tbuckley/cabot-search huggingface dataset:
Treating Disturbances in the Relationship Between Mothers With Bulimic Eating Disorders and Their Infants: A Randomized, Controlled Trial of Video Feedback
Authors: Alan Stein
Journal: American Journal of Psychiatry (2006)

Objective: Maternal eating disorders interfere with parenting, adversely affecting mother-infant interaction and infant outcome. This trial tested whether video-feedback treatment specifically targeting mother-child interaction would be superior to counseling in improving mother-child interaction, especially mealtime conflict, and infant weight and autonomy. Method: The participants were 80 mothers with bulimia nervosa or similar eating disorder who were attending routine baby clinics and whose infants were 4–6 months old. They were randomly assigned to video-feedback interactional treatment or supportive counseling. Both groups also received guided cognitive behavior self-help for their eating disorder. Each group received 13 sessions. The primary outcome measure was mealtime conflict; secondary outcome measures were infant weight, aspects of mother-infant interaction, and infant autonomy. Results: Seventy-seven mothers were followed up when their infants were 13 months old. The video-feedback group exhibited significantly less mealtime conflict than the control subjects. Nine of 38 (23.7%) in the video-feedback group showed episodes of marked or severe conflict, compared with 21 of 39 (53.8%) control subjects (odds ratio=0.27, 95% confidence interval=0.10 to 0.73). Video feedback produced significant improvements in several other interaction measures and greater infant autonomy. Both groups maintained good infant weight, with no differences between groups. Maternal eating psychopathology was reduced across both groups. Conclusions: Video-feedback treatment focusing on mother-infant interaction produced improvements in interaction and infant autonomy, and both groups maintained adequate infant weight. To the authors’ knowledge, this is the first controlled trial to show key improvements in interaction between mothers with postnatal psychiatric disorders and their infants.
Vesicular Glutamate Transport at a Central Synapse Limits the Acuity of Visual Perception in Zebrafish
Authors: Matthew C. Smear, Huizhong W. Tao, Wendy Staub, Michael B. Orger, Nathan J. Gosse, Yan Liu, Koji Takahashi, Mu-ming Poo, Herwig Baier
Journal: Neuron (2007)
Antitumor Activity in <i>RAS</i>-Driven Tumors by Blocking AKT and MEK
Authors: Anthony W. Tolcher, Khurum Khan, Michael Ong, Udai Banerji, Vassiliki Papadimitrakopoulou, David R. Gandara, Amita Patnaik, Richard D. Baird, David Olmos, Christopher R. Garrett, Jeffrey M. Skolnik, Eric H. Rubin, Paul D. Smith, Pearl Huang, Maria Learoyd, Keith A. Shannon, Anne Morosky, Ernestina Tetteh, Ying-Ming Jou, Kyriakos P. Papadopoulos, Victor Moreno, Brianne Kaiser, Timothy A. Yap, Li Yan, Johann S. de Bono
Journal: Clinical Cancer Research (2014)

KRAS is the most commonly mutated oncogene in human tumors. KRAS-mutant cells may exhibit resistance to the allosteric MEK1/2 inhibitor selumetinib (AZD6244; ARRY-142886) and allosteric AKT inhibitors (such as MK-2206), the combination of which may overcome resistance to both monotherapies.
RBCK1 Drives Breast Cancer Cell Proliferation by Promoting Transcription of Estrogen Receptor α and Cyclin B1
Authors: Nina Gustafsson, Chunyan Zhao, Jan-Åke Gustafsson, Karin Dahlman-Wright
Journal: Cancer Research (2010)

Abstract Cell cycle regulatory pathways in breast cancer are incompletely described. Here, we report an important role in estrogen receptor α (ERα)–positive breast cancer cells for the protein kinase C1 (PKC1)–interacting protein RBCK1 in supporting cell cycle progression by driving transcription of ERα and cyclin B1. RBCK1-depleted cells exhibited increased accumulation in G2-M phase of the cell cycle, decreased proliferation, and reduced mRNA levels for ERα and its target genes cyclin D1 and c-myc. Chromatin immunoprecipitation revealed that ERα transcription is associated with RBCK1 recruitment to the ERα promoter, suggesting that transcriptional regulation is one mechanism by which RBCK1 affects ERα mRNA levels. G2-M phase arrest was mediated independently from reduced ERα levels, instead associated with transcriptional inhibition of the key G2-M regulator cyclin B1. In breast tumor samples, there was a positive correlation between levels of RBCK1, ERα, and cyclin B1 mRNA levels. Our findings suggest that RBCK1 regulates cell cycle progression and proliferation of ERα-positive breast cancer cells by supporting transcription of ERα and cyclin B1. Cancer Res; 70(3); 1265–74
Altered balance between matrix gelatinases (MMP‐2 and MMP‐9) and their tissue inhibitors in human dilated cardiomyopathy: potential role of MMP‐9 in myosin‐heavy chain degradation
Authors: Patricia Rouet‐Benzineb, Jean‐Marie Buhler, Patrick Dreyfus, Annick Delcourt, Richard Dorent, Jeannine Perennec, Bertrand Crozatier, Alain Harf, Chantal Lafuma
Journal: European Journal of Heart Failure (1999)
Microwave hyperthermia treatment increases heat shock proteins in human skeletal muscle
Authors: Yuji Ogura, Hisashi Naito, Toshihiro Tsurukawa, Noriko Ichinoseki-Sekine, Norio Saga, Takao Sugiura, Shizuo Katamoto
Journal: British Journal of Sports Medicine (2007)

To test the hypothesis that microwave hyperthermia treatment (MHT) increases heat shock proteins (HSPs) in the human vastus lateralis muscle.Four untrained healthy male volunteers participated in this study. The lateral side of the thigh of one leg (heated leg) was heated with a microwave generator (2.5 GHz, 150 W) for 20 min. At 1 day after the MHT, a muscle sample was taken from the heated leg. A control sample was taken from the unheated leg on another day of the MHT. For both legs, HSP90, HSP72 and HSP27 levels were compared.The HSP90, HSP72 and HSP27 levels in heated legs were significantly higher than those in control legs (p<0.05).Application of MHT can increase the levels of several HSPs in human skeletal muscle.
Abstract 5054: The interplay between Disabled-2 and protein kinase C epsilon in the regulation of prostate cancer cell survival
Authors: Wei-Lien Tseng, Yan-Yu Chen, Ju-Chien Cheng, Ching-Ping Tseng
Journal: Cancer Research (2010)

Abstract Prostate cancer is the leading cause of cancer-related death in men in the world. Previous studies have demonstrated that Disabled-2 (DAB2) is a tumor suppressor and down-regulation of DAB2 expression is accompanied with prostate cancer progression. On the other hands, protein kinase C epsilon (PKCε) functions as an oncogene and promotes human prostate cancer cell survival upon treatment of methyseleninic acid (MSA), an anti-cancer agent that induces prostate cancer cell apoptosis. However, little is known whether there is a crosstalk between DAB2 and PKCε. In this study, we first analyzed DAB2 and PKCε protein expression in three prostate cancer cell lines DU145, PC3 and C4-2. Western blot analysis revealed that DAB2 was relatively abundant in PC3 when compared with the DU145 and C4-2 cells. In contrast, the expression of PKCε was higher in DU145 and C4-2 cells when compared with the PC3 cells. Consistent with these findings, ectopic expression of DAB2 resulted in down-regulation of PKCε. These observations implicate a reverse association of DAB2 and PKCε and suggest that DAB2 is a regulator of PKCε expression. To further explore the interplay between DAB2 and PKCε, we determined the effect of DAB2 overexpression on DU145 cell susceptibility to MSA-induced cell death. Consistent with a previous report, overexpression of PKCε increased DU145 cell survival and knockdown of PKCε by small interfering RNA augmented cell death upon treatment of MSA but not Ibupofen. Accordingly, expression of DAB2 down-regulated PKCε and increased in cell susceptibility to MSA that resulted in a 40% decrease of cell survival. These findings suggest that DAB2 modulates PKCε expression and affects prostate cancer cell susceptibility to selective anti-cancer agents. This study represents the first report to unveil the interplay between DAB2, PKCε and prostate cancer cell survival. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5054.
Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes
Authors: Timothy A. Bauer, Jane E.B. Reusch, Moshe Levi, Judith G. Regensteiner
Journal: Diabetes Care (2007)

OBJECTIVE—People with type 2 diabetes have impaired exercise responses even in the absence of cardiovascular complications. One key factor associated with the exercise intolerance is abnormally slowed oxygen uptake (V̇o2) kinetics during submaximal exercise. The mechanisms of this delayed adaptation during exercise are unclear but probably relate to impairments in skeletal muscle blood flow. This study was conducted to compare skeletal muscle deoxygenation (deoxygenated hemoglobin/myoglobin [HHb]) responses and estimated microvascular blood flow (Qm) kinetics in type 2 diabetic and healthy subjects after the onset of moderate exercise. RESEARCH DESIGN AND METHODS—Pulmonary V̇o2 kinetics and [HHb] (using near-infrared spectroscopy) were measured in 11 type 2 diabetic and 11 healthy subjects during exercise transitions from unloaded to moderate cycling exercise. Qm responses were calculated using V̇o2 kinetics and [HHb] responses via rearrangement of the Fick principle. RESULTS—V̇o2 kinetics were slowed in type 2 diabetic compared with control subjects (43.8 ± 9.6 vs. 34.2 ± 8.2 s, P &amp;lt; 0.05), and the initial [HHb] response after the onset of exercise exceeded the steady-state level of oxygen extraction in type 2 diabetic compared with control subjects. The mean response time of the estimated Qm increase was prolonged in type 2 diabetic compared with healthy subjects (47.7 ± 14.3 vs. 35.8 ± 10.7 s, P &amp;lt; 0.05). CONCLUSIONS—Type 2 diabetic skeletal muscle demonstrates a transient imbalance of muscle O2 delivery relative to O2 uptake after onset of exercise, suggesting a slowed Qm increase in type 2 diabetic muscle. Impaired vasodilatation due to vascular dysfunction in type 2 diabetes during exercise may contribute to this observation. Further study of the mechanisms leading to impaired muscle oxygen delivery may help explain the abnormal exercise responses in type 2 diabetes.
Parent Conversations About Healthful Eating and Weight
Authors: Jerica M. Berge, Rich MacLehose, Katie A. Loth, Marla Eisenberg, Michaela M. Bucchianeri, Dianne Neumark-Sztainer
Journal: JAMA Pediatrics (2013)

The prevalence of weight-related problems in adolescents is high. Parents of adolescents may wonder whether talking about eating habits and weight is useful or detrimental.To examine the associations between parent conversations about healthful eating and weight and adolescent disordered eating behaviors.Cross-sectional analysis using data from 2 linked multilevel population-based studies.Anthropometric assessments and surveys completed at school by adolescents and surveys completed at home by parents in 2009-2010.Socioeconomically and racially/ethnically diverse sample (81% ethnic minority; 60% low income) of adolescents from Eating and Activity in Teens 2010 (EAT 2010) (n = 2793; mean age, 14.4 years) and parents from Project Families and Eating and Activity in Teens (Project F-EAT) (n = 3709; mean age, 42.3 years). EXPOSURE Parent conversations about healthful eating and weight/size.Adolescent dieting, unhealthy weight-control behaviors, and binge eating.Mothers and fathers who engaged in weight-related conversations had adolescents who were more likely to diet, use unhealthy weight-control behaviors, and engage in binge eating. Overweight or obese adolescents whose mothers engaged in conversations that were focused only on healthful eating behaviors were less likely to diet and use unhealthy weight-control behaviors. Additionally, subanalyses with adolescents with data from 2 parents showed that when both parents engaged in healthful eating conversations, their overweight or obese adolescent children were less likely to diet and use unhealthy weight-control behaviors.Parent conversations focused on weight/size are associated with increased risk for adolescent disordered eating behaviors, whereas conversations focused on healthful eating are protective against disordered eating behaviors.
A Novel HSV-1 Virus, JS1/34.5−/47−, Purges Contaminating Breast Cancer Cells From Bone Marrow
Authors: Jennifer C. Hu, Matthew J. Booth, Gopichand Tripuraneni, Derek Davies, Syed A.A. Zaidi, Manuela Tamburo de Bella, Martin J. Slade, Stephen B. Marley, Myrtle Y.A. Gordon, Robert S. Coffin, R. Charles Coombes, Tahereh Kamalati
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Oncolytic herpes simplex virus type 1 (HSV-1) vectors show considerable promise as agents for cancer therapy. We have developed a novel recombinant HSV-1 virus (JS1/34.5−/47−) for purging of occult breast cancer cells from bone marrow of patients. Here, we evaluate the therapeutic efficacy of this oncolytic virus. Experimental Design: Electron microscopy was used to determine whether human breast cancer and bone marrow cells are permissive for JS1/34.5−/47− infection. Subsequently, the biological effects of JS1/34.5−/47− infection on human breast cancer cells and bone marrow were established using cell proliferation and colony formation assays, and the efficiency of cell kill was evaluated. Finally, the efficiency of JS1/34.5−/47− purging of breast cancer cells was examined in cocultures of breast cancer cells with bone marrow as well as bone marrow samples from high-risk breast cancer patients. Results: We show effective killing of human breast cancer cell lines with the JS1/34.5−/47− virus. Furthermore, we show that treatment with JS1/34.5−/47− can significantly inhibit the growth of breast cancer cell lines without affecting cocultured mononuclear hematopoietic cells. Finally, we have found that the virus is effective in destroying disseminated tumors cells in bone marrow taken from breast cancer patients, without affecting the hematopoietic contents in these samples. Conclusion: Collectively, our data show that the JS1/34.5−/47− virus can selectively target breast cancer cells while sparing hematopoietic cells, suggesting that JS1/34.5−/47− can be used to purge contaminating breast cancer cells from human bone marrow in the setting of autologous hematopoietic cell transplantation.
Laboratory and febrile features after joint surgery in patients with rheumatoid arthritis treated with tocilizumab
Authors: M Hirao, J Hashimoto, H Tsuboi, A Nampei, H Nakahara, N Yoshio, T Mima, H Yoshikawa, N Nishimoto
Journal: Annals of the Rheumatic Diseases (2008)

Objectives: To understand the acute phase responses to surgical intervention in patients with rheumatoid arthritis (RA) treated with the anti-interleukin (IL)6 receptor antibody, tocilizumab. Methods: In a retrospective 1:1 pair-matched case-control study, 22 tocilizumab-treated RA cases and 22 cases treated with conventional disease-modifying antirheumatic drugs (DMARDs) and matched for type of surgery, age and sex were evaluated for body temperature every day, and blood C-reactive protein (CRP) levels and white blood cell (WBC), neutrophil and lymphocyte counts on days −1, 1, 3 and weeks 1 and 2 after joint surgery. Safety issues were also monitored. Results: No complications of infection or delay of wound healing occurred in either patient group. Tocilizumab partially, but significantly, suppressed the increase in body temperature on postoperative days 1 and 2, compared with DMARDs (average (SD) maximum increase in temperature was 0.45 (0.1)°C in the tocilizumab group and 0.78 (0.1)°C in the DMARD group; p&lt;0.01). Tocilizumab completely suppressed the increase in CRP after surgery, whereas all cases treated with DMARDs showed a significant increase of CRP at postoperative day 1 (5.5 (0.6) mg/dl; p&lt;0.001). WBC, neutrophil and lymphocyte counts showed no remarkable change after surgery, and there was no significant difference in any cell counts between the patient groups. Conclusions: Within this small number of cases, safe operations on patients were performed during tocilizumab treatment. Tocilizumab suppressed fever and increase of CRP after surgery, whereas there was no influence on the transition in number of leukocytes. This characteristic postoperative response should be considered during tocilizumab treatment.
Mucosal surface pH of the large intestine of the rat and of normal and inflamed large intestine in man.
Authors: N I McNeil, K L Ling, J Wager
Journal: Gut (1987)

The surface pH of rat distal colonic mucosa and human rectal mucosa was measured in vitro using first a small pH electrode with a flattened tip. In buffer with pH 7.56 the mean rat colonic surface pH was 6.72. Lowering the buffer pH in steps resulted in a small fall in surface pH, the values being buffer pH 7.06 surface pH 6.64, buffer pH 6.58 surface pH 6.61 and finally buffer pH 6.09 surface pH 6.39. Similar results were obtained with a buffer where butyrate, 30 mmol/l replaced chloride and when a CO2/bicarbonate buffer was used. During the time taken for the study transmural potential difference only changed by 1-2 mV. Serosal surface pH changed with buffer pH, suggesting that the maintained surface pH is a property of the mucosal surface only. The surface pH of human rectal mucosa was similar to that of rat distal colonic mucosa. As buffer pH fell from pH 7.51 to 5.96 mucosal surface pH only fell from pH 6.80 to 6.26. The values obtained in ulcerative proctitis did not differ from normal mucosa. Secondly pH microelectrodes were used to measure the juxta mucosal pH and the pH-microclimate thickness when luminal pH was controlled. The microclimate had a pH 6.63 adjacent to the mucosa with a thickness of 840 micron. The importance of mucus in maintaining the microclimate was shown by n-acetyl cysteine thinning and prostaglandin E2 thickening the layer. These results describe a surface microclimate in the large intestine of appreciable thickness and a constant juxta mucosal pH. Luminal pH changes produce only a small change in microclimate pH.
Low molecular weight IgM in primary biliary cirrhosis.
Authors: P J Roberts-Thomson, K Shepherd
Journal: Gut (1990)

Low molecular weight IgM is the monomeric subunit of pentameric IgM and is not generally found in the blood of healthy individuals. Using a sensitive immunoblotting technique, low molecular weight IgM was detected in all 17 patients with primary biliary cirrhosis and constituted up to 5% of the total circulating IgM. This low molecular weight IgM moiety correlated significantly with total IgM (p less than 0.01) but not with the specific biliary cirrhosis mitochondrial autoantibody anti-M2. Furthermore it was not possible to show that a partially purified sample of low molecular weight IgM contained M2 binding activity. Mitogen stimulated peripheral blood mononuclear cells from two of four patients were observed to secrete low molecular weight IgM in vitro, a finding seen in only one of six healthy subjects. Immunoblot analysis of patients sera revealed the presence of other oligomers of IgM in addition to low molecular weight IgM. In conclusion this study suggests that during the enhanced IgM synthesis observed in primary biliary cirrhosis a defect occurs in the assembly of the IgM pentamer with release of monomeric and oligomeric IgM into the circulation. The pathogenic significance of these circulating low molecular weight IgM species is unknown.
Effects of Atorvastatin on Early Recurrent Ischemic Events in Acute Coronary Syndromes&lt;SUBTITLE&gt;The MIRACL Study: A Randomized Controlled Trial&lt;/SUBTITLE&gt;
Authors: Gregory G. Schwartz
Journal: JAMA (2001)

Reduction with Aggressive Cholesterol Lowering (MIRACL) Study Investigators B2][3] Previous trials excluded patients who had experienced recent unstable angina or acute myocardial infarction (MI).However, it is within the early period after an acute coronary syndrome (ACS) that patients experience the highest rate of death and recurrent ischemic events. 4,5o date, it has not been determined whether initiation of treatment with a statin soon after an ACS can reduce the occurrence of these early events.Recent studies indicate that statins have salutary physiologic effects within weeks.In conjunction with lowering total and low-density lipoprotein (LDL) cholesterol, statins may improve endo-
A Case of Congenital Xanthoma Multiplex
Authors: W. D. James
Journal: BMJ (1894)

ORN 8;5 it can account for many, and other circumstances, of which direct and carele s contact with the sick is the most important, will account for many others.It does not exclude the influence of local conditions upon the prevalence of cholera.The epidemic in Rassia has indeed furnished 4strong evidence that local conditions, such as elevation and -dampness of the soil, are important factors in the cholera problem.But to discuss this evidence here would be to enter upon the whole question of the etiology of cholera, and would far exceed the limits of tie pres -nt paper.
StellaTUM: current consensus and discussion on pancreatic stellate cell research
Authors: Mert Erkan, Guido Adler, Minoti V Apte, Max G Bachem, Malte Buchholz, Sönke Detlefsen, Irene Esposito, Helmut Friess, Thomas M Gress, Hans-Joerg Habisch, Rosa F Hwang, Robert Jaster, Jörg Kleeff, Günter Klöppel, Claus Kordes, Craig D Logsdon, Atsushi Masamune, Christoph W Michalski, Junseo Oh, Phoebe A Phillips, Massimo Pinzani, Carolin Reiser-Erkan, Hidekazu Tsukamoto, Jeremy Wilson
Journal: Gut (2011)

The field of pancreatic stellate cell (PSC) biology is very young, as the essential in-vitro tools to study these cells (ie, methods to isolate and culture PSC) were only developed as recently as in 1998. Nonetheless, there has been an exponential increase in research output in this field over the past decade, with numerous research groups around the world focusing their energies into elucidating the biology and function of these cells. It is now well established that PSC are responsible for producing the stromal reaction (fibrosis) of two major diseases of the pancreas—chronic pancreatitis and pancreatic cancer. Despite exponentially increasing data, the methods for studying PSC remain variable. Although within individual laboratories methods are consistent, different methodologies used by various research groups make it difficult to compare results and conclusions. This article is not a review article on the functions of PSC. Instead, members of the Pancreatic Star Alliance (http://www.pancreaticstaralliance.com) discuss here and consolidate current knowledge, to outline and delineate areas of consensus or otherwise (eg, with regard to methodological approaches) and, more importantly, to identify essential directions for future research.

Hepatic stellate cells (HSC) were first described by Karl von Kupffer in 1876; however, similar cells in the pancreas were first observed in the 1980s.1–3 In 1998, Apte et al 4 and Bachem et al 5 isolated and cultured PSC.4 5 In the normal pancreas, PSC are located in close proximity to the basal aspect of pancreatic acinar cells. In sections immunostained for the marker desmin (a cytoskeletal protein), quiescent PSC can be seen as cells with a central cell body and long cytoplasmic projections extending along the base of adjacent acinar cells similar to that of pericytes in the mammary gland. …