tbuckley/cabot-search huggingface dataset:
Utility of the initial therapeutic alliance in evaluating psychiatric patients' risk of violence
Authors: J E Beauford, D E McNiel, R L Binder
Journal: American Journal of Psychiatry (1997)

Evaluation of patients' potential for violence is an important component of care in psychiatric emergency and inpatient settings. Although situational variables are widely acknowledged to influence the risk of violence by psychiatric patients, most past research has been limited to patient attributes and has neglected the interpersonal context in which violence occurs. To the authors' knowledge, this is the first study to assess a new type of situational risk factor, the quality of the initial therapeutic alliance between the therapist and patient, as a predictor of the risk of violent behavior during short-term hospitalization.The admitting physician's written initial evaluation for each of 328 patients hospitalized on a locked inpatient unit was reviewed by using a standardized alliance scale. The checklist measures the patient's level of active collaboration with the treatment process. Acute symptoms were rated at admission by physicians using the Brief Psychiatric Rating Scale. Nurses rated aggressive behavior in the hospital with the Overt Aggression Scale.Patients who had a poorer therapeutic alliance at the time of admission were significantly more likely to display violent behavior during hospitalization. Logistic regression analysis showed that the quality of the initial therapeutic alliance remained a strong predictor of violence even when other clinical and demographic correlates of violence were considered concurrently.The results suggest a new class of situational, interactional variable--reflected in the quality of the therapeutic relationship--that may be useful in evaluating patients' potential for violence. Implications for risk management are discussed.
Relationships Between Low-Density Lipoprotein Particle Size, Plasma Lipoproteins, and Progression of Coronary Artery Disease
Authors: Juha Vakkilainen, George Steiner, Jean-Claude Ansquer, Francois Aubin, Stephanie Rattier, Christelle Foucher, Anders Hamsten, Marja-Riitta Taskinen
Journal: Circulation (2003)

Background— The Diabetes Atherosclerosis Intervention Study showed that treatment with fenofibrate decreases progression of coronary atherosclerosis in subjects with type 2 diabetes. We determined whether on-treatment plasma lipid concentrations and LDL particle size contribute to the favorable effect of fenofibrate on the progression of coronary artery disease (CAD). Methods and Results— A total of 418 subjects with type 2 diabetes were randomly assigned to 200 mg micronized fenofibrate daily or placebo. The mean follow-up time was 39.6 months. LDL peak particle diameter (LDL size) was determined by polyacrylamide gradient gel electrophoresis from 405 subjects at baseline and at the end of the study. Progression of CAD was measured with quantitative coronary angiography. LDL size increased significantly more in the fenofibrate group than in the placebo group (0.98±1.04 versus 0.32±0.92 nm, P &lt;0.001). In the combined group, small LDL size was significantly associated with progression of CAD measured as the increase of percentage diameter stenosis ( r =−0.16, P =0.002) and decreases in minimum ( r =−0.11, P =0.030) and mean ( r =−0.10, P =0.045) lumen diameter. High on-treatment LDL cholesterol, apolipoprotein B, and triglyceride concentrations were also associated with the progression of CAD. In regression analyses, small LDL size added to the effect of LDL cholesterol and apolipoprotein B on the progression of CAD. Similar associations were observed in the fenofibrate group, whereas in the placebo group, lipoprotein variables were not significantly correlated with the progression of CAD. Conclusions— Changes in LDL size and plasma lipid levels account for part of the antiatherogenic effect of fenofibrate in type 2 diabetes.
P2-05-01: Acquired Tamoxifen Resistance Promotes Angiogenic Responses in ER+ Breast Cancer Cells.
Authors: E Hayes, C Smith, RI Nicholson, J Gee, S Hiscox
Journal: Cancer Research (2011)

Abstract Background: In the treatment of pre-menopausal women with oestrogen positive (ER+) breast cancer, tamoxifen represents a first line of adjuvant treatment with demonstrable benefits. Despite this, resistance is frequently acquired to tamoxifen with an associated poor prognosis. Breast cancer cell models have revealed the importance of growth factor signalling networks in sustaining growth of endocrine-resistant cancers and, more recently, their ability to promote a highly migratory and invasive phenotype, together with the expression of genes with pro-angiogenic ontology. The potential of endocrine resistant cells to elicit angiogenic responses, however, remains unknown. Materials and Methods: Real-time PCR was used to validate results from preliminary Affymetrix-based gene profiling of pro-angiogenic gene expression in endocrine-sensitive MCF7 cells and their tamoxifen-resistant (TamR) counterparts. The expression of pro-angiogenic factors in conditioned media (CM) from these cells was assessed by ELISA. The proliferative and migratory effects of MCF7 and TamR CM on vascular endothelial cells (HUVEC and HECV cells), was determined by MTS cell proliferation assay, wound closure assays and Matrigel tubule formation assays. Changes in endothelial cell migration following co-culture with endocrine-resistant cells were examined using Boyden-chamber chemotaxis assays. Growth factor signalling and migration pathway activation in endothelial cells in response to CM was determined by Western blotting. Results: TamR cells were found to express high levels of HIF-1α, IL-8 and VEGF-A at an mRNA level compared with expression in MCF7 cells. High levels of VEGF-A protein were also confirmed in the conditioned media from TamR cells versus their endocrine-sensitive counterparts. TamR conditioned media promoted endothelial cell proliferation, migration and the formation of tubules to a greater extent than that seen in MCF7 CM treated cells. TamR conditioned media was found to stimulate VEGFR2 phosphorylation and downstream activation of MAPK in endothelial cells compared to MCF7 CM. Pharmacological inhibition of VEGFR2 activity in endothelial cells suppressed TamR-induced endothelial cell proliferation and VEGFR phosphorylation. Further pharmacological manipulation of erbB receptors and intracellular kinases in TamR cells revealed an ERGF/Her2-Src kinase dependent mechanism of VEGF-A production in these cells. Discussion: These data suggest acquired tamoxifen resistance is accompanied by development of an erbB receptor/Src kinase-dependant pro-angiogenic phenotype which, if recapitulated in vivo, may promote tumour progression. Therapeutic targeting of erbB/Src axis may prove beneficial in such cases. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-05-01.
Catheter Ablation for Atrial Fibrillation in Patients With Obesity
Authors: Yong-Mei Cha, Paul A. Friedman, Samuel J. Asirvatham, Win-Kuang Shen, Thomas M. Munger, Robert F. Rea, Peter A. Brady, Arshad Jahangir, Kristi H. Monahan, David O. Hodge, Ryan A. Meverden, Bernard J. Gersh, Stephen C. Hammill, Douglas L. Packer
Journal: Circulation (2008)

Background— Obesity is a risk factor for atrial fibrillation and other cardiovascular conditions. Our objective was to determine whether catheter-based ablation effectively treated atrial fibrillation in obese patients. Methods and Results— Five hundred twenty-three consecutive patients with symptomatic, medication-refractory atrial fibrillation underwent catheter ablation. Patients were grouped by body mass index (lean, &lt;25 kg/m 2 ; overweight, 25 to 29.9 kg/m 2 ; obese, ≥30 kg/m 2 ). Outcome and quality of life were measured with a general health survey (Medical Outcomes Study 36-item Short-Form General Health Survey [SF-36]); patients were assessed before ablation and at 3 and 12 months after the procedure. Two hundred twenty-eight study patients (44%) were overweight, and 201 (38%) were obese. Twelve months after curative ablation, 72% of patients were free of atrial fibrillation without the use of antiarrhythmic agents; 84% were arrhythmia free when those receiving medication were included. Atrial fibrillation was eliminated in 75%, 72%, and 70% of the lean, overweight, and obese patients, respectively, at 12 months ( P =0.41, trend test). SF-36 scores were lower for patients with higher body mass index ( P &lt;0.05) at baseline. SF-36 scores improved in every functional domain for all body mass index groups after ablation. The mean SF-36 total physical score increased from 59±20 at baseline to 77±19 in 12 months ( P &lt;0.001). The total mental health score improved from 66±18 to 79±16 in 12 months ( P &lt;0.001). Conclusions— Catheter ablation of atrial fibrillation was effective in obese patients. Coexistence of atrial fibrillation and obesity indicated lower SF-36 scores, but the improvement in quality of life was consistent across all body mass index categories.
NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth
Authors: Irina M. Jaba, Zhen W. Zhuang, Na Li, Yifeng Jiang, Kathleen A. Martin, Albert J. Sinusas, Xenophon Papademetris, Michael Simons, William C. Sessa, Lawrence H. Young, Daniela Tirziu
Journal: Journal of Clinical Investigation (2013)

Myocardial hypertrophy is an adaptation to increased hemodynamic demands. An increase in heart tissue must be matched by a corresponding expansion of the coronary vasculature to maintain and adequate supply of oxygen and nutrients for the heart. The physiological mechanisms that underlie the coordination of angiogenesis and cardiomyocyte growth are unknown. We report that induction of myocardial angiogenesis promotes cardiomyocyte growth and cardiac hypertrophy through a novel NO-dependent mechanism. We used transgenic, conditional overexpression of placental growth factor (PlGF) in murine cardiac tissues to stimulate myocardial angiogenesis and increase endothelial-derived NO release. NO production, in turn, induced myocardial hypertrophy by promoting proteasomal degradation of regulator of G protein signaling type 4 (RGS4), thus relieving the repression of the Gβγ/PI3Kγ/AKT/mTORC1 pathway that stimulates cardiomyocyte growth. This hypertrophic response was prevented by concomitant transgenic expression of RGS4 in cardiomyocytes. NOS inhibitor L-NAME also significantly attenuated RGS4 degradation, and reduced activation of AKT/mTORC1 signaling and induction of myocardial hypertrophy in PlGF transgenic mice, while conditional cardiac-specific PlGF expression in eNOS knockout mice did not induce myocardial hypertrophy. These findings describe a novel NO/RGS4/Gβγ/PI3Kγ/AKT mechanism that couples cardiac vessel growth with myocyte growth and heart size.
The German version of the chronic urticaria quality‐of‐life questionnaire: factor analysis, validation, and initial clinical findings
Authors: A. Młynek, M. Magerl, M. Hanna, S. Lhachimi, I. Baiardini, G. W. Canonica, Z. Brzoza, A. Kasperska‐Zajac, B. Rogala, A. Zalewska‐Janowska, T. Zuberbier, M. Maurer
Journal: Allergy (2009)

Chronic urticaria (CU) is a common skin disorder that causes a substantial burden on patients' quality-of-life (QoL). The aim of this work was to generate and validate a German version of the Chronic Urticaria Quality of Life Questionnaire (CU-Q(2)oL) and to provide reference assessments of QoL.The Italian CU-Q(2)oL was translated into German and administered to 157 CU patients. They also completed two well-established general dermatology QoL questionnaires, the Dermatology Life Quality Index (DLQI) and Skindex-29. Factor analysis was used to identify scales of the German CU-Q(2)oL. Correlation to the DLQI and Skindex-29 was used for validation. Multiple linear regression was used to determine which patient characteristics were associated with which dimensions of QoL.The factor analysis identified six scales of the German CU-Q(2)oL: functioning, sleep, itching/embarrassment, mental status, swelling/eating, and limits looks, which accounted for 70% of the data variance. Five of these six scales showed good internal consistency, and another five demonstrated convergent validity. On a percentile scale, they had these median CU-Q(2)oL scores: 29 functioning, 44 sleep, 50 itching/embarrassment, 50 mental status, 31 swelling/eating, 31 limits looks. Disease severity significantly predicted scores on all scales. Age predicted functioning, sleep, itching/embarrassment, and swelling/eating. Sex predicted itching/embarrassment and limits looks.This study yielded a robust validation of the German version of the CU-Q(2)oL. It confirmed previous studies that CU has a clinically meaningful burden on QoL, especially for sleep and mental health, and that women are more severely affected by pruritus. The German CU-Q(2)oL should be widely adopted in clinical research on the treatment of CU.
P218 Recording of COPD mortality must improve if it is to be a robust outcome measure
Authors: S. Ansari, M. Ali, D. J. Powrie, K. G. Lingam, A. G. Davison
Journal: Thorax (2011)

Statistics for chronic obstructive pulmonary disease (COPD) are dependant on local data collection and have an impact on understanding the morbidity and mortality. This can steer the resources and ought to be robust. Inaccuracies in coding can affect the hospital standardised mortality ratio. The Coalition government9s “Outline Strategy for COPD and Asthma in England” published in 2011, emphasises the focus on outcomes. We examined in-patient mortality of COPD at Southend University Hospital to confirm the accuracy of the data. The coding department provided a list of patients coded with COPD who died in the hospital during the study period of 1 year (1 April 2009 and 31 March 2010). All death certificates for the same period were reviewed and those with cause of death recorded as COPD identified. The two lists were compared. Five consultant respiratory physicians reviewed the notes, independently recorded the cause of death and compared to death certificates. According to death certificates 77 patients died of COPD, whereas a total of 55 COPD related deaths were identified by the coding department. The later was compared with actual death certificates for corroboration: COPD as a disease directly leading to death (Ia) was recorded in 21, as a disease leading to 1a (Ib) in 11, as a disease leading to 1b (Ic) in none and as another significant condition contributing to death (II) in 8. Two were referred to the coroner, no data available for two and no COPD was recorded in the remaining 11. Of the available 41 notes (from the coding department9s list) reviewed by respiratory consultants, COPD as a cause of death in their view was Ia in 13, Ib in 5, Ic in none and II in 10 cases and it was not the cause in the rest. Mortality data from coding, death certification and opinion of auditing senior clinicians exhibited multiple discrepancies. This raises doubts as to the robustness of mortality data. We have identified a need to review the practice including the accurate completion of death certificates.
Targeting the LYN/HS1 signaling axis in chronic lymphocytic leukemia
Authors: Elisa ten Hacken, Cristina Scielzo, Maria T. S. Bertilaccio, Lydia Scarfò, Benedetta Apollonio, Federica Barbaglio, Kostas Stamatopoulos, Maurilio Ponzoni, Paolo Ghia, Federico Caligaris-Cappio
Journal: Blood (2013)
Recurrent somatic mutation of FAT1 in multiple human cancers leads to aberrant Wnt activation
Authors: Luc G T Morris, Andrew M Kaufman, Yongxing Gong, Deepa Ramaswami, Logan A Walsh, Şevin Turcan, Stephanie Eng, Kasthuri Kannan, Yilong Zou, Luke Peng, Victoria E Banuchi, Phillip Paty, Zhaoshi Zeng, Efsevia Vakiani, David Solit, Bhuvanesh Singh, Ian Ganly, Linda Liau, Timothy C Cloughesy, Paul S Mischel, Ingo K Mellinghoff, Timothy A Chan
Journal: Nature Genetics (2013)
Histological Follow-up of Duodenitis
Authors: R. Cheli, H. Aste*, G. Ciancamerla
Journal: Endoscopy (1973)

The histological evolution of 39 cases of duodenitis diagnosed by biopsy (32 cases of superficial duodenitis, 3 of interstitial duodenitis and 4 of atrophic duodenitis) in a period lasting from 6 months to 4 years has been evaluated by the authors. – No remarkable histological change is seen in 53% of patients studied in this follow-up. This statement is completely true only in cases of atrophic duodenitis. To the contrary many cases of superficial and interstititial duodenitis showed a trend to normalization and, rarely, from a superficial to an atrophic stage. Persistent or more severe alterations of duodenal mucosa are frequently shown when coexistent chronic affections in organs of the proximity are present.
Review of Some Common Artifacts in Nuclear Medicine
Authors: AMILCARE GENTILI, STEFAN D. MIRON, LEE P. ADLER
Journal: Clinical Nuclear Medicine (1994)

In nuclear medicine, artifacts may simulate a pathologic process; their recognition is therefore necessary to avoid misdiagnosis. Artifacts may be divided into three groups: 1) camera dependent artifacts; 2) radiopharmaceutical dependent artifacts; and 3) patient-related artifacts. The authors present a variety of artifacts and discusses their possible prevention.
A Look at Ourselves
Authors: Jerome P. Kassirer
Journal: New England Journal of Medicine (1992)

IN previous decades the intricacies of the American health care system were largely irrelevant to a physician's day-to-day work and were easy to ignore. But not today. The progressive decline in doctors' independence and public esteem, the increasing burden of utilization review and paperwork, and the frustration of trying to provide care to uninsured patients are daily reminders of the chaotic structure and function of our system. Despite the large number of health care plans proposed in this election year, it seems virtually certain that none will succeed in dealing effectively with uncontrolled costs, inadequate access, and dispirited physicians.Given . . .
The National Leadership Commission's Health Care Plan
Authors: Arnold S. Relman
Journal: New England Journal of Medicine (1989)

The National Leadership Commission on Health Care, which I have discussed before,1 has just released its final report.2 The report is an effort by a blue ribbon panel of private citizens and health professionals representing most of the important components of the health care system to reach consensus on the goals and general structure of a new national health system. The commission described the problems of the present system in an interim report released in June 1987.3 Now, after another year and a half of deliberations, it presents its recommendations.We have recently published two other important proposals for reforming . . .
Abstract 1974: Functional characterization of Basonuclin 1 (BNC1): a novel tumor suppressor gene commonly downregulated in human prostate cancer.
Authors: Bernard Kwabi-Addo, Songping Wang, Paulett Furbert-Harris, Srinivasan Yegnasubramanian, Joseph Devaney
Journal: Cancer Research (2013)

Abstract Prostate cancer (PCa) harbors a myriad of aberrant genomic and epigenetic alterations. Epigenetic inactivation of genes in PCa is largely based on transcriptional silencing by aberrant CpG methylation of CpG rich promoter regions. To better understand the role of aberrant methylation changes and to identify biological pathways likely to be affected in PCa, we used a genome-wide methylation array from Illumina (Infunium) to identify novel methylated genes associated to PCa. We identified several candidate genes including BNC1 as novel genes which are frequently methylated and whose methylation closely related to inactivation of gene expression in prostate cancer cell lines. Basonuclin1 is a zinc finger transcription factor that interacts with a subset of promoters of genes transcribed by both RNA polymerase-I and -II and has roles in maintaining ribosomal biogenesis and the proliferative potential of immature epithelial cells. We found that the expression of BNC1 negatively correlated with the degree of methylation at the CpG island in prostate tumor samples compared to benign prostate tissues. The forced-expression of BNC1 significantly decreased prostate cancer cell proliferation whereas the siRNA mediated BNC1 knock-down increased prostate cancer cell proliferation. Overall, our data suggest a potential tumor suppressor role for BNC1 that includes regulation of cell proliferation and cell-cell interaction in prostate carcinogenesis. Citation Format: Bernard Kwabi-Addo, Songping Wang, Paulett Furbert-Harris, Srinivasan Yegnasubramanian, Joseph Devaney. Functional characterization of Basonuclin 1 (BNC1): a novel tumor suppressor gene commonly downregulated in human prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1974. doi:10.1158/1538-7445.AM2013-1974
PROBLEM OF EMOTIONAL TRAUMA IN HOSPITAL TREATMENT OF CHILDREN
Authors: Katherine Jackson
Journal: JAMA (1952)

The importance of the emotional needs of the child in the hospital, and especially of the child who is to be operated on, has been receiving more attention in recent years by nurses, pediatricians, surgeons, and psychiatrists. The fact that emotional trauma occurs is widely accepted. The definition of the term, however, and the causes and means of prevention of the condition are sometimes inadequately understood. For the purpose of this discussion, emotional trauma will be defined as the intensification of any feeling that may be deleterious to a satisfactory adjustment to life. Feelings that are likely to be involved in the hospital treatment of children are anxiety, suspiciousness, resentment, hostility, inadequacy, insecurity, and a desire to retaliate. From our study of the psychological aspects of hospitalization, anesthesia, and surgery in a group of children, certain conclusions seem justified concerning the nature, etiology, and prevention of emotional trauma associated with
MPs question health chiefs over troubled NHS computer programme
Authors: M. Cross
Journal: BMJ (2011)

<b>Introduction:</b> Up to 5% to 10% of cases of idiopathic pulmonary fibrosis (IPF) may actually be hypersensitivity pneumonitis (HP) that has been erroneously diagnosed. The hypothesis of this study is that exposure to a feather-filled duvet or pillow can be a cause of pulmonary fibrosis that is erroneously diagnosed as IPF. <b>Material and methods:</b> Between 2004 and 2010, 318 consecutive patients were studied. The diagnosis was based on internationally established criteria. Emphasis was placed on detecting transitory exposure to a possible environmental agent, particularly the use of a feather duvet or pillow. Furthermore, in patients whose questioning revealed exposure to an uncommon causal antigen or low-intensity exposure, specific IgG to antigen extract was determined, and specific bronchial challenge (SBC) were carried out. Surgical lung biopsies (SLB) were reviewed. <b>Results:</b> 60 patients were diagnosed with IPF. 24 patients had previous contact with a feather duvet or pillow for at least one year. In 15 patients the final diagnosis was HP; 8 by SBC and 2 by characteristic pathologic findings. HP was diagnosed in 3 patients with atypical usual interstitial pneumonia in SLB+ positive IgG testing and in 2 patients with bronchoalveolar lavage lymphocytosis (&gt;20%) and positive specific IgG to the causal agent. In 36 patients without previous contact, HP was diagnosed in 8 patients. <b>Conclusion:</b> In IPF, thorough clinical questioning can reveal the existence of a low-intensity, but persistent exposure to a known causal agent. HP due to exposure to a feather duvet can be the cause of some cases of pulmonary fibrosis, a condition that can have different prognosis. This abstract in funded in part by Fis PI1001577
P1123 RESPONSE-GUIDED THERAPY WITH BOCEPREVIR PLUS PEGINTERFERON ALFA-2a (40KD) AND RIBAVIRIN IN TREATMENT-NAIVE PATIENTS INFECTED WITH HCV GENOTYPE 1: INTERIM RESULTS FROM THE TriCo STUDY
Authors: P. Ferenci, R. Flisiak, F.A. Caruntu, G. Lengyel, M. Hohmann, G. Bakalos
Journal: Journal of Hepatology (2014)