tbuckley/cabot-search huggingface dataset:
Depressive symptoms and the self-reported use of alcohol, caffeine, and carbohydrates in normal volunteers and four groups of psychiatric outpatients
Authors: E Leibenluft, P L Fiero, J J Bartko, D E Moul, N E Rosenthal
Journal: American Journal of Psychiatry (1993)

The authors examined the relationship between depressive symptoms and the self-reported use of alcohol, carbohydrates, and caffeine in normal volunteers and four groups of psychiatric outpatients.Outpatients and normal volunteers were given a questionnaire asking about their use of each of the three substances in response to each of the 14 depressive symptoms on the Hamilton Rating Scale for Depression. They also rated how much each substance improved each symptom. Twenty-six normal volunteers, 35 patients with major depression, 117 patients with seasonal affective disorder, 16 patients with alcohol dependence, and 24 patients with comorbid primary depression and secondary alcohol dependence completed the questionnaire. Test-retest reliability was established. Analysis of variance and stepwise multivariate discriminant function analyses were used to determine if diagnostic groups differed in the reported use and effect of each of the three substances.The responses concerning use and effect of alcohol of patients with alcohol dependence with or without depression were indistinguishable from each other. The responses of the patient groups regarding caffeine and carbohydrate use did not differ from each other, but all differed significantly from the responses of normal volunteers. Discriminant function analysis distinguished alcoholics from nonalcoholics in the relationship between drinking and the symptoms of anger and anhedonia.The relationship between symptoms and substance use varied depending on the substance. Alcoholics without depression were as likely to report drinking in response to depressive symptoms as were those who had had depression. Patients of all diagnostic groups were more likely than normal volunteers to report using caffeine and carbohydrates in response to depressive symptoms.
Abstract 14980: ADAMTS1 Play Roles In Endothelial Cell Apoptosis
Authors: Satoshi Hirohata, Masanari Obika, Faruk Hatipoglu, Kunihiko Hatanaka, Toru Miyoshi, Hiroko Ogawa, Kaori Sakamoto, Mehmet Z Cilek, Junko Inagaki, Hiroshi Ito, Shozo Kusachi, Yoshifumi Ninomiya
Journal: Circulation (2011)

Background:  We have previously reported that ADAMTS1 (A disintegrin and metalloprotease with thrombospondin motifs), a member of the metalloproteinase family, acts as anti-angiogenic molecule. This inhibitory effect has been explained by its protease activity including the proteolysis of thrombospondin-1 (TSP-1). The aim of this study was to clarify the biological role of ADAMTS1 on endothelial cells.   Methods:  We produced ADAMTS1 deficient mice (ADAMTS1 KO mice) and aortic endothelial cells were isolated from ADAMTS1 KO mice and wild type mice. We examined the effect on endothelial cell apoptosis by stimulation with tumor necrosis factor-alpha (TNF-α) and ADAMTS1 expression levels were examined by quantitative real-time RT-PCR. We next examined the mRNA expressions of apoptosis-related genes Bax and Bcl-2 in TNF-α-stimulated endothelial cells. Finally, we examined the effect of adenoviral gene transfer of ADAMTS1 on endothelial cells with two constructs, full length of ADAMTS1 and protease domain-truncated ADAMTS1.   Results:  In the wild type endothelial cells, endogenous ADAMTS1 was increased approximately 5-fold by TNF-α stimulation after 24 hrs, while endothelial cells derived from ADAMTS1 KO mice did not produce any ADAMTS1. MTT assay revealed that ADAMTS deficient cell were more viable under TNF-α stimulation. Bax mRNA levels were significantly attenuated in the ADAMTS1 deficient endothelial cells. Adenoviral gene transfer of ADAMTS1 in HUVEC demonstrated that ADAMTS1 overexpression enhanced endothelial cell apoptosis via a protease-independent mechanism. Taken together, we found that the novel inhibitory mechanism of ADAMTS1 on endothelial cells that was mediated in a protease-independent manner.   Conclusion:  ADAMTS1 play roles in endothelial cell apoptosis.
Abstract P263: The Associations of Epithelial Sodium Channel Genes with Blood Pressure Changes and Hypertension Incidence: the GenSalt Study
Authors: Tanika N Kelly, Xueli Yang, Dabeeru C Rao, Dongfeng Gu, James E Hixson, Treva K Rice, Depei Liu, Lawrence C Shimmin, Jiang He
Journal: Circulation (2014)

We examined the associations of common variants in ENaC genes with BP changes and hypertension incidence in a longitudinal family study. A total of 2755 Han Chinese participants of the Genetic Epidemiology Network of Salt Sensitivity (GenSalt) baseline examination were eligible for the current study. The average of nine BP measurements obtained using a random-zero sphygmomanometer at the baseline and each of two follow-up visits were used for the current analysis. The associations of 43 tag-SNPs in ENaC genes with BP changes and hypertension incidence were assessed using mixed models to account for the correlations of repeated measures among individuals and within families. A genotype by time interaction term was used to model differences in BP change according to genotype over time. The false discovery rate (FDR) method was used to adjust for multiple testing. During an average of 7.4 years follow-up, systolic BP (SBP) and diastolic BP (DBP) increased, and approximately 33% of participants developed hypertension. Multiple variants in ENaC genes were significantly associated with longitudinal changes in SBP after adjustment for multiple testing, including SCNN1A SNP rs11064153 ( P interaction = 5.8х10 -4 ; FDR-Q = 0.01); SCNN1G SNPs rs4299163 ( P interaction = 0.011; FDR-Q = 0.05) and rs4401050 ( P interaction = 0.001; FDR-Q = 0.01); and SCNN1B SNP rs1004749 ( P interaction = 0.006; FDR-Q = 0.03). Similar but not significant trends were observed for the associations between both rs11064153 and rs4401050 and DBP changes ( P interaction = 0.024 and 0.005, respectively; FDR-Q = 0.41 and 0.17, respectively) and between rs11604153 and hypertension incidence ( P = 0.017; FDR-Q = 0.19). Our findings indicate that ENaC genes may contribute to longitudinal BP changes in the Han Chinese population. Replication of these findings is warranted.
Abstract 19842: Microvascular Dysfunction in Patients with ST-Elevation Myocardial Infarction after Primary Percutaneous Coronary Intervention: No Sex Disparity
Authors: Annie Y Chou, Graham C Wong, Min S Gao, Julie Park, Carolyn M Taylor, Krishnan Ramanathan
Journal: Circulation (2014)

Background: Microvascular dysfunction is highly prevalent in women and presumed secondary to hormonal fluctuations, increased vascular tone, and endothelial dysfunction. Its contribution has never been examined in the acute setting. Patients with ST-elevation myocardial infarction (STEMI) with persistent ST-elevation (ST-E) post successful primary percutaneous coronary intervention (PPCI) are at risk of in-hospital cardiac events. We used ST-E recovery on ECGs pre and post PPCI to study potential sex differences in microvascular dysfunction, in conjunction with cardiac events in a STEMI population. Methods: Retrospective analysis was conducted on consecutive STEMI patients undergoing PPCI in Vancouver between May 2007 and September 2010 with evaluable ECGs pre and post PPCI. Patients with bundle branch block were excluded. Quantification of ST-E in each lead was done by electronic calipers by investigators blinded to clinical outcomes. Univariate analysis was performed by sex, for the association between ST-E recovery in the lead with maximal ST-E and the composite of in-hospital mortality, heart failure, cardiogenic shock, and reinfarction. Results: Of our 413 patients, 23% were women. In comparing baseline characteristics, age was significantly different (mean age of females = 72 vs. males = 61, p&lt;0.001). More female than male patients had incomplete (&lt;50%) ST-E recovery (20.6% vs. 12.7%, p=0.052). Women with incomplete recovery had an odds ratio of 2.3 for the primary outcome, compared with 1.4 in men, which was not statistically significant between sex. The primary outcome occurred more often in women (29.9% vs. 18.0%, p=0.012), but after adjusting for age, sex difference was no longer significant. Conclusions: Female STEMI patients are older, had more incomplete ST-E recovery after PPCI and had more in-hospital cardiac events, although significance was lost after adjusting for age. The higher prevalence of microvascular dysfunction in stable women may not be a large contributor of persistent ST-E in the acute setting. The higher incidence of incomplete ST-elevation in women may be attributable to the increasing prevalence of endothelial dysfunction with age. This novel interaction should be further examined with objective measures.
Monocytic delivery of therapeutic oxygen bubbles for dual-modality treatment of tumor hypoxia
Authors: Wen-Chia Huang, Ming-Yin Shen, Hsin-Hung Chen, Sung-Chyr Lin, Wen-Hsuan Chiang, Pei-Hsuan Wu, Chien-Wen Chang, Chi-Shiun Chiang, Hsin-Cheng Chiu
Journal: Journal of Controlled Release (2015)
Blocking Platelet-Derived Growth Factor-D/Platelet-Derived Growth Factor Receptor β Signaling Inhibits Human Renal Cell Carcinoma Progression in an Orthotopic Mouse Model
Authors: Lei Xu, Ricky Tong, David M. Cochran, Rakesh K. Jain
Journal: Cancer Research (2005)

Renal cell carcinoma is a highly malignant and often fatal disease of the kidney. It is difficult to treat, often because metastases are common at the time of presentation. Platelet-derived growth factor-D (PDGF-D) is a newly discovered member of the PDGF family; its function in tumor progression is largely unknown. Here, we examined the expression level of PDGF-D in human renal cell carcinoma by immunohistochemical staining using tissue arrays. We showed that human renal cell carcinoma expresses high levels of PDGF-D protein. The human renal cell carcinoma cell line SN12-C was stably transfected with pdgf-d cDNA. Overexpression of PDGF-D in SN12-C cells promoted tumor growth, angiogenesis, and metastasis of human renal cell carcinoma in an orthotopic severe combined immunodeficient (SCID) mouse model. PDGF-D overproduction in SN12-C cells increased the proliferation and migration of mural cells in vitro and improved perivascular cell coverage in vivo. Overexpression of PDGF-D led to increased expression of angiopoietin-1 and matrix metalloproteinase-9 in tumor tissues. ShRNAi and Gleevec were used to block PDGF-D expression and PDGF receptor beta (PDGFRbeta) signaling. Inhibition of PDGF-D expression by short hairpin RNA interference (shRNAi) and blockage of PDGFRbeta signaling by Gleevec inhibited the growth and lung metastasis of SN12-C cells grown orthotopically in SCID mice. Thus, PDGF-D is a potential candidate for controlling the progression of metastatic renal cell carcinoma. This opens up an avenue of investigation into novel therapeutic strategies for the treatment of renal cell carcinoma, including the use of recently developed tyrosine kinase inhibitors, such as Gleevec, which inhibit PDGF activity through inhibition of its receptor tyrosine kinase.
Levels and function of regulatory T cells in patients with polymorphic light eruption: relation to photohardening
Authors: N. Schweintzger, A. Gruber‐Wackernagel, E. Reginato, I. Bambach, F. Quehenberger, S.N. Byrne, P. Wolf
Journal: British Journal of Dermatology (2015)

We hypothesized that regulatory T cells (Tregs) are involved in the immunological abnormalities seen in patients with polymorphic light eruption (PLE). To investigate the number and suppressive function of peripheral Tregs in patients with PLE compared with healthy controls. Blood sampling was done in 30 patients with PLE [seeking or not seeking 311‐nm ultraviolet (UV)B photohardening] as well as 19 healthy controls at two time points: TP1, March to June (before phototherapy); and TP2, May to August (after phototherapy). We compared the number of CD4+CD25highCD127−FoxP3+ Tregs by flow cytometry and their function by assessing FoxP3 mRNA levels and effector T cell/Treg suppression assays. Tregs isolated from healthy controls significantly suppressed the proliferation of effector T cells at TP1 by 68% (P =0·0156). In contrast, Tregs from patients with PLE entirely lacked the capacity to suppress effector T‐cell proliferation at that time point. The medical photohardening seen in 23 patients with PLE resulted in a significant increase in the median percentage of circulating Tregs [both as a proportion of all lymphocytes; 65 6% increase (P =0·0049), and as a proportion of CD4+ T cells; 32.5% increase (P =0·0049)]. This was accompanied by an increase in the expression of FoxP3 mRNA (P =0·0083) and relative immunosuppressive function of Tregs (P =0·083) comparing the two time points in representative subsets of patients with healthy controls tested. Seven patients with PLE not receiving 311‐nm UVB also exhibited an increase in the number of Tregs but this was not statistically significant. No significant differences in Treg numbers were observed in healthy subjects between the two time points. An impaired Treg function is likely to play a role in PLE pathogenesis. A UV‐induced increase in the number of Tregs (either naturally or therapeutically) may be a compensatory mechanism by which the immune system counteracts the susceptibility to PLE.
Immigrant Women's Health
Authors: Meadows Lm, Thurston We, Melton C
Journal: JAMA (2000)

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Abstract 3874: Age Associated Responsiveness to Allogeneic Mesenchymal Stem Cell (MSC) Transplantation After Ischemia-Reperfusion (IR) in Rats
Authors: Rosemeire M Takeuchi, Lauro M Takeuchi, Michael Hurtado, Savannah Moon, Ian McNiece, Qinghua Hu, Joshua M Hare
Journal: Circulation (2009)

Background It is increasingly appreciated that host factors play crucial roles in the responsiveness to cell therapy for ischemic heart disease. We tested the hypothesis that advanced age would imp...
Abstract 2800: Immunotherapy of malignant pleural mesothelioma using MET specific t – cells
Authors: Thivyan Thayaparan, Sjoukje v.d Stegen, Ana C. Parente Pereira, Roseanna Petrovic, James Spicer, John Maher
Journal: Cancer Research (2014)

Abstract Background: Malignant pleural mesothelioma (MPM) is an incurable cancer predominantly induced by asbestos exposure. This aggressive tumor commonly presents at an advanced stage of disease. Although surgery, combination chemotherapy and radiotherapy may be used in disease management, median survival from diagnosis is less than 12 months. New therapeutic approaches are required to improve outcome in this disease. Chimeric antigen receptors (CAR) are fusion molecules that couple the HLA-independent binding of a selected cell surface target antigen to the delivery of a tailored T-cell activating signal. Using CAR technology, we aim to develop a novel immunotherapy for MPM that is both safe and effective. These molecules are delivered to patient T-cells using retroviral gene transfer, thereby stably re-directing their specificity for antigen. The receptor tyrosine kinase MET is overexpressed in &amp;gt;80% of MPM patients making it an attractive candidate for CAR directed immunotherapy. Methods: Three MET-targeted peptide-binding motifs have been incorporated into a second generation CAR framework containing a fused CD28/CD3ζ endodomain. Functional assessment of MET-targeted CARs has been assessed by co-cultivation of genetically enhanced test and control T-cells with MPM cell lines that express MET at various levels. Results: In preliminary studies we have shown that human T-cells engineered to express MET CARs can destroy mesothelioma tumor cell monolayers, accompanied by T-cell proliferation and cytokine production. Xenograft models are currently under development using bioluminescence to further evaluate functionality and toxicity in vivo. Conclusions: These findings demonstrate proof of concept for the utility of CAR engineered T-cells to recognise and destroy MET-expressing MPM tumor cells. We envisage that regional i.e. intrapleural delivery of human CAR positive T-cells could be used to maximise therapeutic index of this approach. Citation Format: Thivyan Thayaparan, Sjoukje v.d Stegen, Ana C. Parente Pereira, Roseanna Petrovic, James Spicer, John Maher. Immunotherapy of malignant pleural mesothelioma using MET specific t – cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2800. doi:10.1158/1538-7445.AM2014-2800
Finer Structure of Hepatic, Intestinal and Renal Cells of the Mouse as Revealed by the Electron Microscope
Authors: Albert J. Dalton, Herbert Kahler, Mart Jo Striebich, Bolivar Lloyd
Journal: JNCI Journal of the National Cancer Institute (1950)

Journal Article Finer Structure of Hepatic, Intestinal and Renal Cells of the Mouse as Revealed by the Electron Microscope Get access Albert J. Dalton, Albert J. Dalton Search for other works by this author on: Oxford Academic PubMed Google Scholar Herbert Kahler, Herbert Kahler Search for other works by this author on: Oxford Academic PubMed Google Scholar Mart Jo Striebich, Mart Jo Striebich Search for other works by this author on: Oxford Academic PubMed Google Scholar Bolivar Lloyd Bolivar Lloyd National Cancer Institute, National Institutes of Health, U. S. Public Health Service, Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 11, Issue 2, October 1950, Pages 439–461, https://doi.org/10.1093/jnci/11.2.439 Published: 01 October 1950 Article history Received: 19 September 1950 Published: 01 October 1950
Retinoic acid enhances lactoferrin-induced IgA responses by increasing betaglycan expression
Authors: Jeong-Min Lee, Young-Saeng Jang, Bo-Ra Jin, Sun-Jin Kim, Hyeon-Jin Kim, Bo-Eun Kwon, Hyun-Jeong Ko, Sung-il Yoon, Geun-Shik Lee, Woan-Sub Kim, Goo-Young Seo, Pyeung-Hyeun Kim
Journal: Cellular and Molecular Immunology (2015)
The cisternae decorating the red blood cell membrane in congenital dyserythropoietic anemia (type II) originate from the endoplasmic reticulum
Authors: N Alloisio, P Texier, L Denoroy, C Berger, E Miraglia del Giudice, S Perrotta, A Iolascon, F Gilsanz, G Berger, J Guichard
Journal: Blood (1996)
Abstract 3586: Alcohol Consumption and One-Year Angina Risk After Myocardial Infarction
Authors: Donna M Buchanan, Surya Mundluru, James H O’Keefe, Kimberly J Reid, Fengmeng Tang, Nazeera Dawood, Eric D Peterson, John A Spertus
Journal: Circulation (2007)

Background: Prior studies show light to moderate alcohol use is associated with reduced mortality and cardiovascular events, whereas heavy use increases mortality and cardiovascular risks. The association of alcohol use and post-myocardial infarction (MI) symptoms is unknown. We explored the association between alcohol use and risk of having angina 1 year after an MI. Methods: Upon enrollment in the 19-center prospective PREMIER registry, acute MI patients (n=2481) were asked about alcohol use. Angina (any vs. none) was assessed at 1 year with the Seattle Angina Questionnaire. The association of alcohol use and 1-year angina was modeled using a hierarchical multivariable modified Poisson regression model. Results: Overall, 47% reported never drinking and others reported having the following # of drinks/day: 42% &lt; 1; 6% 1 to 2; 3% &gt; 2 to 4; 2% &gt; 4. After adjusting for demographic, clinical, and treatment variables, patients that reported never drinking were 45% more likely to have angina than moderate drinkers (1 to 2 drinks/day). However, &gt; drinks/day was associated with an 81% greater risk of angina than moderate alcohol use. Those drinking &lt; 1 drink/day or &gt; 2 to 4 per day had similar angina risk compared to moderate drinkers. Results did not vary by gender (p &gt; .05 for interaction). Conclusions: This study extends prior evidence of a dose-dependent relationship between alcohol use and other cardiovascular benefits/risks to post-MI angina. Moderate alcohol consumption (1 to 2 drinks/day) was associated with reduced risk of angina 1 year after MI compared to abstinence or heavy alcohol consumption. Excessive alcohol use (&gt;4 drinks/day) was associated with increased risk of angina.
Pharmacokinetic strategies to improve drug penetration and entrapment within solid tumors
Authors: Ahmed M. Al-Abd, Zekra K. Aljehani, Rana W. Gazzaz, Sarah H. Fakhri, Aisha H. Jabbad, Abdulrahman M. Alahdal, Vladimir P. Torchilin
Journal: Journal of Controlled Release (2015)