Personality and the bipolar spectrum: normative and classification data for the Eysenck Personality Questionnaire-Revised

Background

Personality traits dispose individuals toward particular affective states and may therefore have an important role in the etiology of affective disorders in particular. Despite being one of the most widely used and well-researched personality instruments, few studies have studied bipolar spectrum disorders using the revised Eysenck Personality Questionnaire (EPQ-R) (Eysenck HJ, Eysenck SBG. The Eysenck Personality Questionnaire-Revised. Sevenoaks: UK; Hodder & Stoughton, 1992).

Methods

The EPQ-R was administered to 50 bipolar patients, 50 unipolar patients, and 50 controls matched on age and sex. Participants in clinical groups were euthymic, and participants in the control groups were screened for symptoms of depression.

Results

The EPQ-R scores were most effective at discriminating unipolar patients from controls, such that unipolar patients were higher on neuroticism and lower on extraversion. Bipolar patients showed a similar personality profile to, but were not clearly distinguished from, unipolar patients.

Conclusions

This research provides preliminary normative data for the EPQ-R that complement previous theoretical and empirical work in this area and suggests the usefulness of this tool in a clinical setting.     

Linear Elastic Properties of the Facial Soft Tissues Using an Aspiration Device: Towards Patient Specific Characterization

Biomechanical modeling of the facial soft tissue behavior is needed in aesthetic or maxillo-facial surgeries where the simulation of the bone displacements cannot accurately predict the visible outcome on the patient’s face. Because these tissues have different nature and elastic properties across the face, depending on their thickness, and their content in fat or muscle, individualizing their mechanical parameters could increase the simulation accuracy. Using a specifically designed aspiration device, the facial soft tissues deformation is measured at four different locations (cheek, cheekbone, forehead, and lower lip) on 16 young subjects. The stiffness is estimated from the deformations generated by a set of negative pressures using an inverse analysis based on a Neo Hookean model. The initial Young’s modulus of the cheek, cheekbone, forehead, and lower lip are respectively estimated to be 31.0 kPa ± 4.6, 34.9 kPa ± 6.6, 17.3 kPa ± 4.1, and 33.7 kPa ± 7.3. Significant intra-subject differences in tissue stiffness are highlighted by these estimations. They also show important inter-subject variability for some locations even when mean stiffness values show no statistical difference. This study stresses the importance of using a measurement device capable of evaluating the patient specific tissue stiffness during an intervention.     

Neuropathy optic glaucomatosa induced by systemic hypertension through activation endothelin-1 signaling pathway in central retinal artery in rats

AIM: To evaluate effect of hypertension on retinal ganglion cell (RGC) apoptosis, intraocular pressure (IOP), and the activation of endothelin-1 (ET-1) signaling pathway in central retinal artery (CRA) in rats. METHODS: The experimental study was performed on 20 male Sprague Dawley rats that were divided into control group, and hypertension groups. The hypertension was induced by subcutaneous deoxycorticoacetate (DOCA) 10 mg/kg twice a week and administered 0.9% NaCl solution daily for 2, 6, and 10wk. Blood pressure (BP) was measured using animal BP analyzer. IOP was measured by handheld tonometry. Retinal tissue preparations by paraffin blocks were made after enucleation. The expression of ET-1, eNOS, ET-1 receptor A (ETRA), ET-1 receptor B (ETRB), and phosphorylated myosin light chain kinase (MLCK), and caldesmon (CaD) in CRA and RGC apoptosis were evaluated through immunofluorescent staining method then observed using laser scanning confocal microscopy. RESULTS: BP significantly increased in all of the hypertension groups compared to control (P=0.001). Peak IOP elevation (7.78±4.14 mm Hg) and RGC apoptosis (576.15±33.28 Au) occurred on 2wk of hypertension. ET-1 expression (1238.6±55.1 Au) and eNOS expression (2814.2±70.7 Au) were found highest in 2wk of hypertension, although the ratio of ET-1/eNOS decreased since 2wk. ETRA reached peak expression in 10wk of hypertension (1219.4±6.3 Au), while ETRB significantly increased only in 2 weeks group (1069.2±9.6 Au). The highest MLCK expression (1190.09±58.32 Au), CaD (1670.28±18.36 Au) were also found in 2wk of hypertension. CONCLUSION: Hypertension effects to activation of ET-1 signaling pathway significantly in CRA, elevation of IOP, and RGC apoptosis. The highest value was achieved at 2wk, which is the development phase of hypertension.     

Changing of hepatitis C virus genotype patterns in France at the beginning of the third millenium: The GEMHEP GenoCII Study

Summary.  This cross-sectional study aimed to investigate, during a short period between 2000 and 2001, in a large population of patients with chronic hepatitis C, the epidemiological characteristics of hepatitis C virus (HCV) genotypes in France. Data from 26 referral centres, corresponding to 1769 patients with chronic hepatitis C were collected consecutively during a 6-month period. HCV genotyping in the 5'-non-coding region (NCR) was performed in each center using the line probe assay (LiPA, in 63% of cases), sequencing (25%) or primer-specific polymerase chain reaction (PCR) (12%). HCV genotypes 1a, 1b, 2, 3, 4, 5, non-subtyped 1 and mixed infection were found in 18, 27, 9, 21, 9, 3, 11 and 1% of our population, respectively. HCV genotype distribution was associated with gender, age, source and duration of infection, alanine aminotransferase (ALT) levels, cirrhosis, alcohol consumption, hepatitis B virus (HBV) and human immunodeficiency virus (HIV) coinfection. In multivariate analysis, only the source of infection was the independent factor significantly associated with genotype ( P  = 0.0001). In conclusion, this study shows a changing pattern of HCV genotypes in France, with i.v. drug abuse as the major risk factor, an increase of genotype 4, and to a lesser extent 1a and 5, and a decrease of genotypes 1b and 2. The modification of the HCV genotype pattern in France in the next 10 years may require new therapeutic strategies, and further survey studies.     

The dependence of human T-lymphocyte migration on the 5-lipoxygenation of endogenous arachidonic acid

Human T lymphocytes in modified Boyden migration chambers exhibited a chemokinetic response, but no detectable chemotaxis, to 5(S),12(R)-dihydroxyeicosa-6, 14-cis-8,10-trans-tetraenoic acid (leukotriene B₄) and to 5(S)-hydroxyeicosatetraenoic acid (5-HETE), which are 5-lipoxygenase products of arachidonic acid, and failed to respond to either leukotriene C₄ or 11-HETE. Concentrations of lymphocyte-derived 15-HETE and of 15-hydroperoxyeicosatetraenoic acid that inhibited the 5-lipoxygenation of endogenous arachidonic acid suppressed significantly both random migration and the chemokinetic responses of T lymphocytes to concanavalin A and -thioglycerol. That the suppressive effect of 15-HETE on T lymphocyte chemokinesis was attributable in part to the inhibition of 5-lipoxygenase was further suggested by the ability of exogenous 5-hydroperoxyeicosatetraenoic acid to restore chemokinetic responsiveness to lymphocytes that had been preincubated with 15-HETE.     

Genomics: the next step to elucidate the etiology of calcific aortic valve stenosis

With the current shift toward an older population, calcific aortic valve stenosis (AVS) is likely to become a major societal and economic burden. For many years, AVS was regarded as a degenerative and nonmodifiable process. However, molecular studies unanimously demonstrated that AVS is an actively regulated disorder with several potential therapeutic targets. Many factors are predicted to cause AVS, and an important genetic predisposition is anticipated. In this review, we describe candidate genes and signaling pathways identified by genetic research and incorporate this new knowledge into a more comprehensive picture of factors involved in the pathogenesis of AVS. We also emphasize the need for additional studies to elucidate its complete genetic architecture. Recent advances in genomic research offer a remarkable opportunity to investigate AVS at the most fundamental level. The benefits of these new approaches can be observed in many complex diseases, but the field of AVS is trailing behind. We discuss the future utility of these new genomic approaches to improve our understanding of AVS and to refine the management of patients in terms of diagnosis, prevention, and treatment.     

The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenes

The V617F activating point mutation in Jak2 is associated with a proportion of myeloproliferative disorders. In normal hematopoietic cells, Jak2 signals only when associated with a growth factor receptor, such as the erythropoietin receptor (EpoR). We sought to identify the molecular requirements for activation of Jak2V617F by introducing a point mutation in the FERM domain (Y114A), required for receptor binding. Whereas BaF3.EpoR cells are readily transformed by Jak2V617F to Epo independence, we found that the addition of the FERM domain mutation blocked transformation and the induction of reactive oxygen species. Further, while cells expressing Jak2V617F had constitutive activation of STAT5, cells expressing Jak2V617F/Y114A did not, suggesting that signaling is defective at a very proximal level. In addition, expression of the Myc and Pim proto-oncogenes by Jak2V617F was found to be FERM domain dependent. An inducible constitutively active STAT5 mutant expressed in BaF3 cells was sufficient to induce Myc and Pim. Finally, the FERM domain in Jak2V617F was also required for abnormal hematopoiesis in transduced primary murine fetal liver cells. Overall, our results suggest that constitutive activation of Jak2 requires an intact FERM domain for a transforming phenotype, and is necessary for activation of the major target of Jak2, STAT5.     

Peripatetic health-care workers as potential superspreaders

Many nosocomial outbreaks exhibit “superspreading events” in which cross-transmission occurs via a single individual to a large number of patients. We investigated how heterogeneity in Health-Care Worker (HCW) behaviors, especially compliance to hand hygiene, may cause superspreading events. In particular, we compared the superspreading potential of peripatetic (noncohorted) HCWs with that of other HCWs. We developed an agent-based model for hand transmission of a pathogen in a hospital ward. Three HCW profiles were allowed: 2 assigned profiles, one with frequent contacts with a limited number of patients, another with fewer contacts but with more patients; and one peripatetic profile, with a single daily contact with all patients. We used data from the literature on common nosocomial pathogens (Staphylococcus aureus, Enterococci). The average number of patients colonized over 1 month increases with noncompliance to hand hygiene. Importantly, we show that this increase depends on the profile of noncompliant HCWs; for instance, it remains low for a single noncompliant assigned HCW but can be quite large for a single noncompliant peripatetic HCW. Outbreaks with this single fully noncompliant peripatetic HCW (representing only 4.5% of the staff) are similar to those predicted when all HCWs are noncompliant following 23% of patient contacts. Noncompliant peripatetic HCWs may play a disproportionate role in disseminating pathogens in a hospital ward. Their unique profile makes them potential superspreaders. This suggests that average compliance to hygiene may not be a good indicator of nosocomial risk in real life health care settings with several HCW profiles.     

Differential MUC 1 expression in normal and neoplastic human pancreatic tissue. An immunohistochemical study of 60 samples.

Neoplastic transformation of epithelial cell sis commonly associated with altered synthesis of mucin glycoproteins. Few studies have been performed on the correlation between MUC 1 expression and pancreatic carcinoma using immunohistochemical methods. We compared the patterns of MUC 1 expression in normal pancreatic tissue, in pancreatic carcinoma, and in chronic pancreatitis. Immunohistochemical studies were performed using 3 monoclonal anti-MUC 1 antibodies (12C10, 1G5, and H23) on surgical specimens and on fine-needle aspiration biopsy specimens. In the neoplastic cells from adenocarcinomas, high levels of cytoplasmic MUC 1 expression were observed, with some membrane staining. No such cytoplasmic expression was observed in normal tissue, tissue from chronic pancreatitis, or benign neoplastic tissue. These data show conspicuous quantitative and qualitative differences between the patterns of MUC 1 expression observed in nonmalignant vs malignant pancreatic tissue and may be useful in the histologic diagnosis of adenocarcinoma in biopsy samples.