tbuckley/cabot-search huggingface dataset:
Circulating tumour-associated microparticles in liver cancer: a question of tumour diameter and volume?
Authors: S.K. Urban, M. Krawczyk, H. Julich-Haertel, A. Willms, W. Patkowski, B. Kruk, M. Krasnodebski, J. Ligocka, A. Klein, M. Casper, F. Lammert, P. Milkiewicz, M. Krawczyk, V. Lukacs-Kornek, M. Kornek
Journal: Journal of Hepatology (2017)
Cerium oxide nanoparticles display anti-tumoral activity and improve survival in experimental hepatocellular carcinoma
Authors: G. Fernandez-Varo, D. Oró, T. Yudina, S. Carvajal, S. Marfà, L. Boix, M. Perramón, L. Oller, G. Casals, M. Morales-Ruiz, P. Casado, P.R. Cutillas, J. Bruix, V. Puntes, W. Jiménez
Journal: Journal of Hepatology (2017)
Abstract 58: Dicarbonyl Stress and Diabetic Heart Failure: The Role of Endothelial Cells
Authors: Branka Vulesevic, Brian McNeill, Ferdinando Giacco, Michael Brownlee, Ross Milne, Erik Suuronen
Journal: Circulation Research (2015)

Dicarbonyl stress (DS) caused by the accumulation of α-oxoaldehyde metabolites, like methylglyoxal (MG), leads to detrimental DNA and protein modifications. Under normal conditions, MG is detoxified by glyoxalase-1 (GLO1) and -2 enzymes, but this system fails in diabetes. While the role of DS in diabetic cardiomyopathy through changes in cardiomyocyte function has been well described, this study aimed to link DS with the development of endothelial dysfunction (ED) and early heart failure in diabetes. Transgenic mice that over-express GLO1 in endothelial cells (ECs) but not in cardiomyocytes, and their wild-type (WT) littermates were treated with STZ to induce hyperglycemia (WT-diabetic and GLO1-diabetic mice) or vehicle (non-diabetic controls). Hyperglycemia increased the circulating levels of ED markers in WT-diabetic (E-selectin 1.5-fold, ICAM 1.4-fold, and VCAM 1.1-fold), but not GLO1-diabetic mice. The number of vWF+ ECs in WT-diabetic hearts was reduced 2-fold compared to other groups, whereas GLO1 over-expression preserved capillary density. Cell death, determined by TUNEL staining, was greater in the hearts of WT-diabetic mice compared to all other groups. GLO1 over-expression resulted in reduced inflammation: TNF-α protein expression was increased in both diabetic groups (≥2-fold), but significantly less so in GLO1-diabetic mice (p=0.03). The preservation of ECs in GLO1-diabetic mice was associated with delayed signs of heart failure. At 4wk of hyperglycemia, WT-diabetic mice had reduced heart function compared to all other groups (p=0.04). At 8wk, cardiac function in GLO-diabetic mice was greater than in WT-diabetic mice, but both were reduced compared to non-diabetic controls (p=0.02; p=0.4). A possible mechanism for EC survival in GLO1 mice despite the presence of inflammation was examined in vitro using human aortic ECs. ECs exposed to high glucose or MG for 24h had increased apoptosis induced by TNF-α compared to cells treated only with TNF-α (by 2- and 3-fold, respectively), suggesting that reduced MG protects ECs from TNF-α mediated death. Taken together, these results suggest that DS in diabetes increases inflammation and ED, leading to the loss of ECs in the heart, which contributes to the development of heart failure.
A Home-Based Intervention to Reduce Depressive Symptoms and Improve Quality of Life in Older African Americans
Authors: Laura N. Gitlin, Lynn Fields Harris, Megan C. McCoy, Nancy L. Chernett, Laura T. Pizzi, Eric Jutkowitz, Edward Hess, Walter W. Hauck
Journal: Annals of Internal Medicine (2013)

African Americans often have limited mental health care options because of system- or patient-level factors. This trial randomly assigned older African Americans with depressive symptoms to a home-...
Evaluation of ligand binding and preclinical pharmacokinetics of Hermodulins: A new class of bi-specific protein antagonists that trap most growth factors for the human EGF receptor (HER) family
Authors: Ying Feng, Malgorzata Beryt, Juan Zhang, Catherine Mastroieni, Jeffrey Higaki, Brett Jorgensen, Francis Lau, James Rozzelle, Peter Lindley, Xiaomei Bai, Jim Liu, Irene Ni, Daniel Maneval, H. Shepard, Pei Jin
Journal: Cancer Research (2008)

4076  Receptor tyrosine kinases such as members of the HER family are well-validated targets for cancer therapy. However, anti-cancer agents directed at only one HER family member often encounter endogenous or acquired resistance due to multiple HER co-activation or increased production of HER1 or HER3 ligands by tumor cells. To target multiple members of the HER family and block their function, we have developed a novel bi-specific HER1/HER3 heterodimeric ligand trap comprised of optimized HER1 and HER3 extracellular domains fused with the Fc portion of human IgG1. We investigated binding activities of a prototypic Hermodulin, RB200, using europium-labeled ligands to compare ligand binding affinities of RB200 with those of Hermodulin variants obtained via a high throughput rational mutagenesis process (optimized Hermodulins). Our data show that RB200 retains specific binding to various HER ligands, such as EGF, TGF-alpha, HB-EGF and neuregulin (NRG1-beta1) (Kd = 10 to 30 nM). Optimized Hermodulins have improved ligand binding affinities (Kd = 0.5 to 2 nM) for both HER1 and HER3 ligands with greater Bmax. We also developed a sensitive ELISA specific for Hermodulins, and studied the pharmacokinetics in rodent models in order to provide dosing strategies and interpret future studies evaluating the efficacy and tolerability of Hermodulins. RB200 was administered as a single iv or ip dose of 15-30 mg/kg in rats and mice, and plasma samples were analyzed via ELISA. RB200 exhibited high bioavailability, a low volume of distribution, and a prolonged terminal half-life consistent with expectations for Fc-fusion proteins and therapeutic monoclonal antibodies. Together these data suggest that Hermodulins act as bi-specific HER1/HER3 ligand traps and have desirable in vivo pharmacokinetic characteristics. These results support continued development of Hermodulins for cancer therapy.
Differential gender-related impact of PNPLA3 and CD14 polymorphism on the risk of developing alcoholic cirrhosis
Authors: M. Mischitelli, R. Mancina, F. Ferri, A. Farcomeni, A. Molinaro, A. Maffongelli, E. Poli, C. Rotondo, C. Codazzo, D. Galli, F. Attilia, M.L. Attilia, S. Romeo, S.G. Corradini
Journal: Journal of Hepatology (2017)
Identification of new biomarkers of leukocyte dysfunction by lipidomics in patients with acute-on-chronic liver failure
Authors: C. López-Vicario, A. Checa, J. Alcaraz-Quiles, E. Titos, M. Casulleras, R. Flores-Costa, M. Pavesi, M. Duran-Güell, R. Moreau, V. Arroyo, C.E. Wheelock, J. Claria
Journal: Journal of Hepatology (2017)
TET1 Promotes Leukemic Growth in T-ALL Via Maintenance of 5-Hydroxymethylation Marks and Can be Antagonized By the PARP Inhibitor Olaparib
Authors: Deniz Sahin, Shiva Bamezai, Fabio Ciccarone, Elena Fischbein, Fabian Mohr, Medhanie A. Mulaw, Alex Pulikkottil Jose, Paola Caiafa, Lüder-Hinrich Meyer, Klaus-Michael Debatin, Geertruy te Kronnie, Konstanze Döhner, Hartmut Döhner, Michaela Feuring-Buske, Christian Buske, Vijay P.S. Rawat
Journal: Blood (2016)
Direct acting antivirals did not increase early recurrences after curative treatment of HCV related hepatocellular carcinoma in comparison with IFN-based treatment
Authors: Y. Yasui, M. Kurosaki, W. Wang, M. Okada, Y. Kubota, T. Goto, Y. Komiyama, M. Higuchi, K. Takaura, T. Hayashi, H. Takada, N. Tamaki, K. Tsuchiya, H. Nakanishi, J. Itakura, N. Izumi
Journal: Journal of Hepatology (2017)
Abstract P150: Estrogen Protects Against and Reverses Adverse Ventricular Remodeling in Pulmonary Hypertension-Induced Right Ventricular Failure
Authors: Rangarajan D Nadadur, Soban Umar, Andrea Iorga, Humann Matori, Rod Partow-Navid, Mansoureh Eghbali
Journal: Circulation Research (2011)

Pulmonary hypertension (PH) leads to right-ventricular failure (RVF). RVF is characterized by adverse RV remodeling including hypertrophy and changes in the cardiac Extracellular Matrix (ECM) such as fibrosis and re-expression of cardiac fetal genes. Among the potentially re-expressed genes are the novel ECM interacting proteins Osteopontin (OPN) and Osteocalcin (OCN). Gender differences found in experimental PH are attributed to protective effects of Estrogen (E2). We hypothesize that gender differences observed in experimental PH are partially due to the effects of E2 on the cardiac ECM, and that exogenous E2 may be able to reverse adverse RV remodeling. Male and female rats received single monocrotaline (MCT, 60mg/kg) injection. Some rats were given E2 (42.5μg/kg/day) from day 21–30. Saline treated rats were controls. Cardiopulmonary hemodynamics were serially monitored and RV pressures (RVP) were recorded terminally. RV fibrosis was assessed by trichrome staining. Gene expression was determined by RT PCR and plasma OPN by ELISA. All rats developed PH by day 21 and RVF by day 30. Male rats developed more severe PH-induced RVF than females (RVP=70 vs. 41.5±5 mmHg; RV/(LV+IVS)= 0.69±0.07 vs. 0.47±0.04; RVEF = 30.4±1.8 vs. 42.8±2% resp., all p&lt;0.05). Males also revealed more severe RV fibrosis and greater re-expression of OPN (4.5 fold vs. females, p&lt;0.05) and OCN (2-fold vs. females, p&lt;0.05). Plasma OPN was also elevated in RVF males (1.00±0.11 in control to 1.47±0.18 pg/ml, p&lt;0.05) but not RVF females (0.848±0.18 in control to 0.859±0.294 pg/ml, p=ns). Since females experienced less severe RV remodeling than males, MCT injected males were treated with exogenous E2 from day 21–30. Some E2 treated male rats were sacrificed at day 30, and some were kept an additional 12 days after E2-withdrawal (E2-W group). E2 reversed PH-induced RVF (RVP=38mmHg; RV/(LV+IVS) = 0.28±0.03; RVEF=61.5±0.8%, all p&lt;0.05 vs. male RVF) and fibrosis. OPN and OCN were fully restored following E2 withdrawal by day 42. E2 therapy also restored circulating OPN levels (p&lt;0.05 vs. RVF) showing that OPN has potential value as a plasma marker for PH-induced RV failure. These results suggest that E2 protects against adverse RV remodeling in females, and reverses adverse RV remodeling in males.
Abstract 16673: Intramyocardial Injection of MSC-derived Extracellular Vesicles Confers Superior Cardiac Repair After a Reperfused Myocardial Infarction
Authors: Guangming Cheng, Anna Labedz-Maslowska, Dominika Berdecka, Yu-Ting Xuan, Anweshan Samanta, Magdy Girgis, Ou-Li Wang, Sylwia Kedracka-Krok, Arash Davani, Robert J Vincent, Yanjuan Yang, Elzbieta Karnas, Michal Sarna, Jeryl Hauptman, Zbigniew Madeja, Buddhadeb Dawn, Ewa Zuba-Surma
Journal: Circulation (2015)

Introduction: Stem cell-derived extracellular vesicles (EVs) are known to facilitate cell-to-cell communication. The potential of mesenchymal stem cell (MSC)-derived EVs for cardiac repair when compared with MSC whole cell injection remains unknown. Hypothesis: We hypothesized that therapy with MSC-EVs after a reperfused myocardial infarction (MI) will result in greater improvement in LV structure and function compared with injection of MSCs. Methods: EVs were collected by sequential centrifugation from culture supernatants of murine bone marrow MSCs. We used tunable resistive pulse sensing technology (TRPS), flow cytometry, real-time qRT-PCR and mass spectrometry to analyze MSC-EVs. Wild-type (C57BL/6) mice underwent a 30-min coronary occlusion followed by reperfusion, and 48 h later received intramyocardial injection of vehicle (PBS, n=14), MSCs (n=14), or MSC-EVs (n=14). Echocardiography was performed 4 d prior to MI (BSL) and at 48 h and 30 d after injection. Mice were sacrificed after 30 d. Results: MSC-EVs were noted to be small vesicles with average size of 233.0 ± 70.2 nm (Fig), and expressed MSC-specific markers, including CD29, CD90.2, CD105, Sca-1 and CD49e (Fig). MSC-EVs were enriched in mRNAs, miRNAs and proteins from donor MSCs; and carried transcripts of genes regulating cardiac/vascular differentiation, such as GATA-4, Nkx2.5, Tie-2, and GATA-2. In vivo, LV ejection fraction (EF) was significantly and similarly reduced in all groups at 48 h after MI (Fig). At 30 d after MI, mice injected with MSC-EVs exhibited significantly higher EF (Fig) and smaller LV end-diastolic volume compared with vehicle-treated and MSC-injected mice. Conclusions: We conclude that MSC-EVs represent natural nanocarriers capable of transferring bioactive contents and inducing cardiac repair following intramyocardial injection after MI in vivo. The use of MSC-EVs may potentially improve the outcomes of cell therapy in humans.
Exercise capacity and exercise hemodynamics in the screening for pulmonary vascular disease (PVD) in patients with portal hypertension – results from a prospective cross-sectional study
Authors: P. Douschan, G. Kovacs, V. Stadlbauer, D. Kniepeiss, E. Krones, F. Durchschein, F. Rainer, W. Spindelböck, M. Wagner, G. Zollner, A. Avian, P. Fickert, A. Olschewski, H. Olschewski, R.E. Stauber
Journal: Journal of Hepatology (2017)
Transjugular intrahepatic portosystemic shunt: impact on systemic haemodynamics and renal and cardiac function in patients with cirrhosis
Authors: T.M. Busk, F. Bendtsen, J.H. Poulsen, J.O. Clemmesen, F.S. Larsen, J.P. Gøtze, J.S. Iversen, M.T. Jensen, R. Møgelvang, E.B. Pedersen, J.N. Bech, S. Møller
Journal: Journal of Hepatology (2017)
Have mortality improvements stalled in England?
Authors: Mark Fransham, Danny Dorling
Journal: BMJ (2017)

Same data—different stories

From 2014 to 2015 the number of deaths in England and Wales rose by 5.6% (by 28 000 to 530 000 in 2015), the largest percentage year on year increase since 1968.1 US life expectancy started to fall in 2016, which was attributed to declining access to healthcare for poorer Americans and wider societal factors.2 For middle aged Americans, death rates have not improved in almost 20 years, owing to “a lack of hope.”3

On 6 April 2017 the UK Office for National Statistics released an analysis of deaths in England from January 2001 to the end of December 2016.4 It said that fewer deaths were registered in 2016 (491 000) than in 2015 and that the death rate in 2016 (958.0 deaths per 100 000 population) was the second lowest since 2001. Life expectancy in 2016 was higher than in 2015, and the number of deaths in 2016 was lower than expected based on the average death rate between 2011 and 2015 (973.3 per 100 000). Death rates have fallen among people aged over 75 since 2001, by almost a …
Effects of metoprolol CR in patients with ischemic and dilated cardiomyopathy: The randomized evaluation of strategies for left ventricular dysfunction pilot study
Authors: M. White, S. Yusuf, R. S. McKelvie, D. Pericak, J. Young, R. Latini, J. Pogue, R. J. Burns, J. Probstfield, R. T. Tsuyuki, A. P. Maggioni, A Jr Avezum, J. L. Rouleau
Journal: Circulation (2000)
The Pathophysiologic Role of JunB in Multiple Myeloma Pathogenesis: Focus on Bone Marrow Angiogenesis
Authors: Stefano Malvestiti, Fengjuan Fan, Muhammad Hasan Bashari, Eugenio Morelli, Sonia Vallet, Martin Sattler, Latifa Bakiri, Anja Seckinger, Dirk Hose, Hartmut Goldschmidt, Inka Zörnig, Martin Pecherstorfer, Erwin Wagner, Pierfrancesco Tassone, Dirk Jäger, Klaus Podar
Journal: Blood (2016)
Telomerase activity: a valuable marker of hepatocelluar carcinoma development in cirrhotic hepatitis C patients
Authors: A.E.-D.M. Abdou, N.M. El-Habachi, A.F. El-Shayeb, A.R. Mansour, E. ElKhouly, A. Gowily, M.S. Zaghloul
Journal: Journal of Hepatology (2017)
The Conducted Vasomotor Response: Function, Biophysical Basis, and Pharmacological Control
Authors: Donald G. Welsh, Cam Ha T. Tran, Bjorn O. Hald, Maria Sancho
Journal: The Annual Review of Pharmacology and Toxicology (2017)

Arterial tone is coordinated among vessel segments to optimize nutrient transport and organ function. Coordinated vasomotor activity is remarkable to observe and depends on stimuli, sparsely generated in tissue, eliciting electrical responses that conduct lengthwise among electrically coupled vascular cells. The conducted response is the focus of this topical review, and in this regard, the authors highlight literature that advances an appreciation of functional significance, cellular mechanisms, and biophysical principles. Of particular note, this review stresses that conduction is enabled by a defined pattern of charge movement along the arterial wall as set by three key parameters (tissue structure, gap junctional resistivity, and ion channel activity). The impact of disease on conduction is carefully discussed, as are potential strategies to restore this key biological response and, along with it, the match of blood flow delivery with tissue energetic demand.
Next government must tackle public health “ticking time bomb,” says BMA
Authors: Jacqui Wise
Journal: BMJ (2017)

The BMA has called on politicians who form the next government to make tackling the crisis in public health a priority, with tighter regulation of the food and soft drinks industries, a minimum unit price on alcohol, and support for people to quit smoking.

The BMA warned of a “ticking time bomb” resulting from cuts to public health budgets and rising demand for services. It highlighted the government’s lack of commitment to deliver evidence based measures to improve public health—citing the watered down childhood …
Brigatinib in ALK+ NSCLC pts with intracranial CNS metastases in 2 clinical trials
Authors: M. Tiseo, R.M. Huber, M.J. Hochmair, L.A. Bazhenova, S.-H.I. Ou, W. Reichmann, J. Haney, D. Kerstein, D.R. Camidge, S.N. Gettinger
Journal: Annals of Oncology (2017)
Simple sugar consumption associated abnormal aminotransferase activity without intrahepatic fat: a cross sectional observational study
Authors: H.W. Oh, D.W. Jun, S.B. Ahn, W.K. Saeed, J.S. Lee, Y.J. Chae, J.Y. Jeong, H.T. Kang, J.H. Sohn, E.C. Jang, B.-K. Kang
Journal: Journal of Hepatology (2017)
Sarcoma Eradication by Doxorubicin and Targeted TNF Relies upon CD8+ T-cell Recognition of a Retroviral Antigen
Authors: Philipp Probst, Janine Kopp, Annette Oxenius, Mario P. Colombo, Danilo Ritz, Tim Fugmann, Dario Neri
Journal: Cancer Research (2017)

Antibody-cytokine complexes may offer new tools to treat cancer. Here, we show how TNF-linked antibodies, which recognize tumor-selective splice isoforms of fibronectin (F8-TNF), can be exploited to eradicate sarcomas in immunocompetent mice. We treated mice bearing WEHI-164 fibrosarcoma with a combination of F8-TNF and doxorubicin, curing the majority of treated animals (29/37). Notably, cured mice were resistant to rechallenge not only by WEHI-164 cells but also heterologous C51 or CT26 colorectal tumor cells in a CD8+ T-cell-dependent process. Mechanistic analyses revealed that each tumor cell line presented AH1, a common endogenous retroviral peptide. Numbers of AH1-specific CD8+ T cells exhibiting cytotoxic capacity were increased by F8-TNF plus doxorubicin treatment, arguing that cognate CD8+ T cells contributed to tumor eradication. Sequence analysis of T-cell receptors of CD8+ T cells revealed the presence of H-2Ld/AH1-specific T cells and an expansion of sequence diversity in treated mice. Overall, our findings provide evidence that retroviral genes contribute to tumoral immunosurveillance in a process that can be generally boosted by F8-TNF and doxorubicin treatment. Cancer Res; 77(13); 3644-54. ©2017 AACR.
Associations Between Short or Long Length of Stay and 30-Day Readmission and Mortality in Hospitalized Patients With Heart Failure
Authors: Maneesh Sud, Bing Yu, Harindra C. Wijeysundera, Peter C. Austin, Dennis T. Ko, Juarez Braga, Peter Cram, John A. Spertus, Michael Domanski, Douglas S. Lee
Journal: JACC Heart Failure (2017)

This study sought to examine the associations between heart failure (HF)-related hospital length of stay and 30-day readmissions and HF hospital length of stay and mortality rates. Although reducing HF readmission and mortality rates are health care priorities, how HF-related hospital length of stay affects these outcomes is not fully known. A population-level, multicenter cohort study of 58,230 patients with HF (age >65 years) was conducted in Ontario, Canada between April 1, 2003 and March 31, 2012. When length of stay was modeled as continuous variable, its association with the rate of cardiovascular readmission was nonlinear (p < 0.001 for nonlinearity) and U-shaped. When analyzed as a categorical variable, there was a higher rate of cardiovascular readmission for short (1 to 2 days; adjusted hazard ratio [HR]: 1.12; 95% confidence interval [CI]: 1.04 to 1.21; p = 0.003) and long (9 to 14 days; HR: 1.11; 95% CI: 1.04 to 1.19; p = 0.002) lengths of stay as compared with 5 to 6 days (reference). Hospital readmissions for HF demonstrated a similar nonlinear (p = 0.005 for nonlinearity) U-shaped relationship with increased rates for short (HR: 1.15; 95% CI: 1.04 to 1.27; p = 0.006) and long (HR: 1.14; 95% CI: 1.04 to 1.25; p = 0.004) lengths of stay. Noncardiovascular readmissions demonstrated increased rates with long (HR: 1.17; 95% CI: 1.07 to 1.29; p < 0.001) and decreased rates with short (HR: 0.87; 95% CI: 0.79 to 0.96; p = 0.006) lengths of stay (p = 0.53 for nonlinearity). The 30-day mortality risk was highest after a long length of stay (HR: 1.28; 95% CI: 1.14 to 1.43; p < 0.001). A short length of stay after hospitalization for HF is associated with increased rates of cardiovascular and HF readmissions but lower rates of noncardiovascular readmissions. A long length of stay is associated with increased rates of all types of readmission and mortality.
Whole-genome sequencing of patients achieving hepatitis B virus serum antigen loss following tenofovir disoproxil fumerate (TDF) and/or pegylated-interferon α-2a (PEG) therapy
Authors: S.E. Kleinstein, P. Marcellin, H.L. Chan, P.R. Shea, A. Gaggar, K. Kitrinos, B. Jump, G.M. Subramanian, J. Peterson, D.B. Goldstein
Journal: Journal of Hepatology (2017)
A phase I-II clinical trial to evaluate the safety, pharmacokinetics and efficacy of high dose intravenous ascorbic acid synergy with mEHT in Chinese patients with stage III-IV non-small cell lung cancer
Authors: J. Ou, X. Zhu, Y. Lu, C. Zhao, H. Zhang, X. Gui, X. Wang, X. Zhang, T. Zhang, C.L.K. Pang
Journal: Annals of Oncology (2017)
Inhibition of IL-1b/STAT3/β-catenin-dependent stimulation of the CXCL10/CXCR3 axis prevents macrophage recruitment and progression of the disease in Pkhd1del4/del4 mice, a model of congenital hepatic fibrosis
Authors: E. Kaffe, F. Pellegrino, V. Mariotti, L. Fabris, M. Cadamuro, M. Amenduni, R. Fiorotto, M. Strazzabosco, C. Spirli
Journal: Journal of Hepatology (2017)
Haemodynamically proven pulmonary hypertension in a patient with GATA2 deficiency-associated pulmonary alveolar proteinosis and fibrosis
Authors: Sébastien Sanges, Anne Prévotat, Marie Fertin, Louis Terriou, Guillaume Lefèvre, Bruno Quesnel, Pierre-Yves Hatron, Éric Hachulla, Marie-Christine Copin, David Launay
Journal: European Respiratory Journal (2017)

We read with great interest the article by Ballerie et al. [1], which describes the occurrence of pulmonary alveolar proteinosis and fibrosis in a patient with GATA2 deficiency. Interestingly, our team recently managed a similar case, in which the interstitial lung disease eventually led to pulmonary hypertension (PH). Pulmonary hypertension can occur in GATA2 deficiency-associated pulmonary alveolar proteinosis and fibrosis <http://ow.ly/aHv430aAZct>
Reversal of gene dysregulation in cultured cytotrophoblasts reveals possible causes of preeclampsia
Authors: Yan Zhou, Matthew J. Gormley, Nathan M. Hunkapiller, Mirhan Kapidzic, Yana Stolyarov, Victoria Feng, Masakazu Nishida, Penelope M. Drake, Katherine Bianco, Fei Wang, Michael T. McMaster, Susan J. Fisher
Journal: Journal of Clinical Investigation (2013)