tbuckley/cabot-search huggingface dataset:
Changes in Intrinsic Coronary Circulation and Segmental Ventricular Motion after Saphenous-Vein Coronary Bypass Graft Surgery
Authors: Lawrence S.C. Griffith, Stephen C. Achuff, C. Richard Conti, J. O'Neal Humphries, Robert K. Brawley, Vincent L. Gott, Richard S. Ross
Journal: New England Journal of Medicine (1973)

Occlusive changes in the intrinsic coronary arterial circulation were found in 50 of 71 patients 6.1 ± 0.8(± S.E.M.) after saphenous-vein bypass surgery. A new total arterial occlusion was found in 57 (30 per cent) of 188 major coronary arteries. These occlusions occurred in 29 per cent (20 of 68) of intrinsic coronary arteries with a patent graft, in 62 per cent (24 of 39) of those with an occluded graft, and in 16 per cent (13 of 81) of arteries not bypassed. A comparable reduction in segmental left ventricular motion was noted. Eighty-six per cent of the 71 patients had symptomatic improvement of angina; 60 per cent were asymptomatic. Thus, change in the intrinsic coronary circulation after bypass procedures is not inconsistent with relief of angina and must be considered in the evaluation of this operation.
Abstract 4799: Promoter methylation of leukemia inhibitory factor receptor gene in colorectal carcinoma
Authors: Xiaofei Chang, Yong G. Cho, Il-Seok Park, Chunbo Shao, Patrick Ha, Sara I. Pai, David Sidransky, Myoung S. Kim
Journal: Cancer Research (2011)

Abstract Aberrant methylation of gene promoters and corresponding loss of gene expression plays a critical role in the initiation and progression of colorectal cancer. An IL-6-type cytokine receptor, leukemia inhibitory factor receptor (LIFR), is a component of cell-surface receptor complexes for multifunctional cytokines such as LIF. Herein, we report that LIFR is methylated in human colon cancer. LIFR promoter was methylated in primary tumor tissues with high frequency (65%, 52/80). Quantitative methylation-specific PCR (TaqMan-MSP) demonstrated differential promoter methylation of LIFR in primary colorectal cancer tissues as compared to normal colon tissues (5%, 4/80). LIFR methylation was not detectable in 13 normal colon mucosa samples obtained from patients without cancer. The mRNA expression of LIFR was significantly down-regulated in colon cancer tissues as compared to corresponding normal tissues. A strong expression of LIFR protein was observed in all non-malignant normal and adjacent normal colon mucosa tissues whereas down-regulated LIFR protein expression was observed in primary tumors. These results implicate that cancer-specific methylation and a specific decrease of LIFR expression are a common inactivation event in colon cancer development. 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 4799. doi:10.1158/1538-7445.AM2011-4799
Abstract LB-59: Progressing Forward in Timely Fashion
Authors: Peg Ford
Journal: Cancer Research (2012)

Abstract Peg Ford, Chair, and Kathy Hagan, Co-Chair, caregiver who lost her mother to ovarian cancer, formalized Peg's advocacy efforts in launching the Ovarian Cancer Advocacy Alliance (OCAA) of San Diego in May 2011. OCAA's Mission was formulated in three aspects of Advocacy: 1) Affect change in the way medical doctors approach diagnosis and treatment of ovarian cancer by education of the medical community, patient organizations, and the community at large to achieve early diagnosis and improved treatment options; 2) advance ovarian cancer research toward early diagnosis and improved quality of care; and 3) Address legislative issues that affect ovarian cancer care and research. From becoming a proud partner of the Ovarian Cancer National Alliance (OCNA); successfully expanding OCNA's “Survivors Teaching Students: Saving Women's Lives®” Program to Schools of Nursing; publishing articles; and actively participation in legislative actions, 2011 was a banner year. The poster reflects the continued outstanding success of the STS Program, and Peg Ford, OCAA Chair's, commitment to pursue her initiative to blossom into a voice as a Research Advocate for the ovarian cancer community on a local, state, national and international level, as a guest speaker, facilitator, or writer for community outreach efforts. Progressing forward in a timely fashion will continue to set the initiatives to strengthen Ovarian Cancer Advocacy Alliance's (OCAA) vision of patient advocates as the bridge between the patient community and the scientific/medical world, working hand-in-hand to advance research and impact changes to better serve both communities. 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 LB-59. doi:1538-7445.AM2012-LB-59
Lactic Acidosis in Patients with Diabetes Treated with Metformin
Authors: Robert I. Misbin, Lanh Green, Bruce V. Stadel, John L. Gueriguian, Ananda Gubbi, G. Alexander Fleming
Journal: New England Journal of Medicine (1998)

To the Editor: From May 1995, when metformin was introduced in the United States, through June 30, 1996, the Food and Drug Administration (FDA) received reports of lactic acidosis in 66 patients treated with metformin. In 47 patients, the diagnosis was confirmed on the basis of circulating lactate values (>5 mmol per liter), in accordance with established criteria for the diagnosis of lactic acidosis (Table 1).1,2 Of the 47 patients with confirmed diagnoses, 43 had one or more risk factors for lactic acidosis. Thirty (64 percent) had preexisting cardiac disease, of whom 18 had histories of congestive heart failure. . . .
Abstract P2-06-02: Genomic evolution from primary breast cancers to distant metastases
Authors: LDC Hoefnagel, CB Moelans, P van der Groep, E van der Wall, PJ van Diest
Journal: Cancer Research (2012)

Abstract Purpose: Genomic evolution is an accepted concept during cancer development and progression. However, little is known about the changes that occur during the metastatic process despite the fact that breast cancer metastases are the leading cause of death in breast cancer patients. The purpose of this study was therefore to investigate whether distant breast cancer metastases show progression in copy number changes of onco- and tumor suppressor genes compared to their primary tumor. Material and methods: Multiplex ligation-dependent probe amplification (MLPA) was used to compare copy number of 21 established oncogenes and tumor suppressor genes between primary breast cancer samples and corresponding distant metastases in 55 patients. Genes studied were ESR1, EGFR, FGFR1, ADAM 9, IKBKB, PRDM14, MTDH, MYC, CCND1, EMSY, CDH1, TRAF4, CPD, MED1, HER2, CDC6, TOP2A, MAPT, BIRC5, CCNE1 and AURKA. Results: Overall, there was no significant difference in mean copy number between primary tumors (1.26 +/− 0.6) and metastases (1.27 +/− 0.64) (p = 0.826), but on the individual gene level, mean copy number for PRDM14 (p = 0,023), MED1 (p = 0.001) and CCNE1 (p = 0.039) were significantly higher while TRAF4 (p = 0.038) copy number was significantly lower in the metastases. Using dichotomized MLPA data, MTDH amplifications were significantly more frequent in the primary cancers compared to the metastases (27.3% vs.14.6%, p = 0.039), while significantly more CDH1 losses were found in the metastases compared to the primary tumor (23.6% vs. 9.1%, p = 0.039). Conclusion: Distant breast cancer metastases show genomic evolution from the primary cancer as reflected by copy number changes in several established onco- and tumor suppressor genes. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P2-06-02.
Abstract 3979: Ethnic polymorphisms in the GGAA microsatellite response element of key Ewing's sarcoma EWS/FLI-target genes
Authors: Michael J. Monument, Robert Beck, W. Scott Watkins, Lynn B. Jorde, R. Lor Randall, Stephen L. Lessnick
Journal: Cancer Research (2012)

Abstract Study Rationale: Unlike other cancer models, the risk factors predisposing patients to the development of Ewing's sarcoma and predicting subsequent disease behavior are largely unknown. Interestingly, the incidence of Ewing's sarcoma is highest in populations of European descent, which is 10X higher than the incidence observed in those of African descent. Furthermore, cure rates and overall survival are significantly worse in patients of African descent. Recently, it has been shown that the EWS/FLI fusion product selectively binds to a (GGAA)n microsatellite response element embedded within the promoter region of key EWS/FLI-target oncogenes. An increasing number of these repeats also appears to positively affect DNA binding and gene activation. We hypothesize that differences in polymorphic GGAA microsatellites within the promoter regions of key EWS/FLI-target genes may exist in African and European populations, contributing to observed differences in Ewing's sarcoma incidence and outcomes. Methods: Genomic DNA samples were obtained from 100 subjects each of African and European descent. The microsatellite regions within the promoter elements of two key EWS/FLI target genes (NR0B1 and CAV1) were PCR amplified, cloned and sequenced. Microsatellite sequences were analyzed and the overall length of the microsatellite, the total number of GGAA repeats and the maximal number of consecutive repeats were quantified. Data was statistically interpreted using a comparative two-tailed t-test. Results: Measurements of the CAV1 microsatellite response element were quite similar for both African and European subjects. In sharp contrast, marked inter-ethnic variation was observed for the NR0B1 GGAA microsatellite response element. African samples had a significantly longer GGAA microsatellite, a greater number of total (GGAA)n repeats and longer consecutive (GGAA)n repeats (p&amp;lt;0.0001). Conclusions: These data demonstrate a marked inter-ethnic variation in the genetic constitution of the Ewing's sarcoma EWS/FLI-response element within the NR0B1 promoter. Given the epidemiological differences of Ewing's sarcoma susceptibility and disease outcome in these divergent populations and the importance of NR0B1 dysregulation in Ewing's sarcoma oncogenesis, this novel finding warrants further functional investigation. 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 3979. doi:1538-7445.AM2012-3979
PRO-OXIDANT HDL PREDICTS POOR OUTCOME IN PATIENTS WITH ST-ELEVATION ACUTE CORONARY SYNDROME
Authors: Klaus Distelmaier, Lore Schrutka, Veronika Seidl, Max P. Winter, Raphael Wurm, Andreas Mangold, Gerald Maurer, Christopher Adlbrecht, Irene M. Lang
Journal: Journal of the American College of Cardiology (2015)
Primary small-bowel adult T-cell leukemia/lymphoma with gastric AL amyloidosis
Authors: Hiroki Yaita, Shotaro Nakamura, Koichi Kurahara, Tomohiro Nagasue, Shuji Kochi, Yumi Oshiro, Koichi Ohshima, Yuichi Ikeda, Tadahiko Fuchigami
Journal: Endoscopy (2014)

An 86-year-old man was admitted because of small-bowel wall thickening and mesenteric lymphadenopathy. Neither peripheral lymphadenopathy nor hepatosplenomegaly was noted. The leukocyte count was 7930/mm3, and no abnormal lymphocytes were found. The result of testing for serum antihuman T-lymphotropic virus type 1 (HTLV-1) antibody was positive. A bone marrow biopsy was normal without evidence of lymphoid infiltration. Small-bowel enteroclysis demonstrated a narrowing, edematous lesion with multiple ulcerations in the jejunum ([Fig. 1]). Capsule endoscopy ([Fig. 2]) and double-balloon endoscopy ([Fig. 3]) showed enlarged Kerckring folds with annular and irregularly shaped shallow ulcers. Biopsy specimens from the ulcers revealed diffuse infiltration of medium to large pleomorphic lymphoid cells with CD3 +, CD4 +, CD5 +, CD25 +, CCR4 +, FoxP3 +, CD8 –, CD20 –, CD56 –, and TIA1 – immunophenotype ([Fig. 4]). Biopsy specimens from the stomach, duodenum, ileum, and colon showed no lymphoma cells. Fluorodeoxyglucose F 18 positron emission tomography showed abnormal uptake in the jejunal mass, wide areas of mesentery, and para-aortic lymph nodes. Esophagogastroduodenoscopy with chromoendoscopy revealed granular stomach mucosa and swollen folds in the corpus, with pan-atrophic gastritis ([Fig. 5]). Biopsy from the granular mucosa and folds showed massive amyloid deposits of homogeneous acidophilic substances in the submucosa and around the muscularis mucosae ([Fig. 6]), which were immunohistochemically positive for λ light chain. Amyloid deposits were not observed in any specimen taken from the duodenum, jejunum, ileum, and colon. Therefore, the patient's diagnosis was stage IIE (Lugano classification) small-bowel adult T-cell leukemia/lymphoma (ATLL) accompanied by gastric AL amyloidosis.
Normal Tc-99m Tetrofosmin Cardiac SPECT Images With Three-Vessel Coronary Artery Disease
Authors: Christopher Allen, Wei-Jen Shih
Journal: Clinical Nuclear Medicine (2010)

Normal myocardial perfusion stress imaging with Tc-99m perfusion agents provides an excellent prognosis and suggests the absence of life-threatening coronary artery disease (CAD); however, on rare occasions there have been false-negative stress Tc-99m tetrofosmin cardiac SPECT that showed no perfusion abnormalities in patients demonstrated to have multivessel CAD. The presence of ancillary imaging parameters such as dilation of the left ventricular cavity and pulmonary uptake and nonimaging markers of CAD such as stress-induced chest pain and associated ST-segment depressions should alert the physician to the possibility of significant CAD. We present such a case of nonperfusion abnormalities on a Tc-99m tetrofosmin SPECT study.
916 BOCEPREVIR AND TELAPREVIR BASED TRIPLE THERAPY FOR CHRONIC HEPATITIS C: ON-TREATMENT EFFICACY AND IMPACT ON KIDNEY FUNCTION AND MELD SCORE
Authors: V. Virlogeux, F. Gonçalves, P. Pradat, M. Maynard, K. Hartig- Lavie, M. Amiri, C. Scholtes, P. André, F. Bailly, F. Zoulim
Journal: Journal of Hepatology (2013)
Increased Bone Marrow Uptake of Ga-67 in Patients With Fever of Unknown Origin
Authors: LEO G. FLORES, SEISHI JINNOUCHI, SHIGEKI NAGAMACHI, TAKASHI OHNISHI, SHIGEMI FUTAMI, KATSUSHI WATANABE
Journal: Clinical Nuclear Medicine (1996)

The relationships of clinical diagnosis, the effect of blood chemistry, and the clinical implication of increased Ga-67 citrate uptake in the bone marrow of patients with signs and symptoms of fever of unknown origin were studied. Based on intensity of Ga-67 citrate uptake in bone marrow, patients were classified as follows: type 1 when there was no evidence or very faint bone marrow uptake in the vertebrae, type 2 when mild to moderate, type 3 when uptake was severe. The relationships of WBC count, hemoglobin, hematocrit, serum iron, and unsaturated iron-binding capacity with the occurrence of increased bone marrow uptake in the different groups were noted. Analysis of variance with Fisher's protected least significant difference was used. A P value of less than 0.05 was considered significant. The results showed significant differences between types 1 and 2 and between types 1 and 3 for WBC counts, hemoglobin, and hematocrit levels. Serum iron concentration and unsaturated iron-binding capacity, however, did not show any significant differences. Significant changes in WBC count, hemoglobin and hematocrit in patients with fever of unknown origin were accompanied by a varying intensity of Ga-67 citrate uptake in the bone marrow.
Abstract P5-06-13: Reduced NIMA Related Kinase 2 (Nek2) Expression Level Enhances Anti-Cancer Drug Sensitivity in the Breast Cancer Cells
Authors: J Lee, K Lee, L. Gollahon
Journal: Cancer Research (2010)

Abstract Although the anticancer drugs paclitaxel and doxorubicin are commonly used to treat many types of solid tumors, their effectiveness is highly variable due to tumor cell resistance. Therefore, it is important to find mechanisms that can be targeted to increase the sensitivity of cancer cells to antitumor agents such as paclitaxel and doxorubicin. NIMA related kinase 2 (Nek2), a serine/threonine kinase is emerging as an important oncogene because of its regulatory role in mammalian cell mitosis. Thus, regulation of the Nek2 expression levels may prove important as a target for cancer treatment. In this study, we investigated whether drug sensitivity was increased in the triple negative breast cancer cell line MDA-MB-468 by using antisense oligonucleotides (ASOs) and siRNA against Nek2. MDA-MB-468 breast cancer cells transfected with Nek2 siRNA or ASO were exposed to various concentrations of paclitaxel and doxorubicin. Cell viability, cell cycle distribution, and apoptosis were evaluated. We observed that drug susceptibility in these transfected cells was dramatically increased compared with either agent alone. Interestingly, the cell proliferation of the Nek2 ASO transfected breast cancer cells was much lower than the Nek2 siRNA transfected breast cancer cells. Our FACS data showed paclitaxel and doxorubicin treated cells transfected with ASOs arrested in G2/M phase as expected due to Nek2 regulatory function in centrosome duplication. We observed that ASOs and siRNA against Nek2 work with paclitaxel and doxorubicin by arresting cells at G2/M and progressing the cells to apoptosis. Our results suggest that these drugs in combination with Nek2 siRNA or Nek2 ASO treatment greatly improve the sensitivity of cancer cells. Thus, these results provide a possible new strategy for the treatment of breast cancer. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P5-06-13.
The case for mental duality: Evidence from split-brain data and other considerations
Authors: Roland Puccetti
Journal: Behavioral and Brain Sciences (1981)

Abstract Contrary to received opinion among philosophers, psychologists, and neuroscientists, conscious duality as a principle of brain organization is neither incoherent nor demonstrably false. The present paper begins by reviewing the history of the theory and its anatomical basis and defending it against the claim that it rests upon an arbitrary decision as to what constitutes the biological substratum of mind or person. It then moves on to provide a dynamic model for double consciousness in vertebrate brain organization, giving an evolutionary account that explains why, although each of the two cerebral hemispheres benefits from sensory input from the other for representation of the ipsilateral half of corporeal and extracorporeal space, it was important that conscious experience be confined to each rather than spanning the two. This interhemispheric duplication effect for sensory representation has been known for years but hitherto considered mysterious, or ignored on grounds that integration must be achieved at a higher level of processing. The paper then attempts to resolve a puzzle about split-brain patients in testing situations, namely why it is that in spite of the speaking hemisphere's denial of any independent perception and agency in the mute hemisphere, which would explain its role in cross-cuing, the latter never seems to resent this, but instead continues to be cooperative and helpful. It is suggested that on the hypothesis of mental duality this is understandable, for the nonverbal hemisphere would have known prior to the surgery that it is not generating linguistic behavior. Finally, the essay examines two kinds of bitemporal defects, one due to callosal and the other to chiasmal disruptions. On the present theory a bitemporal defect should be demonstrable in the former case when both eyes are open, because in the absence of a corpus callosum and other forebrain commissures the interhemispheric duplication effect is abolished; in the latter case interhemispheric duplication is preserved, and so the defect should be demonstrable only by testing each eye independently. This is indeed what the evidence indicates, so it appears that, contrary to the prevalent view, the function of the corpus callosum is not to integrate and unify conscious experience between the hemispheres but to duplicate this, in accord with the model of mental duality.
Pericardial Mucinous Adenocarcinoma on 18F-FDG PET/CT
Authors: Guojian Zhang, Xuemei Wang, Hongwei Yuan, Tao Zhang
Journal: Clinical Nuclear Medicine (2014)

A 56-year-old woman presented a history of left chest discomfort for 6 months. A prior CT revealed pericardial thickening, and malignancy cannot be excluded. For this reason, an FDG PET/CT scan was performed, which revealed abnormal activity inside the pericardium. The pathologic examination results after surgery demonstrated a mucinous adenocarcinoma.
Abstract 1079: Targeted disruption of Nemo-like kinase inhibits tumor cell growth by simultaneous suppression of cyclin D1 and CDK2 in human hepatocellular carcinoma
Authors: Kwang Hwa Jung, eong Kyu Kim, Ji Hein Noh, Jung Woo Eun, Hyun JIn Bae, Hong Jian Xie, Wong Sang Park, Jung Young Lee, Suk Woo Nam
Journal: Cancer Research (2010)

Abstract The wnt/β-catenin signaling pathway regulates various aspects of development and plays important role in human carcinogenesis. Nemo-like kinase (NLK), which is mediator of wnt/β-catenin signaling pathway, phosphorylates T-cell factor/lymphoid enhancer factor (TCF/LEF) factor and inhibits interaction of β-catenin/TCF complex. Although, NLK is known to be a tumor suppressor in wnt/β-catenin signaling pathway of colon cancer, the other events occurring downstream of NLK pathways in other types of cancer remain unclear. In the present study, we identified that expression of NLK was significantly up-regulated in the HCCs compared to corresponding normal tissues in five selected tissue samples. Immunhistochemical analysis showed significant over-expression of NLK in the HCCs. Targeted-disruption of NLK suppressed cell growth and arrested cell-cycle transition. Suppression of NLK elicited anti-mitogenic properties of the Hep3B cells by simultaneous inhibition of cyclinD1 and CDK2. The results of this study suggest that NLK is aberrantly regulated in HCC, which might contribute to the mitogenic potential of tumor cells during the initiation and progression of hepatocellular carcinoma; this process appears to involve the induction of CDK2 and cyclin D1 and might provide a novel target for therapeutic intervention in patients with liver cancer. 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 1079.