A Low-Cost Instrumentation System for Seismic Hazard Assessment in Urban Areas.

The development and application of a low-cost instrumentation system for seismic hazard assessment in urban areas are described in the present study. The system comprises a number of autonomous triaxial accelerographs, designed and manufactured in house and together with dedicated software for device configuration, data collection and further postprocessing. The main objective is to produce a detailed view of strong motion variability in urban areas, for at least light intensity strong motion events. The overall cost of the developed devices is at least ten times lower than the respective commercial units, hence their deployment as an ultra-dense network over the area of interest can be significantly cost-effective. This approach is considered an efficient complement to traditional microzonation procedures, which are typically based on relatively few actual recordings and the application of theoretical methodologies to assess the strong motion distribution. The manufactured devices adopt micro-electro-mechanical (MEMS) digital sensor technology for recording acceleration, whereas the accompanying software suite provides various configuration options, quick browsing, analyzing and exporting of the recorded events, as well as GIS type functionality for seamlessly producing explicit seismic hazard maps of the considered area. The evaluation of system performance was based on shaking table and real field comparisons against high accuracy commercial accelerographs. The study concludes with a real application of the proposed system in the form of an ultra-dense network installed at the city of Lefkada, an earthquake prone urban area in Greece, and the following compilation of explicit shakemaps.

Theory of Mind impairment in focal versus generalized epilepsy.

Theory of Mind (ToM) is a critical component of social cognition, and thus, its impairment may adversely affect social functioning and quality of life. Recent evidence has suggested that it is impaired in epilepsy. What is not clear, however, is whether it is related to particular types of epilepsy or other factors. We undertook the present study to explore ToM in patients with focal versus those with generalized epilepsy, the particular pattern of ToM deficits, and the potential influence of antiepileptic medication load. Our sample included 149 adults: 79 patients with epilepsy (34 with generalized epilepsy and 45 with focal epilepsy) and 70 healthy controls. Theory of Mind tasks included a) comprehension of hinting, b) comprehension of sarcasm and metaphor, c) comprehension of false beliefs and deception, d) recognition of faux pas, and e) a visual ToM task in cartoon form. We found significant ToM impairment in the group with focal epilepsy relative to the performance of both the healthy group and the group with generalized epilepsy on all tasks, with the exception of faux pas, on which the group with generalized epilepsy also performed more poorly than the healthy group. Additionally, early age at seizure onset, but not antiepileptic drug (AED) load, was associated with ToM performance. Our findings suggest that focal temporal and frontal lobe, but not generalized, epilepsies were associated with impaired ToM. This may reflect the neuroanatomical abnormalities in the relevant neuronal networks and may have implications for differential cognitive-behavioral interventions based on epilepsy type.

The effect of parental presence on the child's perception and co-operation during dental treatment.

AIM: This was to study the influence of parental presence during dental treatment on children's behaviour and perception. METHODS: Parents of 100 patients (mean age 7 ± 2.2 years) who visited the Postgraduate Paediatric Dental Clinic were randomly divided into two equal groups during one familiarisation and two treatment sessions: (1) parent present in the surgery/operatory and (2) parent absent (with their child observed through a window). Both an independent paediatric dentist and the parent rated the child's behaviour using the Venham scale. The child's perception was measured using the Wong-Baker Faces Rating Scale (FPRS) at the end of every session. Statistical analysis was performed with the IBM Statistics SPSS 22.0 (p < 0.05). Comparisons between variables were performed with the Mann-Whitney U, Wilcoxon and Friedman's tests. RESULTS: According to the paediatric dentist's rating, children's behaviour was worse when the parent was absent, with a significant difference only for the second restorative treatment session (p = 0.011). There was no difference on parents' rating child behaviour scores between the two groups. There was no difference of children's own perception between the two groups, except for any increased discomfort found at the second treatment (p = 0.021) when the parent was present. In both groups, the dentist rated lower Venham scores (better child behaviour), than parents did (presence: p = 0.001, absence: p = 0.038). Children recorded worse scores than both parents and the paediatric dentist. CONCLUSION: The only significant finding lay in the antithesis of how children perceived their last treatment session and how the dentist rated children's behaviour regarding parental presence. Parents' scores of their child's behaviour were unrelated to parental presence.

Basement membrane distortions impair lung lobation and capillary organization in the mouse model for fraser syndrome.

Fras1 is a putative extracellular matrix protein that has been implicated in the structural adhesion of embryonic epidermis to dermis. Moreover, mutations in Fras1/FRAS1 have been associated with the mouse blebbed phenotype and the human rare genetic disorder Fraser syndrome, respectively. Here we report the mapping of Fras1 within the extracellular space and evaluate the effects of Fras1 deficiency on lung development in the mouse. Expression of Fras1 was detected in the mesothelial cells of the visceral pleura and in the conducting airway epithelia. Immunogold histochemistry identified Fras1 as a component of the extracellular matrix localized below the lamina densa of epithelial basement membranes in the embryonic lung. Embryos homozygous for a targeted mutation of Fras1 exhibited fused pulmonary lobes resulting from incomplete separation during development as well as a profound disarrangement of blood capillaries in the terminal air sacs. We demonstrate that loss of Fras1 causes alterations in the molecular composition of basement membranes, concomitant with local disruptions of epithelial-endothelial contacts and extravasation of erythrocytes into the embryonic respiratory lumen. Thus, our findings identify Fras1 as an important structural component of the sub-lamina densa of basement membranes required for lobar septation and the organization of blood capillaries in the peripheral lung.

Evaluation of vertical accuracy of interocclusal records.

PURPOSE: The aim of this study was to evaluate four recording materials (polyether, polyvinyl siloxane, acrylic resin, and wax) for their ability to accurately record, maintain, and reproduce the vertical interocclusal relationship. MATERIALS AND METHODS: A metallic apparatus was used to represent the opposing arches; its epoxy resin duplicate represented the working casts. The vertical discrepancies produced because of the presence of the records were measured both after repositioning them on the metal apparatus and after transferring them onto the casts. Two-way ANOVA was performed. RESULTS: Closure through the interocclusal recording materials produced small vertical discrepancies ranging from 24 to 74 microm. When repositioned on the apparatus, the vertical discrepancies were greater. The lowest discrepancy was displayed by polyvinyl siloxane (101 microm) and polyether (107 microm), and the greatest was displayed by wax (168 microm). When records were transferred onto casts, the discrepancies were approximately 0.5 mm, without significant differences among materials. CONCLUSION: Closure through interocclusal recording materials and removal and repositioning of the records on the apparatus produced small vertical discrepancies with clinically insignificant differences between the materials tested. When records of all materials tested were transferred onto casts, vertical discrepancies of approximately 0.5 mm were found, which is of clinical concern.

Myocardial infarction under the age of 36: prevalence of thrombophilic disorders.

It has been suggested that thrombotic tendency increases the risk of myocardial infarction (MI). To investigate the association between the risk of MI at a young age and genetic thrombogenic disorders (G20210A mutation in the prothrombin gene, G1691A mutation in the factor V gene and deficiencies of protein C, protein S and antithrombin III) we conducted a case-control study among 70 survivors of MI who had experienced the event before the age of 36 and 260 healthy subjects. The G20210A mutation in the prothrombin gene was found more often in young patients with MI than among controls (11.4 versus 3.1%). The odds ratio (OR) for MI for carriers versus non-carriers was 4 (95% confidence interval [CI], 1.5 to 11.3). The adjusted OR for major cardiovascular risk factors (smoking, hypecholesterolaemia, diabetes mellitus, hypertension and obesity) was 4.3 (95% CI, 1.3 to 14). The simultaneous presence of both G20210A mutation in the prothrombin gene and smoking further increased the risk of MI compared with nonsmokers and non-carriers (OR, 58; 95% CI, 11.4-294). The G1691A mutation in factor V gene was not associated with an increased relative risk for MI (OR, 0.87; 95% CI, 0.26 to 2.5). Finally, there was no significant difference in the prevalence of deficiencies of protein C, protein S and antithrombin III between cases and controls. In conclusion, our data indicate that the G20210A mutation in the prothrombin gene was the only genetic prothrombotic risk factor associated with the risk of developing MI under the age of 36 years.

Fras1 deficiency results in cryptophthalmos, renal agenesis and blebbed phenotype in mice.

Loss of tight association between epidermis and dermis underlies several blistering disorders and is frequently caused by impaired function of extracellular matrix (ECM) proteins. Here we describe a new protein in mouse, Fras1, that is specifically detected in a linear fashion underlying the epidermis and the basal surface of other epithelia in embryos. Loss of Fras1 function results in the formation of subepidermal hemorrhagic blisters as well as unilateral or bilateral renal agenesis during mouse embryogenesis. Postnatally, homozygous Fras1 mutants have fusion of the eyelids and digits and unilateral renal agenesis or dysplasia. The defects observed in Fras1-/- mice phenocopy those of the existing bl (blebbed) mouse mutants, which have been considered a model for the human genetic disorder Fraser syndrome. We show that bl/bl homozygous embryos are devoid of Fras1 protein, consistent with the finding that Fras1 is mutated in these mice. In sum, our data suggest that perturbations in the composition of the extracellular space underlying epithelia could account for the onset of the blebbed phenotype in mouse and Fraser syndrome manifestation in human.

The progression in the mouse skin carcinogenesis model correlates with ERK1/2 signaling.

BACKGROUND: The ras family of proto-oncogenes encodes for small GTPases that play critical roles in cell-cycle progression and cellular transformation. ERK1/2 MAP kinases are major ras effectors. Tumors in chemically treated mouse skin contain mutations in the Ha-ras proto- oncogene. Amplification and mutation of Ha-ras has been shown to correlate with malignant progression of these tumors. Cell lines isolated from mouse skin tumors represent the stages of tumor development, such as the PDV:PDVC57 cell line pair and B9 squamous carcinoma and A5 spindle cells. PDVC57 cells were selected from PDV cells, which were transformed with dimethyl-benzanthracene (DMBA) in vitro and then transplanted in adult syngeneic mice. The PDV:PDVC57 pair contains ratio of normal:mutant Ha-ras 2:1 and 1:2, respectively. This genetic alteration correlates with more advanced tumorigenic characteristics of PDVC57 compared to PDV. The squamous carcinoma B9 cell clone was isolated from the same primary tumor as A5 spindle cell line. The mutant Ha-ras allele, also present in B9, is amplified and overexpressed in A5 cells. Therefore these cell line pairs represent an in vivo model for studies of Ha-ras and ERK1/2 signaling in mouse tumorigenesis. MATERIALS AND METHODS: The ERK1/2 status in the above mouse cell lines was examined by using various molecular techniques. For the study of the tumorigenic properties and the role of the ras/MEK/ERK1/2 pathway in the cell lines mentioned, phenotypic characteristics, colony formation assay, anchorage-independent growth, and gelatin zymography were assessed, after or without treatment with the MEK inhibitor, PD98059. RESULTS: ERK1/2 phosphorylation was found to be increased in PDVC57 when compared to PDV. This also applies to A5 spindle carcinoma cells when compared to squamous carcinoma and papilloma cells. The above finding was reproduced when transfecting human activated Ha-ras allele into PDV, thus demonstrating that Ha-ras enhances ERK1/2 signaling. To further test whether ERK1/2 activation was required for growth we used the MEK-1 inhibitor, PD98059. The latter inhibited cell proliferation and anchorage-independent growth of squamous and spindle cells. In addition, PD98059 treatment partially reverted the spindle morphology of A5 cells. CONCLUSIONS: These data suggest, for the first time, that oncogenicity and the degree of progression in the mouse skin carcinogenesis model correlates with ERK1/2 signaling.