Patterns of change in cortical morphometry following traumatic brain injury in adults

Progressive cortical volumetric loss following moderate–severe traumatic brain injury (TBI) has been observed; however, regionally specific changes in the structural determinants of cortical volume, namely, cortical thickness (CT) and cortical surface area (CSA), are unknown and may inform the patterns and neural substrates of neurodegeneration and plasticity following injury. We aimed to (a) assess differences in CT and CSA between TBI participants and controls in the early chronic stage post‐injury, (b) describe longitudinal changes in cortical morphometry following TBI, and (c) examine how regional changes in CT and CSA are associated. We acquired magnetic resonance images for 67 participants with TBI at up to 4 time‐points spanning 5 months to 7 years post‐injury, and 18 controls at 2 time‐points. In the early chronic stage, TBI participants displayed thinner cortices than controls, predominantly in frontal regions, but no CSA differences. Throughout the chronic period, TBI participants showed widespread CT reductions in posterior cingulate/precuneus regions and moderate CT increase in frontal regions. Additionally, CSA showed a significant decrease in the orbitofrontal cortex and circumscribed increase in posterior regions. No changes were identified in controls. Relationships between regional cortical changes in the same morphological measure revealed coordinated patterns within participants, whereas correlations between regions with CT and CSA change yielded bi‐directional relationships. This suggests that these measures may be differentially affected by neurodegenerative mechanisms such as transneuronal degeneration following TBI and that degeneration may be localized to the depths of cortical sulci. These findings emphasize the importance of dissecting morphometric contributions to cortical volume change.     

Viscoelastic Polyurethane Foams with Reduced Flammability and Cytotoxicity

Consistent and proper use of respiratory protective devices (RPD) is one of the essential actions that can be taken to reduce the risk of exposure to airborne hazards, i.e., biological and nonbiological aerosols, vapours, and gases. Proper fit of the facepiece and comfort properties of RPDs play a crucial role in effective protection and acceptance of RPDs by workers. The objective of the present paper was to develop viscoelastic polyurethane foams for use in RPD seals characterised by proper elasticity, allowing for the enhancement of the device fit to the face and the capability of removing moisture from the skin in order to improve the comfort of RPD use. Moreover, it was pivotal to ensure the non-flammability of the foams, as well as a simultaneous reduction in their cytotoxicity. The obtained foams were characterised using scanning electron microscopy, infrared spectroscopy, thermogravimetry, and differential scanning calorimetry. Measurements also involved gel fraction, apparent density, compression set, rebound resilience, wettability, flammability, and cytotoxicity. The results are discussed in the context of the impact of modifications to the foam formulation (i.e., flame-retardant type and content) on the desired foam properties. The test results set directions for future works aimed to develop viscoelastic polyurethane foams that could be applied in the design of respiratory protective devices.     

Reductive Modification of Carbon Nitride Structure by Metals—The Influence on Structure and Photocatalytic Hydrogen Evolution

Pt, Ru, and Ir were introduced onto the surface of graphitic carbon nitride (g-C₃N₄) using the wet impregnation method. A reduction of these photocatalysts with hydrogen causes several changes, such as a significant increase in the specific surface area, a C/N atomic ratio, a number of defects in the crystalline structure of g-C₃N₄, and the contribution of nitrogen bound to the amino and imino groups. According to the X-ray photoelectron spectroscopy results, a transition layer is formed at the g-C₃N₄/metal nanoparticle interphase, which contains metal at a positive degree of oxidation bonded to nitrogen. These structural changes significantly enhanced the photocatalytic activity in the production of hydrogen through the water-splitting reaction. The activity of the platinum photocatalyst was 24 times greater than that of pristine g-C₃N₄. Moreover, the enhanced activity was attributed to significantly better separation of photogenerated electron–hole pairs on metal nanoparticles and structural distortions of g-C₃N₄.     

Immunity in young adult survivors of childhood leukemia is similar to the elderly rather than age‐matched controls: Role of cytomegalovirus

Many treatment complications that occur late in childhood cancer survivors resemble age‐related comorbidities observed in the elderly. An immune phenotype characterized by increased immune activation, systemic inflammation, and accumulation of late‐differentiated memory CD57⁺CD28^? T cells has been associated with comorbidities in the elderly. Here, we explored if this phenotype was present in young adult leukemia survivors following an average of 19 years from chemotherapy and/or radiotherapy completion, and compared this with that in age‐matched controls. We found that markers of systemic inflammation—IL‐6 and human C‐reactive protein and immune activation—CD38 and HLA‐DR on T cells, soluble CD (sCD)163 from monocytes and macrophages—were increased in survivors compared to controls. T‐cell responses specific to cytomegalovirus (CMV) were also increased in survivors compared to controls while CMV IgG levels in survivors were comparable to levels measured in the elderly (>50years) and correlated with IL‐6, human C‐reactive protein, sCD163, and CD57⁺CD28^? memory T cells. Immune activation and inflammation markers correlated poorly with prior chemotherapy and radiotherapy exposure. These data suggest that CMV infection/reactivation is strongly correlated with the immunological phenotype seen in young childhood leukemia survivors and these changes may be associated with the early onset of age‐related comorbidities in this group.     

Etiology of familial aggregation in melanoma and squamous cell carcinoma of the skin.

BACKGROUND: Melanoma and squamous cell carcinoma of the skin (SCC) have been previously shown to coaggregate in families. To shed light on the etiology, we estimated the relative contributions of genetic and environmental factors on the occurrence of each disease, in addition to their influence on coaggregation of the two diseases. Because the malignancies are dependent on UV radiation, we did separate analyses for sun-covered and sun-exposed sites. METHODS: Our Swedish population-based data included 11 million individuals in 3 million families. We used an extended generalized linear mixed model to estimate the genetic and environmental contribution. RESULTS: In melanoma, the genetic contribution was 18% [95% confidence interval (95% CI), 13-22%] in the all-sites analysis, whereas the family-shared contribution was slightly higher in the sun-covered compared with sun-exposed sites analysis. SCC revealed very similar estimates in all analyses for both the genetic effects estimated to 8% (95% CI, 4-12%) and family-shared environmental factors at 18% (95% CI, 16-19%), respectively. In the coaggregation analysis, genetic and family-shared environmental components were estimated at 47% (95% CI, 43-51%) and 36% (95% CI, 33-39%), respectively. CONCLUSIONS: Genetic factors are important in familial aggregation of melanoma and the higher sun-covered compared with sun-exposed site estimate of family-shared environment may convey benefit from cautious sunbathing. In SCC, we observed the highest contribution of family-shared environmental effects in cancer to date, implicating the importance of familial habits. Moreover, we elucidate the potential involvement of genetic variability in the familial coaggregation of melanoma and SCC.     

7-Alkylguanine adducts of styrene oxide determined by 32P-postlabelling in DNA and human embryonal lung fibroblasts (HEL)

The modified ³²P-postlabelling method was used for the detectionof N-7-(2-hydroxy-phenylethyl) guanine adducts in DNA and humanembryonal lung (HEL) cells treated in vitro with styrene oxide(SO). The total recovery of 7-alkylguanine adducts of styreneoxide in DNA analysed by ³²P-postlabelling assay was 4.1±0.6%.The disappearance of 7-alkyldeoxyguanosine monophosphate adductsfrom SO-modified DNA at 37°C showed a half-life of 19 h.The levels of 7-alkylguanine DNA adducts and single-strand breaks(SSBs) in DNA were determined in HEL cells treated with SO for3 and 18 h. In the 3 h treatment there was a concentration-dependentincrease of both 7-alkylguanine adducts and SSBs in DNA (r =0.98, P = 0.012 and r = 0.99, P = 0.003, respectively). We founda significant correlation between 7-alkylguanine DNA adductsand SSBs in DNA (r = 0.98, P = 0.011). In HEL cells     

Associative processes disorders in schizophrenia

This paper tries to approach and systematize knowledge about the character of associative process disorders in schizophrenia. In considering schizophrenia as an illness composed of various symptoms which may lead to different clinical progress, the paper is mainly focused on disorganization of thinking and, consequently, speaking and communication disorders. Authors reviewed various concept of pathogenesis and course of associative process disorders in schizophrenic patients. Special attention was paid to a connectionist model of disturbed associations. This model originates from cognitive psychology and assumes that concepts are represented as networks in the mental lexicon. Following from this model, a hypothesis was presented, claiming that disturbed associations in schizophrenia may be related to abnormalities in semantic networks. Results of research, supporting this hypothesis, were referred. Moreover, authors tried to describe the relationship between associative processes disorders in schizophrenia and abnormalities in neurophysiological (event--related potentials) and neuropathological (MRI) examinations. At least hypotheses describing the role of neurotransmission disorders was presented.     

Time trends and familial risks in squamous cell carcinoma of the skin

OBJECTIVES: To study time trends and familial clustering of invasive and in situ squamous cell skin cancers (SCC), with particular reference to sun-exposed and covered sites of the body. DESIGN: Epidemiologic follow-up study of the whole population. SETTING: The Swedish Family-Cancer Database from the year 2000, to cover individuals born after 1931 with their biological parents, totaling 10.2 million persons. PATIENTS: Cancer data were obtained from the Swedish Cancer Registry from 1961 through 1998 and included 1907 invasive SCCs in offspring and 12,702 and 7167 in fathers and mothers, respectively. The numbers of patients affected by in situ SCC were 2666, 13,739, and 13,321, respectively. MAIN OUTCOME MEASURES: Standardized incidence ratios and 95% confidence intervals were calculated for SCC in offspring when parents had SCC. Incidence rates were calculated for the population in the Database. RESULTS: Incidence trends showed a large increase in reported cases of SCC and particularly of in situ SCC. Among invasive cases, the increase was largest among covered sites. A clear cohort effect was observed particularly for SCC on covered sites. Familial standardized incidence ratios for offspring combining invasive and in situ SCC were 2.25 (95% confidence interval, 1.93-2.59) for concordant exposed sites and 2.60 (95% confidence interval, 1.38-4.20) for concordant covered sites, suggesting no difference between the body parts within the present statistical power. CONCLUSIONS: The higher increase in incidence on covered sites and the strong cohort effect suggest a contribution by intentional tanning. The observed equal increase in the familial effect on exposed and covered sites suggests that familial risk increases proportionately to the background rate.