tbuckley/cabot-search huggingface dataset:
A Prospective Study of Marine Phytoplankton and Reported Illness Among Recreational Beachgoers in Puerto Rico, 2009
Authors: Cynthia J. Lin, Timothy J. Wade, Elizabeth A. Sams, Alfred P. Dufour, Andrew D. Chapman, Elizabeth D. Hilborn
Journal: Environmental Health Perspectives (2015)

Background:Blooms of marine phytoplankton may adversely affect human health. The potential public health impact of low-level exposures is not well established, and few prospective cohort studies of recreational exposures to marine phytoplankton have been conducted.Objective:We evaluated the association between phytoplankton cell counts and subsequent illness among recreational beachgoers.Methods:We recruited beachgoers at Boquerón Beach, Puerto Rico, during the summer of 2009. We conducted interviews at three time points to assess baseline health, water activities, and subsequent illness. Daily water samples were quantitatively assayed for phytoplankton cell count. Logistic regression models, adjusted for age and sex, were used to assess the association between exposure to three categories of phytoplankton concentration and subsequent illness.Results:During 26 study days, 15,726 individuals successfully completed all three interviews. Daily total phytoplankton cell counts ranged from 346 to 2,012 cells/mL (median, 712 cells/mL). The category with the highest (≥ 75th percentile) total phytoplankton cell count was associated with eye irritation [adjusted odds ratio (OR) = 1.30; 95% confidence interval (CI): 1.01, 1.66], rash (OR = 1.27; 95% CI: 1.02, 1.57), and earache (OR = 1.25; 95% CI: 0.88, 1.77). In phytoplankton group-specific analyses, the category with the highest Cyanobacteria counts was associated with respiratory illness (OR = 1.37; 95% CI: 1.12, 1.67), rash (OR = 1.32; 95% CI: 1.05, 1.66), eye irritation (OR = 1.25; 95% CI: 0.97, 1.62), and earache (OR = 1.35; 95% CI: 0.95, 1.93).Conclusions:We found associations between recreational exposure to marine phytoplankton and reports of eye irritation, respiratory illness, and rash. We also found that associations varied by phytoplankton group, with Cyanobacteria having the strongest and most consistent associations.Citation:Lin CJ, Wade TJ, Sams EA, Dufour AP, Chapman AD, Hilborn ED. 2016. A prospective study of marine phytoplankton and reported illness among recreational beachgoers in Puerto Rico, 2009. Environ Health Perspect 124:477–483; http://dx.doi.org/10.1289/ehp.1409558
Motor learning and synaptic plasticity in the cerebellum
Authors: Richard F. Thompson
Journal: Behavioral and Brain Sciences (1996)

For reasons I have never understood, some students of the cerebellum have been unwilling to accept the now overwhelming evidence that the cerebellum exhibits lasting synaptic plasticity and plays an essential role in some forms of learning and memory. With a few exceptions (e.g., target article by SIMPSON et al.) this is no longer the case, as is clear in the excellent target articles on cerebellar LTD and the excellent target review by HOUK et al. [CRÉPEL et al.; HOUR et al.; KANO; LINDEN; SIMPSON et al.; SMITH; VINCENT]
Abstract 587: A novel non-COX-inhibitory sulindac derivative induces autophagic cell death by inhibiting Akt signaling in lung cancer cells.
Authors: Evrim Gurpinar, William E. Grizzle, John J. Shacka, Nan Li, Adam B. Keeton, Gary A. Piazza
Journal: Cancer Research (2013)

Abstract Nonsteroidal anti-inflammatory drugs (NSAIDs) such as sulindac sulfide (SS) have shown promising antineoplastic activity in multiple tumor types, but toxicities resulting from cyclooxygenase (COX) inhibition limit their chronic use for chemoprevention. We recently described a N,N-dimethylethyl amine derivative of SS referred to as sulindac sulfide amide (SSA) that does not inhibit COX-1 or -2, yet displays potent tumor cell growth inhibitory activity. Here, we studied the basis for the growth inhibitory effects of SSA on human lung adenocarcinoma cell lines. SSA potently inhibited the growth of lung tumor cells with IC50 values of 2-5 μM compared with 44-52 μM for SS. SSA also suppressed DNA synthesis and caused a G0/G1 cell cycle arrest more potently than SS. SSA-induced cell death was associated with characteristics of autophagy, including an increase in acidic vesicular organelle content, elevation of the levels of LC3-II, and an increase in autophagic flux. siRNA knockdown of Atg7 attenuated SSA-induced autophagy and cell death. Surface exposure of phosphatidylserine, cleavage of caspases 3 and 7, as well as PARP were detectable with SSA treatment, although the pan-caspase inhibitor, ZVAD was not able to rescue viability. SSA treatment also inhibited Akt/mTOR signaling and the expression of downstream proteins that are regulated by this pathway. Overexpression of a constitutively active form of Akt was able to reduce autophagy markers and confer resistance to SSA-induced cell death. Our findings provide evidence that SSA induces autophagic cell death in lung cancer cell lines by suppressing Akt/mTOR signaling. This unique mechanism of action along with its increased potency and lack of cyclooxygenase inhibition support the development of SSA or related analogs for the prevention and/or treatment of lung cancer. Funding provided by NIH/NCI grants CA131378 and CA148817. Citation Format: Evrim Gurpinar, William E. Grizzle, John J. Shacka, Nan Li, Adam B. Keeton, Gary A. Piazza. A novel non-COX-inhibitory sulindac derivative induces autophagic cell death by inhibiting Akt signaling in lung cancer cells. [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 587. doi:10.1158/1538-7445.AM2013-587
Increased Costs and Rates of Use in the California Workers' Compensation System as a Result of Self-Referral by Physicians
Authors: Alex Swedlow, Gregory Johnson, Neil Smithline, Arnold Milstein
Journal: New England Journal of Medicine (1992)

There is widespread concern that ownership by physicians of testing or treatment facilities to which they refer patients leads to overuse of such facilities. We determined the patterns of use of three services--physical therapy, psychiatric evaluation, and magnetic resonance imaging (MRI)--among physicians treating patients whose care was covered under workers' compensation. We then compared the rates of use among physicians who referred patients to facilities of which they were owners (self-referral group) with the rates among physicians who referred patients to independent facilities (independent-referral group).We used a large data base to analyze claims under workers' compensation in California from October 1, 1990, through June 30, 1991, to determine the frequency and cost of these three selected services and determined whether the referring physicians were practicing self-referral or independent referral. We evaluated the cost per case for all three services, measured the frequency with which physical therapy was initiated, and evaluated the medical appropriateness of MRI.We found that physical therapy was initiated 2.3 times more often by the physicians in the self-referral group (68 percent) than by those in the independent-referral group (30 percent; P < 0.01). The mean cost per case for physical therapy was significantly lower in the self-referral group ($404 +/- 102) than in the independent-referral group ($440 +/- 167; P < 0.01). The mean cost of psychiatric evaluation services was significantly higher in the self-referral group than in the independent-referral group (psychometric testing, $1,165 +/- 728 vs. $870 +/- 482; P < 0.01, psychiatric evaluation reports, $2,056 +/- 1,063 vs. $1,680 +/- 578; P < 0.01). The total cost per case of psychiatric evaluation services was 26.3 percent higher in the self-referral group ($3,222 +/- 1,451) than in the independent-referral group ($2,550 +/- 742; P < 0.01). Of all the MRI scans requested by the self-referring physicians, 38 percent were found to be medically inappropriate, as compared with 28 percent of those requested by physicians in the independent-referral group (P < 0.05). There was no significant difference in the cost per case between the two groups.This study demonstrates that self-referral increases the cost of medical care covered by workers' compensation for each of the three types of service studied.
Detection of the WT1 transcript by RT-PCR in complete remission has no prognostic relevance in de novo acute myeloid leukemia
Authors: A Gaiger, D Schmid, G Heinze, B Linnerth, H Greinix, P Kalhs, K Tisljar, S Priglinger, K Laczika, M Mitterbauer, M Novak, G Mitterbauer, C Mannhalter, OA Haas, K Lechner, U Jäger
Journal: Leukemia (1998)
P182 VIRAL PARTICLES CONTAINING HBVRNA ARE PRESENT IN PLASMA BEFORE AND DURING NUCLEOS(T)IDE ANALOGUE TREATMENT OF CHRONIC HEPATITIS B PATIENTS
Authors: L. Jansen, K.A. van Dort, N.A. Kootstra, H.W. Reesink, H.L. Zaaijer
Journal: Journal of Hepatology (2014)
LIGADURA ENDOSCOPICA CON BANDAS COMO TRATAMIENTO ALTERNATIVO DE LAS ECTASIAS VASCULARES ANTRALES
Authors: A Rincon, JM Alcívar, R León, S Sobrino, JA Caballero, TJ López, JM Bozada
Journal: Endoscopy (2014)

Introducción: Las ectasias vasculares antrales (GAVE) son un causa infrecuente de sangrado gastrointestinal. El tratamiento endoscópico tradicional se basa en coagulación con argón plasma (APC). Recientemente se han publicado trabajos sobre la ligadura endoscópica con bandas (LEB) como alternativa al tratamiento convencional.
Abstract 1990: GNMT activates mTOR/Raptor signaling and delays G2/M progression through interacting with DEPTOR
Authors: Chia-hung Yen, Yao-Cheng Lu, Chung-Hsien Li, Cheng-Ming Lee, Chia-Yen Chen, Ming-Yuan Cheng, Shiu-Feng Huang, Yan-Hwa Wu Lee, Yi-Ming A. Chen
Journal: Cancer Research (2011)

Abstract GNMT is a tumor suppressor for hepatocellular carcinoma (HCC). We found that DEPTOR, a novel mTOR binding protein, interacts with GNMT through its PDZ domain. DEPTOR expression is significantly increased in HCC, especially among patients with HCV infection. Loss of DEPTOR in HuH-7 cells activates S6K but reduces Akt activation and cell growth. DEPTOR overexpression activates Akt and extends survival of HCC cells. Overexpression of GNMT counteracts DEPTOR induced Akt activation and activates mTORC1 downstream signaling via disruption of the DEPTOR-mTOR interaction. Moreover, GNMT overexpression delays G2/M progression, which causes senescence and slows proliferation of HuH-7 cells, sensitizing them to rapamycin. We suggest that GNMT by interacting with DEPTOR regulates the cellular homeostasis of hepatocytes through modulation of Akt/mTORC1 signaling. 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 1990. doi:10.1158/1538-7445.AM2011-1990
Ubiquitous Heat Shock Proteins Deal With Stress, Cancer
Authors: L. Seachrist
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Ubiquitous Heat Shock Proteins Deal With Stress, Cancer Get access Lisa Seachrist Lisa Seachrist Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 19, 6 October 1993, Pages 1551–1552, https://doi.org/10.1093/jnci/85.19.1551 Published: 06 October 1993
Universal Hepatitis B Vaccination in Taiwan and the Incidence of Hepatocellular Carcinoma in Children
Authors: Mei-Hwei Chang, Chien-Jen Chen, Mei-Shu Lai, Hsu-Mei Hsu, Tzee-Chung Wu, Man-Shan Kong, Der-Cherng Liang, Wen-Yi Shau, Ding-Shinn Chen
Journal: New England Journal of Medicine (1997)

A nationwide hepatitis B vaccination program was implemented in Taiwan in July 1984. To assess the effect of the program on the development of hepatocellular carcinoma, we studied the incidence of this cancer in children in Taiwan from 1981 to 1994.
Natural History, Diagnostic Approaches, and Therapeutic Strategies for Patients With Asymptomatic Severe Aortic Stenosis
Authors: Philippe Généreux, Gregg W. Stone, Patrick T. O’Gara, Guillaume Marquis-Gravel, Björn Redfors, Gennaro Giustino, Philippe Pibarot, Jeroen J. Bax, Robert O. Bonow, Martin B. Leon
Journal: Journal of the American College of Cardiology (2016)
Abstract 5552: Manganese porphyrins in combination with ascorbate act as pro-oxidants and mediate caspase-independent cancer cell death.
Authors: Myron Evans, Artak Tovmasyan, Ines Batinic-Haberle, Gayathri Devi
Journal: Cancer Research (2013)

Abstract Resistance to therapy-mediated apoptosis in inflammatory breast cancer (IBC), an aggressive and distinct subtype of breast cancer was recently attributed to increased antioxidant expression (superoxide dismutase [SOD]; reduced glutathione) and decreased accumulation of reactive oxygen species (ROS) resulting in redox adaptation and increased cell survival. Mn porphyrins (MnPs) are amongst the most potent synthetic mimics of the antioxidant, superoxide dismutase (SOD). In the present study, we demonstrate the unique ability of two Mn porphyrin (MnP)-based SOD mimics (MnTE-2-PyP5+ and MnTnBuOE-2-PyP5+) to act as pro-oxidants when combined with ascorbate (vitamin C) and enhance ROS-mediated cell death. We identified that the ethyl species, MnTE-2-PyP5+, was less stable than its butoxyethyl analog, MnTnBuOE-2-PyP5+, resulting in greater potency in inducing cytotoxicity via radical-driven oxidative degradation in cellular models of IBC isolated from patient tumors and an isogenic derivative with acquired resistance to therapeutic apoptosis. The combination of MnP and ascorbate induced accumulation of mitochondrial superoxide and H2O2-derived radicals in both therapy-sensitive and therapy-resistant cell lines. High intracellular ROS resulted in decreases in both pro-survival signaling (pNF-κB, pERK1/2) and expression of X-linked inhibitor of apoptosis protein (XIAP), the most potent caspase inhibitor. Although markers of classical apoptosis were observed, including PARP cleavage and Annexin V staining, administration of a pan-caspase inhibitor (QVD-OPh) did not reverse the observed cytotoxicity. Nuclear translocation of apoptosis inducing factor (AIF) was observed, suggesting a caspase-independent cell death following mitochondrial outer membrane permeabilization after treatment with this combination. In conclusion, this study provides the molecular basis of a novel MnP-based anti-cancer strategy and suggests the feasibility of using MnPs to sensitize cancer cells to many chemotherapies and radiotherapy that are dependent on potent induction of the oxidative stress response. Citation Format: Myron Evans, Artak Tovmasyan, Ines Batinic-Haberle, Gayathri Devi. Manganese porphyrins in combination with ascorbate act as pro-oxidants and mediate caspase-independent cancer cell death. [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 5552. doi:10.1158/1538-7445.AM2013-5552 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Risk of Second Cancers after Treatment for Hodgkin's Disease
Authors: M A Tucker, C N Coleman, R S Cox, A Varghese, S A Rosenberg
Journal: New England Journal of Medicine (1988)

We estimated the risk of second cancers among 1507 patients with Hodgkin's disease treated at Stanford University Medical Center since 1968. Eight-three second cancers occurred more than one year after diagnosis, as compared with 15.9 expected on the basis of rates in the general population (relative risk, 5.2; 95 percent confidence interval, 4.2 to 6.5). The mean (+/- SE) 15-year actuarial risk of all second cancers was 17.6 +/- 3.1 percent, of which 13.2 +/- 3.1 percent was due to solid tumors. The risk of leukemia appeared to reach a plateau level of 3.3 +/- 0.6 percent at 10 years, whereas non-Hodgkin's lymphoma continued to increase, to 1.6 +/- 0.7 percent by the end of the follow-up period. The risk of solid tumors did not vary significantly according to treatment category, with the array of neoplasms resembling that previously observed in populations exposed to radiation and in immunosuppressed groups. The risk of leukemia, although elevated after radiation therapy alone (relative risk, 11; 95 percent confidence interval, 1.2 to 38), was much higher after either adjuvant chemotherapy (relative risk, 117; 95 percent confidence interval, 69 to 185) or chemotherapy alone (relative risk, 130; 95 percent confidence interval, 26 to 380). These data suggest that the risk of solid tumors after therapy for Hodgkin's disease continues to increase with time.
An Adenovirus with Enhanced Infectivity Mediates Molecular Chemotherapy of Ovarian Cancer Cells and Allows Imaging of Gene Expression
Authors: Akseli Hemminki, Natalya Belousova, Kurt R. Zinn, Bin Liu, Minghui Wang, Tandra R. Chaudhuri, Buck E. Rogers, Donald J. Buchsbaum, Gene P. Siegal, Mack N. Barnes, Jesus Gomez-Navarro, David T. Curiel, Ronald D. Alvarez
Journal: Molecular Therapy (2001)

The adenovirus (Ad) is a useful vector for cancer gene therapy due to its unparalleled gene transfer efficiency to dividing and quiescent cells. Primary cancer cells, however, often have highly variable or low levels of the requisite coxsackie-adenovirus receptor (CAR). Also, assessment of gene transfer and vector persistence has been logistically difficult in human clinical trials. We describe here two novel bicistronic adenoviral (Ad) vectors, AdTKSSTR and RGDTKSSTR, which contain the herpes simplex virus thymidine kinase gene (TK) for molecular chemotherapy and bystander effect. In addition, the viruses contain the human somatostatin receptor subtype-2 gene (SSTR2), the expression of which can be noninvasively imaged. We enhanced the infectivity of RGDTKSSTR by genetically incorporating the RGD-4C motif into the HI-loop of the fiber. This allows the virus to circumvent CAR deficiency by binding to αvβ3 and αvβ5 integrins, which are highly expressed on most ovarian cancers. The expanded tropism of RGDTKSSTR results in increased infectivity of purified primary ovarian cancer cells and allows enhanced gene transfer in the presence of malignant ascites containing anti-Ad antibodies. RGDTKSSTR may be a useful agent for treating ovarian cancer in clinical trials.
Abstract 2002: Prevention of gastric cancers induced by <i>Helicobacter pylori</i> infection with a DNA demethylating reagent, 5-aza-2′-deoxycytidine
Authors: Tohru Niwa, Takeshi Toyoda, Tetsuya Tsukamoto, Akiko Mori, Masae Tatematsu, Toshikazu Ushijima
Journal: Cancer Research (2011)

Abstract Aberrant DNA methylation is deeply involved in carcinogenesis, and Helicobacter pylori infection, a Group-I carcinogen according to IARC classification, is known to induce aberrant methylation in gastric epithelial cells. Therefore, it is likely that methylation induction is the major mechanism by which H. pylori infection induces gastric cancers. In this study, using a Mongolian gerbil model, we aimed to clarify whether a DNA demethylating reagent, 5-aza-2′-deoxycytidine (5-aza-dC), can prevent H. pylori-induced gastric cancers. Administration of N-methyl-N-nitrosourea (20 p.p.m. by drinking water from 5 to 25 weeks of age) and H. pylori infection (∼108 CFU, at 5 weeks of age) induced gastric cancers in 55.2% of the gerbils at 55 weeks of age. By intraperitoneal infection of 5-aza-dC (0.125 mg/kg body weight, twice a week from 5 to 55 weeks of age), the incidence decreased significantly to 23.3% (P&amp;lt;0.05). Methylation levels of two CpG islands in gastric epithelial cells decreased to 46-69% of those of the infected gerbils without 5-aza-dC treatment (P&amp;lt;0.05). Also, the global methylation level decreased from 83.0% to 80.3% by 5-aza-dC as measured by luminometric methylation assay (P&amp;lt;0.05). At the same time, 5-aza-dC treatment tended to reduce expression of inflammation-related genes (Il1b and Nos2) in the stomach, suggesting that 5-aza-dC treatment can also modulate inflammatory responses. These results showed that H. pylori infection-induced gastric cancers could be suppressed by 5-aza-dC, and suggested that inhibition of methylation induction and/or immunomodulation by 5-aza-dC were the mechanisms of the suppression. Suppression of epigenetic alterations is a promising target for cancer prevention. 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 2002. doi:10.1158/1538-7445.AM2011-2002
Instruments for the Functional Assessment of Older Patients
Authors: Jane F. Desforges, William B. Applegate, John P. Blass, T. Franklin Williams
Journal: New England Journal of Medicine (1990)

COMPREHENSIVE functional assessment of elderly patients in clinical settings is becoming essential for optimal clinical management.1 Frail elderly patients present with multiple interrelated problems, some of which often go undetected.2 Comprehensive assessment cuts across disease categories, addressing physical, cognitive, emotional, and social function.3 Many of these problems can be detected by thorough history-taking and physical examination. Others, however, may fall outside the traditional clinical evaluation and therefore receive little attention from physicians.4 , 5 Recent studies have underscored the importance of focusing on functional status in assessing patients and predicting outcomes,6 , 7 and structured assessments can easily complement the standard clinical evaluation.4 , 8 , 9 The . . .
Comments on "Analysis of systolic bulging: mechanical characteristics of acutely ischemic myocardium in the conscious dog".
Authors: R M Norris, M A Brown, M Takayama
Journal: Circulation Research (1987)

Dr. Akaishi and colleagues have provided valuable data on the relationship between systolic bulging and loading conditions in experimental myocardial ischemia.However, there are two aspects of their paper that we think merit further discussion.In our own (unpublished) experiments, we have found that the magnitude of systolic bulge of severely ischemic myocardial segments in open-chest anesthetized dogs declines by about 50%, compared with the extent of bulging immediately after coronary artery ligation, over approximately 90 minutes.We attribute this to gradual reduction in compliance of the infarcting tissue.'In the experiments of Akaishi et al, unloading (venesection) always preceded loading (infusion) by a time that is not stated but must have exceeded 30 minutes because infusion was given over this time.Thus, it is possible that the reduction in bulge that the authors found after infusion was due in part to time-dependent fall in compliance after coronary artery ligation.Our second criticism concerns the acceptance by the authors on the basis of their data that shortening of the ischemic myocardial segment that occurs after ejection is a purely passive phenomenon.We agree that the exponential downstroke of the tension-length loop, which is superimposed on the upstroke and does not vary with loading, suggests that shortening during isovolumic relaxation (late systolic shortening) is passive.But shortening continues after mitral valve opening (shown in Figure 1 of the paper of Akaishi and colleagues), and therefore must extend into the phase of ventricular filling (postsystolic shortening).Shortening of ischemic segments during early ventricular fill ing has been described in the intact human ventricle. 2Moreover, late systolic shortening is a well-recognized phenomenon in isolated papillary muscle and occurs both during and after ischemia. 3-4 The cause of postsystolic shortening is unknown, but could be active (delayed relaxation) or passive (elastic recoil).However, the presence of latent contractile function in severely ischemic myocardium' suggests that an active process may exist.We think that it would be premature, on the basis of the data submitted by Akaishi et al, to conclude that al 1 of the shortening of severely ischemic myocardium is a completely passive phenomenon.