tbuckley/cabot-search huggingface dataset:
Abstract 20343: Leptin and the Developmental Origins of Hypertension
Authors: Kate M Pitz, Veronica A Peotta, Kenneth A Volk, Kamal Rahmouni, Robert D Roghair
Journal: Circulation (2014)

Introduction: Individuals with growth restriction through 2 years of age are relatively protected from adult obesity, but they are at increased risk of adult hypertension. Modeling this in mice, neonatal growth restriction (GR) leads to neonatal leptin deficiency, impaired neurodevelopment, adult growth restriction and adult hypertension. Hypothesis: We hypothesized that neonatal leptin deficiency during a window of developmental plasticity permanently increases central leptin sensitivity with subsequent renal sympathetic over-activation and hypertension. Methods: From day 4 to 14, C57BL/6 mice were randomized to vehicle (0.9% NaCl) or leptin at a dose shown to normalize the plasma levels of GR mice without impacting neonatal growth (1 mg/kg/d, intraperitoneal). GR mice were identified by weanling weights below the 10th percentile. Beginning at 4 months, adult phenotypes were assessed. Results: Compared to normal weight controls, adult GR mice had significantly increased leptin receptor mRNA expression within the arcuate nucleus of the hypothalamus (ARC), decreased adult food intake (0.09±0.01 vs. 0.13±0.02g/g/d; p&lt;0.05), decreased adult body weight, and exaggerated leptin-triggered increases in both renal sympathetic nerve activity (29+/-11 vs. -9+/-6% change from baseline, p&lt;0.01 for GR versus control) and systolic blood pressure (8+/-3 vs. -1+/-6% change from baseline, p&lt;0.05 for icv leptin versus icv saline in GR mice). Leptin supplementation normalized the hypothalamic gene expression and leptin responsiveness of GR adult mice in association with a programmed suppression in leptin-triggered activation of signal transducer and activator of transcription 3 (STAT3). Conclusions: Neonatal GR-related leptin deficiency is associated with a sustained increase in ARC leptin receptor expression and enhanced adult leptin responsiveness. This heightened central leptin responsiveness may contribute to the increased risk of hypertension seen patients with a history of perinatal growth restriction. We are currently assessing the effects of neonatal GR and neonatal leptin administration on cell-specific leptin-mediated hypothalamic signaling pathways.
Investigation of the spread of brucellosis among human and animal populations in southeastern Bulgaria, 2007
Authors: V Tzaneva, S Ivanova, M Georgieva, E Tasheva
Journal: Eurosurveillance (2009)

Three human cases of brucellosis were reported in summer 2007 in the region of Haskovo in southeastern Bulgaria. Subsequently, the regional veterinary and public health authorities carried out investigations to determine the spread of infection in domestic animals and in the human population. As a result, over 90,000 animals were tested, and 410 were found infected with brucellosis. The screening of 561 people believed to have been at risk of infection yielded 47 positive results. The majority of these persons had direct contact with domestic animals or had consumed unpasteurised dairy products. The investigations revealed evidence of disease among animals in the region and a considerable risk to humans, thus emphasising the need for effective prevention and control programmes.
Dexamethasone suppression in dementia, depression, and normal aging
Authors: A Georgotas, R E McCue, O M Kim, W E Hapworth, B Reisberg, P M Stoll, E Sinaiko, C Fanelli, P E Stokes
Journal: American Journal of Psychiatry (1986)

Dexamethasone suppression tests (DSTs) were performed for 18 moderately demented elderly patients, 66 depressed elderly outpatients, and 25 age- and sex-matched healthy elderly control subjects. Seventeen percent of the demented patients and 4% of the normal subjects were DST nonsuppressors, compared to 38% of the total depressed group. The postdexamethasone plasma cortisol levels of the dementia group fell between those of the normal and the depressed subjects. In addition, demented patients had postdexamethasone cortisol levels significantly lower than those of depressed patients with high Hamilton depression scores. Older subjects in all diagnostic categories, including normal subjects, had higher postdexamethasone plasma cortisol levels.
Nightmares and trauma: a comparison of nightmares after combat with lifelong nightmares in veterans
Authors: B van der Kolk, R Blitz, W Burr, S Sherry, E Hartmann
Journal: American Journal of Psychiatry (1984)

In this study the chronic traumatic nightmares of men who had been in combat were found to differ from the lifelong nightmares of veterans with no combat experience in that they tended to occur earlier in the sleep cycle, were more likely to be replicas of actual events, and were more commonly accompanied by gross body movements. Traumatic nightmares may arise out of varying stages of sleep and are not confined to REM sleep alone. The group with lifelong nightmares showed evidence of thought disorder on the Rorschach. The men with posttraumatic stress disorder had failed to psychologically integrate their traumatic experiences and used dissociation as a way of dealing with strong affects.
Adiponectin is a potent inhibitor of gastric cancer.
Authors: Joji Kitayama, Makoto Ishikawa, Toshimasa Yamauchi, Takashi Kadowaki, Hiroharu Yamashita, Hirokazu Nagawa
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

5350 

Background: Recent epidemiologic studies have shown a positive association between adiposity and increased risk of various cancers. Adiponectin, a circulating peptide hormone secreted mainly in adipose tissue, is supposed to be closely related with the adiposity-related carcinogenesis, although the mechanism has not been clarified yet. Method: In this study, we characterized the expressions of receptor adiponectin (AdipoR1 AdipoR2) both with RT-PCR and western blotting in 6 gastric cancer cell lines (MKN1, MKN45, MKN74, HGC27 MKN28, AZ521). The effects of adiponectin on cell growth and apoptosis were examined by MTS assay and FACS, respectively. In vivo effects were evaluated by inoculation of AZ521 in nude mice. Results: All the 6 cell lines expressed significant and variable levels of mRNA and protein of both receptors. In vitro experiments using AZ521 and HGC27 revealed that adiponectin, at the μM order, potently inhibited the proliferation through the induction of apoptosis, At the concentration of 30 μM, adiponectin inhibited the proliferation of the 2 cell lines to 39% and 10% of controls, respectively. Moreover, the growth inhibitory effects were significantly returned by the suppression of either AdipoR1 or AdipoR2 with siRNA. The effect of siRNA of AdipoR1 tended to be stronger than that of AdipoR2. In vivo mice model, administration of 50 μg adiponectin every 3 days significantly inhibited the growth of subcutaneously inoculated AZ521. When AZ521 was intraperitoneally inoculated, continuous infusion of adiponectin into peritoneal cavity with micropump strongly reduced the number and size of peritoneal metastasis. Conclusion: Adiponectin potently inhibits the growth of gastric cancer possibly through AdipoR1 and AdipoR2 on cancer cells, and thus could be used as an effective anti-cancer drugs in gastric cancer.
2008 George E. Brown Memorial Lecture—Flow-Induced Vasodilation in the Human Heart: Unique Endothelial Mechanisms and Clinical Insights
Authors: David Gutterman
Journal: Circulation (2008)

The most physiologically important stimulus for endothelium-dependent dilation is shear stress. Flow across the endothelial surface triggers a mechanochemical signal transduction pathway that results in release of nitric oxide (NO), prostacyclin, and/or endothelial-derived hyperpolarizing factors (EDHFs) such as hydrogen peroxide (H 2 O 2 ) and epoxyeicosatrienoic acid (EET). In most normal arteries, NO is the prominent mediator; however, in disease states, NO may be quenched by an elevation in superoxide. In these situations, compensatory dilator mechanisms may emerge, using EDHFs. One mechanism of this compensation may involve an important dilator pathway interaction whereby NO inhibits CYP450 monooxygenase. This is particularly prominent in the microcirculation, where disease-induced loss of NO often results in enhanced endothelial CYP450 activity and generation of EET as an alternate dilator. Recent data indicate that H 2 O 2 can also inhibit CYP450. In the human coronary microcirculation from subjects with coronary artery disease, NO and prostacyclin play little role in the dilation to most pharmacological agonists or to shear stress. Instead, EETs and H 2 O 2 are critical mediators of flow-induced dilation. Interestingly, the dilation requires ROS generation from the endothelial mitochondrial electron transport chain. Dual vessel bioassay studies suggest that H 2 O 2 is the transferable compound responsible for hyperpolarizing and relaxing the underlying vascular smooth muscle cells. In contrast, dilation to bradykinin also involves both H 2 O 2 and EET, but the H 2 O 2 originates from endothelial nicotinamide adenine dinucleotide phosphateoxidase oxidase, and EETs serve as an important transferable dilator agent. Endothelial release of NO, EET, and H 2 O 2 has implications beyond vasodilation. NO and EETs have potent antiatherosclerotic properties. Hydrogen peroxide, on the other hand, although a potent dilator, has proatherogenic properties. Therefore, it is hypothesized that the profile of endothelial factors released by shear stress and other stimuli may help determine the balance between proatherosclerotic and anti-atherosclerotic factors in vascular homeostasis.
Abstract 12694: Extent of Late Gadolinium Enhancement on Cardiovascular Magnetic Resonance Predicts Improvement in Left Ventricular Function and Adverse Outcomes After Steroid Therapy in Patients with Cardiac Sarcoidosis
Authors: Takayuki Ise, Takuya Hasegawa, Yoshiaki Morita, Naoaki Yamada, Akira Funada, Hiroyuki Takahama, Makoto Amaki, Hideaki Kanzaki, Hideo Okamura, Shiro Kamakura, Masafumi Kitakaze
Journal: Circulation (2011)

Background: Gadolinium-enhanced cardiac magnetic resonance imaging is an emerging tool for the diagnosis of cardiac sarcoidosis (CS). Although the presence of late gadolinium enhancement (LGE) refl...
Abstract 2691: Prophylactic Implantable Defibrillator in Patients with Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia and No Prior Sustained Ventricular Tachyarrhythmias: Therapy-Based Risk Stratification During a Long Term Follow-up
Authors: Domenico Corrado, Loira Leoni, Hugh Calkins, Stefano Favale, Deirdre Ward, Giuseppe Boriani, Mark S Link, Stefano Ricci, Jonathan P Piccini, Cristina Basso, Darshan Dalal, N.A Mark Estes, Massimo Santini, Gianfranco Buja, William J McKenna, Gaetano Thiene, Sabino Iliceto
Journal: Circulation (2006)

Background: patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) who survived an episode of cardiac arrest have a risk of recurrent ventricular tachycardia/ fibrillation...
Abstract 4366: Influence of Strut Width on Neointimal Coverage After Sirolimus-Eluting Stent Implantation Assessed by Optical Coherence Tomography
Authors: Shimpei Nakatani, Osaka Rosai Hosp
Journal: Circulation (2009)

Background: Sirolimus-eluting stents (SES) have reduced in-stent restenosis, but late stent thrombosis remains as the most major complication. Some reports suggest that optimal neointimal coverage ...
Accuracy of Doppler Catheter Measurements: Effect of Inhomogeneous Beam Power Distribution on Mean and Peak Velocity 11All editorial decisions for this article, including selection of referees, were made by a Guest Editor. This policy applies to all articles with authors from the University of California, San Francisco.
Authors: Scott J Denardo, Lawrence Talbot, Victor K Hargrave, Alan R Selfridge, Thomas A Ports, Paul G Yock
Journal: Journal of the American College of Cardiology (1997)
Relationship between hypomania and personality disorders before and after successful treatment
Authors: E D Peselow, M P Sanfilipo, R R Fieve
Journal: American Journal of Psychiatry (1995)

To examine the effect of hypomanic states on maladaptive personality traits and personality disorders, the authors evaluated personality traits and disorders of patients during an episode of hypomania and after successful somatic treatment.The authors used the Structured Interview for DSM-III Personality Disorders to study 66 outpatients who had a lifetime diagnosis of bipolar disorder and who met the minimum Research Diagnostic Criteria for hypomania. All patients had a knowledgeable informant separately undergo the Structured Interview for DSM-III Personality Disorders during the patient's hypomanic state. Outpatients who successfully recovered from the hypomanic episode (N = 47) and their informants were read-ministered the interview 4-8 weeks after the initial assessment.During the hypomanic state, informants generally reported higher levels of maladaptive personality traits among patients than patients themselves. For the patients who recovered successfully from the hypomanic episode, a reduction in all maladaptive personality traits except schizoid and dependent traits was reported by both patients and their informants; however, the decrease reported by patients generally was much greater than that reported by informants. In addition, schizoid traits actually increased after successful treatment according to patient reports but were unchanged according to informant reports.Hypomania may be associated with an exacerbation of maladaptive personality traits, which may be attenuated after successful treatment. Even with the attainment of euthymic mood, however, about 50% of the cohort had at least one personality disorder, which suggests that a high degree of comorbidity may exist between bipolar disorders and maladaptive personality traits or personality disorders.
Planum temporale asymmetry reversal in schizophrenia: replication and relationship to gray matter abnormalities
Authors: P E Barta, G D Pearlson, L B Brill, R Royall, I K McGilchrist, A E Pulver, R E Powers, M F Casanova, A Y Tien, S Frangou, R G Petty
Journal: American Journal of Psychiatry (1997)

Objective: The planum temporale, the posterior superior surface of the superior temporal gyrus, is a highly lateralized brain structure involved with language.In schizophrenic patients the authors previously found consistent reversal of the normal left-larger-than-right asymmetry of planum temporale surface area.The original subjects plus new patients and comparison subjects participated in this effort to replicate and extend the prior study.Method: High-resolution magnetic resonance imaging of 28 schizophrenic patients and 32 group-matched normal subjects was performed.The authors measured planum temporale surface area, gray matter volume underlying the planum temporale, and gray matter thickness.Asymmetry indices for areas and volumes were calculated.Results: Overall gray matter and total brain volume were not significantly smaller in the patients than in the comparison subjects.As previously reported, there was striking reversal of the normal asymmetry for planum temporale surface area in the male and female schizophrenic subjects.Bilaterally, gray matter volume beneath the planum temporale was smaller in the schizophrenic patients, and the gray matter thickness of the right planum temporale was only 50% of the comparison value.Volume of planum temporale gray matter did not show significant asymmetry in either group.Conclusions: This study extends the finding of reversed planum temporale surface area asymmetry in schizophrenic patients and clarifies its relationship to underlying gray matter volume.Although right planum temporale surface area is larger than normal in schizophrenia, gray matter volume is less than the comparison value; thus, gray matter thickness is substantially less than normal.
Abstract 14688: Submuscular is Superior to Subcutaneous Implantation for Subcutaneous Implantable Cardioverter Defibrillator
Authors: Joachim Winter, Harald Clahsen, Dong-In Shin, Stephen O’Connor
Journal: Circulation (2013)

Objectives: The incidence of electrode problems in the subcutaneous ICD (S-ICD) system appears to be rare but an improvement upon conventional transvenous systems. Recent publications of subcutaneo...
Abstract 2069: Reducing Door-to-Balloon Times: Hospital Strategies That Work
Authors: Elizabeth H Bradley, Jeptha P Curtis, Jeph Herrin, Yongfei Wang, Barbara A Barton, Tashonna Webster, Jennifer Mattera, Brahmajee Nallamothu, Sarah A Roumanis, David J Magid, Robert L McNamara, Janet Parkosewich, Jerod M Loeb, Harlan M Krumholz
Journal: Circulation (2006)
Abstract 1507: Disruption of KCNH2 Trafficking May Contribute to Severe Clinical Phenotype of Trafficking Deficient Long-QT Type-1 Mutation KCNQ1-T587M
Authors: Peter Biliczki, Zenawit Girmatsion, Ralf P Brandes, Isabelle Baro, Stefan H Hohnloser, Terence E Hebert, Stanley Nattel, Joachim R Ehrlich
Journal: Circulation (2008)

Background: The trafficking deficient long QT syndrome (LQTS)-associated KCNQ1 mutation T587M has previously been associated with a severe clinical phenotype that was not explained by biophysical characteristics of the mutation per se . Objective: We have previously shown significant interactions between KCNQ1 and KCNH2 and speculated that T587M-KCNQ1 might affect this interaction. We therefore compared the effects of KCNQ1 and T587M-KCNQ1 on KCNH2 trafficking and function. Methods/Results: While heterologous co-expression of wildtype (WT) KCNQ1 and KCNH2 in CHO cells increased KCNH2 current (H2+Q1, Fig. A , *P&lt;0.05) in comparison to KCNH2 expressed alone (H2), co-transfection of KCNH2 with T587M-KCNQ1 failed to increase I KCNH2 . Immunoblots of specific plasma membrane preparations (Fig. B ) and confocal microscopy indicated increased KCNH2 membrane localization in KCNQ1 co-transfected cells, while total KCNH2 expression remained unaffected. These results indicated a chaperone effect as the potential underlying mechanism. Furthermore, effective co-immunoprecipitation of WT channels occurred. T587M-KCNQ1 also co-precipitated with KCNH2, but the LQTS mutant was retained perinuclearly (Fig. C ) and additionally failed to increase membrane KCNH2 expression (Fig. B ), abolishing the WT KCNQ1 chaperone function. Conclusions: Trafficking-deficient T587M-KCNQ1 lacks the KCNH2 chaperone function that occurs with WT KCNQ1, limiting KCNH2 membrane localization and potentially explaining the malignant LQTS phenotype. Consideration of KCNQ1-KCNH2 interactions may be important for understanding mutation-specific clinical variability in LQTS presentations.
Abstract 11433: Postinfarction Cardiac Remodeling Normally Proceeds in Granulocyte Colony-Stimulating Factor Knockout Mice
Authors: Kentaro Morishita, Genzou Takemura, Akiko Tsujimoto, Hiromitsu Kanamori, Itta Kawamura, Atsushi Mikami, Hideshi Okada, Toshiaki Takeyama, Tomonori Kawaguchi, Takatomo Watanabe, Kazuko Goto, Atsushi Ogino, Megumi Morishita, Hiroaki Ushikoshi, Masanori Kawasaki, Shinji Ogura, Shinya Minatoguchi
Journal: Circulation (2014)

Treatment with granulocyte colony-stimulating factor (G-CSF) has been reported to mitigate postinfarction cardiac remodeling. We here examined how the postinfarction remodeling proceeds in the hearts of G-CSF-null mice, of which outcome we hypothesized to be miserable. We generated myocardial infarction in G-CSF-knockout (KO) mice and wild-type (WT) mice by ligation of the left coronary artery. The acute infarct size was similar at 24 h after ligation between the groups, where the incidence of in situ nick-end labeling (TUNEL)-positive cardiomyocytes was similar while the infiltrating leukocytes were significantly fewer in KO mice (n = 6 each). Somewhat surprisingly, at the chronic stage (4 weeks postinfarction), there was no difference in the left ventricular dimension, function and histological findings including the infarct size and myocardial vascular density between the groups (n = 6 each). Because it was contrary to our hypothesis, we next investigated the changes in major angiogenesis growth factors such as angiopoientin-1, hepatocyte growth factor, hypoxia induced factor-1 alpha, insulin-like growth factor-1, vascular endothelial growth factor (VEGF) in postinfarction hearts. As a result, biochemical analyses revealed a markedly increased expression of VEGF in the hearts of KO mice compared with WT mice (n = 6 each). The findings suggest a possibility that overexpressed VEGF might have compensated for the defect of G-CSF in KO mice. To check this hypothesis, we next inhibited the VEGF signal using an anti-VEGF antibody bevacizumab. Then the cardiac remodeling was significantly aggravated at the chronic stage, and the immunostaining showed scarce vascular development, reduced cell proliferation activity, and increased apoptosis in the granulation tissue of the bevacizumab-treated hearts at the subacute stage (4 days postinfarction), which might have contributed to the aggravation of cardiac remodeling during the chronic stage. In conclusion, G-CSF-KO mice unexpectedly displayed normal process of postinfarction cardiac remodeling. Overexpressed VEGF in the KO mice is suggested to compensate for the deficit of G-CSF through enhancement of neovascularization in the postinfarction heart.
Abstract 17621: Octogenarians Who Can Exercise During Stress Testing Have Better Outcomes: A Stress Echocardiography Study
Authors: Neel P Chokshi, Shiv K Agarwal, Azhar Supariwala, Ganesh S Kamath, Ahmed Otokiti, Dan G Halpern, Wallacy Garcia, Farooq A Chaudhry
Journal: Circulation (2012)
NF-κB/RelA and Nrf2 cooperate to maintain hepatocyte integrity and to prevent development of hepatocellular adenoma
Authors: Ulrike A. Köhler, Friederike Böhm, Frank Rolfs, Michèle Egger, Thorsten Hornemann, Manolis Pasparakis, Achim Weber, Sabine Werner
Journal: Journal of Hepatology (2015)