tbuckley/cabot-search huggingface dataset:
Analysis of fracture prevalence in kidney-pancreas allograft recipients.
Authors: M Y Chiu, S M Sprague, D S Bruce, E S Woodle, J R Thistlethwaite, M A Josephson
Journal: Journal of the American Society of Nephrology (1998)

Fractures occur in 11 to 26% of renal allograft recipients after transplantation despite improvements in bone and mineral disorders. This high fracture rate is likely a consequence of accelerated osteopenia. The cause of posttransplant bone loss is multifactorial, and patients with insulin-dependent diabetes mellitus and renal failure may have additional fracture risks such as low turnover bone disease. This retrospective cohort study was undertaken to determine the long-term incidence and the potential risk factors of posttransplant fractures in patients with insulin-dependent diabetes mellitus undergoing combined kidney-pancreas allograft transplantation. Thirty-five patients with insulin-dependent diabetes mellitus who received a combined kidney-pancreas allograft between 1987 and 1992 were evaluated. Thirty-five kidney allograft recipients matched for age, gender, and the date of transplant were also reviewed. The fracture incidence in the kidney-pancreas group was 49% after transplantation. The rate of first fracture after kidney-pancreas transplantation was 12.1% per patient year, resulting in a 5-yr fracture-free rate of 48%. The initial fracture occurred at a mean of 31.06 +/- 19.9 mo. Steroid exposure was found to increase the risk of fracture, and analysis by means of a Cox regression model estimated that an increase in cumulative steroid exposure of 10 mg/kg at any given month increased the hazard of sustaining a fracture by 9% (95% confidence interval for hazard ratio, 1.01 to 1.18; P = 0.031). This analysis suggests that kidney-pancreas recipients are at significant risk of sustaining a fracture within a few years after transplantation.
Pulmonary leukostasis without hyperleukocytosis: A clinicopathologic study of 16 cases
Authors: Fernando Augusto Soares, Glaucia A. Magnani Landell, Maria Camila de Miranda Cardoso
Journal: American Journal of Hematology (1992)

Abstract Pulmonary leukostasis is a serious, almost always fatal, complication usually reported to occur in patients with acute granulocy tic leukemias when the peripheral white blood cells exceed 50,000/mm 3 . We report a Clinicopathologic study of 16 leukemic patients with pulmonary leukostasis and with &lt; 50,000/mm 3 circulating leukocytes. The results demonstrated that hyperleukocytosis per se cannot be the cause of pulmonary leukostasis, but that other factors, such as the presence of circulating blasts and the affinity of neoplastic cells for the pulmonary endothelium, may be related to the development of acute respiratory distress in patients with leukemia. © 1992 Wiley‐Liss, Inc.
Revisions of the international criteria for neuroblastoma diagnosis, staging, and response to treatment.
Authors: G M Brodeur, J Pritchard, F Berthold, N L Carlsen, V Castel, R P Castelberry, B De Bernardi, A E Evans, M Favrot, F Hedborg
Journal: Journal of Clinical Oncology (1993)

PURPOSE AND METHODS: Based on preliminary experience, there was a need for modifications and clarifications in the International Neuroblastoma Staging System (INSS) and International Neuroblastoma Response Criteria (INRC). In 1988, a proposal was made to establish an internationally accepted staging system for neuroblastoma, as well as consistent criteria for confirming the diagnosis and determining response to therapy (Brodeur GM, et al: J Clin Oncol 6:1874-1881, 1988). A meeting was held to review experience with the INSS and INRC and to revise or clarify the language and intent of the originally proposed criteria. Substantial changes included a redefinition of the midline, restrictions on age and bone marrow involvement for stage 4S, and the recommendation that meta-iodobenzylguanidine (MIBG) scanning be implemented for evaluating the extent of disease. Other modifications and clarifications of the INSS and INRC are presented. In addition, the criteria for the diagnosis of neuroblastoma were modified. Finally, proposals were made for the development of risk groups that incorporate both clinical and biologic features in the prediction of prognosis. The biologic features that were deemed important to evaluate prospectively included serum ferritin, neuron-specific enolase (NSE), and lactic dehydrogenase (LDH); tumor histology; tumor-cell DNA content; assessment of N-myc copy number; assessment of 1p deletion by cytogenetic or molecular methods; and TRK-A expression. RESULTS AND CONCLUSION: Modifications of the INSS and INRC made at this conference are presented. In addition, proposals are made for future modifications in these criteria and for the development of International Neuroblastoma Risk Groups.
Phase II study of tailored chemotherapy for advanced colorectal cancer with either 5-fluouracil and leucovorin or oxaliplatin and irinotecan based on the expression of thymidylate synthase and dihydropyrimidine dehydrogenase
Authors: C.H. Smorenburg, G.J. Peters, C.J. van Groeningen, P. Noordhuis, K. Smid, A.M.G.H. van Riel, W. Dercksen, H.M. Pinedo, G. Giaccone
Journal: Annals of Oncology (2005)
Cell-specific microarray profiling experiments reveal a comprehensive picture of gene expression in the C. elegans nervous system
Authors: Stephen E Von Stetina, Joseph D Watson, Rebecca M Fox, Kellen L Olszewski, W Clay Spencer, Peter J Roy, David M Miller
Journal: Genome biology (2007)

Abstract Background With its fully sequenced genome and simple, well-defined nervous system, the nematode Caenorhabditis elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and, thereby, link comprehensive profiles of neuronal transcription to key developmental and functional properties of the nervous system. Results We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Microarray Profiling C. elegans cells) method, we used fluorescence activated cell sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (for example, transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. Of particular interest are 19 conserved transcripts of unknown function that are also expressed in the mammalian brain. In addition to utilizing these profiling approaches to define stage-specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and, therefore, provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system.
Predictors of Marijuana Use in Adolescents Before and After Licit Drug Use: Examination of the Gateway Hypothesis
Authors: Ralph Tarter
Journal: American Journal of Psychiatry (2006)

Objective: The authors investigated whether the transition from licit drug use to marijuana use is determined by particular risk factors, as specified by the gateway hypothesis. They also evaluated the accuracy of the "gateway sequence" (illicit drug use following licit drugs) for predicting a diagnosis of substance use disorder. Method: Boys who consumed licit drugs only (N=99), boys who consumed licit drugs and then transitioned to marijuana use (gateway sequence) (N=97), and boys who used marijuana before using licit substances (alternative sequence) (N=28) were prospectively studied from ages 10–12 years through 22 years to determine whether specific factors were associated with each drug use pattern. The groups were compared on 35 variables measuring psychological, family, peer, school, and neighborhood characteristics. In addition, the utility of the gateway and alternative sequences in predicting substance use disorder was compared to assess their clinical informativeness. Results: Twenty-eight (22.4%) of the participants who used marijuana did not exhibit the gateway sequence, thereby demonstrating that this pattern is not invariant in drug-using youths. Among youths who did exhibit the gateway pattern, only delinquency was more strongly related to marijuana use than licit drug use. Specific risk factors associated with transition from licit to illicit drugs were not revealed. The alternative sequence had the same accuracy for predicting substance use disorder as the gateway sequence. Conclusions: Proneness to deviancy and drug availability in the neighborhood promote marijuana use. These findings support the common liability model of substance use behavior and substance use disorder.
Tumor αvβ3 Integrin Is a Therapeutic Target for Breast Cancer Bone Metastases
Authors: Yingshe Zhao, Richard Bachelier, Isabelle Treilleux, Philippe Pujuguet, Olivier Peyruchaud, Roland Baron, Philippe Clément-Lacroix, Philippe Clézardin
Journal: Cancer Research (2007)

Abstract In breast cancer bone metastasis, tumor cells stimulate osteoclast-mediated bone resorption, and bone-derived growth factors released from resorbed bone stimulate tumor growth. The αvβ3 integrin is an adhesion receptor expressed by breast cancer cells and osteoclasts. It is implicated in tumor cell invasion and osteoclast-mediated bone resorption. Here, we hypothesized that the therapeutic targeting of tumor αvβ3 integrin would prevent bone metastasis formation. We first showed that, compared with mock-transfected cells, the i.v. inoculation of αvβ3-overexpressing MDA-MB-231 breast cancer cells in animals increased bone metastasis incidence and promoted both skeletal tumor burden and bone destruction. The direct inoculation of αvβ3-overexpressing transfectants into the tibial bone marrow cavity did not however enhance skeletal tumor burden and bone destruction, suggesting that αvβ3 controls earlier events during bone metastasis formation. We next examined whether a nonpeptide antagonist of αvβ3 (PSK1404) exhibits meaningful antitumor effects in experimental breast and ovarian cancer bone metastasis. A continuous PSK1404 treatment, which inhibited osteoclast-mediated bone resorption in an animal model of bone loss, substantially reduced bone destruction and decreased skeletal tumor burden. Importantly, a short-term PSK1404 treatment that did not inhibit osteoclast activity also decreased skeletal tumor burden and bone destruction. This dosing regimen caused a profound and specific inhibition of bone marrow colonization by green fluorescent protein, αvβ3-expressing tumor cells in vivo and blocked tumor cell invasion in vitro. Overall, our data show that tumor αvβ3 integrin stands as a therapeutic target for the prevention of skeletal metastases. [Cancer Res 2007;67(12):5821–30]
Enhanced Expression of Vascular Endothelial Growth Factor in Pulmonary Arteries of Smokers and Patients with Moderate Chronic Obstructive Pulmonary Disease
Authors: Salud Santos, Victor I. Peinado, Josep Ramírez, Jaime Morales-Blanhir, Ricardo Bastos, Josep Roca, Robert Rodriguez-Roisin, Joan A. Barberà
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

Chronic obstructive pulmonary disease (COPD) is associated with structural and functional changes in the pulmonary circulation that commence at an early stage. To investigate whether vascular endothelial growth factor (VEGF) might be implicated as a mediator in COPD-associated pulmonary vascular changes, we studied surgical specimens obtained from 19 nonsmokers, 21 smokers with normal lung function, 28 patients with moderate COPD, and 10 patients with severe emphysema. The expression of VEGF in pulmonary muscular arteries was evaluated by immunohistochemistry, its protein content in lung tissue by Western blot analysis, and VEGF mRNA and its isoforms were analyzed by reverse transcription-polymerase chain reaction. The immunohistochemical expression of VEGF was increased in pulmonary arteries of smokers (median, 68% [interquartile range, 60–88]) and patients with moderate COPD (77% [63–82]), compared with nonsmokers (53% [40–63]) (p < 0.05 each). The expression of VEGF in smooth muscle cells correlated with the thickness of the vessel wall (r = 0.38, p < 0.01). VEGF protein content in lung tissue was reduced in severe emphysema, where reverse transcription-polymerase chain reaction demonstrated a lower proportion of the VEGF189 isoform. In conclusion, the expression of VEGF varies according to the severity of COPD and might be involved in the pathogenesis of pulmonary vascular remodeling at early stages of the disease.
Genome-Wide Analysis of Aromatase Inhibitor-Resistant, Tamoxifen-Resistant, and Long-Term Estrogen-Deprived Cells Reveals a Role for Estrogen Receptor
Authors: Selma Masri, Sheryl Phung, Xin Wang, Xiwei Wu, Yate-Ching Yuan, Lawrence Wagman, Shiuan Chen
Journal: Cancer Research (2008)

Acquired resistance to either tamoxifen or aromatase inhibitors (AI) develops after prolonged treatment in a majority of hormone-responsive breast cancers. In an attempt to further elucidate mechanisms of acquired resistance to AIs, MCF-7aro cells resistant to letrozole (T+LET R), anastrozole (T+ANA R), and exemestane (T+EXE R), as well as long-term estrogen deprived (LTEDaro) and tamoxifen-resistant (T+TAM R) lines were generated. This is the first complete panel of endocrine therapy-resistant cell lines, which were generated as multiple independent biological replicates for unbiased genome-wide analysis using affymetrix microarrays. Although similarities are apparent, microarray results clearly show gene signatures unique to AI-resistance were inherently different from LTEDaro and T+TAM R gene expression profiles. Based on hierarchical clustering, unique estrogen-responsive gene signatures vary depending on cell line, with some genes up-regulated in all lines versus other genes up-regulated only in the AI-resistant lines. Characterization of these resistant lines showed that LTEDaro, T+LET R, and T+ANA R cells contained a constitutively active estrogen receptor (ER)alpha that does not require estrogen for activation. This ligand-independent activation of ER was not observed in the parental cells, as well as T+EXE R and T+TAM R cells. Further characterization of these resistant lines was performed using cell cycle analysis, immunofluorescence experiments to visualize ER subcellular localization, as well as cross-resistance studies to determine second-line inhibitor response. Using this well-defined model system, our studies provide important information regarding differences in resistance mechanisms to AIs, TAM, and LTEDaro, which are critical in overcoming resistance when treating hormone-responsive breast cancers.
IL-10 Alters Immunoproteostasis in APP Mice, Increasing Plaque Burden and Worsening Cognitive Behavior
Authors: Paramita Chakrabarty, Andrew Li, Carolina Ceballos-Diaz, James A Eddy, Cory C Funk, Brenda Moore, Nadia DiNunno, Awilda M Rosario, Pedro E Cruz, Christophe Verbeeck, Amanda Sacino, Sarah Nix, Christopher Janus, Nathan D Price, Pritam Das, Todd E Golde
Journal: Neuron (2015)
Unique blood culture for diagnosis of bloodstream infections in emergency departments: a prospective multicentre study
Authors: S. Dargère, J.-J. Parienti, E. Roupie, P.-E. Gancel, E. Wiel, N. Smaiti, C. Loiez, L.-M. Joly, L. Lemée, M. Pestel-Caron, D. du Cheyron, R. Verdon, R. Leclercq, V. Cattoir
Journal: Clinical Microbiology and Infection (2014)
Longitudinal evaluation of vitamin D plasma levels during anthracycline- and docetaxel-based adjuvant chemotherapy in early-stage breast cancer patients
Authors: D. Santini, S. Galluzzo, B. Vincenzi, A. Zoccoli, E. Ferraro, C. Lippi, V. Altomare, G. Tonini, F. Bertoldo
Journal: Annals of Oncology (2009)
Neuronal calcium sensor-1 enhancement of InsP3 receptor activity is inhibited by therapeutic levels of lithium
Authors: Christina Schlecker, Wolfgang Boehmerle, Andreas Jeromin, Brenda DeGray, Anurag Varshney, Yogendra Sharma, Klara Szigeti-Buck, Barbara E. Ehrlich
Journal: Journal of Clinical Investigation (2006)

Regulation and dysregulation of intracellular calcium (Ca2+) signaling via the inositol 1,4,5-trisphosphate receptor (InsP3R) has been linked to many cellular processes and pathological conditions. In the present study, addition of neuronal calcium sensor-1 (NCS-1), a high-affinity, low-capacity, calcium-binding protein, to purified InsP3R type 1 (InsP3R1) increased the channel activity in both a calcium-dependent and -independent manner. In intact cells, enhanced expression of NCS-1 resulted in increased intracellular calcium release upon stimulation of the phosphoinositide signaling pathway. To determine whether InsP3R1/NCS-1 interaction could be functionally relevant in bipolar disorders, conditions in which NCS-1 is highly expressed, we tested the effect of lithium, a salt widely used for treatment of bipolar disorders. Lithium inhibited the enhancing effect of NCS-1 on InsP3R1 function, suggesting that InsP3R1/NCS-1 interaction is an essential component of the pathomechanism of bipolar disorder.
Bevacizumab plus high-dose ifosfamide, etoposide and carboplatin (HD-ICE) as third-line salvage chemotherapy induced an unexpected dramatic response in highly platinum refractory germ-cell cancer
Authors: W. Voigt, T. Kegel, G. Maher, K. Jordan, L. Müller, H.-J. Schmoll
Journal: Annals of Oncology (2005)
Exemption from compulsory wearing of seat belts--medical indications.
Authors: M S Christian
Journal: BMJ (1979)

Reference is made to the delay in the introduction of seat-belt legislation in Britain, the knowledge that the observance of such a law would lead to a dramatic reduction in deaths and serious injuries in those wearing seat-belts, and the demand for exemptions for certain categories of people on medical grounds. The medical reasons for exemptions are discussed by reference to road accident traffic victims received at a particular hospital, and categories of medical conditions sometimes claimed to constitute ground for exemption. The case of disabled drivers is considered. General observations and suggestions indicate that the general consensus of informed medical opinion indicates that there are no medical conditions that would be seriously aggravated by wearing a seat belt. It is considered that any conditions that could be cited would undoubtedly indicate not only unfitness to wear a seat belt but unfitness to drive. /TRRL/
Patients with rheumatoid arthritis and periodontitis have higher disease activity and a more pronounced antibody response against<i>Porphyromonas gingivalis</i>
Authors: M de Smit, J Westra, A Vissink, B Doornbos-van der Meer, A J van Winkelhoff, E Brouwer
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background</h3> Co-existence of periodontitis and rheumatoid arthritis (RA) has been reported. These diseases have similarities in aetiology, pathogenesis and risk factors. <i>Porphyromonas gingivalis</i> (PG) is a periodontal pathogen that has the ability to citrullinate endogenous proteins, human fibrinogen and α-enolase, which are auto-antigens in RA. This study aimed to assess prevalence of periodontitis, and occurrence of PG and of the antibody response against PG in RA patients. <h3>Methods</h3> In 95 consecutive dentate RA patients, periodontal condition was examined using the Dutch Periodontal Screening Index for treatment needs (DPSI). DPSI category A patients have no periodontitis, category B patients suffer from moderate periodontitis and category C patients have severe periodontitis. Prevalence of periodontitis was compared to a control population consisting of 500 age- and gender matched individuals attending a general dental practice in the same geographic area of the Netherlands. RA disease activity was scored with the disease activity score-28 (DAS28). Serum was investigated for C reactive protein (CRP), immunoglobulin M rheumatoid factor (IgM-RF) and anticitrullinated peptide antibodies (ACPA). IgG- and IgM antibody titres to PG were measured by an inhouse ELISA. Subgingival plaque samples were tested for presence of PG by culture technique. Serum and subgingival plaque measures were compared to a second control group, matched for age, gender, smoking- and periodontal status without RA or other systemic diseases (n=44). <h3>Results</h3> 27% of the RA patients had severe periodontitis, which is significantly higher than the 11% found in the control population (p&lt;0.0001). Within the RA patients group C had higher DAS28-scores (p&lt;0.001), higher CRP-levels (p&lt;0.05) and were older (p&lt;0.01) than group A and B, although RA disease duration was equal. RA patients group C had higher IgG-anti PG titres (p&lt;0.05) than group A and B. No differences were seen in IgM-RF, ACPA and IgM-anti PG titres within the groups. Prevalence of PG in subgingival plaque samples was not different in RA patients compared to matched healthy controls (n=44). RA patients with severe periodontitis showed both higher IgM- and IgG- anti PG titres (p&lt;0.01 resp. p&lt;0.05) compared to severe periodontitis patients without RA. There was a significant difference between PG culture positive and negative RA patients, but not in controls, concerning IgM- and IgG- anti-PG titres (p&lt;0.01 resp. p&lt;0.001). <h3>Conclusions</h3> Prevalence of severe periodontitis is high in RA patients. These patients have higher disease activity of RA and a more pronounced antibody response against PG. These findings support the view that both PG and periodontitis attribute to RA disease activity.