tbuckley/cabot-search huggingface dataset:
Personality Profiles in Eating Disorders: Rethinking the Distinction Between Axis I and Axis II
Authors: Drew Westen, Jennifer Harnden-Fischer
Journal: American Journal of Psychiatry (2001)

OBJECTIVE: Like other DSM-IV axis I syndromes, eating disorders are diagnosed without respect to personality, which is coded on axis II. The authors assessed the utility of segregating eating disorders and personality pathology and examined the extent to which personality patterns account for meaningful variation within axis I eating disorder diagnoses. METHOD: One hundred three experienced psychiatrists and psychologists used a Q-sort procedure (the Shedler-Westen Assessment Procedure-200) that assesses personality and personality pathology to describe a patient they were currently treating for bulimia or anorexia. Data were subjected to a cluster-analytic procedure (Q-analysis) to determine whether patients clustered into coherent groupings on the basis of their personality profiles. Categorical and dimensional personality diagnoses were then used to predict measures relevant to adaptation and etiology, controlling for axis I diagnosis. RESULTS: Three categories of patients emerged: a high-functioning/perfectionistic group, a constricted/overcontrolled group, and an emotionally dysregulated/undercontrolled group. This categorization demonstrated substantial incremental validity beyond axis I diagnosis in predicting eating disorder symptoms, adaptive functioning (Global Assessment of Functioning scores and history of psychiatric hospitalization), and etiological variables (sexual abuse history). CONCLUSIONS: Axis I symptoms are a useful component, but only one component, in the accurate diagnosis of eating disorders. Classifying patients with eating disorders by eating symptoms alone groups together patients with anorexic symptoms who are high functioning and self-critical with those who are highly disturbed, constricted, and avoidant, and groups together patients with bulimic symptoms who are high functioning and self-critical with those who are highly disturbed, impulsive, and emotionally dysregulated. These distinctions may be relevant to etiology, prognosis, and treatment.
Principles of Genetic Murine Models for Cardiac Disease
Authors: Katherine E. Yutzey, Jeffrey Robbins
Journal: Circulation (2007)

It was only ≈15 years ago that methodologies evolved to the point where we began to manipulate the genetic apparatus of the mouse such that proteins of the investigator’s choice could be expressed in a 4-chambered, mammalian heart. Our abilities to express both normal and mutated proteins in the heart or to create genetic nulls in which the protein is not expressed at all continue to evolve. With the tools now available, one can target protein expression to the different cell types present in the heart, often at a particular time, and, in some cases, turn off the protein as development progresses or the animal ages. These abilities have enabled us to model many of the genetic mutations identified as causative for pediatric and/or adult cardiovascular disease and heart failure. Identifying the primary genetic cause is, more often than not, insufficient for designing effective therapeutics or interventions. Therefore, it is critical to be able to develop animal models that accurately recapitulate the pathogenic processes that ensue as a result of mutant gene expression or loss of protein expression. In this review, we discuss the nature, strengths, and weaknesses of the current set of tools for developing genetically manipulated mouse models, as well as the relevance of these models for understanding cardiovascular disease and illuminating potential therapeutic avenues.
Efficacy and Safety of a New 20% Immunoglobulin Preparation for Subcutaneous Administration, IgPro20, in Patients with Primary Immunodeficiency
Authors: J. Hagan, M.B. Fasano, S. Spector, R.L. Wasserman, I. Melamed, M.A. Rojavin, O. Zenker, J.S. Orange
Journal: Journal of Allergy and Clinical Immunology (2010)
58 LY-6C INTERMEDIATE AND LY-6C LO INTRAHEPATIC MACROPHAGE SUBSETS ORCHESTRATE RESOLUTION OF HEPATIC FIBROSIS FOLLOWING CHRONIC INJURY
Authors: P. Ramachandran, A. Pellicoro, M.A. Vernon, S.N. Hartland, A. Ali, R.L. Aucott, S.J. Forbes, J.P. Iredale
Journal: Journal of Hepatology (2011)
Role of Dietary Proteins and Amino Acids in the Pathogenesis of Insulin Resistance
Authors: Frédéric Tremblay, Charles Lavigne, Hélène Jacques, André Marette
Journal: Annual Review of Nutrition (2007)

Dietary proteins and amino acids are important modulators of glucose metabolism and insulin sensitivity. Although high intake of dietary proteins has positive effects on energy homeostasis by inducing satiety and possibly increasing energy expenditure, it has detrimental effects on glucose homeostasis by promoting insulin resistance and increasing gluconeogenesis. Varying the quality rather than the quantity of proteins has been shown to modulate insulin resistance induced by Western diets and has revealed that proteins derived from fish might have the most desirable effects on insulin sensitivity. In vitro and in vivo data also support an important role of amino acids in glucose homeostasis through modulation of insulin action on muscle glucose transport and hepatic glucose production, secretion of insulin and glucagon, as well as gene and protein expression in various tissues. Moreover, amino acid signaling is integrated by mammalian target of rapamycin, a nutrient sensor that operates a negative feedback loop toward insulin receptor substrate 1 signaling, promoting insulin resistance for glucose metabolism. This integration suggests that modulating dietary proteins and the flux of circulating amino acids generated by their consumption and digestion might underlie powerful new approaches to treat various metabolic diseases such as obesity and diabetes.
Alternate Ranging Methods for Cancer Mortality Maps
Authors: D. J. Grauman
Journal: JNCI Journal of the National Cancer Institute (2000)

Mapping techniques can highlight the spatial or temporal variations in rates of cancer mortality. In mapping geographic patterns of cancer mortality, spatial units are grouped into categories defined by specified rate ranges, and then the units in each category are assigned a particular color in the map. We examined the consequences of using different ranging methods when comparing maps over several time intervals.Maps of mortality rates for cancers of the breast, lung (including the lung, trachea, bronchus, and pleura), and cervix uteri in the United States by county or state economic area are created for different time intervals between 1950 and 1994. Two ranging methods are employed: 1) Ranges are defined for individual time interval by the deciles of rates in that interval (ranging within intervals), and 2) constant ranges for all time intervals are defined by the deciles of rates for the entire 45-year period from 1950 through 1994 (ranging across intervals). The time intervals from 1950 through 1969 and from 1970 through 1994 were chosen to accommodate the availability of detailed county-level population estimates specifically for blacks starting in 1970.The ranging method has little impact on maps for breast cancer mortality, which changed little over time. For lung cancer, which increased over time, and cervix uteri cancer, which decreased over time, ranging within time intervals shows the geographic variability but does not convey the temporal trends. Trends are evident when ranging across time intervals is employed; however, geographic variability is partially obscured by the predominance of spatial units in the highest rate categories in the recent time intervals for lung cancer and in the early time intervals for cervix uteri cancer.Ranging within time intervals displays geographic patterns and changes in geographic patterns, regardless of time trends in rates. Ranging across time intervals shows temporal changes in rates but with some loss of information about geographic variability.
Dietary Flaxseed Alters Tumor Biological Markers in Postmenopausal Breast Cancer
Authors: Lilian U. Thompson, Jian Min Chen, Tong Li, Kathrin Strasser-Weippl, Paul E. Goss
Journal: Clinical Cancer Research (2005)

Abstract Purpose: Flaxseed, the richest source of mammalian lignan precursors, has previously been shown to reduce the growth of tumors in rats. This study examined, in a randomized double-blind placebo-controlled clinical trial, the effects of dietary flaxseed on tumor biological markers and urinary lignan excretion in postmenopausal patients with newly diagnosed breast cancer. Experimental Design: Patients were randomized to daily intake of either a 25 g flaxseed-containing muffin (n = 19) or a control (placebo) muffin (n = 13). At the time of diagnosis and again at definitive surgery, tumor tissue was analyzed for the rate of tumor cell proliferation (Ki-67 labeling index, primary end point), apoptosis, c-erbB2 expression, and estrogen and progesterone receptor levels. Twenty-four–hour urine samples were analyzed for lignans, and 3-day diet records were evaluated for macronutrient and caloric intake. Mean treatment times were 39 and 32 days in the placebo and flaxseed groups, respectively. Results: Reductions in Ki-67 labeling index (34.2%; P = 0.001) and in c-erbB2 expression (71.0%; P = 0.003) and an increase in apoptosis (30.7%; P = 0.007) were observed in the flaxseed, but not in the placebo group. No significant differences in caloric and macronutrient intake were seen between groups and between pre- and posttreatment periods. A significant increase in mean urinary lignan excretion was observed in the flaxseed group (1,300%; P &amp;lt; 0.01) compared with placebo controls. The total intake of flaxseed was correlated with changes in c-erbB2 score (r = −0.373; P = 0.036) and apoptotic index (r = 0.495; P &amp;lt; 0.004). Conclusion: Dietary flaxseed has the potential to reduce tumor growth in patients with breast cancer.
A vibrating trachea
Authors: M J Doherty, D P S Spence, D Graham, B M G Cheetham, X Q Sun, J E Earis
Journal: Thorax (1998)

A case of relapsing polychondritis presenting as tracheomalacia is reported in which an unusual low pitched sound was heard at the mouth and over the chest wall during expiration. The sound was associated with expiratory airflow limitation and oscillation on the flow trace of approximately 50 Hz. Spectral analysis of the sound showed it to have the characteristics of sounds produced by flutter in flow limited flexible tubes. These observations suggest that the sound was produced by airflow induced flutter in the trachea and main airways and is further evidence in support of the dynamic flutter theory of wheeze production.
Imbalance of M1/M2 alveolar macrophages phenotype in pulmonary sarcodosis
Authors: Svetlana Lyamina, Natalia Demianenko, Svetlana Shelukhina, Olga Lovacheva, Eugeny Shmelev, Igor Malyshev
Journal: European Respiratory Journal (2013)

Imbalance of Th1/Th2 components of the immune system and M1/M2 macrophages phenotype, respectively, play a critical part in pulmonary sarcoidosis (PS) development regardless of the disease state. Objective : assessment of M1/M2 alveolar macrophages (AM) phenotype imbalance in PS of various state and healthy volunteers (HV). Methods : AM phenotype in patients with newly diagnosed PS (n=15, 41,72±3,89 y.o.), recurrent PS (n=15, 44,10±5,06 y.o) and HV (n=10, 51,83±3,52 y.o.) was assessed by flow cytometry (Beckman Coulter FC500) by surface macrophages markers CD80, CD25 and CD163, CD206, typical for M1 and M2 phenotype, respectively. Results : AM population in all patients with PS and HV was not monophenotypical. In newly diagnosed PS percent of M1 markers CD25 and CD80 was 1.3 and 4 times increased vs HV. The content of M2 marker CD163 was not significantly changed, and CD206 was 1.7 times decreased as compared to HV. In recurrent PS CD25 was 1.5 times increased and CD80 – 3.5 times increased vs healthy, and the content of M2 markers was not significantly changed as compared to HV.  Conclusion : In PS regardless of the disease state AM predominantly possess M1 phenotype. Imbalance of M1/M2 AM phenotypes towards M1 macrophages is more expressed in newly diagnosed pulmonary sarcoidosis.
A macrophage colony-stimulating factor receptor–green fluorescent protein transgene is expressed throughout the mononuclear phagocyte system of the mouse
Authors: R. Tedjo Sasmono, Delvac Oceandy, Jeffrey W. Pollard, Wei Tong, Paul Pavli, Brandon J. Wainwright, Michael C. Ostrowski, S. Roy Himes, David A. Hume
Journal: Blood (2003)
Extensor carpi ulnaris injuries in tennis players: a study of 28 cases
Authors: B Montalvan, J Parier, J L Brasseur, D L Viet, J L Drape
Journal: British Journal of Sports Medicine (2006)

Pain on the ulnar side of the wrist is common among elite tennis players. Ten years of experience has allowed identification of a pathology involving the extensor carpi ulnaris (ECU) tendon. On the basis of 28 clinical cases seen over the last five years, three clinical patterns are described: (a) acute instability of the ECU; (b) tendinopathy; (c) ECU rupture. Each of these clinical entities requires a different therapeutic approach. A review of the relevant anatomy is provided.
Validated measurement of periarticular bone mineral density at the knee joint by dual energy x ray absorptiometry
Authors: E Murphy
Journal: Annals of the Rheumatic Diseases (2001)

<h3>OBJECTIVE</h3> The association of inflammatory arthritis with loss of periarticular bone mineral density (BMD) has been well established. However, changes in bone density cannot be quantified by conventional radiography. This study aimed at developing a new technique for measurement of periarticular bone density at the knee joint by dual energy<i>x </i>ray absorptiometry (DXA) and assessing the precision of this technique for selected areas around the knee. <h3>METHODS</h3> To validate this technique for bone density assessment in both patient and control subjects, knee joints from healthy subjects and patients with inflammatory arthritis were selected for study. Posteroanterior (PA) and lateral scans of both knees were acquired with the Hologic 4500 elite bone densitometer. Each scan was repeated three times, with repositioning between scans. Knee scans were obtained with the forearm software and evaluated by subregion analysis. Seven femoral and seven tibial subregions of interest (ROIs) were selected on PA scans. Six ROIs were selected on lateral scans. Precision was determined for each ROI selected. <h3>RESULTS</h3> 14 knee joints were studied in each group. Precision, expressed as percentage coefficient of variation (CV%), varied widely between subregions. PA scans were most appropriate for measurement of femoral bone density (CV% = 1.89–2.64%), whereas the best value obtained for ROIs within the tibia was on the lateral scan, where CV% for measurement of the proximal 5 mm was 2.67% in the patient group. CV% for BMD of the patella was excellent at 0.84% in the patient group. <h3>CONCLUSION</h3> This new application of DXA can be used to measure periarticular bone density at the knee joint. Regions within the distal femur and patella have been identified as the optimal areas to study
Deoxyhaemoglobin concentrations in the detection of central cyanosis.
Authors: G A Goss, J A Hayes, J G Burdon
Journal: Thorax (1988)

Central cyanosis is an important clinical sign because it indicates the presence of appreciable arterial hypoxaemia.According to classical textbook teaching, concentrations of deoxyhaemoglobin of about 5 g/dl are necessary before central cyanosis is clinically detectable.This figure has recently been questioned and thought to be a considerable overestimation.The aim of this study was to re-examine the relationship between deoxyhaemoglobin concentration and central cyanosis and to determine the minimum deoxy- haemoglobin concentration required for the detection of central cyanosis. MethodsEighty normothermic patients (60 of them male) with various acute and chronic respiratory disorders referred for routine arterial blood gas analysis were studied during normal working hours.Most patients were breathing air when the samples were taken but 20 were receiving supplemental oxygen.Pigment disorders (methaemoglobin or sulphaemoglobin) were not present in any patient.Arterial blood was collected in preheparinised syringes by standard techniques and delivered immediately to the laboratory in ice for analysis.Oxygen and carbon dioxide tensions and pH were measured with a blood gas analyser (Radiometer BMS
Effect of a lifestyle intervention on weight change in south Asian individuals in the UK at high risk of type 2 diabetes: a family-cluster randomised controlled trial
Authors: Raj S Bhopal, Anne Douglas, Sunita Wallia, John F Forbes, Michael E J Lean, Jason M R Gill, John A McKnight, Naveed Sattar, Aziz Sheikh, Sarah H Wild, Jaakko Tuomilehto, Anu Sharma, Ruby Bhopal, Joel B E Smith, Isabella Butcher, Gordon D Murray
Journal: The Lancet Diabetes & Endocrinology (2013)

Background The susceptibility to type 2 diabetes of people of south Asian descent is established, but there is little trial-based evidence for interventions to tackle this problem.We assessed a weight control and physical activity intervention in south Asian individuals in the UK.Methods We did this non-blinded trial in two National Health Service (NHS) regions in Scotland (UK).Between July 1, 2007, and Oct 31, 2009, we recruited men and women of Indian and Pakistani origin, aged 35 years or older, with waist circumference 90 cm or greater in men or 80 cm or greater in women, and with impaired glucose tolerance or impaired fasting glucose determined by oral glucose tolerance test.Families were randomised (using a random number generator program, with permuted blocks of random size, stratifi ed by location [Edinburgh or Glasgow], ethnic group [Indian or Pakistani], and number of participants in the family [one vs more than one]) to intervention or control.Participants in the same family were not randomised separately.The intervention group received 15 visits from a dietitian over 3 years and the control group received four visits in the same period.The primary outcome was weight change at 3 years.Analysis was by modifi ed intention to treat, excluding participants who died or were lost to follow-up.We used linear regression models to provide mean diff erences in baseline-adjusted weight at 3 years.This trial is registered, number ISRCTN25729565.Findings Of 1319 people who were screened with an oral glucose tolerance test, 196 (15%) had impaired glucose tolerance or impaired fasting glucose and 171 entered the trial.Participants were in 156 family clusters that were randomised (78 families with 85 participants were allocated to intervention; 78 families with 86 participants were allocated to control).167 (98%) participants in 152 families completed the trial.Mean weight loss in the intervention group was 1•13 kg (SD 4•12), compared with a mean weight gain of 0•51 kg (3•65) in the control group, an adjusted mean diff erence of -1•64 kg (95% CI -2•83 to -0•44).Interpretation Modest, medium-term changes in weight are achievable as a component of lifestyle-change strategies, which might control or prevent adiposity-related diseases.
Clonal Interference Is Alleviated by High Mutation Rates in Large Populations
Authors: Jonathan P. Bollback, John P. Huelsenbeck
Journal: Molecular Biology and Evolution (2007)

When a beneficial mutation is fixed in a population that lacks recombination, the genetic background linked to that mutation is fixed. As a result, beneficial mutations on different backgrounds experience competition, or "clonal interference," that can cause asexual populations to evolve more slowly than their sexual counterparts. Factors such as a large population size (N) and high mutation rates (μ) increase the number of competing beneficial mutations, and hence are expected to increase the intensity of clonal interference. However, recent theory suggests that, with very large values of Nμ, the severity of clonal interference may instead decline. The reason is that, with large Nμ, genomes including both beneficial mutations are rapidly created by recurrent mutation, obviating the need for recombination. Here, we analyze data from experimentally evolved asexual populations of a bacteriophage and find that, in these nonrecombining populations with very large Nμ, recurrent mutation does appear to ameliorate this cost of asexuality.
AGE AND SUSCEPTIBILITY OF MICE TO COXSACKIE A VIRUSES
Authors: A. Martin Lerner, Howard S. Levin, Maxwell Finland
Journal: The Journal of Experimental Medicine (1962)

Mice varying in age from 1 day to 8 months were inoculated intraperitoneally with Coxsackie A virus, type 9 and studies were made of the quantity of virus in striated muscle and myocardium, the presence of neutralizing antibody in the serum, and the pathological changes in the tissues. The hind limbs of young (1- to 20-day-old) mice yielded high titers of virus and showed diffuse myositis, whereas only low yields of virus and focal myositis were obtained in older mice. In the 20-day-old mice the skeletal lesions were not accompanied by manifest symptoms and histologically showed evidence of regeneration progressing from the 3rd to the 11th day after inoculation. Older mice showed no symptoms and only focal myositis and low yields of virus were found in their hind limbs. Coxsackie A9 virus replicated to relatively low titers in the hearts of young (1- to 40-day-old) mice without producing any demonstrable lesions whereas frank myocarditis with high yields of virus were demonstrated in mice infected at 8 months of age. The data suggest that at least for the 2 strains used, the adult mouse should be considered susceptible to subclinical infection with Coxsackie A9 virus. Neither subclinical infection, nor antibody formation was demonstrable in young adult mice inoculated with a strain of Coxsackie A4 virus.
Prostate cancer ETS rearrangements switch a cell migration gene expression program from RAS/ERK to PI3K/AKT regulation
Authors: Nagarathinam Selvaraj, Justin A Budka, Mary W Ferris, Travis J Jerde, Peter C Hollenhorst
Journal: Molecular Cancer (2014)

The RAS/ERK and PI3K/AKT pathways induce oncogenic gene expression programs and are commonly activated together in cancer cells. Often, RAS/ERK signaling is activated by mutation of the RAS or RAF oncogenes, and PI3K/AKT is activated by loss of the tumor suppressor PTEN. In prostate cancer, PTEN deletions are common, but, unlike other carcinomas, RAS and RAF mutations are rare. We have previously shown that over-expression of "oncogenic" ETS transcription factors, which occurs in about one-half of prostate tumors due to chromosome rearrangement, can bypass the need for RAS/ERK signaling in the activation of a cell migration gene expression program. In this study we test the role of RAS/ERK and PI3K/AKT signaling in the function of oncogenic ETS proteins. We find that oncogenic ETS expression negatively correlates with RAS and RAF mutations in prostate tumors. Furthermore, the oncogenic ETS transcription factors only increased cell migration in the absence of RAS/ERK activation. In contrast to RAS/ERK, it has been reported that oncogenic ETS expression positively correlates with PI3K/AKT activation. We identified a mechanistic explanation for this finding by showing that oncogenic ETS proteins required AKT signaling to activate a cell migration gene expression program through ETS/AP-1 binding sequences. Levels of pAKT correlated with the ability of oncogenic ETS proteins to increase cell migration, but this process did not require mTORC1. Our findings indicate that oncogenic ETS rearrangements cause a cell migration gene expression program to switch from RAS/ERK control to PI3K/AKT control and provide a possible explanation for the high frequency of PTEN, but not RAS/RAF mutations in prostate cancer.
Analysis of 3D bone ingrowth into polymer scaffolds via micro-computed tomography imaging
Authors: Anthony C. Jones, Bruce Milthorpe, Holger Averdunk, Ajay Limaye, Tim J. Senden, Arthur Sakellariou, Adrian P. Sheppard, Rob M. Sok, Mark A. Knackstedt, Arthur Brandwood, Dennis Rohner, Dietmar W. Hutmacher
Journal: Biomaterials (2004)