tbuckley/cabot-search huggingface dataset:
<i>Staphylococcus aureus</i>Infections
Authors: F D Lowy
Journal: New England Journal of Medicine (1998)

Micrococcus, which, when limited in its extent and activity, causes acute suppurative inflammation (phlegmon), produces, when more extensive and intense in its action on the human system, the most virulent forms of septicæmia and pyæmia.1 In an elegant series of clinical observations and laboratory studies published in 1880 and 1882, Ogston described staphylococcal disease and its role in sepsis and abscess formation.1,2 More than 100 years later, Staphylococcus aureus remains a versatile and dangerous pathogen in humans. The frequencies of both community-acquired and hospital-acquired staphylococcal infections have increased steadily, with little change in overall mortality. Treatment of these infections . . .
A CASE OF ACUTE CORONARY SYNDROME IN A 62 YEAR OLD FEMALE WITH A LOW PRETEST PROBABILITY OF CORONARY ARTERY DISEASE
Authors: Abdallah El Sabbagh, Abdallah El Sabbagh, Mackram Eleid, Mohammed Al-Hijji, Rajiv Gulati, Mandeep Singh
Journal: Journal of the American College of Cardiology (2015)
Abstract 1825: Maternal alcohol consumption and childhood acute myeloid leukemia risk
Authors: Minkyo Song, Kyoung-Mu Lee, Sohee Han, Sue K. Park, Hyo Seop Ahn, Hee Young Shin, Hyoung Jin Kang, Hong Hoe Koo, Jong Jin Seo, Ji Eun Choi, Yoon-Ok Ahn, Daehee Kang
Journal: Cancer Research (2010)

Abstract Background: Leukemia is the most common malignancy in children. The etiology of childhood leukemia is mostly unknown, although some environmental factors such as ionizing radiation and parental alcohol and tobacco use may play a causative role in leukemia. Methods: To investigate the association between parental alcohol consumption and childhood leukemia in a hospital-based case-control study in Korea, histologically-confirmed incident childhood leukemia cases (n=365) aged 0-18 years old were recruited from three teaching hospitals located in Seoul, Korea, between May 2003 and August 2008. Non-cancer controls (n=558) aged 0-18 years old without medical history of childhood cancer were recruited from the Department of Pediatrics of the same hospitals. Controls were frequency-matched to cases by 5-year age intervals and sex (cases: controls=1:1). Leukemia risks were estimated as odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression analysis adjusted for age, sex, parent's education, and birth weight (&amp;lt;3.25, 3.25-3.70, ≥3.70 kg). In addition to conducting analyses of all childhood leukemia, we calculated histologic subtype-specific ORs for acute lymphoblastic leukemia (ALL; n=200) and acute myeloid leukemia (AML; n=88). Results: Among general characteristics, higher birth weight and parental education were associated with childhood leukemia risk (P&amp;lt;0.05). The proportion of drinking mothers was significantly higher among all leukemia cases than controls (58% vs. 49%: OR=1.4, 95% CI=1.00-1.83), whereas no association was observed for paternal alcohol consumption (87% vs. 83%). When the analysis was restricted to AML cases, the association between maternal drinking and cancer risk became stronger (OR=1.8, 95% CI=1.06-2.90). Drinking frequency of the mothers was also associated with the increased risk. (≥1/month vs. &amp;lt;1/month; OR=1.7, 95% CI=1.10-2.28). Also, drinking duration of more than one year before pregnancy increased the risk of AML (OR=1.7, 95% CI= 1.00-2.85). No association was found between parental alcohol consumption and ALL risk. Conclusion: Our results suggest that maternal alcohol consumption is associated with AML among Korean children. However, larger studies need to be conducted to replicate our findings. 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 1825.
AIDS-Related Cancers Emerging as a Second Epidemic
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article AIDS-Related Cancers Emerging as a Second Epidemic Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 17, 1 September 1993, Pages 1369–1370, https://doi.org/10.1093/jnci/85.17.1369 Published: 01 September 1993
PWE-275 Multiple organ dysfunction syndrome (MODS), rather than the need for renal replacement therapy per se, dictates poor prognosis in patients with cirrhosis admitted to ICU
Authors: R D Abeles, D L Shawcross, M J McPhail, A Yeoman, N Taylor, A Portal, M J Austin, G Auzinger, C Willars, W Bernal, J A Wendon
Journal: Gut (2012)

<h3>Introduction</h3> Critically ill cirrhotics admitted to ICU who receive renal replacement therapy (RRT) have a poor prognosis. It is unclear whether prognosis relates to renal dysfunction per se or whether RRT is one facet of MODS. We report the 7-year experience of outcomes and physiological disturbances in cirrhotics admitted to ICU who received RRT. <h3>Methods</h3> We analysed physiological and biochemical variables on admission for 478 cirrhotic patients admitted to ICU, excluding those transplanted during that hospital admission. Patients were cohorted on RRT requirement (RRT<sup>+</sup>/RRT<sup>−</sup>) at any point during ICU admission. Outcome, organ failure scores and utilisation of organ support were recorded. <h3>Results</h3> Of 253 RRT+ patients, 22% survived ICU and 13% survived hospital. Of 225 RRT<sup>−</sup>, 81% survived ICU and 59% survived hospital (p. On day 1 of admission, RRT+ had a higher prevalence of systemic inflammatory response syndrome (76% vs 62%), Child-Pugh (12 vs 11), MELD (32 vs 17) and SOFA scores (13 vs 11) (pEven when the renal component was removed from the SOFA score (SOFAminusRENAL), RRT+ had higher scores than RRT- (9 vs 7) (p. 23% of RRT+ commenced RRT after day 3 of admission; this did not affect ICU or hospital survival compared to those that commenced RRT before day 3. RRT+ survivors required less ventilation (39% vs 93%) and vasopressors (52% vs 89%) than RRT+ non-survivors and had lower Child-Pugh (12 vs 13), SOFA (12 vs 14) and SOFAminusRENAL (8 vs 10) scores (p=1 of admission. 23 patients required RRT but no other organ support, 18/23 (78%) survived to ICU discharge and 11/23 (48%) to hospital discharge. <h3>Conclusion</h3> The extent of MODS, rather than requirement of RRT per se, dictates poor prognosis in cirrhotics needing RRT in ICU. Requirement for RRT should not preclude admission to ICU, rather, prognostication should take into account other elements of MODS; in particular a concomitant requirement for circulatory and respiratory support. <h3>Competing interests</h3> None declared.
Abstract 1736: Mitochondrial priming of apoptotic machinery in pancreatic cancer by BPM 31510 to enhance efficacy of chemotherapy.
Authors: Niven R. Narain, Tony E. Walshe, Arleide Lee, Rakib Ouro-Djoba, Lucia Mauro, Adel Yunis, Vivek K. Vishnudas, Rangaprasad Sarangarjan, Joaquin J. Jimenez
Journal: Cancer Research (2013)

Abstract Recent evidence suggests that the cytotoxic effects of chemotherapy, specifically in cancer cells is a consequence of “pre-treatment priming” event wherein exposure to the chemotherapeutic agents pushes the cancer cells beyond an apoptotic threshold to effectuate cell death. (Letai, A et. al, Science. 2011 Nov 25;334 (6059) BPM 31510 is a ubidecarenone containing proprietary formulation that effectuates a metabolic switch from glycolysis towards enhanced mitochondrial oxidative phosphorylation resulting in the recapitulation of apoptosis in cancer. The current study was aimed at investigating whether pretreatment with BPM 31510 results in mitochondrial priming, thereby augmenting the cytotoxic effect of standard of care chemotherapeutic agents. The human derived pancreatic cancer cell line Mia-Paca-2 was subjected to either (a) pretreatment with BPM 31510 followed by co-treatment with gemcitabine or (b) co-treatment with BPM 31510 and gemcitabine. BPM 31510 exposure resulted in decreased cell proliferation rates that were significantly higher than gemcitabine alone in Mia-Paca-2 cell line. Pre-treatment with BPM 31510 augmented the cytotoxic potential of gemcitabine, a phenomenon that was also observed in the co-treatment regimen. In vivo pancreatic cancer model using Mia-Paca-2 cell lines were developed to further investigate the priming effect of BPM 31510. Results demonstrate that 1-week and 2-week pretreatment with intravenous BPM 31510 followed by gemcitabine results in improved survival in the pancreatic cancer model compared to the co-treatment regimen. The data demonstrates that addition of BPM 31510 synergizes the cytotoxic effect of gemcitabine in pancreatic cancer. In addition, pretreatment with BPM 31510 followed by gemcitabine treatment is associated with improved survival. Taken together, the data suggest that BPM 31510 may be a viable mitochondrial priming agent to sensitize cancer cells to the cytotoxic effects of gemcitabine in pancreatic cancer. Citation Format: Niven R. Narain, Tony E. Walshe, Arleide Lee, Rakib Ouro-Djoba, Lucia Mauro, Adel Yunis, Vivek K. Vishnudas, Rangaprasad Sarangarjan, Joaquin J. Jimenez. Mitochondrial priming of apoptotic machinery in pancreatic cancer by BPM 31510 to enhance efficacy of chemotherapy. [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 1736. doi:10.1158/1538-7445.AM2013-1736
Abstract 2202: Classification of DPYD variations using an isogenic system of expression.
Authors: Steven M. Offer, Natalie J. Wegner, Croix Fossum, Robert D. Diasio
Journal: Cancer Research (2013)

Abstract The pyrimidine analog 5-fluorouracil (5-FU) was developed in the 1950s and remains one of the most widely used chemotherapy drugs in use today. A significant portion of patients who receive 5-FU suffer severe adverse toxicities, and, in extreme cases, death. Dihydropyrimidine dehydrogenase (DPD, encoded by the DPYD gene) rapidly degrades 85% of administered 5-FU, and as such, limits the amount of drug available for conversion into active metabolites. Genetic variations in DPYD have been suggested to increase the risk of 5-FU toxicity. Large-scale sequencing efforts have identified nearly 100 missense and nonsense DPYD variations, however only a handful of alleles have been studied for their association with 5-FU toxicity. Most studies have focused on a single allele (DPYD*2A), which only accounts for a small fraction of DPD deficiencies. Further complicating the interpretation of DPYD alleles, many individuals carry multiple variations within the DPYD gene. The purpose of this study was to identify missense variants that affect the enzyme function of DPD using a mammalian isogenic system of expression. Expression vectors encoding missense DPYD variations were generated by site directed mutagenesis and the expressed protein assayed for enzyme activity. Cells expressing selected variants were also teasted for sensitivity to 5-FU using a novel implementation of electrical impedance based realtime cellular analysis. The results of functional studies are compared to in silico predictions used to classify variants as deleterious or benign. An appreciable fraction of DPD variants showed enzyme activity that was significantly lower than that of wildtype protein. Within the deficient group of variants, a gradient of activities was noted, prompting the grouping of variants as mildly, moderately, and severely impaired. In addition to loss-of-function variations, a few hyperactive DPYD alleles were identified. This novel class of DPYD variants may be protective against 5-FU toxicity at the cost of treatment efficacy. The further evaluation of hyperactive alleles in clinical studies will be necessary to determine their impact on patient outcomes. Overall these data will facilitate the development of predictive tests for 5-FU toxicity by allowing researchers to prioritize variations for association studies. Citation Format: Steven M. Offer, Natalie J. Wegner, Croix Fossum, Robert D. Diasio. Classification of DPYD variations using an isogenic system of expression. [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 2202. doi:10.1158/1538-7445.AM2013-2202
Abstract SY02-02: Interaction of MMPs with oncogenic signaling: Disruption of dynamic reciprocity and tissue polarity
Authors: Alain Beliveau, Joni Mott, Alvin Lo, Emily Chen, John Muschler, Virginia Spencer, Mina J. Bissell
Journal: Cancer Research (2011)

Abstract Whether or not epithelial cells organize into three-dimensional structures defines their normal or invasive and malignant status. In a model of human breast morphogenesis, we have shown that inhibiting key signaling pathways in breast cancer cells leads to phenotypic reversion of the malignant cells. Using intact architecture or invasive behavior as an endpoint, we report that in all cases, signaling through Raf/MEK/ERK disrupts tissue polarity via MMP9 activity. Induction of Raf or activation of an engineered functionally inducible MMP9 in nonmalignant cells leads to loss of tissue polarity and reinitiates proliferation. Conversely, inhibition of Raf or MMP9 with small molecule inhibitors or shRNAs restores the ability of cancer cells to form polarized quiescent structures. Silencing MMP9 expression reduces tumor growth dramatically in a murine xenograft model. LC-MS/MS analysis comparing secreted proteins from nonmalignant cells – with or without active MMP9 – reveals laminin 111 (LN1) as a prominent target of MMP9. LN1 is shown to be necessary for acinar morphogenesis; thus its degradation by MMP9 provides the molecular mechanism by which tissue polarity is lost and growth and invasion reinitiated. These findings underscore the essential dynamic reciprocity between ECM integrity, tissue polarity, and suppression of Raf/MEK/ERK and MMP9 activities: the correct balance is essential to homeostasis, whereas imbalance leads to malignant progression. 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 SY02-02. doi:10.1158/1538-7445.AM2011-SY02-02
Abstract 1491: CEA interacts with TGF-β receptor and inhibits TGF-β signaling in colorectal cancers
Authors: Hong Cao, Ying Li, Wenguo Yao, Wilma Jogunoori, Arun Thenappan, Lopa Mishra
Journal: Cancer Research (2010)

Abstract Carcinoembryonic antigen (CEA) is a tumor marker for the clinical management of colorectal cancer (CRC). The elevated blood levels of CEA are associated with metastasis and poor prognosis in CRC. There is mounting evidence that CEA enhances the metastatic potential of cancer cells. CEA increases the ability of weakly metastatic CRC to colonize the liver and to develop spontaneous hematogeneous liver and lung metastases. CEA expression has also been related with resistance to cytotoxic chemotherapy and to anoikis, a form of apoptosis caused by detachment from cell matrix. Yet the mechanism of CEA mediated metastasis is only partially understood. The TGF-β (transforming growth factor beta) signaling pathway contributes to tumorigenesis by controlling several biological processes, including cell proliferation, differentiation, migration and apoptosis. It has been reported that TGF-β regulates CEA transcription and secretion, however, little is known about the effects of CEA on TGF-β signaling. Aims: Based on the above facts, we focused on the influence of CEA on the TGF-β signaling in both normal cells and colorectal cancer cells. Results: Our preliminary data showed that CEA directly interacted with TGF-β receptors. Overexpression of CEA blocked TGF-β induced SMAD3 phosphorylation, SMAD3 translocation to nuclear and the downregulation of c-myc transcription. Targeting CEA with anti-CEA antibody rescued TGF-β response in CRC cell lines with elevated CEA expression, thereby restoring the inhibitory effects of TGF-β on the proliferation of these cancer cells. Finally, in animal experiment, we found that CEA enhanced survival of colorectal cancer cell in both local colonization and liver metastasis. Conclusion: Since CEA is a well-characterized tumor-associated antigen that is frequently overexpressed in tumors, specific antibodies targeting CEA have been developed as a novel therapeutic approach for treatment of tumors expressing CEA on their surface. Based on our study, it may be helpful to combine CEA antibody and TGF-β to inhibit cancer cell proliferation and metastasis in some cases. 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 1491.
OP0031 Tocilizumab is Associated with Higher CDai/Sdai Remission in Biologic-Naïve Rheumatoid Arthritis Patients – Data from Reuma.Pt: Table 1.
Authors: V. Romao, M. Santos, J. Polido-Pereira, C. Duarte, P. Nero, C. Miguel, J. Costa, F. Pimentel-Santos, F. Barcelos, L. Costa, J. Melo Gomes, J. Pereira da Silva, J. Branco, J. Canas da Silva, J. Da Silva, J. Fonseca, H. Canhao
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Tocilizumab (TCZ), an interleukin-6 receptor blocker, and anti-tumor necrosis factor (TNF) biologic agents are key therapies in the management of rheumatoid arthritis (RA). They are considered to be equally effective and very few head-to-head comparisons have been published. <h3>Objectives</h3> To compare remission rates in RA patients treated with anti-TNF agents and TCZ and assess the impact of previous biologic therapies in treatment response. <h3>Methods</h3> We included RA patients registered in the Rheumatic Diseases Portuguese Register, Reuma.pt, who started anti-TNF or TCZ after January 1, 2008, were treated for at least 6 months and had available DAS28 scores at baseline and at 6 months. Our primary outcome was the proportion of patients who achieved remission at 6 months by DAS28, CDAI, SDAI and Boolean remission criteria. Logistic regressions were performed to compare the groups and subgroup analyses of biologic-naïve patients were conducted. <h3>Results</h3> 524 RA patients were enrolled, (106 adalimumab, 202 etanercept, 43 golimumab, 78 infliximab, 95 TCZ). At baseline, the groups were similar except for proportion of biologic-naïve patients (lower in TCZ group, p&lt;0.0001) and mean DAS28, CDAI and swollen joint count, all higher in the TCZ group (respectively: p=0.0005, p=0.037 and p&lt;0.0001). At 6 months, more TCZ-treated patients were in DAS28 remission, with no differences for CDAI, SDAI or Boolean remission. Considering only naïve patients, DAS28, CDAI and SDAI remission were significantly higher in the TCZ group compared to anti-TNF, with similar rates of Boolean remission. This was confirmed in the multivariate logistic regression, adjusting for age, gender, number of previous biologics and baseline disease activity: DAS28 OR 10.8 (5.9-19.7), CDAI OR 2.9 (1.3-6.5), SDAI OR 4.1 (1.8-9.5), Boolean OR 1.9 (0.88-4.3). <h3>Conclusions</h3> TCZ treatment was associated with higher rate of DAS28 remission at 6 months and previous biologic therapy significantly affected CDAI/SDAI remission. Naïve patients treated with TCZ had better DAS28, CDAI and SDAI remission rates compared to those treated with TNF inhibitors, whereas the more stringent Boolean remission was similar among all groups. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2668
Long-Term Follow-up after Partial Removal of a Solitary Kidney
Authors: Andrew C. Novick, Gordon Gephardt, Brian Guz, Donald Steinmuller, Raymond R. Tubbs
Journal: New England Journal of Medicine (1991)

The removal of more than one kidney in animals leads to proteinuria and progressive renal failure due to focal segmental glomerulosclerosis. This injury may be the result of chronic glomerular hyperfiltration. The purpose of this study was to determine the effect of a reduction in renal mass of more than 50 percent on residual renal function and morphology in humans.
Unusual Finding of a Tumor Thrombus Arising From Osteosarcoma Detected on 18F-NaF PET/CT
Authors: Priyanka Verma, Nilendu Purandare, Archi Agrawal, Sneha Shah, Venkatesh Rangarajan
Journal: Clinical Nuclear Medicine (2016)

Osteosarcoma is the most common bone sarcoma in adolescents and children. Tumor thrombus arising from osteosarcoma is rare. We describe the case of a 13-year-old girl with osteosarcoma of the right femur, in whom the F-NaF PET/CT was done for initial staging to look for skeletal metastases. The scan showed abnormal increased tracer uptake in the primary tumor and the right common femoral and external iliac vein representing a tumor thrombus. Our case emphasizes the importance of extraosseous findings on F-NaF PET/CT, which may result in important management changes.
A NOVEL IGG AUTOANTIBODY, LO9, REACTS SPECIFICALLY WITH ADHERENT LOW DENSITY LIPOPROTEIN (LDL), TARGETS LDL IN ATHEROSCLEROSIS IN VIVO AND STIMULATES MACROPHAGE TNFα RELEASE
Authors: Ramzi Yousef Khamis, Kevin Woollard, Chiari Kojima, Mikhail Caga-Anan, Gareth Hyde, Chang Shang-Hung, Oliver Gale-Grant, Michael Johns, Joseph Boyle, Jason Johnson, Dorian Haskard
Journal: Journal of the American College of Cardiology (2016)