tbuckley/cabot-search huggingface dataset:
P430RP105 deficiency aggravates cardiac dysfunction after myocardial infarction in mice
Authors: MC Louwe, JC Karper, MR De Vries, AJNM Bastiaansen, JWA Van Der Hoorn, K Willems Van Dijk, PCN Rensen, P Steendijk, JWA Smit, PHA Quax
Journal: Cardiovascular Research (2014)

Purpose: Toll-like receptor-4 (TLR4), a receptor of the innate immune system, is suggested to have detrimental effects on cardiac function after myocardial infarction (MI). RP105 (CD180) is a TLR4 homolog lacking the intracellular signalling domain that competitively inhibits TLR4-signalling. Thus, we hypothesized that RP105 deficiency, by amplifying TLR4 signalling, would lead to aggravated cardiac dysfunction after MI. Methods and Results: First, whole blood from RP105-/- and wild-type (WT) male C57Bl/6N mice was stimulated with LPS, which induced a strong inflammatory TNFα response in RP105-/- mice. Then, baseline heart function was assessed by left ventricular pressure-volume relationships which were not different between RP105-/- and WT mice. Permanent ligation of the left anterior descending coronary artery was performed to induce MI. Infarct sizes were analysed by (immuno)histology and did not differ. Fifteen days post MI heart function was assessed and RP105-/- mice had significantly higher heart rate (+21%,P<0.01), end systolic volume index (+57%,P<0.05), end systolic pressure (+22%,P<0.05) and lower relaxation time constant tau (-12%,P<0.05), and a tendency for increased end diastolic volume index (+42%,P<0.06), compared to WT mice. In the area adjacent to the infarct zone, compared to the healthy myocardium, levels of RP105, TLR4 and the endogenous TLR4 ligand fibronectin-EDA were increased as well as the number of macrophages, however this was not different between both groups. Conclusion: Deficiency of the endogenous TLR4 inhibitor RP105 leads to an enhanced inflammatory status and more pronounced cardiac dilatation after induction of MI, underscoring the role of the TLR4 pathway in post-infarction remodelling.
Abstract 4700: Acrolein-deoxyguanosine DNA adduct formation and lung cancer
Authors: Yu Hu, William Rom, Harvey I. Pass, Simon D Spivack, Moon-shong Tang
Journal: Cancer Research (2010)

Abstract Cigarette smoke (CS) contains 1,000-10,000 fold more acrolein (Acr) and crotonaldehyde (Crot) than polycyclic aromatic hydrocarbons (PAHs). These aldehydes can induce propanoldeoxyguanosine (propanol-dG) DNA adducts formation in cultured normal human lung epithelial cells. Previously, we have found that the distribution of Acr-dG in the p53 gene coincides with the lung cancer p53 mutational spectrum of cigarette smokers, and that Acr-dG induces similar level of G to T transversion and G to A transition mutations as in lung cancer of cigarette smokers. Hence, we have proposed that Acr is a major etiological agent of CS related lung cancer. We developed a 32P-postlabelling method in combination with 2D TLC/HPLC method to quantify propanol-dG formation in human lung tissue. To date we have determined Acr-dG and Crot-dG in the lung tissue of cigarette smokers (n=27) and nonsmokers (n=25) with lung cancer. We found that 1) both α- and γ-Acr-dG are formed in lung tissues of smokers and nonsmokers, and the level of these two types of adduct in lung tissue varies from 10-4,510, and 0-1,900 fmole/μmole, respectively; and 2) smokers appear to have a higher level of γ-Acr-dG than nonsmokers although the differences have not reached statistical significance (p=0.1854); 3) the level of Crot-dG in smokers is significant higher than that in nonsmokers (p=0.0279). These results indicate a substantial amount of Acr-dG and Crot-dG formed in lung tissue of lung cancer. Key words: α, β-unsaturated aldehydes, cigarette smoking, DNA adducts, lung cancer. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 4700.
Active Chronic Pyelonephritis without Evidence of Bacterial Infection
Authors: Marcia E. Angell, Arnold S. Relman, Stanley L. Robbins
Journal: New England Journal of Medicine (1968)

The clinical records of 20 patients with histologically proved, nonobstructive "active chronic pyelonephritis" as their sole renal lesion were selected for study. Six had chronic or recurrent urinary-tract infection, and two gave a history of possible past infection. The remaining 12 had no clinical or bacteriologic evidence of either past or current infection. In four cases renal insufficiency progressed to a fatal termination, over a period during which repeated urine cultures remained negative. The possibility that prior asymptomatic bacterial infection was indirectly involved cannot be ruled out by these observations, but the data suggest that many examples of the lesion now called "active chronic pyelonephritis" may be of nonbacterial origin. These observations show that progression of this disease does not require the presence of demonstrable bacteria.
Case 38-1966
Authors: Edwin P. Maynard, Benjamin Castleman
Journal: New England Journal of Medicine (1966)

Presentation of Case First admission. A fifty-two-year-old woman was admitted to the hospital because of a lump in the breast.One year previously she felt a lump in the right breast but did not seek medical advice until two weeks before entry, when she became aware of tenderness in the right axilla. A hysterectomy had been performed eleven years earlier.Physical examination revealed an obese woman who appeared well. A stony-hard mass, 4 by 3 cm., was palpable in the upper outer quadrant of the right breast; 3 hard lymph nodes were felt in the right axilla. The lungs, heart . . .
Usefulness of three dimensional endoscopic ultrasonography assisting at endoscopic resection for rectal carcinoids
Authors: T Abe, S Itoh, Y Nemoto, T Kakemura, S Fujinuma
Journal: Endoscopy (2006)

Background: Recent progress in colonoscopic examination has facilitated the diagnosis of many rectal carcinoids. Rectal carcinoids less than or equal to 1cm in diameter and the depth of invasion to submucosal layer are perfomed local excision adequate. Endoscopic complete resection of rectal carcinoids is difficult during conventional endoscopic polypectomy. This problem stimulated an exploration of new endoscopic technique, such as two-channel endosope method, aspiration lumpectomy, band-snare resection and so on. Though we treated rectal carcinoids by endoscopic mucosal resection with a ligation device (EMR-L), a few cases were not complet resection. So we perfomed EMR-L assisted with three dimensional endoscopic ultrasonography (3D EUS) at saline injection into the submucosal layer and before snaring resection. Aim: We evaluated the usefulness of assisting the 3D EUS when rectal carcinoids were resected by EMR-L. Patients and Method: We perfomed endoscopic resection 26 rectal carcinoids during Mar 1998 through Dec 2005. 12 lesions were resected by EMR-L not assited with 3D EUS. 14 lesions were resected by EMR-L assited with 3D EUS. 3D EUS was carried out using 3D ultrasonic probe at 12MHz or 20MHz and 3D display software (MAJ1330, Olympus). Results: There were no differences between the two groups in terms of age, gender, or tumor size. For three patients (25%) in EMR-L not assited with 3D EUS group, there was tumor involvement at margin of resection specimen. Whereas all tumors removed by EMR-L assisted with 3D EUS had histopathologically proven negative margins (P<0.05). There was no complication of any procedure. For all lesions, the depth of invasion by 3D EUS and by pathological diagnosis were corresponding. Conclucion: It was useful to assist 3D EUS at EMR-L for small rectal carcinoids and diagnose the depth of invasion.
The Hot Rectus Abdominis Muscle Sign
Authors: ETHEL V. SABNIS, MICHAEL J. BLEND, DAN G. PAVEL
Journal: Clinical Nuclear Medicine (1999)

Uptake of bone-seeking agents in muscle has been described in conditions associated with muscular damage, including rhabdomyolysis, overexertion, polymyositis, myositis ossificans, ischemia, and electric burns. Uptake of Tc-99m phosphate compounds may occur secondary to binding to tissue hormone receptors, tissue calcium, denatured proteins, iron deposits, or all of these. The authors describe a patient with increased rectus abdominis uptake secondary to vigorous sit-up exercises.
Tc-99m Depreotide Scintigraphy of Breast Carcinoma
Authors: JAIME L. MONTILLA-SOLER, ROBERT S. BRIDWELL
Journal: Clinical Nuclear Medicine (2002)

From the Nuclear Medicine Service, Department of Radiology, Walter Reed Army Medical Center, Washington, DC Received for publication March 7, 2001. Revision accepted October 4, 2001. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the United States Department of the Army or the Department of Defense. Reprint requests: Jaime L. Montilla-Soler, Nuclear Medicine Service, Department of Radiology, Walter Reed Army Medical Center, Washington, DC 20307-5001.
Abstract 255: Identification of a novel TRAIL sensitizer in TRAIL-resistant cancer cells
Authors: So Jung Park, Yoon Kyung Jo, Ye Jin Ha, Jin Cheon Kim, Dong-Hyung Cho
Journal: Cancer Research (2012)

Abstract The Tumor Necrosis Factor Related Apoptosis Inducing Ligand (TRAIL), a TNF-family member is a highly promising agent for cancer therapy as it selectively induces apoptosis in various cancer cells but not in normal cells. However, many primary tumors are resistant to TRAIL-induced apoptosis and the resistant mechanisms are not fully understood. To identify novel TRAIL signaling regulatory molecules, we screened a siRNA library that target 719 whole human protein kinases in TRAIL-resistant lung cancer cell line (A549 cell). As a screening result, we identified a member of NIMA-related kinases as a new regulator of TRAIL-induced cell death. NEK family play key role in controlling mitosis but the role in TRAIL signaling was not elucidated. Down-regulation of NEK by siRNA dramatically increased TRAIL-induced apoptosis in TRAIL resistant cancer cells including A549 cells. However it was not effective on both etoposide and TNF/CHX-mediated apoptosis. In addition, inhibition of NEK highly activated caspase-3 in response to TRAIL. On the other hand, over-expression of NEK reduced TRAIL-induced apoptosis in TRAIL sensitive cells. Our findings suggest that NEK is a novel negative modulator of TRAIL-induced apoptosis in cancer cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 255. doi:1538-7445.AM2012-255
Abstract 1064: Numb, a progenitor cell fate determinant and intrinsic inhibitor of Notch signaling, is cell cycle regulated and required for proper mitotic entry and progression in melanoma cells
Authors: Travis L. Schmit, Vijayasaradhi Setaluri, Vladimir S. Spiegelman, Nihal Ahmad
Journal: Cancer Research (2010)

Abstract Proper regulation of the cell cycle, particularly DNA replication and cell division, are crucial for correct cell ploidy and genomic integrity. Loss of various regulators, often tumor suppressors, during these processes leads to either cell cycle arrest or unregulated progression through mitosis. This may result in aneuploidy and neoplastic transformation. Therefore, defining the mechanisms by which various tumor suppressors exert their regulatory functions is essential for understanding cancer development as well as developing novel target-based therapies to combat cancer progression. We found that Numb expression is cell cycle regulated and that its expression is required for proper mitotic entry and exit in melanoma cells. Using a double thymidine arrest and release protocol, we evaluated the expression of Numb during the cell cycle. Numb mRNA and protein expression was found to be maintained at a low steady state level in asynchronous A375 and HS294T melanoma cells. However, as cells entered S phase Numb levels were found to increase, peak during mitosis and then rapidly decline at mitotic exit when the cells reentered G1 Phase. This cycling of Numb mirrored the mitotic specific expression of both Plk1 and CyclinB1, however Numb showed an expression pattern with an increase beginning slightly earlier (as early as S phase). Plk1 inhibition (via shRNA as well as a small molecule inhibitor) and nocodazole-mediated mitotic arrest was also found to be accompanied with an increase in Numb expression. Additionally, we found that Plk1 and Numb co-immunoprecipitated and Plk1 was capable of phosphorylating Numb indicating a possible regulation of Numb by Plk1. Further, surprisingly, we found that lentiviral shRNA mediated knockdown of Numb resulted in a G2/M cell cycle arrest (using FACS analysis) and a significant reduction in cell growth (using Trypan blue exclusion) in both melanoma cell lines. Overall, our observations suggests that Numb is a regulator of proper cell cycle progression and may possess tumor suppressor functions. 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 1064.
Screening for CDKN2A Mutations in Hereditary Melanoma
Authors: A. M. Goldstein, M. A. Tucker
Journal: JNCI Journal of the National Cancer Institute (1997)

Cutaneous malignant melanoma (CMM) is a potentially fatal form of skin cancer whose etiology is heterogeneous and complex.Approximately 10% of the cases of CMM occur in persons with a familial predisposition (1), often in association with clinically dysplastic or atypical nevi (2).In 1993, a low-molecular-weight protein p16 INK4A was shown to inhibit the activity of the cyclin D1-cyclin-dependent kinase 4 or 6 (CDK4 or CDK6) complex (3).This complex phosphorylates the retinoblastoma protein, allowing the cell to pass through the G1 cell-cycle checkpoint.The CDKN2A gene that encodes p16 INK4A was localized to chromosome 9p21 (4,5), a region that has been implicated in melanoma by linkage, cytogenetic, and loss-of-heterozygosity studies (6)(7)(8)(9)(10)(11). Somatic mutations in this gene have frequently been detected in many melanoma cell lines (4,5).Although initial reports of germline mutations in melanomaprone families (selected for genetic analyses) suggested that the p16 INK4A protein might be important in approximately one half of inherited melanoma (12-14), subsequent studies have revealed lower frequencies of mutations.To date, germline CDKN2A mutations have been detected in approximately one fourth of melanoma-prone kindreds (defined as having two or more first-degree relatives with confirmed CMM) from North America, Europe, and Australia (12-21).In this issue of the Journal, Platz et al. ( 22) present the first report of screening for germline mutations in a population-based cohort of melanoma-prone families.The results provide further evidence that CDKN2A mutations may not be as prevalent as originally thought.Platz et al. ( 22) identified 177 melanoma-prone families, defined by the occurrence of two or more relatives (including first-, second-, and third-degree relatives) with histopathologically confirmed CMM, in the County of Stockholm, Sweden.A representative selection of 181 individuals with CMM, from 100 of these families, was screened for germline mutations in CDKN2A.Of the 100 families, 64 kindreds had at least two cases of melanoma in first-degree relatives; 24 kindreds had melanoma in two or more second-degree relatives; and 12 kindreds had melanomas in third-degree or more distant relatives.Both direct sequencing and single-strand conformation polymorphism (SSCP) analyses of exons 1 and 2 were conducted.Of the 64 families with two or more first-degree relatives with CMM, five (7.8%) had potentially disease-related mutations.Four of the five families with mutations had more than the
KRAS status and risk of venous thromboembolic events in patients with metastatic colorectal cancer: a case-control study
Authors: K. Rihawi, C. Fontanella, D. Rossini, M. Schirripa, E. De Carlo, L. Salvatore, E. Ongaro, M. Casagrande, L. Ferrari, N. Pella, G.G. Cardellino, M. Giovannoni, E. Iaiza, P. Ermacora, F. Puglisi, F. Loupakis, A. Falcone, F.E. Pisa, G. Aprile, G. Fasola
Journal: Annals of Oncology (2015)
AB0579 The relationship between visceral adiposity index and disability function in a cohort of psoriatic arthritis patients
Authors: G. Pistone, P. Vitale, M. Catanoso, P. Macchioni, S. Corrao, C. Salvarani
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> <b>Background:</b> : Psoriatic arthritis (PsA) is an inflammatory musculoskeletal disease associated with psoriasis. PsA patients have a higher prevalence of some comorbidities (obesity, metabolic syndrome, depression and premature cardiovascular disease). Recent data suggest a link between fat-mediated inflammation and joint involvement in PsA. Visceral adiposity index (VAI) has been used as a surrogate of visceral adiposity. <h3>Objectives</h3> <b>Objective:</b> To examine if VAI is correlated to disability and/or cutaneous involvement in PsA patients. <h3>Methods</h3> <b>Material and methods</b>: Prospective study on 88 (37 M/51 W) consecutive PsA fulfilled CASPAR criteria. All the patients were evaluated according to a predefined protocol that included:rheumatology and dermatology clinical evaluation and functional disability ( Health Assessment Questionnaire, HAQ, quality of life score- Short Form36, SF36), PASI and VAI based on Waist Circumference (WC), Body Mass Index (BMI), triglycerides (TG) and HDL cholesterol (HDL) levels. BMI was calculeted in 4 standard categories according to WHO criteria and WC was calculeted according to WHO (cut points 94 cm for men and 80 cm for women). <h3>Results</h3> <b>Results:</b> Our results demonstrated that WC was significantly associated with disability function (HAQ) even after adjustment for BMI; patients in the highest versus the lowest quartiles of WC had approximately 125% and 275% increases in the odds of HAQ among men and women, respectively (OR 2.33, 95% CI 1.08 to 4.66, OR 3.64, 95% CI 1.38 to 9.48). In contrast, there was no evidence of a significant association between HAQ and VAI index, with or without adjustment for WC. <h3>Conclusions</h3> <b>Conclusions:</b> WC was found, independent of VAI, to be a risk factor for disability function in PSA patients among both men and women. Future evaluations are needed since some authors supported that abdominal obesity may also determine an increased risk of not achieving minimal disease activity in PsA patients, highlighting the role of abdominal fat accumulation as a negative predictor of good clinical response to biologic agents <h3>References</h3> Amato MC, Giordano C, Galia M et al:. Diabetes Care 2010, 33:920-922 Cañete JD, Mease P. Ann Rheum Dis. 2012 Aug;71(8):1265-6. Taylor WJ. Curr Rheumatol Rep. 2012 Aug;14(4):369-74 Russolillo A, Iervolino S, Peluso et al. Rheumatology (Oxford). 2013 Jan;52(1):62-7 <h3>Disclosure of Interest</h3> None Declared
Abstract 188: EphrinA1 induces microRNA-302b expression in malignant mesothelioma cells and suppresses tumor growth via repression of Mcl-1 gene
Authors: Nazli Khodayari, Kamal A. Mohammed, Eugene P. Goldberg, Michael A. Jantz, Najmunnisa Nasreen
Journal: Cancer Research (2012)

Abstract Introduction: EphA2 is a receptor tyrosine kinase (RTK) and is over expressed in malignant mesothelioma (MM). In earlier studies we demonstrated that receptor EphA2 activation with ephrinA1 suppressed growth of MM. In addition there is evidence that ephrin ligand induces some MicroRNAs expression in cancer cells. MicroRNAs belonging to the miR-302 family are emerging as key players in the control of proliferation and cell fate determination during differentiation. However, the mechanisms whereby EphrinA1 activation attenuates the MM cell growth are not clear. Our study identified a novel mechanism of Ephrin-A1 tumor suppressor signaling in MM cells. Ephrin-A1 activation up regulates miR-302b expression in MM cells and attenuates tumor growth via repression of Mcl-1. Methods: MM cell lines (CRL-2081 and CRL-5830) were activated with recombinant-Ephrin-A1 for the indicated period of time. The expression of miR-302b was analyzed by quantitative real time RT-PCR, and the expression Mcl-1 was analyzed by RT-PCR, immuno-blotting and Immunofluorescence staining. To confirm that Ephrin-A1 regulates the expression of Mcl-1 mRNA through miR302-b up regulation, cultured cells were transfected with and without miR302-b and miR-302b inhibitor prior to activation. The cell proliferation and tumor growth was measured by WST-1 and 3 D matrigel assay in vitro assays respectively. Luciferase assay was performed to confirm the binding of miR-302b to the 3′UTR of Human Mcl-1. Results: Ephrin-A1 activation induced several fold increases of miR-302b expression in MM cells when compared to resting cells. In Ephrin-A1 activated MM cells, Mcl-1 expression was significantly down regulated when compared to resting cells. Moreover, Ephrin-A1 activation significantly inhibited MM cell proliferation and tumor growth. The present data suggests that Ephrin-A1 targets MM cells by inducing the expression of miR-302b and inhibits MM cell and tumor growth by targeting Mcl-1 protein. Conclusion: Our data suggest that over expression of Mcl-1 enhances tumor proliferation in MM cells. During Ephrin-A1 activation miR-302b expression is up regulated in MM cells. The up regulation of miR-302b leads to repression of Mcl-1 gene and attenuation of tumor growth. EphrinA1 could be a promising therapeutic agent for the treatment of MM. Funding Source: NIR and RC1 Department of Health Florida; VA Merit Review Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 188. doi:1538-7445.AM2012-188
254 SINGLE HEPATOCELLULAR CARCINOMA SMALLER THAN 2 cm: ARE PERCUTANEOUS ETHANOL INJECTION AND RADIOFREQUENCY ABLATION EQUALLY EFFECTIVE?
Authors: N. de Matthaeis, A. Saviano, I. De Sio, G. Francica, F. Brunello, A. Cantamessa, A. Giorgio, U. Scognamiglio, F. Fornari, F. Giangregorio, F. Piscaglia, S. Gualandi, E. Caturelli, P. Roselli, G.L. Rapaccini, M. Pompili
Journal: Journal of Hepatology (2013)