Impact of depressive symptoms on adult asthma outcomes.

BACKGROUND: Psychological disorders, including depression, are common in adults with asthma. Although depression is treatable, its impact on longitudinal asthma outcomes is not clear. OBJECTIVE: To elucidate the impact of depressive symptoms on patient-centered outcomes and emergency health care use in adults with asthma. METHODS: We conducted a prospective cohort study of 743 adults with asthma who were recruited after hospitalization for asthma. Depressive symptoms were defined as having a score of 16 or more on the Center for Epidemiologic Studies Depression Scale. We examined the impact of depressive symptoms on patient-centered outcomes (validated severity-of-asthma score, Marks Asthma Quality of Life Questionnaire, and 12-Item Short-Form Health Survey physical component summary score) and on future emergency health care use for asthma ascertained from computerized databases. RESULTS: The prevalence of depressive symptoms was 18% (95% confidence interval [CI], 15%-21%) among adults with asthma. Depressive symptoms were associated with greater severity-of-asthma scores after controlling for age, sex, race/ ethnicity, educational attainment, and cigarette smoking (mean score increment, 2.6 points; 95% CI, 1.8-3.4 points). Furthermore, depressive symptoms were associated with poorer asthma-specific quality of life (mean score increment, 19.9 points; 95% CI, 17.7-22.1 points) and poorer physical health status (mean score decrement, 3.7 points; 95% CI, 1.5-5.8 points). Depressive symptoms were associated with a greater longitudinal risk of hospitalization for asthma (hazard ratio, 1.34; 95% CI, 0.98-1.84). After controlling for differences in preventive care for asthma, the relationship was stronger (hazard ratio, 1.45; 95% CI, 1.05-2.0). CONCLUSION: Depressive symptoms are common in adults with asthma and are associated with poorer health outcomes, including greater asthma severity and risk of hospitalization for asthma.     

Effects of air pollution on cup a 3 allergen in Cupressus arizonica pollen grains.

BACKGROUND: Cupressaceae is a family of plants resistant to airborne contamination, and its pollen is the main cause of winter allergic respiratory diseases, especially in North America, Japan, and Mediterranean countries. Recently, a major allergen from Cupressus arizonica pollen grains, Cup a 3, was cloned and expressed. OBJECTIVE: To study the effects of air pollution on the expression of Cup a 3, a thaumatinlike protein, in C. arizonica pollen grains using a combination of transmission electron microscopy and immunocytochemical techniques. METHODS: Observations were made in mature and hydrated C. arizonica pollen grains from various regions in Spain with different degrees of air pollution. Specimens were fixed using freezing protocols, and ultrathin sections were incubated with anti-rCup a 3 rabbit polyclonal antibodies. RESULTS: Labeling of Cup a 3 was detected in mature and hydrated C. arizonica pollen grains. It was more intense in pollen from polluted air regions, and abundant gold particles were observed as they were released through the pollen grain walls. Furthermore, gold particles remained abundant in the pollen cytoplasm. The labeling was noticeably lower in pollen grains from unpolluted air regions. CONCLUSIONS: Cup a 3 is present in the cytoplasm and walls of cypress pollen grains during the air dispersion and hydration stages. The abundance of Cup a 3 in pollen grains under polluted air conditions indicates that these cypresses intensify their activity as a defense from environmental pollution, thus strengthening their allergenicity.     

Differences in hormonal and inflammatory parameters in male Lewis and Long Evans rats with adjuvant arthritis

The purpose of the present study was (i) to compare secretory responses of prolactin and corticosterone to the acute stress of immobilization in male rats of the Lewis and Long Evans strains and (ii) to compare secretion of the two hormones in rats with fully developed adjuvant arthritis (AA) and their relationship with the intensity of the inflammatory reaction. A short immobilization of 5 min induced equal elevations of both hormones in both strains, but 20-min immobilization produced significantly stronger responses in Long Evans rats than in Lewis rats. AA inhibited prolactin secretion equally in both strains (from 11.6 +/- 1.3 ng/ml to 4.2 +/- 0.6 ng/ml in Lewis rats, p < 0.01, and from 3.7 +/- 0.6 to 2.12 +/- 0.1 ng/ml in Long Evans rats, p < 0.05), but caused a conspiciously larger elevation of corticosterone in the Long Evans than in the Lewis animals (11.5 +/- 1.2 microg/dl in Long Evans rats versus 5.1 +/- 0.5 microg/dl in Lewis rats, p < 0.01) while basal levels were similar. The larger corticosterone response in the Long Evans rats was associated with a stronger inflammatory reaction assessed by hind paw swelling (2.3 +/- 0.1 ml for Long Evans rats versus 1.8 +/- 0.08 ml for Lewis rats, p < 0.01) and plasma levels of nitric oxide (47.5 +/- 5.7 microM for Long Evans rats versus 28.7 +/- 2.5 microM for Lewis rats, p < 0.01) than in the Lewis males with lower corticosterone levels. In conclusion, there are significant, obviously genetically based, differences in the corticosterone responses to both immobilization and AA between the two strains, with the Long Evans rats reacting more strongly than the Lewis rats. The lack of the expected inverse relationship between corticosterone levels and the intensity of the inflammation indicates that the activity of corticosterone is not its primary determinant and that other important factors are involved.     

Magnetic resonance microscopy versus light microscopy in human embryology teaching

A study was carried out on the application of magnetic resonance microscopy (MRM) in teaching prenatal human development. Human embryos measuring 8 mm, 15 mm, 18.5 mm, and 22 mm were fixed in a 4% paraformaldehyde solution and sections obtained with magnetic resonance imaging (MRI) were compared to those prepared for light microscopy (LM), using the same embryos. The MRM and LM slices were of a similar quality. In the MRM sections, embryonic organs and systems were clearly visible, particularly the peripheral and central nervous systems, and the cardiovascular and digestive systems. The digitalization and clarity of the MRM images make them an ideal teaching aid that is suitable for students during the first years of a health-science degree, particularly medicine. As well as providing students with their first experience of MRM, these images allow students to access, at any time, all embryos used, to assess changes in the positions of different organs throughout their stages of development, and to acquire spatial vision, an absolute requirement in the study of human anatomy. We recommend that this technique be incorporated into the wealth of standard embryonic teaching methods already in use.     

Vortex Shedding in Steady Flow Through a Model of an Arterial Stenosis and Its Relevance to Mural Platelet Deposition

In this study, the development of unsteady vortical formations in the separated flow region distal to a stenosis throat is presented and compared with the platelet deposition measurements, to enhance our understanding of the mechanisms involved in platelet kinetics in flowing blood. Qualitative and quantitative flow visualization and numerical simulations were performed in a model of a streamlined axisymmetric stenosis with an area reduction of 84% at the throat of the stenosis. Measurements were performed at Reynolds numbers (Re), based on upstream diameter and average velocity, ranging from 300 to 1800. Both the digital particle image visualization method employed and the numerical simulations were able to capture the motion of the vortices through the separated flow region. Periodic shedding of vortices began at approximately Re=375 and continued for the full range of Re studied. The locales at which these vortices are initiated, their size, and their life span, were a function of Re. The numerical simulations of turbulent flow through the stenosis model entailed a detailed depiction of the process of vortex shedding in the separated flow region downstream of the stenosis. These flow patterns were used to elucidate the mechanisms involved in blood platelet kinetics and deposition in the area in and around an arterial stenosis. The unsteady flow development in the recirculation region is hypothesized as the mechanism for observed changes in the distribution of mural platelet deposition between Re=300, 900, and 1800, despite only a marginal variation in the size and shape of the recirculation zone under these flow conditions. © 1999 Biomedical Engineering Society. PAC99: 8719Uv, 8710+e     

Adrenocortical adenoma and carcinoma: histopathological and molecular comparative analysis.

We compared histomorphological features and molecular expression profiles of adrenocortical adenomas (ACAd) and carcinomas (ACCa). A critical histopathological review (mean, 11 slides per patient) was conducted of 37 ACAd and 67 ACCa. Paraffin-embedded tissue cores of ACAd (n = 33) and ACCa (n = 38) were arrayed in triplicate on tissue microarrays. Expression profiles of p53, mdm-2, p21, Bcl-2, cyclin D1, p27, and Ki-67 were investigated by immunohistochemistry and correlated with histopathology and patient outcome using standard statistical methodology. Median follow-up period was 5 years. Tumor necrosis, atypical mitoses, and >1 mitosis per 50 high-power fields were factors that were highly specific for ACCa (P <.001). Number (0 to 4) of unfavorable markers [Ki-67 (+), p21 (+), p27 (+), mdm-2(-)] expressed was significantly associated with mitotic activity and morphologic index (i.e., number of adverse morphologic features) and highly predictive of malignancy (P <.001). Ki-67 overexpression occurred in 0 ACAd and 36% ACCa (P <.001) and was significantly associated with mitotic rate and unfavorable morphologic index (P <.001). Tumor necrosis, atypical mitoses, >5 mitoses per 50 high-power fields, sinusoidal invasion, histologic index of >5, and presence of more than two unfavorable molecular markers were associated significantly with metastasis in ACCa. Well-established histopathologic criteria and Ki-67 can specifically distinguish ACCAd from ACCa. Tumor cell proliferation (Ki-67) correlates with mitotic activity and morphologic index. Tumor morphology is a better predictor of metastatic risk in ACCa than current immunohistochemistry-detected cell cycle regulatory and proliferation-associated proteins.     

E-cadherin germline missense mutations and cell phenotype: evidence for the independence of cell invasion on the motile capabilities of the cells

In Hereditary Diffuse Gastric Cancer syndrome, E-cadherin germline mutations of the missense type harbour significant functional consequences. In this study, we have characterised the effect of T340A, A617T, A634V and V832M E-cadherin germline missense mutations on cell morphology, motility and proliferation. Wild-type E-cadherin and A617T expressing cells have an epithelial-like morphology, with polarised cells migrating unidirectionally. T340A and A634V expressing cells, fibroblast-like, have a high motile phenotype. We show that this phenotype is dependent on an increased level of active RhoA. V832M expressing cells grow in piled-up structure of round cells, as an effect of the disturbance of the binding between alpha-catenin and beta-catenin. The destabilisation of the adhesion complex is shown to hamper the motile capabilities of these cells. We did not observe any effect of the E-cadherin mutations on cell proliferation. We show the existence of a genotype-phenotype correlation between different E-cadherin mutations and cell behaviour. However, we demonstrate that the ability of cells expressing the different E-cadherin mutations to invade is independent on their motile capabilities, providing evidence that motility is neither necessary nor sufficient for cells to invade. Our data give new insights into the understanding of the mechanisms linking invasion and E-cadherin mutations in diffuse gastric cancer.     

Encuesta nacional sobre valoración de la actividad de los médicos internos residentes en los servicios de urgencias españoles

Introduction

The care activity of internal resident doctors is common to practically all medical and surgical training programs; however, there are no national data available regarding the situation of this activity from the perspective of the resident. The present study has sought to collect the opinion of the resident internal physicians on the health care performance and the teaching character that links them to their corresponding emergency departments, in the following areas: overall training value, appreciation of the workload, characteristics of the morning rotation, supervision or tutoring, etc.

Family-based and case-control studies reveal no association of lipocalin-type prostaglandin D2 synthase with schizophrenia.

Several observations point to the involvement of disturbed lipid biology in schizophrenia. Reduced response to niacin flushing test, which involves vasodilatation induced by prostaglandin D2 (PGD2), is among the evidences, together with decreased CSF levels of lipocalin-type prostaglandin D2 synthase (PTGDS), the enzyme responsible for the synthesis of PGD2 in the brain. Since PTGDS is also a carrier for lipophilic molecules such as retinoids and thyroid hormones, altered PTGDS levels might influence both PGD2-mediated signaling, and vitamin A and thyroid hormone availability. To test whether genetic variants of PTGDS are involved in the etiology of schizophrenia, we searched for variants in the coding and regulatory regions of the gene. We identified four previously described polymorphisms. Using two case-control samples from Portugal and Brazil, none of the polymorphisms tested was associated with the disease. In addition, no transmission distortion was observed in an independent parents-offspring sample from the Azorean Islands. Our data do not support the involvement of the PTGDS gene in the etiology of schizophrenia.     

Cohesin component dynamics during meiotic prophase I in mammalian oocytes

Cohesins are chromosomal proteins that form complexes involved in the maintenance of sister chromatid cohesion during division of somatic and germ cells. Three meiosis-specific cohesin subunits have been reported in mammals, REC8, STAG3 and SMC1 beta; their expression in mouse spermatocytes has also been described. Here we studied the localization of different meiotic and mitotic cohesin components during prophase I in human and murine female germ cells. In normal and atretic human fetal oocytes, from leptotene to diplotene stages, REC8 and STAG3 colocalize in fibers. In murine oocytes, SMC1beta, SMC3 and STAG3 are localized along fibers that correspond first to the chromosome axis and then to the synaptonemal complex in pachytene. Mitotic cohesin subunit RAD21 is also found in fibers that decorate the SC during prophase I in mouse oocytes, suggesting a role for this cohesin in mammalian sister chromatid cohesion in female meiosis. We observed that, unlike human oocytes, murine synaptonemal complex protein SYCP3 localizes to nucleoli throughout prophase I stages, and centromeres cluster in discrete locations from leptotene to dictyate. At difference from meiosis in male mice, the cohesin axis is progressively lost during the first week after birth in females with a parallel destruction of the axial elements at dictyate arrest, demonstrating sexual dimorphism in sister chromatid cohesion in meiosis.