Insight dimensions and cognitive function in psychosis: a longitudinal study

BACKGROUND: It has been reported that lack of insight is significantly associated with cognitive disturbance in schizophrenia. This study examines the longitudinal relationships between insight dimensions and cognitive performance in psychosis. METHODS: Participants were 75 consecutively admitted inpatients with schizophrenia, affective disorder with psychotic symptoms or schizoaffective disorder. Assessments were conducted at two time points during the study: at the time of hospital discharge after an acute psychotic episode and at a follow-up time that occurred more than 6 months after discharge. A multidimensional approach of insight was chosen and three instruments for its assessment were used: the Scale to Assess Unawareness of Mental Disorder (SUMD), three items concerning insight on the Assessment and Documentation in Psychopathology (AMDP) system and the Insight and Treatment Attitudes Questionnaire. The neuropsychological battery included a wide range of tests that assessed global cognitive function, attention, memory, and executive functions. RESULTS: After conducting adequate statistical correction to avoid Type I bias, insight dimensions and cognitive performance were not found to be significantly associated at cross-sectional and longitudinal assessments. In addition, baseline cognitive performance did not explain changes in insight dimensions at follow-up. Similar results were found in the subset of patients with schizophrenia (n = 37). The possibility of a Type II error might have increased due to sample attrition at follow-up. CONCLUSION: These results suggest that lack of insight dimensions and cognitive functioning may be unrelated phenomena in psychosis

CRP polymorphisms and chronic kidney disease in the third national health and nutrition examination survey

<p>Abstract</p> <p>Background</p> <p><it>CRP </it>gene polymorphisms are associated with serum C-reactive protein concentrations and may play a role in chronic kidney disease (CKD) progression. We recently reported an association between the gene variant rs2808630 and CKD progression in African Americans with hypertensive kidney disease. This association has not been studied in other ethnic groups.</p> <p>Methods</p> <p>We used data from 5955 participants from Phase 2 of The Third National Health and Nutrition Examination Survey (1991-1994) to study the association between <it>CRP </it>polymorphisms and CKD prevalence in a population-based sample. The primary outcome was CKD defined as estimated glomerular filtration rate (eGFR) <60 ml/min or the presence of albuminuria. Secondary outcomes were the presence of albuminuria (any degree) and continuous eGFR. Six single nucleotide polymorphisms (SNPs) from the <it>CRP </it>gene, rs2808630, rs1205, rs3093066, rs1417938, rs3093058, and rs1800947, were evaluated.</p> <p>Results</p> <p><it>CRP </it>rs2808630 AG compared to the referent AA genotype was associated with CKD in non-Hispanic blacks (n = 1649, 293 of whom had CKD) with an adjusted odds ratio (OR) of 3.09 (95% CI 1.65-5.8; p = 0.001). For the secondary outcomes, rs2808630 AG compared to the referent AA genotype was associated with albuminuria with an adjusted OR of 3.07 (95% CI 1.59-5.94; p = 0.002), however not with eGFR. There was no association between the SNPs and CKD, albuminuria or eGFR in non-Hispanic whites or Mexicans Americans.</p> <p>Conclusions</p> <p>In this cross-sectional study, the 3' flanking <it>CRP </it>gene variant rs2808630 was associated with CKD, mainly through its association with albuminuria in the non-Hispanic blacks. Despite not finding an association with eGFR, our results support our previous study demonstrating an association between <it>CRP </it>gene variant rs2808630 and CKD progression in a longitudinal cohort of African American with hypertensive kidney disease.</p

Photoacclimation strategies in northeastern Atlantic seagrasses: Integrating responses across plant organizational levels

Seagrasses live in highly variable light environments and adjust to these variations by expressing acclimatory responses at different plant organizational levels (meadow, shoot, leaf and chloroplast level). Yet, comparative studies, to identify species' strategies, and integration of the relative importance of photoacclimatory adjustments at different levels are still missing. The variation in photoacclimatory responses at the chloroplast and leaf level were studied along individual leaves of Cymodocea nodosa, Zostera marina and Z. noltei, including measurements of variable chlorophyll fluorescence, photosynthesis, photoprotective capacities, non-photochemical quenching and D1-protein repair, and assessments of variation in leaf anatomy and chloroplast distribution. Our results show that the slower-growing C. nodosa expressed rather limited physiological and biochemical adjustments in response to light availability, while both species of faster-growing Zostera showed high variability along the leaves. In contrast, the inverse pattern was found for leaf anatomical adjustments in response to light availability, which were more pronounced in C. nodosa. This integrative plant organizational level approach shows that seagrasses differ in their photoacclimatory strategies and that these are linked to the species' life history strategies, information that will be critical for predicting the responses of seagrasses to disturbances and to accordingly develop adequate management strategies.Fundacao para a Ciencia e Tecnologia (FCT), Portugal [PTDC/MAR-EST/4257/2014

A novel xylan degrading β-D-xylosidase: purification and biochemical characterization

Aspergillus ochraceus, a thermotolerant fungus isolated in Brazil from decomposing materials, produced an extracellular b-xylosidase that was purified using DEAE-cellulose ion exchange chromatography, Sephadex G-100 and Biogel P-60 gel filtration. b-xylosidase is a glycoprotein (39 % carbohydrate content) and has a molecular mass of 137 kDa by SDS-PAGE, with optimal temperature and pH at 70 C and 3.0–5.5, respectively.b-xylosidase was stable in acidic pH (3.0–6.0) and 70 C for 1 h. The enzyme was activated by 5 mM MnCl2 (28 %)and MgCl2 (20 %) salts. The b-xylosidase produced by A. ochraceus preferentially hydrolyzed p-nitrophenyl-b- D-xylopyranoside, exhibiting apparent Km and Vmax values of 0.66 mM and 39 U (mg protein)-1 respectively, and to a lesser extent p-nitrophenyl-b-D-glucopyranoside. The enzyme was able to hydrolyze xylan from different sources,suggesting a novel b-D-xylosidase that degrades xylan. HPLC analysis revealed xylans of different compositions which allowed explaining the differences in specificity observed by b-xylosidase. TLC confirmed the capacity.This work was supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), and the Conselho de Desenvolvimento Científico e Tecnológico (CNPq). J. A. J. and M. L. T. M. P are Research Fellows of CNPq. M. M. was a recipient of a FAPESP fellowship and this work is part of her Doctoral Thesis. It is also part of the project SISBIOTA CNPq: 563260/2010-6 and FAPESP: 2010/52322-3

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

Cell-cell adhesion is an elementary process in normal epithelial cellular architecture. Several studies have shown the role mediated by cadherins in this process, besides their role in the maintenance of cell polarity, differentiation and cell growth. However, during tumour progression, these molecules are frequently altered. In breast cancer, tumours that overexpress P-cadherin usually present a high histological grade, show decreased cell polarity and are associated with worse patient survival. However, little is known about how this protein dictates the very aggressive behaviour of these tumours. To achieve this goal, we set up two breast cancer cell models, where P-cadherin expression was differently modulated and analysed in terms of cell invasion, motility and migration. We show that P-cadherin overexpression, in breast cancer cells with wild-type E-cadherin, promotes cell invasion, motility and migration. Moreover, we found that the overexpression of P-cadherin induces the secretion of matrix metalloproteases, specifically MMP-1 and MMP-2, which then lead to P-cadherin ectodomain cleavage. Further, we showed that soluble P-cadherin fragment is able to induce in vitro invasion of breast cancer cells. Overall, our results contribute to elucidate the mechanism underlying the invasive behaviour of P-cadherin expressing breast tumours.scientific project (POCI/BIA-BCM/59252/2004) financed by the Portuguese Science and Technology Foundation (FCT). FCT also provided research grants as follows: Programa Ciência 2007 (FCT) for Joana Paredes, and PhD research grants for Ana Sofia Ribeiro (SFRH/BD/36096/2007) and André Albergaria (SFRH/BD/15316/2005)

ZIP8 Zinc Transporter: Indispensable Role for Both Multiple-Organ Organogenesis and Hematopoiesis In Utero

Previously this laboratory characterized Slc39a8-encoded ZIP8 as a Zn2+/(HCO3–)2 symporter; yet, the overall physiological importance of ZIP8 at the whole-organism level remains unclear. Herein we describe the phenotype of the hypomorphic Slc39a8(neo/neo) mouse which has retained the neomycin-resistance gene in intron 3, hence causing significantly decreased ZIP8 mRNA and protein levels in embryo, fetus, placenta, yolk sac, and several tissues of neonates. The Slc39a8(neo) allele is associated with diminished zinc and iron uptake in mouse fetal fibroblast and liver-derived cultures; consequently, Slc39a8(neo/neo) newborns exhibit diminished zinc and iron levels in several tissues. Slc39a8(neo/neo) homozygotes from gestational day(GD)-11.5 onward are pale, growth-stunted, and die between GD18.5 and 48 h postnatally. Defects include: severely hypoplastic spleen; hypoplasia of liver, kidney, lung, and lower limbs. Histologically, Slc39a8(neo/neo) neonates show decreased numbers of hematopoietic islands in yolk sac and liver. Low hemoglobin, hematocrit, red cell count, serum iron, and total iron-binding capacity confirmed severe anemia. Flow cytometry of fetal liver cells revealed the erythroid series strikingly affected in the hypomorph. Zinc-dependent 5-aminolevulinic acid dehydratase, required for heme synthesis, was not different between Slc39a8(+/+) and Slc39a8(neo/neo) offspring. To demonstrate further that the mouse phenotype is due to ZIP8 deficiency, we bred Slc39a8(+/neo) with BAC-transgenic BTZIP8-3 line (carrying three extra copies of the Slc39a8 allele); this cross generated viable Slc39a8(neo/neo)_BTZIP8-3(+/+) pups showing none of the above-mentioned congenital defects–proving Slc39a8(neo/neo) causes the described phenotype. Our study demonstrates that ZIP8-mediated zinc transport plays an unappreciated critical role during in utero and neonatal growth, organ morphogenesis, and hematopoiesis