tbuckley/cabot-search huggingface dataset:
Abstract 371: PGI2 analog enhances endothelial-pericyte interactions and suppresses lung metastasis.
Authors: Yoshinori Minami, Takaaki Sasaki, Satoshi Endo, Kiyoko Shibukawa, Yoshinobu Ohsaki
Journal: Cancer Research (2013)

Abstract Background: Endothelial cells (ECs) express IP (prostaglandin I2 (PGI2) specific receptor) and are playing important role in tumor angiogenesis. We have reported that the PGI2-IP system is necessary for vascular remodeling and angiogenesis. Additionally, we have reported that the knockdown of IP increases tumor metastasis in mouse models. Objectives: In this study, we examined whether the activated PGI2-IP signaling could enhance EC-PC interactions and suppress tumor metastasis. Materials &amp; Methods: Mouse-derived Lewis lung carcinoma (LLC) cells were used for a mouse lung metastatic model, and were injected from the tail vein of mice (c57BL/6J). Beraprost sodium (BPS; PGI2 analog) was continuously administered for 3 weeks. Tumor metastasis to lung was assessed by using hematoxylin-eosin staining. The a-SMA and the NG2 as a pericyte marker and the endomucin as an endothelial cell marker were analyzed by immunofluorescence to evaluate angiogenesis in metastatic lung tumors. The structure of the tumor blood vessels was analyzed by scanning electron microscopy (SEM). Results: The size and number of lung metastatic nodules were significantly decreased in BPS group compared with in control group assessed by the mice lung metastatic model. Immunofluorescence analysis revealed that the number of vessel-associated a-SMA+ cells was significantly increased by BPS administration. Scanning electron microscopy revealed that pericytes covering the tumor blood vessels increased in BPS group. Conclusions: The present study demonstrated that BPS suppresses lung metastasis in our model. These results also suggested that the maturation of tumor blood vessels by pericytes may decrease tumor metastasis. Finally, we propose that BPS would be a novel therapeutic target in lung metastasis. Citation Format: Yoshinori Minami, Takaaki Sasaki, Satoshi Endo, Kiyoko Shibukawa, Yoshinobu Ohsaki. PGI2 analog enhances endothelial-pericyte interactions and suppresses lung metastasis. [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 371. doi:10.1158/1538-7445.AM2013-371
Targeting distinct tumor-infiltrating myeloid cells by inhibiting CSF-1 receptor: combating tumor evasion of antiangiogenic therapy
Authors: Saul J. Priceman, James L. Sung, Zory Shaposhnik, Jeremy B. Burton, Antoni X. Torres-Collado, Diana L. Moughon, Mai Johnson, Aldons J. Lusis, Donald A. Cohen, M. Luisa Iruela-Arispe, Lily Wu
Journal: Blood (2009)
Detection of Cutaneous Metastatic Melanoma With Tl-201 Scintigraphy
Authors: LUKAS RETTENBACHER, JOSEF KOLLER, GÜNTHER GALVAN
Journal: Clinical Nuclear Medicine (1996)

This case demonstrates successful localization of cutaneous metastatic melanoma with Tl-201 scintigraphy. The good tumor-to-background ratio suggests that further studies may be promising.
A Cross-sectional Study of a Prototype Carcinogenic Human Papillomavirus E6/E7 Messenger RNA Assay for Detection of Cervical Precancer and Cancer
Authors: Philip E. Castle, Janel Dockter, Cristina Giachetti, Francisco A.R. Garcia, Mary Kay McCormick, Amy L. Mitchell, E. Blair Holladay, Daniel P. Kolk
Journal: Clinical Cancer Research (2007)

Abstract Purpose: To evaluate carcinogenic human papillomavirus (HPV) mRNA for E6 and E7 mRNA detection on clinical specimens to identify women with cervical precancer and cancer. Experimental Design: We evaluated a prototype assay that collectively detects oncogenes E6/E7 mRNA for 14 carcinogenic HPV genotypes on a sample of liquid cytology specimens (n = 531), masked to clinical data and to the presence of HPV genotypes detected by PGMY09/11 L1 consensus primer PCR assay. Results: We found an increasing likelihood of testing positive for carcinogenic HPV E6/E7 mRNA with increasing severity of cytology (PTrend &amp;lt; 0.0001) and histology (PTrend &amp;lt; 0.0001), with 94% of cervical intraepithelial neoplasia grade 3 (CIN3) histology cases (46 of 49) and all five cancer cases testing positive for carcinogenic HPV E6/E7 mRNA. Overall, fewer specimens tested positive for carcinogenic HPV E6/E7 mRNA than for carcinogenic HPV DNA (P &amp;lt; 0.0001, McNemar's χ2 test), especially in women with &amp;lt;CIN1 (P &amp;lt; 0.0001). We also found that using a higher positive cutpoint for detection of carcinogenic HPV E6/E7 mRNA improved the association of positive test results with cervical precancer and cancer by reducing the number of test positives in women without precancer without reducing clinical sensitivity for cervical precancer and cancer compared with detection of carcinogenic HPV E6/E7 mRNA using a lower positive cutpoint by the same assay and with detection of carcinogenic HPV DNA. Conclusions: We found that carcinogenic HPV E6/E7 mRNA is a potentially useful biomarker for detection of cervical precancer and cancer and warrants further evaluation.
Hepatic regulatory T cells and Kupffer cells are crucial mediators of systemic T cell tolerance to antigens targeting murine liver
Authors: Ekaterina Breous, Suryanarayan Somanathan, Luk H. Vandenberghe, James M. Wilson
Journal: Hepatology (2009)

The mechanisms of tolerance in the liver that limit susceptibility to food allergy and that mediate the acceptance of liver transplants, even with a complete major histocompatibility complex (MHC) mismatch, remain poorly defined. Here we report that in a model of liver-directed gene transfer, cytotoxic T lymphocyte (CTL) responses to non-self antigens are controlled by hepatic regulatory T cells (Tregs) that secrete the immunosuppressive cytokine interleukin (IL)-10 in response to the antigen. In addition, Kupffer cells (KCs), normally thought to initiate immune responses, are rendered tolerogenic in this context. The depletion of KCs results in a complete abrogation of IL-10 production by hepatic Tregs, indicating an interaction between Tregs and KCs in the induction of tolerance.Our study suggests that hepatic Tregs together with KCs create a local suppressive microenvironment that prevents the establishment of the CTL response. These mechanisms provide pivotal insights and may prove instrumental in the tolerization toward non-self therapeutic proteins delivered to the liver.
Abstract 3457: Galectin-1 suppression enhances combined anti-EGFR and radiation-therapy of NSCLC
Authors: Michael Siedow, Arnab Chakravarti, Tim Lautenschlaeger
Journal: Cancer Research (2012)

Abstract Lung cancer remains the leading cause of cancer related death worldwide and will account for nearly 160,000 deaths in the United States alone in 2010. Between 80-90% of all cases diagnosed are classified as non-small cell lung cancer (NSCLC). Recent studies have shown a significant subpopulation of patients diagnosed with NSCLC have an activation of the epidermal growth factor receptor (EGFR) domain resulting from gene amplification, overexpression, or kinse-domain activating mutations. EGFR inhibitors such as Erlotinib and Gefitnib have shown promising results in this subpopulation of patients however median overall survival remains poor. LSGAL1, Galectin-1 (GAL1), is a beta-galactoside-binding protein we recently identified to play an important role in the activation of the PI3-Kinase pathway located directly downstream of EGFR. Silencing Galectin-1 in combination with an EGFR-inhibitor and radiation therapy may be a promising therapeutic strategy for patients with NSCLC. Using a short-hairpin RNA strategy we silenced GAL1 expression in four different NCSLC cell lines and assessed their relative radioresistance via clonogenic survival assay in the presence and absence of an EGFR inhibitor. In order to elucidate the mechanism between GAL1 and EGFR, western blotting and QPRC analysis was performed on downstream pathway members, specifically the RAS/PI3-Kinase and RAS/ERK signaling cascades. Functional assays focusing on proliferation/survival were carried out to determine the effect silencing GAL1 had on the combination of EGFR inhibition and radiation therapy in our NSCLC cell lines. Our preliminary results suggest silencing GAL1 reduces the clonogenic survival of NSCLC cells when used in combination with an EGFR inhibitor following irradiation. In addition well known players within PI3-Kinase pathway such as pAKT S473 appear to be altered in the absence of GAL1. Our preliminary findings suggest GAL1 is a promising therapeutic target in NSCLC when used in combination with an EGFR inhibitor and radiation therapy and is worthy of further 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 3457. doi:1538-7445.AM2012-3457
Measurement of offline exhaled nitric oxide in a study of community exposure to air pollution.
Authors: J Q Koenig, K Jansen, T F Mar, T Lumley, J Kaufman, C A Trenga, J Sullivan, L-J S Liu, G G Shapiro, T V Larson
Journal: Environmental Health Perspectives (2003)

As part of a large panel study in Seattle, Washington, we measured levels of exhaled nitric oxide (eNO) in children's homes and fixed-site particulate matter with aerodynamic diameters of 2.5 micro m or less (PM(2.5)) outside and inside the homes as well as personal PM(2.5) during winter and spring sessions of 2000-2001. Nineteen subjects 6-13 years of age participated; 9 of the 19 were on inhaled corticosteroid (ICS) therapy. Exhaled breath measurements were collected offline into a Mylar balloon for up to 10 consecutive days. Mean eNO values were 19.1 (SD +/- 11.4) ppb in winter sessions and 12.5 +/- 6.6 ppb in spring sessions. Fixed-site PM(2.5) mean concentrations were 10.1 +/- 5.7 microg/m(3) outside homes and 13.3 +/- 1.4 inside homes; the personal PM(2.5) mean was 13.4 +/- 3.2 microg/m(3). We used a linear mixed-effects model with random intercept and an interaction term for medications to test for within-subject-within-session associations between eNO and various PM(2.5) values. We found a 10 microg/m(3) increase in PM(2.5) from the outdoor, indoor, personal, and central-site measurements that was associated with increases in eNO in all subjects at lag day zero. The effect was 4.3 ppb [95% confidence interval (CI), 1.4-7.29] with the outdoor monitor, 4.2 ppb (95% CI, 1.02-7.4) for the indoor monitor, 4.5 ppb (95% CI, 1.02-7.9) with the personal monitor, and 3.8 ppb (95% CI, 1.2-6.4) for the central monitors. The interaction term for medication category (ICS users vs. nonusers) was significant in all analyses. These findings suggest that eNO can be used as an assessment tool in epidemiologic studies of health effects of air pollution.
Gas Gangrene from Parenteral Injection
Authors: Thomas A. Koons
Journal: JAMA (1961)

THE POSSIBILITY of gas gangrene is always thought of in connection with extensive contaminated wounds of the battlefield or in connection with injuries with extensive areas of devitalized tissue resulting from civil accidents. Every surgeon is acquainted with the potential dangers of these injuries, and intensive therapy is instituted at the first sign of gas or extending cellulitis. The potential hazard of parenteral medication as a source of gas gangrene is not recognized in this country. We can find no case reports in the American literature. There are 2 case reports from Britain,<sup>1-3</sup>1 from Australia,<sup>4</sup>"more than 30 cases" from Brazil,<sup>5</sup>and 83 cases collected by Touraine from France, Germany, and Italy.<sup>6</sup>The following case is reported to bring attention to this unfortunate complication of parenteral therapy so that awareness may lead to early diagnosis and treatment and possibly lower the extremely high mortality experienced
Cholesterol nucleation time in gallbladder bile of patients with solitary or multiple cholesterol gallstones
Authors: Dieter Jüngst, Thomas Lang, Christoph von Ritter, Ekkehard Pratschke, Gustav Paumgartner
Journal: Hepatology (1992)

Patients with multiple cholesterol gallbladder stones have been found to be at a higher risk for the recurrence of gallstones after successful nonsurgical treatment than those with a solitary stone. Cholesterol gallstone recurrence, like primary gallstone formation, probably involves a triple defect with supersaturation, abnormally rapid nucleation of cholesterol in bile and altered gallbladder motor function. We investigated whether the increased recurrence rate of patients with multiple stones might be caused by more rapid nucleation. Therefore the time required for cholesterol monohydrate crystals to appear in ultracentrifuged bile of patients with solitary (n = 71) or multiple (n = 42) cholesterol gallstones was determined. The cholesterol nucleation time was significantly (p less than 0.01) longer in the bile from patients with solitary stones (less than 1 to 16 days, median = 2.0 days) than in the bile from patients with multiple stones (less than 1 to 8 days, median = 1.0 days). Moreover, 15 of 71 (21.1%) patients with solitary cholesterol stones but only 1 of 42 (2.4%) patients with multiple cholesterol stones showed a normal (greater than 4 days) nucleation time. However, no difference in the cholesterol saturation index was found between the bile samples from patients with solitary stones and the bile samples from patients with multiple stones (1.55 +/- 0.65 vs. 1.54 +/- 0.59, mean +/- S.D., respectively). The more rapid cholesterol nucleation in gallbladder bile may, therefore, be the major risk factor causing the higher percentage of stone recurrence in patients with multiple cholesterol stones as compared with patients with solitary cholesterol stones.
<i>Gut</i> boldly goes where others have gone before:www.gutjnl.com
Authors: MICHAEL FARTHING
Journal: Gut (1998)

The dawn of a new age in the dissemination of and access to information will not have escaped your notice. I refer, of course, to the world wide web. The Internet has developed and grown so rapidly that neither publishers nor editors of journals can afford to ignore it. It is definitely not going to go away. Gut has had an Internet presence for some years now but it has been a …
Viral Vector–mediated and Cell-based Therapies for Treatment of Cystic Fibrosis
Authors: Terence R Flotte, Philip Ng, Doug E Dylla, Paul B McCray, Guoshun Wang, Jay K Kolls, Jim Hu
Journal: Molecular Therapy (2007)

Gene and cell-based therapies are considered to be potentially powerful new approaches for the management of cystic fibrosis (CF) lung disease. Despite tremendous efforts that have been made, especially in studies to understand the obstacles to gene delivery, major challenges to the application of these approaches remain to be solved. This article will review the advancements made and challenges remaining in the development of viral vector-mediated and cell-based approaches to treat patients with CF.
Measles Vaccination in Infants
Authors: Phillip H. Jones
Journal: JAMA (1982)

<h3>To the Editor.—</h3> On May 15, 1981, the Centers for Disease Control (CDC) reported an outbreak of measles among the children of migrant farm workers in Texas. Among these were 42 infants younger than 15 months. The CDC and the Office of Migrant Health recommended that "infants ages 6 months through 14 months be vaccinated."<sup>1</sup> In June of this year a message was sent by the CDC to migrant health clinics throughout the country: "Infants, six to 11 months of age, up to first birthday, should receive one dose of single antigen measles vaccine. These infants must be revaccinated at 15 months with trivalent measles, mumps, [and] rubella vaccine to assure continued protection, since some children vaccinated prior to their first birthday will not be effectively immunized." This was a poor recommendation for nationwide distribution. Any physician participating in immunization programs should be aware that immunization against measles at
Race/Ethnicity–Specific Associations of Urinary Phthalates with Childhood Body Mass in a Nationally Representative Sample
Authors: Leonardo Trasande, Teresa M. Attina, Sheela Sathyanarayana, Adam J. Spanier, Jan Blustein
Journal: Environmental Health Perspectives (2013)

Phthalates have antiandrogenic effects and may disrupt lipid and carbohydrate metabolism. Racial/ethnic subpopulations have been documented to have varying urinary phthalate concentrations and prevalences of childhood obesity.We examined associations between urinary phthalate metabolites and body mass outcomes in a nationally representative sample of U.S. children and adolescents.We performed stratified and whole-sample cross-sectional analyses of 2,884 children 6-19 years of age who participated in the 2003-2008 National Health and Nutrition Examination Survey. Multivariable linear and logistic analyses of body mass index z-score, overweight, and obesity were performed against molar concentrations of low-molecular-weight (LMW), high-molecular-weight (HMW), and di-2-ethylhexylphthalate (DEHP) metabolites, controlling for sex, television watching, caregiver education, caloric intake, poverty-income ratio, race/ethnicity, serum cotinine, and age group. We used sensitivity analysis to examine robustness of results to removing sample weighting, normalizing phthalate concentrations for molecular weight, and examining different dietary intake covariates.In stratified, multivariable models, each log unit (roughly 3-fold) increase in LMW metabolites was associated with 21% and 22% increases in odds (95% CI: 1.05-1.39 and 1.07-1.39, respectively) of overweight and obesity, and a 0.090-SD unit increase in BMI z-score (95% CI: 0.003-0.18), among non-Hispanic blacks. Significant associations were not identified in any other racial/ethnic subgroup or in the study sample as a whole after controlling for potential confounders, associations were not significant for HMW or DEHP metabolites, and results did not change substantially with sensitivity analysis.We identified a race/ethnicity-specific association of phthalates with childhood obesity in a nationally representative sample. Further study is needed to corroborate the association and evaluate genetic/epigenomic predisposition and/or increased phthalate exposure as possible explanations for differences among racial/ethnic subgroups.
Abstract B8: FOXD3 enhances expression of ERBB3 and promotes resistance to vemurafenib
Authors: Kevin J. Basile, Ethan V. Abel, Andrew E. Aplin
Journal: Clinical Cancer Research (2012)

Abstract Melanoma cells driven by mutant B-RAF are sensitive to vemurafenib (PLX4032), which selectively inhibits BRAF/MEK/ERK1/2 signaling. Despite initial tumor shrinkage, most responders in the trials experienced tumor relapse over time. Furthermore, approximately 5–15% of patients show tumor progression. These findings indicate that resistance mechanisms will hamper the clinical efficacy of vemurafenib. We have previously shown that a stemness factor, FOXD3, is upregulated following inhibition of B-RAF-MEK signaling in mutant B-RAF melanoma cells. Here, we show that siRNA-mediated knockdown of FOXD3 significantly enhanced the cell death response after PLX4032 treatment in mutant B-RAF melanoma cell lines. Additionally, ectopic expression of FOXD3 in nonadherent cells significantly reduced cell death in response to PLX4720 treatment. Genome wide analyses revealed that FOXD3 significantly increased expression of ERBB3 through direct binding to a known enhancer region of the ERBB3 gene. Knockdown of endogenous FOXD3 reduced ERBB3 upregulation after treatment with PLX4032. Furthermore, activation of ERBB3 in the presence of ligand was enhanced by B-RAF inhibition in an ERBB2-dependent manner. Treatment with the EGFR/ERBB2 inhibitor, lapatinib, in combination with PLX4032/4720 significantly reduced viability in both in vitro and in vivo assays. These data indicate that upregulation of FOXD3 is an adaptive response to B-RAF inhibitors that enhances ERBB3 signaling and promotes a state of drug resistance.
Lessons From the Health Sector in Afghanistan
Authors: Benjamin Loevinsohn, Ghulam Dastagir Sayed
Journal: JAMA (2008)

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A "SCHREIBER" ADAPTER FOR INTRAVENOUS INJECTIONS
Authors: J. H. Stokes
Journal: JAMA (1918)

Those who appreciate the good qualities of the Schreiber needle in meeting the difficulties of intravenous injection technic will appreciate the serviceability of the device here illustrated, which has been in use in my service for several months. The Schreiber needle is made in only one, or at most two sizes. This adapter makes possible the use of a needle of any size desired to meet the indications in a particular case. The needle proper is attached to the standard Lüer hub of the adapter, and adapter and needle are then used together as one instrument, in accordance with a technic that I have already described.<sup>1</sup>The device was developed in cooperation with Mr. P. L. Pinkerton of the Precious Metals Tempering Company, who submitted a sketch and later a specimen for clinical trial. Whenever, for any reason, it is found necessary to inject amounts of solution too large
Protection and in Vivo Selection of Hematopoietic Stem Cells Using Temozolomide, O6-Benzylguanine, and an Alkyltransferase-Expressing Retroviral Vector
Authors: Nobukuni Sawai, Sheng Zhou, Elio F. Vanin, Peter Houghton, Thomas P. Brent, Brian P. Sorrentino
Journal: Molecular Therapy (2001)

Transfer of drug resistance genes to hematopoietic stem cells offers the potential to protect cancer patients from drug-induced myelosuppression and to increase the number of gene-modified cells by in vivo selection. In this study, a retroviral vector expressing both a P140K variant of human O6-methylguanine-DNA methyltransferase (MGMT) and an EGFP reporter gene was evaluated for stem cell protection in a murine transplant model. Mice transplanted with vector-transduced cells showed significant resistance to the myelosuppressive effects of temozolomide (TMZ), an orally administered DNA-methylating drug, and O6-benzylguanine (BG), a drug that depletes cells of wild-type MGMT activity. Following drug treatment, increases in EGFP(+) peripheral blood cells were seen in all peripheral blood lineages, and secondary transplant experiments proved that selection had occurred at the stem cell level. In a second set of experiments in which transduced cells were diluted with unmarked cells, efficient stem cell selection was noted together with progressive marrow protection with repeated treatment courses. Altogether, these results show that P140K MGMT gene transfer can protect stem cells against the toxic effects of TMZ and BG and that this vector/drug system may be useful for clinical myeloprotection and for in vivo selection of transduced stem cells.