tbuckley/cabot-search huggingface dataset:
THE ADJUNCTIVE USE OF ANGIO-SEAL IN FEMORAL VASCULAR CLOSURE FOLLOWING PERCUTANEOUS TRANSCATHETER AORTIC VALVE REPLACEMENT
Authors: Sarkis Kiramijyan, Marco Magalhaes Pereira, Itsik Ben-Dor, Edward Koifman, Ricardo Escarcega Alarcon, Nevin Baker, Smita Negi, Romain Didier, Won Yu Kang, Sa’ar Minha, Rebecca Torguson, Petros Okubagzi, Nelson Bernardo, Lowell Satler, Augusto Pichard, Ron Waksman
Journal: Journal of the American College of Cardiology (2016)
Abstract 456: 25-Hydroxyvitamin D3 inhibits clonogenic growth and regulates expression of multiple cytokines/chemokines in co-culture of colon cancer and macrophage-like THP-1 cells
Authors: Xinjian Peng, Fatouma Alimirah, Sarbani Roy, Liang Yuan, Genoveva Murillo, Rajeshwari R. Mehta, Rajendra G. Mehta
Journal: Cancer Research (2011)

Abstract Colon cancer cells interact with immune cells in vivo, creating a microenvironment which affects both tumor growth and treatment. Macrophages are often the most abundant immune cells in the tumor microenvironment and are involved in inflammation. Since inflammation is tightly associated with colon carcinogenesis, it is important to understand how vitamin D affects the interaction between colon epithelial cells and macrophages. In this study, we used a co-culture system to examine the role of 25-hydroxyvitamin D3 (25(OH)D3) on the clonogenic growth of colon cancer cells and on the profiling of cytokines/chemokines. 25(OH)D3 at 250 nM had minor effect on clonogenic growth in CaCo-2 cells, co-culture of macrophage-like THP-1 cells with CaCo-2 cells significantly stimulated the clonogenic growth of CaCo-2 cells in the absence of 25(OH)D3. However, in the presence of 25(OH)D3, THP-1 cells failed to stimulate the the clonogenic growth of CaCo-2 cells. Cytokine antibody array demonstrated that several cytokines were differentially expressed in the medium after co-culture of the two cell lines for 2 days in the absence of 25(OH)D3. These include increased expression of GROα, MCP-1 and decreased expression of TNFα, Angiogenin; however, in the presence of 25(OH)D3, MCP-2 and MDC were significantly induced and TNFα level was restored. Proliferation assay showed that MCP-2 and MDC had minor or no effect on cell proliferation in CaCo-2 cells, suggesting that these chemokines mainly target macrophages. 25(OH)D3 treatment of THP-1 cells for 24h also induced CYP24, an immediate vitamin D target gene and enhanced MDC and MCP-2 expression as evaluated by qRT-PCR. These results demonstrate that 25(OH)D3 at 250 nM might selectively target macrophages in a co-culture system with colon cells and block the interaction between colon cancer cells and macrophages, which may result in prevention of inflammation. [Supported by NCI R01 CA121157]. 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 456. doi:10.1158/1538-7445.AM2011-456
Endoscopic removal of a partial denture lodged in the jejunum, using single balloon enteroscopy
Authors: L. Fry, Q. Akbar, C. von Gruchalla, K. Mönkemüller
Journal: Endoscopy (2012)

A 48-year-old man accidentally swallowed his upper partial denture while asleep, at about 4 o'clock in the morning. He thought he was dreaming and continued to sleep. However, when he woke up around 7 o'clock, he realized that he was missing his upper denture, and 1 hour later, he presented to our emergency room. A plain film of the abdomen confirmed his fear ([Fig.1]). On physical examination the patient appeared poorly groomed and disheveled but in no apparent distress. The abdomen was soft and nontender, and bowel sounds were normal. An esophagogastroduodenoscopy (EGD) did not reveal any foreign body in the entire stomach or duodenum. Thus we carried out a small-bowel enteroscopy, using the single balloon technique (i. e., only using the overtube balloon but not placing a balloon on the scope; Fujinon EN-450T5; Fuji, Fujinon Corp., Tokyo, Japan). The missing denture was found at approximately 35 cm from the pylorus ([Fig. 2]). The overtube was advanced towards the tip of the endoscope, and the balloon of the overtube was inflated to provide stability to the small bowel. With an assistant holding the overtube in a straight position, we could easily torque and manipulate the scope in a to-and-fro manner. Once an adequate endoscopic position was achieved, we used a standard oval snare ([Fig. 3 a]) to grasp the most proximal part of the denture ([Fig. 3 b]), which was then pulled out under direct and continuous endoscopic visualization. As the denture could not be brought inside the overtube, we proceeded in the following stepwise fashion: (1) we kept the tip of the overtube close to the tip of the enteroscope; (2) the balloon of the overtube was inflated and deflated while pulling out of small bowel; and (3) we kept insufflating the small bowel. We speculated that with this method, the dilated bowel lumen on the proximal side (overtube and partially inflated balloon) and on the distal side (dilated through air insufflation) would minimize impaction and/or laceration potential of the prosthesis while it was being pulled out. Whereas in the stomach there was a minimal chance of impaction, at the level of the cardia and esophageal sphincter we again carefully inflated and deflated the balloon of the overtube to repeat the maneuver used within the small bowel. The denture was thus successfully removed and returned to the patient, who had it re-cemented by his dentist after discharge.
Abstract 2086: Evaluation of a promoter methylation panel in plasma cell-free DNA to screen for colorectal cancer in Hispanics
Authors: Maria del Mar Gonzalez-Pons, Heriberto M. Rodríguez, Patricia Delgado, Francisco Velazquez, Mercedes Y. Y. Lacourt, Alberto Cardona, Raúl D. Bernabe, Marcia R. Cruz-Correa
Journal: Cancer Research (2012)

Abstract Introduction: Detection of quantitative and qualitative changes in cell-free, tumor-derived nucleic acids in cancer patients are being evaluated as potential screening, monitoring and diagnostic tools. Genetic and epigenetic changes in cell-free plasma DNA (cfpDNA) have been studied as non-invasive colorectal cancer (CRC) diagnostic markers, but a gene panel with the diagnostic accuracy necessary for clinical use has not been defined. The CpG island methylator phenotype (CIMP), characterized by hypermethylation in promoter-associated regions, is one of the molecular mechanisms resulting in CRC. We evaluated the detection of promoter hypermethylation in a gene panel previously used to define CIMP in CRC tumors, as plasma biomarkers. Methods: Methylation specific PCR was used to analyze eight CIMP-specific gene promoters (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1, hMLH1, p16, CRABP1) in cfpDNA. Forty age-and-gender matched plasma samples (20 CRC and 20 controls) were evaluated. Samples were classified as methylated, unmethylated or not detected if not amplified by either primer set. Results: Methylation patterns of eight genes in 40 subjects (20 CRC and 20 controls; mean age 67 ± 12.2 years; 20 females) were examined. Five genes revealed a 100% unmethylation pattern. p16 was found to be more likely methylated in controls (11%) whereas NEUROG1 and CRABP1 were more likely to be methylated in CRC cases (6% and 33%, respectively). 53.3% of CRC and 48% controls had β1 methylated genes (OR = 1.24, 95% CI 0.34-4.46). The use of β1 methylated genes detected CRC with 40% sensitivity and 65% specificity. Discussion: We report the first evaluation of the methylation pattern of an eight-gene panel as CRC biomarkers in Hispanics. Our preliminary findings showed that genes were mostly unmethylated in cases and controls. NEUROG1 and CRAP1 were found to be most likely methylated in CRC patients, but the diagnostic accuracy of this panel was poor as a CRC screening biomarker. 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 2086. doi:1538-7445.AM2012-2086
Successfully widening access to medicine. Part 1: recruitment and admissions
Authors: Sally Curtis, Carolyn Blundell, Christine Platz, Linda Turner
Journal: Journal of the Royal Society of Medicine (2014)

Widening access programmes aim to create a more diverse and representative workforce. Some, but not all of these programmes are focused on increasing the representation from low socioeconomic backgrounds, and increasing social mobility.1 The Social Mobility and Child Poverty Commission highlight the need for Russell Group universities to do more to increase fair access to higher education (HE) and the medical profession.1–4 A key recommendation of the commission’s most recent report, State of the Nation 2013,4 is ‘We urge the professions to open their doors to a wider pool of talent… We urge top universities to do the same by using contextual data’. The Medical Schools Council’s (MSC) newly formed Selecting for Excellence Executive Group5 aims to determine how to implement recommendations from these key reports regarding selection and widening access to medicine.

A key aim of the BM6 widening access to medicine programme delivered by the Faculty of Medicine at the University of Southampton, a member of the Russell Group, is to increase representation of lower socioeconomic groups in its medical school while providing the appropriate level of education and support to enable these students to succeed in their studies and future profession, thereby increasing social mobility. Cleland et al.6 state that ‘When a society is mobile, individuals have an equal chance of progressing in terms of income or occupation’.

For the past 12 years, the BM6 programme has been demonstrating many areas of best practice in accessing HE and medicine for students from low socioeconomic backgrounds. This paper aims to add to the limited existing literature in this area and illustrate key aspects of the BM6 programme’s recruitment and admissions process that supports students from low socioeconomic backgrounds in accessing medical school.
Sphenoid Wing Meningioma Behavior on 11C-PiB and 18F-FDG PET
Authors: Hernan Chaves, Yanina Bergamo, Santiago Paz, Flavio Sanchez, Silvia Vazquez
Journal: Clinical Nuclear Medicine (2014)

Two patients with mild cognitive impairment underwent 11C-PiB and 18F-FDG brain PET. Both patients had previously gone through a contrast-enhanced MRI scan that revealed extra-axial tumors next to the sphenoid wing, suggestive of meningiomas. 11C-PiB PET images showed a highly increased uptake by the extra-axial masses. These 2 cases represent 1.2% of our 11C-PiB population (n = 163). No meningioma was found with negative 11C-PiB uptake. The 18F-FDG concentration was not increased within the lesions. 11C-PiB could be used as a meningioma marker.
Case 21-2002
Authors: Simon M. Helfgott, R. Neal Smith
Journal: New England Journal of Medicine (2002)

Presentation of CaseA 21-year-old man was admitted to the hospital because of inflammatory lesions of the foot.The patient had been well until 15 months before admission. At that time, while he was at home in Indonesia, he had diarrhea with fever for several weeks. A diagnosis of typhoid fever was made on the basis of a positive result on Widal's test. Several antibiotics were given, and his symptoms resolved. A few weeks later, migratory polyarthritis developed, but it subsided after one to two months. Thirteen months before admission, the patient came to this hospital while he was taking . . .
Abstract P1-04-06: Insertional mutagenesis identifies HACE1 as a HER2/Neu Cooperating Breast Cancer Tumor Suppressor Gene
Authors: E Goka, P Miller, K Baker, G Stark, ME Lippman
Journal: Cancer Research (2012)

Abstract The development of human breast cancer is a multi-step process leading from normal epithelium to fully transformed breast cancer. Early genetic changes result in hyperplasias which evolves into ductal carcinoma in situ (DCIS) and culminates as invasive ductal carcinoma. The transition from DCIS to invasive disease has been implicated as the key transition in breast cancer progression. Specific genomic, transcriptomic, and proteomic alterations responsible for this transition process have yet to been elucidated. HER2/Neu, a member of the EGFR family of receptor tyrosine kinases, is associated with poor clinical outcome. HER2/Neu overexpression/amplification is commonly seen (50–60%) in non-invasive lesions but is significantly less common (20–30%) in invasive and metastatic breast carcinoma. This indicates that HER2/Neu gives normal epithelium a proliferative advantage but additional genetic alterations are required for full malignant transformation. This idea is supported by the fact that transgenic mice that overexpress HER2/Neu develop spontaneous mammary tumors but only after a prolonged latency period. Recent forward genetic approaches use insertional mutagenesis to randomly integrate a strong promoter into the genome, activating downstream gene transcription that can lead to either gain or loss-of-function mutations based on the integration site. We used this insertional mutagenesis approach to induce anchorage-independent growth of isolated murine HER2/Neu over-expressing mammary epithelial cells. We identified HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1 (HACE1) as a putative breast tumor suppressor protein whose loss leads to the formation of anchorage-independent colonies. Loss of HACE1 expression is commonly seen in breast cancer patients [as well as other tumor types] supporting the role of HACE1 as a breast tumor suppressor gene. Knockdown of HACE1 in human mammary epithelial cells (HMECs) results in the acquisition of anchorage-independent growth. Moreover, knockdown of HACE1 in established breast cancer cell lines that express moderate levels of HACE1 results in enhanced cloniginicity. Therefore, we propose that the loss of HACE1 can potentially be used as a predictive marker for breast cancer progression. Additional studies investigating the mechanism of HACE1 action may also identify therapeutic targets that counteract HACE1 loss. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-04-06.
P2-05-10: Brain-Derived Neurotrophic Factor, BDNF, and Its Biological Impact on Vascular Endothelial Cells.
Authors: WG Jiang, L Ye, X Yang, RE Mansel
Journal: Cancer Research (2011)

Abstract Background: BDNF, Brain-derived neurotrophic factor is a member of the neurotrophin superfamily and is a known growth factor for both central and peripheral nervous systems. While BDNF has been shown to play a role in the development of a number clinical condition including epilepsy, Alzheimer's and Parkinson's disease, it has recently been implicated in human cancers, primarily in neurological related malignancies, as well as ovarian cancer, lung cancer and skin malignancies. We have recently reported a pivotal relationship between BDNF and disease progression and clinical outcome in human breast cancer. Certain members of the neurotrophin family have also been shown to play a role in the regulation of angiogenesis. In the present study, we examined the impact of BDNF on the biological behaviour of vascular endothelia cells. Materials and methods. Human vascular endothelial cells were used in the present study. A human BDNF expression plasmid was constructed from a cDNA library of normal tissues. Anti-BDNF transgenes were constructed based on the secondary structure of human BDNF and used to knockdown the expression of BDNF from the cells. Vascular endothelial cells with differential expression of BDNF were generated using the expression construct. Cell-matrix adhesion, cell migration and growth were determined. Results. Human vascular endothelial cells (HECV) expressed very low levels of BDNF, traceable by PCR method. The cells were transfected with BDNF expression plasmid, which allowed establishment of BDNF over-expressing sublines, HECVBDNFexp. Expression of BDNF had a marked influence on matrix adhesion of the endothelial cells (adhesion indices for control and HECVBDNFexp cells being 3.3± 0.83 and 2.18± 0.94, respectively, p=0.01). It is interesting to note that the change of adhesion was likely to involve the focal adhesion (FAK) pathway as a FAK inhibitor, PF573228, had a profound impact on the adhesion of both control and HECVBDNFexp cells. Manipulation of BDNF in endothelial cells had a similar effect on the cellular migration, although to a lesser degree. Conclusions. Brain-derived neurotrophic factor, BDNF, has a profound impact on the biological functions of vascular endothelial cells. This may have implications in the angiogenic process seen in solid tumours. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-05-10.
Optimization of Gross Tumour Volume Definition and Treatment Planning in Lung-Sparing Volumetric Modulated Arc Therapy for Pleural Mesothelioma
Authors: A. Botticella, G. Defraene, K. Nackaerts, C. Deroose, J. Coolen, P. Nafteux, S. Peeters, D. De Ruysscher
Journal: Annals of Oncology (2015)
Abstract 3020: Transcriptional repressive H3K9 and H3K27 methylations are essential for DNMT1-mediated DNA methylation recovery
Authors: Chun-Ming Wong, Irene Oi-Lin Ng
Journal: Cancer Research (2011)

Abstract DNA methylation and histone modifications are two major epigenetic events regulating gene expression and chromatin structure, and their alterations are linked to human carcinogenesis. DNA methylation plays an important role in tumor suppressor gene inactivation, and can be revised by DNA methylation inhibitors. The reversible nature of DNA methylation forms the basis of epigenetic cancer therapy. However, it has been reported that DNA re-methylation and gene re-silencing could occur after removal of demethylation treatment and this may significantly hamper the therapeutic value of DNA methylation inhibitors. In this study we have provided detailed evidence demonstrating that mammalian cells possess a bona fide DNA methylation recovery system. We have also shown that DNA methylation recovery was mediated by the major human DNA methyltransferase, DNMT1. Moreover, the DNA methylation recovery function of DNMT1 was cell division-independent and likely to be distinct from its conventional “maintenance” DNA methyltransferase function. In addition, we found that H3K9-tri-methylation and H3K27-tri-methylation were closely associated with this DNA methylation recovery. These persistent transcriptional repressive histone modifications may have a crucial role in regulating DNMT1-mediated DNA methylation recovery. Our findings may have important implications towards a better understanding of epigenetic regulation and future development of epigenetic therapeutic intervention. 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 3020. doi:10.1158/1538-7445.AM2011-3020
Therapy of<i>Haemophilus influenzae</i>Meningitis Reconsidered
Authors: Penelope G. Shackelford, John E. Bobinski, Ralph D. Feigin, James D. Cherry
Journal: New England Journal of Medicine (1972)

Ampicillin and chloramphenicol therapy for Haemophilus influenzae meningitis was compared, retrospectively. The 136 ampicillin recipients and 116 chloramphenicol-treated patients proved to be well matched in relation to age, duration of symptoms before treatment, and initial cerebrospinal-fluid findings. Fever was prolonged in a significant number (p less than 0.0025) and was of greater magnitude (p less than 0.0025) in ampicillin recipients. No significant differences were apparent in mortality or other infection-associated complications except for bacteriologic relapse, which occurred in six ampicillin recipients, some of whom received ampicillin intravenously in high dosage and for a prolonged time. Four additional ampicillin recipients had slow bacteriologic responses. Low cerebrospinal-fluid ampicillin concentration was documented in patients receiving ampicillin in a dose of 300 mg per kilogram per day intravenously. Low cerebrospinal-fluid glucose concentrations after therapy were frequently noted with both therapeutic regimens and did not signify persistent bacterial disease; other spinal-fluid findings were comparable.
Use of the Initial Electrocardiogram to Predict In-Hospital Complications of Acute Myocardial Infarction
Authors: John E. Brush, Donald A. Brand, Denise Acampora, Bruce Chalmer, Frans J. Wackers
Journal: New England Journal of Medicine (1985)

We evaluated the initial electrocardiogram as a predictor of complications in 469 patients with suspected acute myocardial infarction. An electrocardiogram was classified as positive if it showed one or more of the following: evidence of infarction, ischemia, or strain; left ventricular hypertrophy; left bundle-branch block; or paced rhythm. Forty-two (14 per cent) of 302 patients with positive electrocardiograms had at least one life-threatening complication (ventricular fibrillation, sustained ventricular tachycardia, or heart block), as compared with 1 (0.6 per cent) of 167 patients with a negative electrocardiogram. Life-threatening complications were therefore 23 times more likely if the initial electrocardiogram was positive (P less than 0.001). Other complications were 3 to 10 times more likely (P less than 0.01), interventions were 4 to 10 times more likely (P less than 0.05), and death was 17 times more likely (P less than 0.001) in patients with a positive electrocardiogram. We conclude that patients with a negative initial electrocardiogram have a low likelihood of complications and could be admitted to an intermediate care unit instead of a coronary care unit. This would reduce admissions to the coronary care unit by 36 per cent and thereby save considerable hospital costs without compromising patient care.
Kidney-Related Munchausen's Syndrome
Authors: Onyekachi Ifudu, Sharon L. Kolasinski, Eli A. Friedman
Journal: New England Journal of Medicine (1992)

MUNCHAUSEN'S syndrome, originally described in 1951,1 is the term applied to persons who seek medical care by feigning illness in the absence of any organic medical or surgical disease. Some persons with the syndrome pretend to have disorders known to require invasive diagnostic procedures and undergo multiple surgical interventions. Although the cause of Munchausen's syndrome is unknown, psychiatric evaluation is recommended whenever it is identified.2 Since the first report of the syndrome, many case reports3 4 5 6 7 have documented the performance of unneeded operations and the administration of dangerous drugs in these patients. We have not, however, seen any reports of the . . .