tbuckley/cabot-search huggingface dataset:
P38 Is it possible to predict ambulatory oxygen (AO) requirements?
Authors: L Cornish, F Dyer, K Cheema, J Bott
Journal: Thorax (2013)

<h3>Aim</h3> To determine whether AO flow rate requirements can be predicted in patients with chronic lung diseas. <h3>Background</h3> The process for AO assessment as per current UK guidance can be extremely time consuming, necessitating multiple walking tests with significant rest periods between walks. We set out to explore whether a model could accurately predict the AO flow rate required to abolish/minimise desaturation, thus simplifying the process. <h3>Method</h3> Retrospectivedatawere analysed for all patients who attended AO clinic from April 2009 to January 2013. AO needs were assessed as per current UK guidance. For those who met the criteria for AO (n = 100), resting Sp02, desaturation on the endurance shuttle walk test (ESWT) and AO flow rate required to minimise this desaturation were recorded, along with age and diagnosis. <h3>Results</h3> Multiple regression analysis was undertaken to test how well the variables included in the data could predict the likely level of AO required. A range of models were constructed and tested against the actual AO flow rate that had been required. The model which accounted for the greatest proportion of the variance (r = 0.671, F = 79.40, p &lt; 0.05) included only one variable, the level of oxygen desaturation on room air post ESWT. Adding additional variable to the model, such as age and resting SpO2 did not add significantly to the predictive power of the model. <h3>Conclusion</h3> Using this model, 91% of patients were predicted correctly with an error of +/- 1L of the actual flow rate. It would therefore, 9 times out of 10, give a flow rate that was either correct ( +/- 1L). Use of this model will reduce the number of walking tests required when performing AO assessment, saving both time and valuable healthcare resources.
Abstract 1744: Hsp27 overexpression enhances the chemosensitivity to MCF7 doxorubicin resistance cells
Authors: Ragu Kanagasabai, Karthikeyan Krishnamurthy, Govindasamy Ilangovan
Journal: Cancer Research (2011)

Abstract Multidrug resistance (MDR) is a major obstacle in cancer chemotherapy and its inhibition is an effective way to reverse cancer drug resistance. In the present study we report that over expression of HSP27 down-regulated MDR1 expression in MCF7/Doxorubicin (MCF7/DOX), a human breast MDR cancer cell line. In MCF7/Dox cells, mutant p53 was found to be accumulated, whereas Hsp27 level is completely depleted. Since Hsp27 was shown to enhance Akt phosphorylation and G2/M cell cycle arrest, a common pathway of Dox-induced cell death in MCF7 cells, we hypothesized that over expression of Hsp27 in resistant cell will sensitize for chemotherapy. HSP27 over expression significantly inhibited mutant p53 and MDR1 (P-gp) expression and MDR1 mRNA. The suppression of MDR1 was accompanied by partial recovery of intracellular drug accumulation and increased cytotoxicity of Doxorubicin, indicating that HSP27 reversed the MDR phenotype by inhibiting the drug efflux function of MDR1. Moreover, nuclear factor-KB activity and IKB degradation were inhibited by HSP27 over expression through down regulation of mutant p53. Interestingly, the over expression of HSP27 negatively regulated the cell growth with significant G2/M arrest of cell cycle, and it could up-regulate endogenous p21 in a p53 independent manner leading to enhanced caspase activation to promote intracellular apoptotic signaling for cell death. Taken together, our results suggested that HSP27 is down regulated in MCF7/Dox resistant cells, and when re-expressed, it down regulates MDR1 expression via p53 and NF-KB., which results in growth suppression and higher sensitivity to Doxorubicin. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1744. doi:10.1158/1538-7445.AM2011-1744
A Comparison of Two Regimens for the Treatment of<i>Mycobacterium avium</i>Complex Bacteremia in AIDS: Rifabutin, Ethambutol, and Clarithromycin versus Rifampin, Ethambutol, Clofazimine, and Ciprofloxacin
Authors: Stephen D. Shafran, Joel Singer, Donald P. Zarowny, Peter Phillips, Irving Salit, Sharon L. Walmsley, Ignatius W. Fong, M. John Gill, Anita R. Rachlis, Richard G. Lalonde, Mary M. Fanning, Christos M. Tsoukas
Journal: New England Journal of Medicine (1996)

Bacteremia with the Mycobacterium avium complex is common in patients with the acquired immunodeficiency syndrome (AIDS), but the most effective treatment for this infection remains unclear.
AB0049 TH17 but not TH22 cells display direct pathological behaviour in arthritis
Authors: J.P. van Hamburg, O.B. Corneth, S.M. Paulissen, N. Davelaar, P.S. Asmawidjaja, E. Lubberts
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Th17 cells (IL-17+IL-22+) are critically involved in the induction and progression of arthritis. Recently, Th22 cells were discovered, which were characterized by IL-22 expression in the absence of IL-17. However, it remains unclear whether IL-22 and Th22 cells, directly contribute to synovial inflammation. <h3>Objectives</h3> Therfore, we examined the potency of Th22 cells to activate synovial fibroblasts. In addition, it was investigated whether IL-22 is critical in Th17-mediated experimental arthritis. <h3>Methods</h3> Th17 (CD4+CD45RO+CD25-CCR6+CCR4+CCR10-) and Th22 (CD4+CD45RO+CD25-CCR6+CCR4+CCR10-) cells were analyzed in peripheral blood of treatment-naïve RA patients in comparison to age and sex matched healthy controls by flow cytometry. Furthermore, synovial fluid of patients with established RA was analysed for the presence of Th17 and Th22 cells. To test the contribution of IL-22 or Th22 in synovial inflammation, co-culture experiments of RA synovial fibroblasts (RASF) with Th22 and Th17 cells were performed. The <i>in vivo</i> relevance of IL-22 in synovial inflammation was investigated in a T cell-mediated arthritis model using mice deficient for IL-22. <h3>Results</h3> Both Th17 and Th22 cell populations were present in synovial fluid of patients with rheumatoid arthritis (RA) and were increased in peripheral blood of these patients compared to healthy controls. Upon interaction with RA synovial fibroblasts (RASF), Th17 cells induce activation of RASF resulting in an inflammatory feedback loop including autocrine IL-17A production. In Th17-RASF co-cultures, neutralisation of IL-22 resulted in increased RASF activation whereas the opposite was found by FICZ-induced IL-22 production. Moreover, Th17 cells were markedly more potent than Th22 cells in RASF activation. In addition, no difference in T cell-mediated experimental arthritis severity was found between IL-22 deficient mice compared to wild type mice. <h3>Conclusions</h3> These findings show that IL-22 and Th22 cells are less potent in inducing synovial inflammation compared to Th17 cells. These data imply that targeting Th17 cells rather than Th22 cells should be the focus for the treatment of T cell mediated joint inflammation. <h3>Disclosure of Interest</h3> None Declared
Rapidly progressive relapsing sclerosing cholangitis following surgery for pancreatic pseudotumor
Authors: I. Hajj, J. Ahmad, A. Slivka
Journal: Endoscopy (2009)

A 52-year-old man presented with painless jaundice and weight loss. A computed tomography (CT) scan of the abdomen revealed an inflammatory mass in the pancreatic head. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated a double duct sign ([Fig. 1]), and a biliary stent was placed. Brush cytology was negative and percutaneous biopsy showed inflammatory changes. Laparotomy confirmed a large inflammatory mass in the pancreatic head, and a cholecystojejunostomy was carried out. Several months later, the patient developed recurrent jaundice and ERCP showed new diffuse strictures involving the intra- and extrahepatic biliary tree ([Fig. 2]). CT abdomen revealed concentric thickening of the common bile duct (CBD) with enlarged periportal nodes ([Fig. 3]), and endoscopic ultrasound with fine-needle aspiration biopsy of the pancreatic head and lymph nodes was benign. A liver biopsy showed bile duct inflammation and marked cholestasis, and ultrasound revealed patent vasculature. Colonoscopy as well as autoimmune serology and IgG4 levels were normal.
HER-2/neu over-expressing DCIS phenotypes and the transition from <i>in situ</i> to invasive breast cancer: implications for breast cancer prevention.
Authors: RE Roses, EC Paulson, A Sharma, JE Schueller, H Nisenbaum, S Weinstein, KR Fox, PJ Zhang, BJ Czerniecki
Journal: Cancer Research (2009)

Abstract Abstract #1161 Background: Prognostically significant invasive breast cancer subtypes, distinguishable through immunohistochemistry for ER, PR and HER-2/neu expression, have recently been identified. The implication of similar phenotypic patterns in ductal carcinoma in situ (DCIS) lesions remains uncertain. The objective of this study was to determine whether DCIS phenotypes are associated with different rates of progression to invasive cancer.&amp;#x2028; Methods: Immunohistochemical staining for ER, PR and HER-2/neu was performed on biopsy and resection specimens from consecutive patients evaluated with DCIS between March 2003 and May 2008. DCIS lesions were characterized as luminal A (ER+ or PR+, HER-2/neu-), luminal B (ER+ or PR+, HER-2/neu+), HER-2/neu positive (ER- and PR-, HER-2/neu+) or basal-like (ER-, PR- and HER-2/neu-). All patients underwent breast MRI and those patients with evidence of invasive disease greater than 1cm in largest dimension were excluded from the analysis. Rates of invasive disease associated with DCIS lesions with different phenotypes were compared using a chi square test. Multivariate logistic regression was used to evaluate the relationship between phenotype and invasion adjusting for patient age, lesion size, nuclear grade, and the presence of comedo necrosis.&amp;#x2028; Results: One hundred and seven patients were included in the analysis. Luminal A was the most common phenotype and accounted for 59% of lesions (63/107). Associated invasive disease was identified in 6 patients with such lesions (10%). The HER-2/neu positive phenotype accounted for 21% of lesions (23/107). Invasive disease was identified in 8 patients with such lesions (35%). Seventeen patients had luminal B DCIS (16%) and 8 of these patients had associated invasive disease (47%). Basal-like lesions were uncommon; only four patients with such lesions were identified. The rates of invasion differed significantly between groups (overall rxc chi square p=0.002). By univariate analysis, the rates of invasion associated with luminal B and HER-2/neu positive phenotypes were significantly higher than the rate of invasion associated with the luminal A phenotype (p&amp;lt;0.001 and p=0.005, respectively). Luminal B DCIS was significantly associated with invasive disease after multivariate adjustment (OR=11.1 p &amp;lt;0.001).&amp;#x2028; Discussion: Invasive foci are more commonly associated with HER-2/neu over-expressing DCIS phenotypes. Moreover, co-expression of HER-2/neu and ER in DCIS lesions is an independent predictor for the presence of associated invasive disease. Novel therapies targeting HER-2/neu in addition to anti-estrogen therapies may, therefore, play a role in breast cancer prevention. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 1161.
OP0055 IL-1 receptor antagonist restores IL-18 nk cell axis in systemic JIA
Authors: W. De Jager, S.J. Vastert, B.J. Noordman, B.J. Prakken, N.M. Wulffraat
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Systemic onset juvenile idiopathic arthritis (SoJIA) is an acquired auto-inflammatory disease characterized by systemic inflammation and innate immune activation reflected in uncontrolled production of cytokines such as IL-1, IL-6 and IL-18. In SoJIA, NK cell function is severely hampered despite high levels of IL-18. We recently found that defective phosphorylation of the IL-18 receptor beta is responsible for the deficient IL-18-NK cell axis in SoJIA <h3>Objectives</h3> To study first line treatment with recombinant IL-1 receptor antagonist (rIL-1RA, Anakinra) in 16 newly systemic onset JIA patients <h3>Methods</h3> Clinical outcome was measured using ACRp70 and ACRp90. Furthermore NK cell function, inflammasome activity and cytokine expression was assed during follow up (max 2 years) <h3>Results</h3> Here we show that patients with SoJIA have increased inflammasome activation leading to elevated IL-18 levels. First line treatment with rIL-1RA effectively down-regulated IL-18 levels through suppression of inflammasome activation and led to rapid resolution of clinical features in 87% (ACRp90) of patients. Furthermore, using rIL-1RA as first line treatment approach the defective IL-18-NK cell axis is restored as shown by resulting in improved lytic NK cell function and regaining of the NK cell responsiveness to IL-18 stimulation. <h3>Conclusions</h3> These data suggest that the mechanisms of inflammatory control induced by rIL-1RA in SoJIA patients involves more than blocking IL-1R signalling, since it seems to restore the IL-18-NK cell route and affecting the inflammasome as well. <h3>Disclosure of Interest</h3> None Declared
Abstract 2260: Modulation of P-glycoprotein expression by a novel nutrient mixture in multidrug-resistant human uterine sarcoma cell line MES-SA/Dx5 but not in drug-sensitive MES-SA cell line
Authors: M. Waheed Roomi, Nusrath W. Roomi, Matthias Rath, Aleksandra Niedzwiecki
Journal: Cancer Research (2010)

Abstract Introduction: We have characterized a nutrient mixture containing lysine, proline, ascorbic acid and green tea extract as a novel antineoplastic agent with a broad spectrum of antitumor activity against a number of cancer cell lines. Objective: We investigated the effect of NM on modulation of P-glycoprotein (Pgp) in the drug-resistant human uterine sarcoma cell line MES-SA/Dx5 and compared it with the effect on drug-sensitive cell line MES-SA. In addition we also studied the effect of NM on MMP expression and Rhodamine-123 accumulation and efflux. Material and Methods: Human drug insensitive uterine sarcoma cell line MES-SA/Dx5 and drug sensitive cell line MES-SA (ATCC) were grown in RPMI 1640 medium supplemented with fetal bovine serum and antibiotics. At near confluence, the cells were tested with NM at 0, 50, 100, 250, 500 and 1000 mcg/ml, in triplicate at each dose. Cell proliferation was evaluated by MTT assay, MMPs by gelatinase zymography, and Pgp expression by Western blot and immunodetection using FITC-conjugated antibody and rhodamine-123 (Rh-123) accumulation and efflux assays. Results: NM exhibited antiproliferative effect on MES-SA/Dx5, by 20% at 50 and 100 mcg/ml and by 40% at 25, 500 and 1000 mcg/ml, whereas in MES-SA cell line, NM showed dose-response toxicity of 40% at 50 and 30% at 1000 mcg/ml. In both cell lines, zymography demonstrated a band corresponding to MMP-2 in normal cells and MMP-9 with PMA treatment. Both MMPs showed dose-response inhibition by NM. NM treatment also showed diminished dose-dependent Pgp expression by MES-SA/Dx5 cell line by Western blot and by immunodetection, whereas MES-SA did not exhibit Pgp by Western blot or by immunostaining. NM enhanced the accumulation and efflux of Pgp substrate Rh-123 in MES-SA/Dx5 uterine sarcoma cell line but not in the drug-sensitive cell line MES-SA. Conclusions: In summary, this study demonstrated that Pgp is modulated by NM, which may be an attractive potential agent for therapeutic use in cancer treatment 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 2260.
TCT-371 Evaluation of Highly Automated Software for Analyzing Intravascular Optical Coherence Tomography Pullbacks of Stents
Authors: Hong Lu, Martin Jakl, Zhao Wang, Kentaro Tanaka, Soumya Ray, Pavel Cervinka, Andrew M. Rollins, Hiram Bezerra, David L Wilson
Journal: Journal of the American College of Cardiology (2014)
Lens Changes and Survival in a Population-Based Study
Authors: Marvin J. Podgor, Gary H. Cassel, William B. Kannel
Journal: New England Journal of Medicine (1985)

The Framingham Heart Study was begun in 1948 to study factors associated with cardiovascular disease. Participants have been reexamined approximately every two years. From 1973 to 1975, the Framingham Eye Study examined the eyes of available Heart Study participants. We used information about nearly 2000 persons from these population-based studies to investigate the relation of lens changes to survival. Follow-up ranged from five to eight years; 312 persons (16 per cent) died. Proportional-hazards regression analyses indicated an overall association of lens changes and decreased survival (P = 0.01), but detailed investigation showed (1) no association of lens changes and decreased survival among persons without diabetes (P = 0.29) and (2) a significant association of lens changes and decreased survival among persons with diabetes (P = 0.001). Diabetic persons with lens changes had an estimated death rate more than twice that of diabetics without lens changes. The duration of diabetes and degree of retinopathy were not associated with survival in this group, most of whom had adult-onset diabetes of short duration. We conclude that lens changes are earlier predictors of death in diabetics than these more traditional variables.
DOES LEFT ATRIAL APPENDAGE CLOSURE IMPROVE THE SUCCESS OF PULMONARY VEIN ISOLATION? RESULTS OF A RANDOMIZED CLINICAL TRIAL
Authors: Alexander Romanov, Evgeny Pokushalov, Sergey Artyomenko, Akmal Yakubov, Ilya Stenin, Evgeny Kretov, Oleg Krestianinov, Igor Grazhdankin, Dejan Risteski, Alexander Karaskov, Jonathan Steinberg
Journal: Journal of the American College of Cardiology (2015)
A Clinical Conundrum Solved with Indium-111 White Blood Cell Scanning
Authors: MAJ SCOTT C. WRIGHT, JEROME L. BILLINGSLEY, LTC HARRIET J. DEISSLER
Journal: Clinical Nuclear Medicine (2002)

WRIGHT, MAJ SCOTT C. M.D.; BILLINGSLEY, JEROME L. M.D.; DEISSLER, LTC HARRIET J. D.O. Author Information
AB0935 Musculoskeletal Involvement in A Study of 50 Patients with Sarcoidosis
Authors: N. Boussetta, R. Dhahri, F. Jaziri, M. Mahfoudhi, S. Barbouchi, S. Turki, K. Ben Abdel Ghani, A. Khedhr
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Sarcoidosis is a multisystem disease of unknown etiology. Patients with sarcoidosis may develop extrapulmonary organ involvement, including rheumatologic complications. Joint manifestations, including arthritis and periarthritis, occur in 14–38%. <h3>Objectives</h3> To analyze the pattern of osteoarticular lesions in patients with sarcoidosis hospitalized in internal medicine departments. <h3>Methods</h3> We carried out a systematic retrospective analysis of cases with sarcoidosis admitted in the last 38 years, using hospital databases. We assessed the following items: distribution of arthritis, chronicity, systemic manifestations, biochemical measures. <h3>Results</h3> We included 50 patients (75% women).Osteoarticular symptoms revealed the disease in 60% of patients. The mean age at the onset of symptoms of sarcoidosis was 42.47 years [18-70]. The average time between onset of symptoms and diagnosis was 17.74 months. Inflammatory polyarthritis was the most common symptom found in 28 patients (56%) mainly affecting the large joints, and were bilateral and symmetrical in all cases. Arthralgia hits both knees in 22 cases, elbows in 16 cases, wrists in 13 cases ankles in 11 cases, and shoulders in 4 cases. Polyarthritis were revealing in 9 cases (18%). They were asymmetric in 3 cases. Acute polyarthritis was noted in 5 cases (10%) and chronic in 4 others (8%).Plain radiographs were performed in 30 cases and no anomalies were found in all cases. Muscle involvement was noted in one case (2%). The diagnosis of sarcoidosis has been selected on clinical and laboratory, radiological and histological findings in all cases. <h3>Conclusions</h3> Rheumatic manifestations have been reported to occur in 4% to 38% of patients and may manifest clinically as inflammatory arthritis, periarticular soft tissue swelling, tenosynovitis, dactylitis, bone involvement, or myopathy. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5703
Case 5-1995: Arteritis with Multiple Cerebral Infarcts
Authors: David Schiff
Journal: New England Journal of Medicine (1995)

To the Editor: In his otherwise superb discussion of Case 5-1995 (Feb. 16 issue),1 Dr. Caplan was inaccurate in stating that ``lymphomatoid granulomatosis does not involve the peripheral nerves.'' In addition to causing intraparenchymal brain masses, this disorder may involve the peripheral nervous system. In the initial report of this condition, 20 percent of patients had evidence of central nervous system disease and 15 percent ``peripheral neuritis,'' and pathological studies revealed lymphocytic infiltration, often atypical, of peripheral and cranial nerves.2 In a larger study, 11 of 152 patients (7 percent) had peripheral neuropathy.3 In that study, both central nervous system . . .
Abstract 651: Insulin-like growth factor 1 receptor antibody induces rhabdomyosarcoma cell death via a process involving AKT and Bcl-xL
Authors: Linnia Mayeenuddin, Yunkai Yu, Zhigang Kang, Lee Helman, Liang Cao
Journal: Cancer Research (2011)

Abstract Insulin-like growth factors (IGFs) and their receptor, IGF-1 receptor (IGF1R), have important roles in growth, development, stress response, aging and cancer. There are many agents that inhibit IGF1R in oncology clinical development, and in some cases, they have been associated with rapid tumor regression. However, it is not clear by which process these targeted agents induce cancer cell death and how to predict such tumor responses. Here, we showed that IGF1R antibody led to rapid cell death and tumor regression in some rhabdomyosarcoma (RMS) cells. Mechanistic analysis revealed a rapid onset of mitochondrial-dependent apoptosis, including mitochondrial depolarization, cytochrome C release and the activation of specific caspases. The antibody sensitive cells had greater dependence on AKT for maintaining downstream signaling and the expression of a constitutively active AKT, which restored AKT-signaling in these cells, inhibited anti-IGF1R induced cell death. Further analysis showed IGF1R antibody-induced hypophosphorylation of BAD and activation of downstream BAX. Interestingly, the examination of RMS cell lines and tumors revealed an inverse correlation between elevated IGF1R and Bcl-2 level (P=0.033), with the sensitive cells lacking Bcl-2 expression. The overexpression of BAD specific target, Bcl-xL, conferred resistance, whereas Bcl-xL knockdown sensitized cells lacking Bcl-2 to anti-IGF1R-induced cell death. We propose that RMS pathogenesis involves increased IGF1R expression that enhances AKT and Bcl-xL-mediated cell survival, and the blockage of IGF1R results in inhibition of survival signal from Bcl-xL and cell death in the sensitive Bcl-2 negative cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 651. doi:10.1158/1538-7445.AM2011-651
982 PERFORMANCE OF RAPID TESTS FOR DETECTION OF HEPATITIS B SURFACE ANTIGEN (HBSAG) AND ANTI HEPATITIS B SURFACE ANTIBODY (ANTI-HBSAB) IN A LARGE COHORT, FRANCE
Authors: J. Bottero, J. Gozlan, A. Boyd, M. Lemoine, A. Collignon, N. Boo, P. Dhotte, B. Varsat, G. Muller, O. Cha, O. Picard, J. Nau, P. Campa, B. Silbermann, M. Bary, P.-M. Girard, K. Lacombe
Journal: Journal of Hepatology (2012)