tbuckley/cabot-search huggingface dataset:
Percutaneous Transluminal Coronary Angioplasty in 1985–1986 and 1977–1981
Authors: Katherine Detre, Richard Holubkov, Sheryl Kelsey, Michael Cowley, Kenneth Kent, David Williams, Richard Myler, David Faxon, David Holmes, Martial Bourassa, Peter Block, Arthur Gosselin, Lamberto Bentivoglio, Louis Leatherman, Gerald Dorros, Spencer King, Joseph Galichia, Mahdi Al-Bassam, Martin Leon, Thomas Robertson, Eugene Passamani
Journal: New England Journal of Medicine (1988)

In August 1985, the Percutaneous Transluminal Coronary Angioplasty Registry of the National Heart, Lung, and Blood Institute reopened at its previous sites to document changes in angioplasty strategy and outcome. The new registry entered 1802 consecutive patients who had not had a myocardial infarction in the 10 days before angioplasty. Patient selection, technical outcome, and short-term major complications were compared with those of the 1977 to 1981 registry cohort. The new-registry patients were older and had a significantly higher proportion of multivessel disease (53 vs. 25 percent, P<0.001), poor left ventricular function (19 vs. 8 percent, P<0.001), previous myocardial infarction (37 vs. 21 percent, P<0.001), and previous coronary bypass surgery (13 vs. 9 percent, P<0.01). The new-registry cohort also had more complex coronary lesions, and angioplasty attempts in these patients involved more multivessel procedures. Despite these differences, the in-hospital outcome in the new cohort was better. Angiographic success rates according to lesion increased from 67 to 88 percent (P<0.001), and overall success rates (measured as a reduction of at least 20 percent in all lesions attempted, without death, myocardial infarction, or coronary bypass surgery) increased from 61 to 78 percent (P<0.001). In-hospital mortality for the new cohort was 1 percent, and the nonfatal myocardial infarction rate was 4.3 percent. Both rates are similar to those for the old registry. The long-term efficacy of current angioplasty remains to be determined. (N Engl J Med 1988; 318:265–70.)
Viral Load and Disease Progression in Infants Infected with Human Immunodeficiency Virus Type 1
Authors: William T. Shearer, Thomas C. Quinn, Philip LaRussa, Judy F. Lew, Lynne Mofenson, Susan Almy, Kenneth Rich, Edward Handelsman, Clemente Diaz, Marcello Pagano, Vincent Smeriglio, Leslie A. Kalish
Journal: New England Journal of Medicine (1997)

There are only limited data on human immunodeficiency virus type 1 (HIV-1) RNA in perinatally infected infants. Understanding the dynamics of HIV-1 infection and its relation to disease progression may help identify opportunities for effective antiviral treatment in infected infants.
Abstract 588: Effect of antibiotic treatment on <i>Salmonella typhimurium</i> A1-R tumor targeting of prostate cancer
Authors: Ming Zhao, Jack Geller, Fang Liu, Lei Zhang, Yong Zhang, Robert M. Hoffman
Journal: Cancer Research (2010)

Abstract We have previously demonstrated that a genetically-altered Salmonella typhimurium, auxotrophic for arginine and leucine, could effectively treat metastatic PC-3 tumors in nude mice and profoundly increase survival. The auxotrophic mutations, induced by nitrosoguamidine, allow the bacteria to grow in tumors but not in normal tissue. Since human prostate cancer eventually becomes non-androgen-dependent similar to PC-3 tumors, bacterial treatment offers a novel treatment for this disease. In the current study, we observed the effect of antibiotic treatment on A1-R bacteria therapy of PC-3 tumors in nude mice. Thirty mice were implanted subcutaneously with PC-3 tumors expressing GFP. Approximately two weeks following implantation, the tumors were externally imageable. Ten of the 30 mice served as untreated control, and 10 mice were given A1 weekly intravenously as treated controls. Ten mice were given A1 intravenously weekly, combined with Gentamicin administered by intra-peritoneal injection at 100 µg daily for 10 day cycles with a two-day break between cycles. The treatment was repeated until the study end. Tumor growth was externally imaged by GFP expression of the tumors. All mice in the untreated group were sacrificed by 6 weeks after tumor implantation due to tumor size of 1.5-2.0 cm diameter. All mice in the A1-R-antibiotic combination group were sacrificed at 8 weeks due to tumor size. At the same time, all mice in the A1-R-only treatment group were alive and well. Currently, 3 treated mice were close to tumor eradication at 16 weeks following implantation and are still being injected weekly with A1-R. These results suggest that the tumor-targeting activity of A1-R bacteria was antibiotic dependent. This study gives proof of principle that A1-R can be regulated by antibiotics, an important safety feature for clinical application. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 588.
P2-09-12: High Resolution Diffusion MRI Characterizes Tumor Stromal Boundaries.
Authors: RL McLaughlin, DC Newitt, LJ Wilmes, S Sinha, DJ Wisner, NM Hylton
Journal: Cancer Research (2011)

Abstract Background: Studies of 3D cell cultures have shown that mammary epithelial cell growth and morphogenesis is regulated by extracellular matrix (ECM) stiffness, linking ECM stiffening to malignant transformation. Tumors are consistently stiffer than normal adjacent tissue, and matrix stiffening is caused by ECM cross-linking and increased deposition of collagen. Some evidence suggests that collagen orientation at tumor boundaries can promote tumor metastasis. Measuring the stiffness of the tumor boundaries and adjacent stromal tissue may give additional information 1) about tumor microenvironment and 2) to guide treatment. Diffusion-weighted imaging (DWI) MRI measures the mobility of water in tissue and may be sensitive to this phenomenon. Material and Methods: MRI data was collected on patients with locally advance breast cancer enrolled in an IRB-approved study at UCSF and signed informed consent. In addition to a standard dynamic contrast enhanced (DCE) MRI, a high-resolution diffusion-weighted image (HR DWI) was acquired with an echo planar imaging sequence and the following parameters: TR/TE=4000/64.8 ms, b=0,600, FOV=70×140mm, matrix=28×64, and voxel size=0.55×0.55×4.0mm. Apparent diffusion coefficient (ADC) maps were created. HR DWI images were segmented into tumor and non-enhancing, surrounding stromal tissue. A proximity mapping method was used to measure ADC values at the inner edge of tumor and at increasing distances from the tumor boundary on HR DWI. The mean was calculated for the voxels in 1 mm increments, starting at 5 mm into the tumor (−5 mm) and ending at 2.5 cm away from the tumor (25 mm). Results: The average of the changes per 1 mm shell was largest for the transition of the tumor boundary (Table 1). In Table 1, the −5 to 0 mm, 0 to 5 mm, and 5 to 25 mm columns represent inside the tumor, tumor boundary, and outside the tumor, respectively. In general, ADC values were consistently lower inside the tumor than outside. The greatest changes per 1 mm shell was seen in the transition from inside to outside tumor, although the values varied among tumor types. Each of the three cases analyzed had different patterns of ADC values. Discussion: These preliminary studies show that water mobility measurements change at the tumor boundary, with different patterns observed among individual patients. We are further investigating the influence of density and tumor margin morphology on these ADC measurements. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-09-12.
OC-094 TGF Beta1 Mediated EMT in CACO2BBE Gut Cells
Authors: L Lee, R Geevarghese, F Heidtbreitch, M Dockrell
Journal: Gut (2013)

<h3>Introduction</h3> Crohn’sDisease is a chronic autoimmune condition characterised by abdominal pain and diarrhoea. 80% of patients will require surgery and half of these will be as a result of stricture formation. Strictures occur as a result of mesenchymalcell proliferation and deposition of extracellular matrix. Epithelial-mesenchymaltransition (EMT) is a novel mechanism theorised to contribute to gut fibrosis and is a potential target to prevent stricture formation. EMT has been noted in vivo and in animal gut models. However, it has been previously shown that CaCo2 cells are non-responsive to TGFbeta1, the principle mediator of EMT. EMT has not been investigated in the CaCo2 BBE cells. <h3>Aims</h3> To determine the cell receptor and signalling phenotype of CaCo2 BBE cells To establish EMT in CaCo2 BBE cells <h3>Methods Cell culture</h3> -CaCo2 BBE cells were grown in DMEM and 10% FBS on plastic wells to 100% confluenencyand allowed to differentiate. <h3>CaCo2 BBE cell phenotype</h3> -Western blotting and immunofluorescence was performed to according to manufacturer protocols to analyse the phenotype of CaCo2 BBE Cells. <h3>TGF-beta mediated EMT</h3> -Cells were exposed to a 1 hour and 4 day treatment with TGF beta. <h3>Results Cell phenotype</h3> Zo1 and E. Cadherinwere expressed on the cell membrane. Alpha-SMA was expressed in the cell nuclei. Intracellularly, vimentinwas not expressed. E. Cadherinand zo1 were constituently expressed. <h3>Cell Signalling</h3> In response to a 1 hour treatment with TGF beta 0.8ng/ml, 2.5ng/ml, 7.5ng/ml, an increase in p-SMAD2 was noted. <h3>Response to TGF-beta</h3> Following a 4 day treatment with TGF beta (2.5ng/ml), no change in expression of alpha-SMA, E.cadherin, Vimentinwas observed by Western Blot or Immunofluorescence. <h3>Conclusion</h3> EMT has been theorisedto play a central role in stricture formation in Crohn’sdisease. However, this mechanism in human gut cells has only demonstrated by one author. This project has demonstrated that whilst CaCo2 BBE cells are able to respond to TGFbetaby increased phosphorylation of SMAD2, we were not able to definitively demonstrate EMT. <h3>Disclosure of Interest</h3> None Declared
Abstract 604: Erucin treatment through induction of thioredoxin reductase may alter tamoxifen resistance in LCC2 cells
Authors: Rosalind B. Penney, Quentin Felty, Joyce Slingerland, Deodutta Roy
Journal: Cancer Research (2010)

Abstract Tamoxifen-resistant growth is a considerable problem in the treatment of estrogen receptor-positive breast cancer. While the mechanisms of tamoxifen do not rely on an increase in oxidants, reactive oxygen species have been shown to increase with tamoxifen treatment, and tamoxifen-resistance coincides with a high intracellular oxidant state. We postulate that the chronic use of tamoxifen leads to a pro-oxidant environment in cells, leading to tamoxifen resistance. Here we present data that show that increasing a reduced state in the cell through an induction of thioredoxin reductase and subsequent reduction of oxidized thioredoxin, may restore tamoxifen sensitivity to previously resistant LCC2 cells. The isothiocyanate erucin has been found to increase thioredoxin reductase in MCF-7 cells. As such, we tested this in the MCF-7 derivative cell line LCC2, which is sensitive to fulvestrant but resistant to tamoxifen. We found that erucin not only increases expression of thioredoxin reductase, but also increased expression of thioredoxin in LCC2 cells. Erucin treatment led to a decrease in DNA synthesis, as measured by BrdU incorporation. In vitro tumor formation, as measured by colony count with soft agar colony formation assay, was also decreased in tamoxifen-treated cells after erucin treatment. Western blotting shows an increase in p27 with erucin treatment, and probing for p27 in a Jab1 immunoprecipitation shows a decrease in p27/Jab1 interactions after erucin treatment, similar to the effects of fulvestrant in these cells. These data support our hypothesis that altering thioredoxin's redox status can affect the sensitivity of tamoxifen to previously resistant cells, and this alteration may be through the p27/Jab1/thioredoxin pathway. Supported by BCRP-funded project W81XWH-07-1-0417, BC060125. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 604.
AB1011 Anti-TNF using ankylosing spondylitis patients may have less severe osteoporosis
Authors: I. Dolasik, F. Cosan, B. Yilmazer, A. Cefle
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Ankylosing spondylitis (AS) is a systemic chronic inflammatory disease characterized with enthesitis. The risk of osteoporosis is increased in AS. Low bone mineral dencity is found associated with systemic inflammation. <h3>Objectives</h3> We aimed in this study to investigate the risk of osteoporosis in AS patients using anti- TNF treatment. <h3>Methods</h3> The study group consisted of 49 AS patients who are using anti-TNF therapy more than 6 months, and the control group 47 AS patients without anti-TNF therapy. Two groups had similar age distribution at the time of bone mineral dansitometry. No patient had received steroid therapy previously. <h3>Results</h3> The total femoral T score was higher in AS group with anti-TNF treatment in comparison to the control group (p=0,033; mean T scores: -0,97 and -1,53, respectively). The T scores of total lomber vertebra was higher in AS group with anti-TNF therapy than the control group (p=0,046, mean T scores: 0,0 and -0,81, respectively). The mean femoral BMD value in the anti-TNF therapy group was 0,92 g/cm<sup>2</sup> (in comparing to 0,78 g/cm<sup>2</sup>) and was signifacantly higher (p=0,002). Moreover the lomber vertebra BMD value was significantly higher in the anti-TNF group (p=0,001, mean BMD values: 1,20 g/cm<sup>2</sup> and 1,03 g/cm<sup>2</sup>, respectively). <h3>Conclusions</h3> Our data revealed that AS patients receiving anti-TNF therapy have more less osteoporosis. The anti-TNF therapy may reduce the risk of osteoporosis in AS patients. <h3>Disclosure of Interest</h3> None Declared
The examination of relationships between linear sprint and angular turns in football players
Authors: A Kamar
Journal: British Journal of Sports Medicine (2011)

Subjects were 26 male football players aged 16±1 y, height 171±7 cm, body mass 64±8 kg, and training age of 6±4 y. The study examined changes in linear and angular sprint performance and the effect of angular factors on sprint speed and anaerobic power. 30 m sprint performance was determined by recording the time in every 10 m, and then the 30 m distance has been measured by 10 m 90 degrees turns, and finally the 30 m distance has been measured by 10 m 180 degrees turns and the sprint values have been determined and the relationships between the three measurements have been examined. While smooth linear acceleration was detected only in 30 m sprint runs (P&lt;0.01),the most loss of speed was detected in the second 10 m of 90 degrees turns (P&lt;0.05) and in the last 10 m in 180 degrees turns (P&lt;0.01). The average 30 m sprint time were increased by 46% compared to 90 degrees average turn time (P&lt;0.01), and were increased by 97% compared to 180 degrees average turn time (P&lt;0.05). When the 90 degrees average turn value and the 180 degrees average turn value were compared, the average value of the increase in the turn angle was increased by 36% (P&lt;0.05). When the 30 m sprint, 90 degrees turn and the 180 degrees turn values of the experimental subjects were examined as anaerobic power, it has been found out that when 30-meter sprint watt value is compared with 90 degrees turn watt value, a % 310,5 of negative effect from the reference value has been determined, whereas the 30 meter sprint watt value has been affected % 775 negatively from the reference value of the anaerobic power when it is compared with 180 degrees turn watt value (P&lt;0.001). When the 90 degrees turn watt value is compared with the 180 degrees turn watt value, it has been found out that the difference in the angle of the turn has affected the average watt value (Anaerobic power) % 250 negatively (P&lt;0.01).
P74 Hepatocyte transplantation in rats with acute liver failure using cells labelled with a clinical grade MRI contrast agent
Authors: J. Puppi, R. D. Hughes, M. Modo, R. R. Mitry, A. Dhawan
Journal: Gut (2011)

<h3>Introduction</h3> Hepatocyte transplantation is being evaluated as an alternative to orthotopic liver transplant. However, the fate of hepatocytes after transplantation is not well defined. <h3>Aim</h3> The aims of the study were to: (1) investigate the possibility of labelling hepatocytes in vitro using superparamagnetic iron oxide nanoparticles (SPIOs), (2) determine the effects of labelling on cell viability and function, and (3) perform in vivo experiments on tracking labelled cells by MRI. <h3>Method</h3> Human and rat hepatocytes were labelled in culture for 16 h with clinical SPIOs (12.5 μg Fe/ml) and protamine sulphate (3 μg/ml) as a transfection agent. Cellular iron uptake was determined using Prussian blue staining, and quantified by a ferrozine-based assay. Cell viability and function were assessed using LDH leakage, mitochondrial dehydrogenase activity, [<sup>14</sup>C]-leucine incorporation, albumin and urea assays. Effects of labelled cells on T2-weighted images were assessed in vitro using a 7-T MR scanner. Intrasplenic transplantation of 2×10<sup>7</sup> male rat hepatocytes labelled with SPIOs (n=4) or non-labelled (n=4) was performed in female recipients 28–30 h after acute liver failure induction by intraperitoneal injection of D-galactosamine. Hepatocytes were also marked with the fluorescent dye CM-DiI. A control group (n=4) received medium injection only. T2*weighted gradient-echo images at 7-T MRI were acquired at day 7 post-acute liver failure induction. Transplanted cells were detected in the liver by PCR for the Y-chromosome (Sry-2 gene) and histological analysis. <h3>Results</h3> Mean intracellular iron concentrations were 11.4±SE1.1 pg/cell in human and 8.6±0.3 pg/cell in rat hepatocytes. Cell viability and metabolic function were not significantly affected at these SPIO concentrations. In vitro MRI of SPIO-labelled cells (2000 cells/μl) induced a 50% change in T2 relaxivity compared to non-labelled cells. SPIOs were detected in rat liver as a decrease in the MRI signal intensity 6 days after transplantation in the three survivors. On histology most of the SPIO particles were located in Kupffer cells, indicating the loss of iron oxide particles from hepatocytes. In keeping with this, labelled cells could not be detected in the liver by the fluorescent dye or by PCR for Sry-2 gene. <h3>Conclusion</h3> Optimum conditions to label human and rat hepatocytes with SPIOs were determined, which did not affect cell viability or metabolic function, and were sufficient for in vitro MRI detection. However, the clearance of hepatocytes after transplantation limits the value of MRI for assessing long-term hepatocyte engraftment.
A cerebellar long-term depression update
Authors: David J. Linden
Journal: Behavioral and Brain Sciences (1996)

Two major themes have emerged in the commentaries elicited by the target articles that concern cerebellar long-term depression (LTD) (CRÉPEL, VINCENT, and LINDEN). First, is a lively debate concerning the potential role of a nitric oxide/cGMP cascade in cerebellar LTD induction. Second is a much broader issue relating to the interchange of information between cerebellar physiologists concerned with mechanisms at a cellular and synaptic level and those working at the level of systems physiology, behavior, or modeling. What contributions can cellular physiologists make to the study of motor learning? Cellular physiologists can provide testable hypotheses to help determine if these synaptic phenomena do underlie particular behaviors (e.g., if cerebellar LTD underlies vestibulo-ocular reflex [VOR] adaptation or eyeblink conditioning, then blockade of cerebellar LTD via, say, mGluRl inhibition, should interfere with these forms of motor learning). In addition, we can provide descriptive parametric information about basal synaptic function and use-dependent synaptic modifications that can constrain the range of models proposed to underlie a given behavior (e.g., are the timing constraints on LTD induction consistent with VOR adaptation or eyeblink conditioning?).
Massive mucinous discharge from a fistula caused by intraductal papillary mucinous neoplasm diagnosed by endoscopic ultrasound
Authors: P. Fusaroli, P. Cecinato, L. Garulli, F. Poli, G. Caletti
Journal: Endoscopy (2011)

A 76-year-old Caucasian man presented to our institution with progressive fatigue and weight loss. He had undergone esophagogastroduodenoscopy 1 year previously, which suggested a large duodenal ulcer [1] [2].
FRI0258 Long-term treatment with mycophenolate versus cyclophosphamide for systemic sclerosis-associated pulmonary fibrosis: A case control retrospective study
Authors: I. Giavri, S. Panopoulos, V.K. Bournia, K. Fragiadaki, G. Trakada, C. Kostopoulos, P.P. Sfikakis
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Evidence from uncontrolled studies suggests that mycophenolate mofetil (MMF), an immunomodulatory agent which inhibits lymphocyte proliferation is beneficial for the treatment of systemic sclerosis (SSc)-associated pulmonary fibrosis. <h3>Objectives</h3> We sought to determine the efficacy and safety profile of long term treatment with MMF or mycophenolate sodium (MS) in SSc patients with pulmonary fibrosis and compare these results to cyclophosphamide (CYC), the gold standard treatment. <h3>Methods</h3> We retrospectively identified our SSc patients with "active" pulmonary fibrosis confirmed by CT scan who were able to perform pulmonary function tests and received MMF or MS for at least one year. Treatment had been always initiated in symptomatic patients with either first-diagnosed pulmonary fibrosis or with a &gt;10% decrease in forced vital capacity (FVC) over the past 12 months. These patients were carefully matched 1:1 for disease characteristics and baseline FVC (±3% of predicted) with patients fulfilling the same criteria but had received CYC. Patients' course, including changes in FVC, total lung capacity (TLC), and diffusion capacity of the lung for carbon monoxide (DLCO) at one and two years of continuous treatment were compared between groups. <h3>Results</h3> Ten patients received MMF (n=3) or MS (n=7), either for first-diagnosed symptomatic pulmonary fibrosis (n=3) or for significant deterioration of FVC, whereas CYC was given in 4 and 6 first-diagnosed or deteriorating patients, respectively.Pulmonary function tests (mean±SD % of predicted) for the MMF/MS group at baseline, at one-year and two-years of treatment were as follows: FVC: 78±14, 80±12 and 82±16, respectively; TLC: 71±16, 74±11, and 72±13, respectively; DLCO: 57±12, 55±10, and 52±8, respectively. The respective values in the CYC group were as follows: FVC: 77±12, 80±12, and 80±11; TLC: 64±15, 69±16 and 71±11; DLCO: 53±15, 56±15 and 57±8. FVC, TLC or DLCO did not change significantly after one- or two years of MMF/MS or CYC therapy. After two years of continuous treatment 6 of 10 patients in each group fulfilled the definition of stable disease by the American Thoracic Society, 3 patients in each group improved (&gt;10% in FVC) and the remaining patient in both groups failed to meet criteria for stability, as FVC decreased by more than 10%. Both drugs were well tolerated in these patients and no serious adverse events occurred in either group. <h3>Conclusions</h3> These results suggest that long term treatment with MMF or MS can be a safe therapeutic modality having a comparable to CYC effect in stabilising pulmonary function in a small cohort of patients with SSc-associated pulmonary fibrosis. <h3>Disclosure of Interest</h3> None Declared