tbuckley/cabot-search huggingface dataset:
Endoscopic Diagnosis of Leukemia in a Child with Acute Abdominal Pain
Authors: L. de Ridder, D. Bosman, M. Benninga, F. ten Kate, V. de Haas, J. Taminiau
Journal: Endoscopy (2004)

Figure 1 A 10-year-old girl with an unremarkable medical history presented with acute abdominal pain. She had had symptoms of general malaise, intermittent fever, and pain in the right-sided maxilla joint and in the elbow joint for 1 month. There was no diarrhea or rectal blood loss. She had lost 4 kg in weight, and was a moderately ill child with pinpoint localized tenderness in the right lower quadrant of the abdomen. A full blood count showed normal leukocyte differentiation. Abdominal ultrasonography revealed some thickening of the ileal wall. Infectious, immunological, and gastrointestinal causes or malignancy were considered. Colonoscopy was carried out to rule out inflammatory bowel disease. A sessile, hyperplastic polypoid lesion in an otherwise unremarkable colon was found, situated opposite the ileocecal valve.
Amenorrhea, Abdominal Pain, and Weight Gain
Authors: Jeroen P H van Wijk, Edith W M T ter Braak
Journal: New England Journal of Medicine (2011)

A 21-year-old woman was referred for secondary amenorrhea, abdominal pain, and weight gain. Laboratory tests showed elevated serum estradiol (23,501 pmol per liter), suppressed luteinizing hormone (<0.1 IU per liter), and inappropriately high follicle-stimulating hormone (27 IU per liter). Pelvic ultrasonography showed bilateral enlarged polycystic ovaries (Panels A and B), which suggested a spontaneous ovarian hyperstimulation syndrome. Subsequent magnetic resonance imaging showed a pituitary macroadenoma with optic chiasm compression (Panel C, arrow). Transsphenoidal resection of the macroadenoma was performed. Immunohistochemical staining was positive for follicle-stimulating hormone, confirming the diagnosis of a follicle-stimulating hormone–secreting pituitary macroadenoma. After the surgery, the patient . . .
Breast Cancer Risk Estimation Using the OncoVue® Model Compared to Combined GWAS Single Nucleotide Polymorphisms.
Authors: E. Jupe, T. Pugh, N. Knowlton, D. Defreese
Journal: Cancer Research (2009)

Abstract Background: We have developed a new breast cancer risk assessment model (OncoVue) that integrates information from 22 single nucleotide polymorphisms (SNPs) and 5 personal risk factors. It has been shown to effectively stratify risk in three independent validation populations. Genome wide association studies (GWAS) have identified seven candidate SNPs independently associated with breast cancer risk. Using estimates of relative risks and allele frequencies derived from these studies, a theoretical examination of these SNPs has concluded that they have the potential to modestly improve clinical risk estimation. We have examined both the OncoVue model and these GWAS SNPs in the same case-control population to determine their utility in risk estimation.Materials and Methods: A randomly selected subset of participants (376 cases and 982 controls) that had enrolled in a larger case-control study conducted in six distinct geographic regions of the United States were examined. DNAs were genotyped for the 22 SNP variants in OncoVue and combined with personal factors to calculate the risk scores for the individual participants. DNAs were also genotyped for the following GWAS SNPs: rs2981582 (FGFR2), rs3817198 (LSP1), rs889312 (MAP3K), rs4415084 (MRPS30), rs13281615 (POU5F1P1), rs13387042 (TNP1), and rs3803662 (TOX3, formerly TNRCR9). Association of individual GWAS SNP genotypes with breast cancer risk was evaluated by calculating odds ratios (ORs). Assuming independent contribution of each SNP to risk, a combined GWAS risk score was calculated using a multiplicative model. Positive likelihood ratios (PLRs) were calculated using a risk threshold of 1.5-fold the control population mean risk to evaluate the proportion of individuals placed at elevated risk by OncoVue compared to the combined GWAS risk scores.Results: OncoVue exhibited significant ability to stratify risk at the 1.5-fold mean with a PLR of 2.2 and at a risk level of 2.5-fold mean the PLR increased to 5.0. In analyses of individual GWAS SNPs, statistically significant associations with breast cancer were identified for homozygous carriers of the rare allele for the FGFR2, MAP3K and TOX3 genes. However, the PLR for the combined GWAS risk scores at 1.5-fold mean was 1.0 indicating no ability to discriminate risk in this study population.Conclusions: In this case-control population OncoVue effectively stratified risk by accurately assigning elevated risk to breast cancer cases. In the same population, a combined risk score produced from seven GWAS SNPs did not effectively stratify risk. These results indicate that the OncoVue model has clinical utility for identifying elevated risk women who might benefit from additional screening and prevention. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 3177.
Ectopic Parathyroid Imaging With Tc-99m Sestamibi
Authors: P Pusuwan, V Ratanamart, P Suwanagool, R Pleehachinda
Journal: Clinical Nuclear Medicine (1996)

A patient with persistent hypercalcemia after failed parathyroidectomy was referred for localization of an abnormal parathyroid gland. Tc-99m sestamibi imaging revealed a focal area of increased uptake involving the left anterior mediastinum, suggesting an ectopic parathyroid gland. The pathologic finding showed an ectopic parathyroid adenoma.
Experimental Cryptococcosis Produced by the Ingestion of Virulent Organisms
Authors: Michael J. Takos
Journal: New England Journal of Medicine (1956)

THE lungs are usually considered to be the primary portal of entry for the pathogenic yeastlike fungus, Cryptococcus neoformans. The appearance of the lungs at autopsy of human beings dying of cryptococcosis has suggested that these organs were the first to become infected. The clinical histories of many patients have offered further evidence, since symptoms of pulmonary disease have often long antedated the terminal signs of Central-nervous-system involvement.1 , 2 However, in some cases, lesions of the lung due to infection by these pathogenic organisms cannot be demonstrated at autopsy, despite extensive tissue involvement elsewhere. Symptoms of meningoencephalitis have frequently been . . .
P423No evidence for activated autophagy in left ventricular myocardium with protection by remote ischemic preconditioning in patients undergoing coronary artery bypass grafting
Authors: N Gedik, M Thielmann, E Kottenberg, J Peters, H Jakob, G Heusch, P Kleinbongard
Journal: Cardiovascular Research (2014)

Objective: Remote ischemic preconditioning (RIPC) by repeated brief limb ischemia/reperfusion reduces myocardial injury in patients undergoing coronary artery bypass grafting (CABG). Activation of signal transducer and activator of transcription 5 (STAT5) in left ventricular (LV) myocardium at early reperfusion is associated with such protection. Autophagy, i.e., removal of dysfunctional cellular components through lysosomes, has been proposed as one mechanism of cardioprotection. Therefore, we analyzed whether or not the protection by RIPC is associated with activated autophagy. Methods: CABG patients were randomized to undergo RIPC (3x5 min blood pressure cuff inflation/5 min deflation) or placebo (cuff deflated) before skin incision (n=10/10). Transmural myocardial biopsies were taken from the LV before cardioplegia (baseline) and at early (5-10 min) reperfusion. RIPC-induced protection was reflected by decreased serum troponin I concentration area under the curve (194±17 versus 709±129 ng/ml x 72 h, p=0.002). Western blotting for beclin-1-phosphorylation and protein expression of autophagy-related gene 5-12 (ATG5-12) complex, light chain 3 (LC3), parkin, and p62 was performed. STAT3- STAT5- and extracellular signal-regulated protein kinase 1/2 (ERK1/2)-phosphorylation was used as positive control to confirm signal activation by ischemia/reperfusion. Results: Signals of all analyzed autophagy proteins did not differ between baseline and early reperfusion and not between RIPC and placebo. STAT5-phosphorylation was greater at early reperfusion only with RIPC (2.2-fold, p=0.02). STAT3- and ERK1/2-phosphorylation were greater at early reperfusion with placebo and RIPC (≥2.7-fold versus baseline, p≤0.05). Conclusion: Protection through RIPC in patients undergoing CABG surgery does not appear to be associated with enhanced autophagy.
SAT0428 Prevalence and severity of insomnia in chronic low back pain patients
Authors: H. Bahouq, H. Rkain, F. Allali, N. Hajjaj Hassouni
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Sleep disturbance is becoming increasingly recognised as a clinically important symptom in people with chronic low back pain (CLBP). However, prevalence and severity of insomnia for patients with CLBP are lacking. Also, it is not known whether high pain intensity, the most relevant condition-specific variable, is associated with higher rates of reported insomnia. <h3>Objectives</h3> The purpose of this study was to assess prevalence and severity of insomnia in participants diagnosed with CLBP and to identify eventual factors associated with this insomnia. <h3>Methods</h3> In this cross sectional study, One hundred patients suffering from CLBP were consecutively included (50 females and 50 males, mean age: 43.28±7.5 years). CLBP, sleep characteristics, types and consequences of insomnia were collected. Insomnia severity was assessed using index of severity of insomnia (ISI) with a global score going from 0 (the best situation) to 28 (the worst situation). Eventual relationship between insomnia and CLBP characteristics was analyzed. <h3>Results</h3> Insomnia was reported by 78% of patients and was caused by pain in 83% of them. Insomnia was early, middle and late in respectively 85, 78 and 46% of insomniac patients. The mean of ISI score was 18.07±7.3. Consequences of this insomnia were dominated by daily activities disturbance (71%), tiredness (63%) and mood disorders (47%). Significant correlations were found between ISI and pain (r=0.587; p&lt;0.0001), fatigue (r=0.495; p&lt;0.0001) and body mass index (r=-0.209; p=0.03). Multiple logistic regression models have shown that only pain (OR=1.293; IC 95% (1.032- 1.618); p=0.02) and fatigue (OR=1.084; IC 95% (1.032- 1.138); p=0.001) were the significant independent factors related to insomnia severity. <h3>Conclusions</h3> Insomnia prevalence seems to be important in patients suffering from CLBP. Consequences of this insomnia are dominated by daily activities disturbance, mood disorders and tiredness. The severity of insomnia appears to be related to pain and fatigue. Assessment of insomnia should be integrated to CLBP management and those results should be confirmed by larger studies. <h3>Disclosure of Interest</h3> None Declared
Abstract P3-09-01: Odds of the triple negative subtype and survival of stages 1–3 breast cancer: Variation by race/ethnicity
Authors: C Parise, V Caggiano
Journal: Cancer Research (2012)

Abstract Background: Triple negative (TN) breast cancer is known to be more common in black and Hispanic women and associated with poor survival. This study assesses the differences in the odds and survival of the TN versus the ER+/PR+/HER2− (the most common subtype) by race/ethnicity separately for AJCC stages 1, 2, and 3. Methods: Using the California Cancer Registry for years 2000–2010, we examined 91,393 cases of stages 1–3 TN and ER+/PR+/HER2− first primary female invasive breast cancer. Race/ethnicity was defined as white, black, Hispanic, and Asian/Pacific Islander (API). Logistic regression was used to assess the association of race with odds of the TN subtype. Kaplan-Meier was used to compute 6-year survival. Cox proportional hazards was used to assess the risk of mortality of the TN subtype by race adjusting for age, grade, year of diagnosis, and socioeconomic status. All analyses were run separately for stages 1, 2, and 3. Results: The table shows the distribution of the TN and ER+/PR+/HER2-subtypes by stage and race/ethnicity. Blacks had increased odds of the TN compared with whites for stages 1 (OR = 2.24; 95%CI=1.96–2.56); 2 (OR = 2.01; 95%CI=1.81–2.25) and 3 (OR = 2.00; 95%CI=1.66–2.40). Hispanics had increased odds for the TN in stages 1 (OR = 1.23; 95%CI=1.11–1.35) and 2(OR = 1.20; 95%CI=1.11–1.31). APIs had decreased odds of the TN in stages 2 (OR = 0.85; 95%CI=0.77–0.93) and 3 (OR = 0.77; 95%CI=0.64–0.92). KM survival showed that APIs had the best 72 month survival for the TN in stages 1 (86%), 2 (78%), and 3(59%). Hazard ratios (HRs) indicated that all races with TN had the same risk of mortality in stage 1. Only in stage 2 did blacks have an increased risk of mortality (HR = 1.17; 95%CI=1.02–1.36) while APIs had a decreased risk (HR = 0.78; 95%CI=0.65–0.94). In stage 3, Hispanics (HR = 0.85; 95%CI=0.72–0.99) and APIs (HR = 0.70; 95%CI=0.55–0.89) had decreased risk of mortality compared with whites. Conclusions: Race/ethnicity is an important factor for survival of the TN subtype: 1. Although blacks and Hispanics are more likely to have the TN subtype, blacks have an increased risk of mortality compared with whites only in stage 2.2. For stage 1, all races have the same risk of mortality.3. Hispanics have decreased risk of mortality in stage 3.4. APIs have decreased risk of mortality in both stages 2 and 3. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P3-09-01.
Psychiatry in a General Hospital of a Small City
Authors: Samuel M. Tarnower
Journal: New England Journal of Medicine (1948)

PSYCHIATRY is slowly becoming part of general-hospital organization. This branch of medicine was preceded by neurology, which is concerned with more obvious physical disease and usually does not involve overt abnormalities of behavior. The patient with a psychiatric diagnosis is not welcome in a general hospital. His diagnosis meets the resistance of outmoded attitudes. His illness is still not devoid of some social stigma. Hospital personnel are too apt to associate memories of excitements and unco-operative behavior with psychiatric disorders. To circumvent such conditions, psychiatric patients are admitted daily to general hospitals with nonpsychiatric diagnoses. Bennett1 reports that in 1940 . . .
68Ga DOTATATE PET/CT in a Rare Coexistence of Pituitary Macroadenoma and Multiple Paragangliomas
Authors: Rahul Vithalrao Parghane, Kanhaiyalal Agrawal, Bhagwant Rai Mittal, Jaya Shukla, Anish Bhattacharya, Kanchan Kumar Mukherjee
Journal: Clinical Nuclear Medicine (2013)

The coexistence of a pituitary neoplasm and pheochromocytoma is a rare condition, which may be another undefined variant of Multiple endocrine neoplasia (MEN) syndrome. Moreover, the coexistence of pituitary macroadenoma and multiple paragangliomas is more uncommon and only few authors have reported these findings. We are reporting the use of Ga DOTATATE PET/CT in a rare case of coexisting pituitary macroadenoma and multiple paragangliomas.
EVALUATION OF LEFT ATRIAL MORPHOLOGY BY A NOVEL VOLUME RENDERED IMAGING BASED ON THREE-DIMENSIONAL TRANSESOPHAGEAL ECHOCARDIOGRAPHY
Authors: Qing Zhou, Hong-Ning Song, Qing Deng, Jin-Ling Chen, Bo Hu, Yi-Jia Wang, Rui-Qiang Guo
Journal: Journal of the American College of Cardiology (2016)
Abstract 1077: Dominant negative PI3-Kinase inhibits UV-induced squamous cell carcinoma in vivo.
Authors: Sally E. Dickinson, Erik R. Olson, Jadrian J. Rusche, P. Jane Criswell, Jack Zhang, Zagong Dong, Chengcheng Hu, Kathylynn Saboda, David S. Alberts, G. Timothy Bowden
Journal: Cancer Research (2013)

Abstract Phosphoinositide-3 Kinase (PI3-Kinase) is an upstream regulator of cellular proliferation and anti-apoptotic signaling that has been implicated in cancer induction in many tissues, including skin. Pharmacological inhibition of PI3-Kinase is effective at inhibiting both chemical and UV-driven skin carcinogenesis. However, the specificity of these pharmacological inhibitors is often questioned. Therefore, specific genetic inhibition of PI3-Kinase in the epidermis needs to be carried out in mice. We report here on the generation of a new transgenic mouse which constitutively expresses the dominant negative mutant form of the regulatory subunit of the PI3-Kinase dimer, p85, in the epidermis under control of the keratin-5 promoter. These p85DN transgenic mice were derived on the SKH-1 hairless genetic background. A chronic UVB exposure experiment showed significant inhibition of both tumor size (p=0.0012) and tumor burden (p=0.0003) for mice carrying the transgene compared to wildtype littermates. The time to first tumor was also delayed in transgenic mice, but with only marginal significance (p=0.07). p85DN mice also showed significant inhibition of epidermal Activator Protein-1 (AP-1) transcription factor activity after acute UVB treatment (p=0.046). UVB induced activation of AP-1 in the epidermis has been shown to play a functional role in UVB mouse skin carcinogenesis. Further analysis of protein expression after acute treatment with UVB suggests that Akt signaling and COX-2 activation are both downregulated in p85DN transgenic mice. To our knowledge, this is the first report of genetic inhibition of PI3-Kinase in mouse skin carcinogenesis studies. Together, these data suggest a functional role of PI3-Kinase in UVB-induced squamous cell carcinoma and support the assertion that inhibition of this pathway is beneficial in chemoprevention of non-melanoma skin cancer. This work was supported in part by the following NIH grants: K07CA132956, K07CA132956-02S1, P01CA27502 and P30CA23074. Citation Format: Sally E. Dickinson, Erik R. Olson, Jadrian J. Rusche, P. Jane Criswell, Jack Zhang, Zagong Dong, Chengcheng Hu, Kathylynn Saboda, David S. Alberts, G. Timothy Bowden. Dominant negative PI3-Kinase inhibits UV-induced squamous cell carcinoma in vivo. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1077. doi:10.1158/1538-7445.AM2013-1077
ASSOCIATIONS OF KNOWN COMPLICATIONS WITH TRANSCATHETER IMPLANTATION OF FIRST-GENERATION BALLOON EXPANDABLE EDWARDS-SAPIEN AORTIC VALVES WITH PERI-PROCEDURAL MORTALITY: AN INSIGHT FROM 2011-2014 REPORTS FROM THE FDA MAUDE DATABASE
Authors: Pragya Ranjan, Saurav Chatterjee, Deepansh Gupta, Partha Sardar, Jay Giri, Jasjit Bhinder, Debrata Mukherjee, Dharam Kumbhani
Journal: Journal of the American College of Cardiology (2015)
Abstract 698: β-arrestin-1 as nuclear signalling element essential for endothelin A receptor-induced epithelial to mesenchymal transition and chemoresistance
Authors: Laura Rosanò, Roberta Cianfrocca, Valeriana Di Castro, Francesca Spinella, Maria Rita Nicotra, Pier Giorgio Natali, Anna Bagnato
Journal: Cancer Research (2011)

Abstract The onset of chemoresistance is the major challenge in epithelial ovarian cancer (EOC). Emerging evidence suggests molecular and phenotypic association between chemoresistance and epithelial-mesenchymal transition (EMT) in cancer. We recently demonstrated that β-arrestin-1, scaffold and signaling protein of G-protein-coupled receptors, is recruited to endothelin A receptor (ETAR) to form molecular signaling complexes which concur to activate β-catenin transcriptional activity, EMT and metastasis. Here, by using biochemical and imaging techniques, we provide evidence that in EOC cells, ETAR activation by endothelin-1 (ET-1) induces nuclear translocation of β-arrestin-1 and its association with β-catenin. ChIP assays demonstrated that following this translocation, β-arrestin-1 was selectively enriched at specific promoters of β-catenin target genes, such as ET-1, MMP-2, cyclin D1. Further experiments showed that ET-1 promotes the nuclear association between histone acetyltransferase p300 and β-arrestin and the recruitment of p300 on these promoters, resulting in H3 and H4 histone acetylation and enhanced gene transcription. In chemoresistant EOC cells, ET-1/ETAR axis is overexpressed associated with EMT marker expression. Most importantly, the transcriptional activity of β-catenin was upregulated in chemoresistant EOC cells, associated with enhanced ETAR and β-arrestin-1 expression, providing molecular evidence that the ETAR/β-arrestin-1-mediated EMT signaling in EOC can represent a “salvage pathway” occurring during chemoresistance development. Interestingly, ETAR blockade with zibotentan, a specific ETAR antagonist, or its silencing with siRNA, abrogates both the engagement of β-arrestin-1 in the nucleus and the interplay between ET-1 and the β-catenin in controlling gene transcription. In vivo, zibotentan inhibited tumor growth of sensitive and resistant EOC xenografts, associated with reduction of EMT markers, and sensitized to chemotherapy. Analysis of EOC human tissues revealed that ETAR is overexpressed in resistant tumors and is associated with EMT phenotype. Our data provide the first evidence that blockade of ETAR/β-arrestin-1-driven EMT can overcome chemoresistance and inhibit tumor progression, improving the outcome of EOC patients’ treatment. Supported by AIRC 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 698. doi:10.1158/1538-7445.AM2011-698
Abstract 5614: Tandutinib (MLN518/CT53518) targeted to stem-like cells by inhibiting the function of ATP-binding cassette subfamily G member 2
Authors: Wen Deng, Chun-Ling Dai, Xiao-qin Zhao, Shinobu Ohnuma, Yong-ju Liang, Zhi-Jie Xiao, Mu-Sheng Zeng, Suresh V. Ambudkar, Li-wu Fu, Zhe-Sheng Chen
Journal: Cancer Research (2012)

Abstract Tandutinib (MLN518/CT53518) is a novel quinazoline-based inhibitor of FMS-like tyrosine kinase 3, platelet-derived growth factor receptor, and KIT. In this study, we evaluated the possible interactions of tandutinib with P-glycoprotein (P-gp/ABCB1), multidrug resistance protein 1 (MRP1/ABCC1), breast cancer resistance protein (BCRP/ABCG2) and MRP4/ABCC4. Our results showed that tandutinib reverses ABCG2-mediated drug resistance in ABCG2-transfected cell lines ABCG2-482-R2, ABCG2-482-G2 and ABCG2-482-T7 and mitoxantrone-induced ABCG2-overexpressing cell line S1-M1-80. On the other hand, tandutinib did not change the sensitivity of all tested ABCG2-overexpressing cell lines and their sensitive parental cell lines to cisplatin (non-substrate of ABCG2) and had no significant reversal effect on ABCB1-, ABCC1- and ABCC4-mediated drug resistance. Tandutinib increased doxorubicin and rhodamine 123 accumulation in S1-M1-80 cells in a dose-dependent manner, but did not change their accumulation in parental S1 cells. Similarly, tandutinib also enhanced [3H]mitoxantone accumulation in ABCG2-transfected cell lines, significantly inhibited mitoxantrone efflux in ABCG2-482-R2 cells, but not in HEK293/pcDNA 3.1 cells. However, tandutinib did not stimulate the ATPase activity of ABCG2 and significantly inhibit the photolabeling of ABCG2 with [125I]Iodoarylazidoprazosin. Tandutinib also did not affect the expression of ABCG2 at mRNA or protein levels. In addition, tandutinib did not block the phosphorylation of Akt and Erk1/2 in S1-M1-80 or S1 cells. Importantly, tandutinib targeted to A549 side population cells and enhanced their sensitivity to mitoxantrone, which was not altered in non-SP cells. Collectively, our results advocate the use of tandutinib as an ABCG2 modulator and stem cell targeted agent to increase efficiency of anticancer drugs in clinic therapy. 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 5614. doi:1538-7445.AM2012-5614