowel syndrome exhibited a 100% response rate. This study confirms the successful effect of hypnotherapy in a larger series of patients with irritable bowel syndrome and defines some subgroup variations.
Renal Tubular Transport of Proline, Hydroxyproline, and Glycine in Health and in Familial Hyperprolinemia *
Authors: Charles R. Scriver, Mary L. Efron, Irwin A. Schafer
Journal: Journal of Clinical Investigation (1964)

In man (2) and other mammals (3), most of the amino acid load in the glomerular filtrate is reabsorbed from the proximal tubule against a chemical gradient (4, 5).There are indications that human tubular absorption of the different chemical groups of amino acids occurs by means of several transport mechanisms.In cystinuria, for example, transport of only the di-amino acids, cystine, lysine, ornithine, and arginine, is im- paired (6-9).In familial glycinuria (10) only glycine reabsorption is abnormal.In Hartnup disease (11, 12) there is impaired transport of most of the neutral amino acids; there is, however, relatively little impairment in absorption of the cystinuric group of amino acids or of the imino acids and glycine.The presence, in patients with familial hyperprolinemia (13, 14), of a specific hyperaminoaciduria comprising proline, hydroxyproline, and glycine raised the possibility of a transport mech- anism selective for these three compounds.In this disease we observed that prolinuria occurred only when the plasma proline concentration was greater than 0.8 mM (normal, < 0.3 mM); at this point hydroxyprolinuria and increased glycine excretion also appeared despite normal plasma concentrations of the latter two compounds.Pre- sumably under these circumstances, the amount of proline in the glomerular filtrate exceeded its ca-
Vascular Adhesion Protein 1 (VAP-1) Mediates Lymphocyte Subtype-specific, Selectin-independent Recognition of Vascular Endothelium in Human Lymph Nodes
Authors: Marko Salmi, Sami Tohka, Ellen L. Berg, Eugene C. Butcher, Sirpa Jalkanen
Journal: The Journal of Experimental Medicine (1997)

Interactions between lymphocyte surface receptors and their ligands on vascular endothelial cells regulate the exit of lymphocytes from the circulation. Distinct subsets of mononuclear cells bind to high endothelial venules (HEVs) in different lymphoid organs to a different extent, but the molecular mechanisms behind this selectivity have remained poorly characterized. Here we show that vascular adhesion protein-1 (VAP-1) mediates subtype-specific binding of CD8-positive T cells and natural killer cells to human endothelium. VAP-1–dependent, oligosaccharide-dependent peripheral lymph node (PLN) HEV adhesion under shear was independent of L-selectin, P-selectin glycoprotein ligand 1, and α4 integrins, the known lymphocyte receptors involved in the initial recognition of endothelial cells. PLN HEV adhesion was also critically dependent on peripheral lymph node vascular addressins (PNAds), but lymphocyte L-selectin was absolutely required for PNAd binding. Most lymphocytes relied on both PNAd and VAP-1 in HEV binding. The overlapping function of L-selectin ligands and VAP-1 in PLN introduces a new control point into the lymphocyte extravasation process. Finally, intravital microscopy revealed that VAP-1 is involved in initial interactions between human lymphocytes and endothelial cells in inflamed rabbit mesenterial venules in vivo. In conclusion, VAP-1 is a novel contact-initiating ligand that discriminates between different subpopulations of mononuclear cells and is an appealing target for selective modulation of adhesion of CD8- and CD16-positive effector cells.
Parathyroid Hormone–Related Protein Drives a CD11b+Gr1+ Cell–Mediated Positive Feedback Loop to Support Prostate Cancer Growth
Authors: Serk In Park, Changki Lee, W. David Sadler, Amy J. Koh, Jacqueline Jones, Jung Won Seo, Fabiana N. Soki, Sun Wook Cho, Stephanie D. Daignault, Laurie K. McCauley
Journal: Cancer Research (2013)

In the tumor microenvironment, CD11b(+)Gr1(+) bone marrow-derived cells are a predominant source of protumorigenic factors such as matrix metalloproteinases (MMP), but how distal tumors regulate these cells in the bone marrow is unclear. Here we addressed the hypothesis that the parathyroid hormone-related protein (PTHrP) potentiates CD11b(+)Gr1(+) cells in the bone marrow of prostate tumor hosts. In two xenograft models of prostate cancer, levels of tumor-derived PTHrP correlated with CD11b(+)Gr1(+) cell recruitment and microvessel density in the tumor tissue, with evidence for mediation of CD11b(+)Gr1(+) cell-derived MMP-9 but not tumor-derived VEGF-A. CD11b(+)Gr1(+) cells isolated from mice with PTHrP-overexpressing tumors exhibited relatively increased proangiogenic potential, suggesting that prostate tumor-derived PTHrP potentiates this activity of CD11b(+)Gr1(+) cells. Administration of neutralizing PTHrP monoclonal antibody reduced CD11b(+)Gr1(+) cells and MMP-9 in the tumors. Mechanistic investigations in vivo revealed that PTHrP elevated Y418 phosphorylation levels in Src family kinases in CD11b(+)Gr1(+) cells via osteoblast-derived interleukin-6 and VEGF-A, thereby upregulating MMP-9. Taken together, our results showed that prostate cancer-derived PTHrP acts in the bone marrow to potentiate CD11b(+)Gr1(+) cells, which are recruited to tumor tissue where they contribute to tumor angiogenesis and growth.
Secretory low-molecular-weight phospholipases A2 and their specific receptor in bile ducts of patients with intrahepatic calculi: Factors of chronic proliferative cholangitis
Authors: Junichi Shoda, Masahito Kano, Toru Asano, Tatsuro Irimura, Tetsuya Ueda, Ryu Iwasaki, Masato Furukawa, Junichi Kamiya, Yuji Nimura, Takeshi Todoroki, Yasushi Matsuzaki, Naomi Tanaka
Journal: Hepatology (1999)

Intrahepatic calculi is characterized by an intractable course and frequent recurrences, requiring multiple operative interventions. Chronic proliferative cholangitis, an active and long–standing inflammation of the stone–containing bile ducts with the hyperplasia of epithelia and the proliferation of the duct–associated mucus glands, may underlie the complex nature of the disease. In terms of the pathophysiology, interest has been focused on the role of secretory low-molecular–weight phospholipases A 2 (sPLA 2 s) as inflammatory mediators or factors modulating cell functions via their specific sPLA 2 –receptor, and also on the production and secretion of altered mucin molecules from the inflamed bile ducts. In search of factors involving chronic proliferative cholangitis, the sPLA 2 isoforms in the bile such as the pancreatic–type sPLA 2 (group IB sPLA 2 ) and the arthritic–type sPLA 2 (group IIA sPLA 2 ), were assayed to correlate protein masses of the sPLA 2 s with alterations in biliary composition. Furthermore, the steady–state messenger RNA (mRNA) levels of the sPLA 2 s, the membrane–bound sPLA 2 –receptor, cystic fibrosis transmembrane conductance regulator (CFTR), and mucin core polypeptide (MUC) genes in the bile ducts were assayed by reverse– transcriptase polymerase chain reaction (RT–PCR). Immunoreactive sPLA 2 –IB and sPLA 2 –IIA levels were significantly higher in the bile from the stone–containing hepatic ducts (2315 ± 677 for sPLA 2 –IB; 281 ± 42 for sPLA 2 –IIA ng/dL, mean ± SEM; n = 20) than in the ductal bile from gallbladder stone patients (609 ± 92, P &lt; .01; 22 ± 2, P &lt; .01; n = 24). The increased sPLA 2 levels were associated with a concomitant increase in lysophosphatidylcholine, prostaglandin E 2 (PGE 2 ), and total mucin concentrations. The affected bile ducts showed an increased mRNA level of sPLA 2 –IB and sPLA 2 –IIA compared with the ducts from control subjects, in whom the mRNAs of the sPLA 2 –receptor and other sPLA 2 isoforms, such as groups V and X sPLA 2 s, were coincidently expressed. Reflecting the increased amounts of total biliary mucins, the affected ducts showed an increase in mRNA levels of CFTR as well as MUC2, MUC3, MUC5AC, MUC5B, and MUC6 compared with the ducts from control subjects. In intrahepatic calculi, an enhanced expression of the sPLA 2 s and their possible cross–talk via sPLA 2 –receptor may be of pathophysiological significance for the chronic proliferative cholangitis, in association with the enhanced CFTR expression and the alterations in mucin gene expression in the bile ducts, probably through potentiating arachidonate metabolism with associated biliary alterations favoring growth of preexisting stones and even further progressions. (Hepatology 1999;29:1026–1036.)
The Matter of Bias in the American Board of Psychiatry and Neurology
Authors: LAWRENCE C. KOLB
Journal: American Journal of Psychiatry (1969)

The author considers charges that the American Board of Psychiatry and Neurology is biased against examination candidates who are trained in state hospitals or abroad, or who are members of minority groups. He concludes that bias does not exist and that efforts should be made to improve the preparation of these groups so that they will be more successful in the examinations.
G<scp>ENERATING THE</scp> C<scp>EREBRAL</scp> C<scp>ORTICAL</scp> A<scp>REA</scp> M<scp>AP</scp>
Authors: Elizabeth A. Grove, Tomomi Fukuchi-Shimogori
Journal: Annual Review of Neuroscience (2003)

▪ Abstract The view that the cortical primordium is initially patterned in similar ways to the rest of the embryo has been a conceptual breakthrough. We now have a new starting point for understanding how the cortical area map is established and how maps may change and evolve. Here we review findings that signaling molecules secreted from distinct cortical signaling centers establish positional information in the cortical primordium and regulate regional growth. In other embryonic systems, positional signals would regulate the patterned expression of transcription factors, leading, in a gene regulatory cascade, to the patterned differentiation of the tissue. We discuss candidate transcription factors with respect to such a model of cortical patterning. Finally, embryonic structures interact to pattern one another. We review data suggesting that the thalamus and cortex are patterned independently then interact to generate the final cortical area map.