Social media and children: what is the paediatrician’s role?

Social media use has become an integral part of children’s and adolescents’ lives. It has become a novel way of interaction among people and influences people’s social lives and public opinion as well as people’s purchasing decisions and businesses. Any website or platform that allows social interaction is considered to be a social media site. Social media use among children in 25 European countries has been reported to be 38% among 9–12 year olds and 77% among those aged 13–16 years. All these children report having their own profile on at least one social network site. While social networking provides children and adolescents with many opportunities and benefits, it also carries many risks. Among the benefits are socialization and communication enhancement, improving learning skills, positive impact on education and getting health information. Potential risks of social media use include falsifying age and identity, cyberbullying, sexting, Facebook depression, gamification, glamourization, cyberostracism and sleep disturbances.

Conclusion: Paediatricians play a vital role in promoting the physical, mental and social welfare of all children. There is a critical need for paediatricians to play an active role, guiding children and families appropriately through the impact of social networking, in order to become a real driver of children’s development.

     

Effect of Aryl Substituents and Fluorine Addition on the Optoelectronic Properties and Organic Solar Cell Performance of a High Efficiency Indacenodithienothiophene‐alt‐Quinoxaline π‐Conjugated Polymer

A series of donor‐acceptor (D‐A) π‐conjugated polymers, based on indacenodithienothiophene (IDTT) as an electron‐donating unit and quinoxaline as an electron‐deficient moiety, are synthesized via a Pd‐catalyzed Stille cross‐coupling polymerization. Molecular characteristics, photovoltaic parameters, and optoelectronic properties are examined through structural differences corresponding to thienyl versus phenyl side group substitutions on the IDTT and the non‐fluorinated versus the monofluoro quinoxaline derivatives. One of the most important outcome is that the power conversion efficiency (PCE) in the studied polymers is more device architecture dependent (conventional vs inverted) rather than chemical structure dependent. From single junction solar cells based on bulk heterojunction polymer:[6,6]‐phenyl‐C₇₁‐butyric acid methyl ester (PC₇₁BM) systems as the active layer, a maximum PCE of 5.33% has been achieved from the polymer containing the thienyl substituent on the IDTT and one fluorine atom on the quinoxaline. This demonstrates that finding the optimum molecular weight of ThIDTT‐QF or introducing the monofluoro‐quinoxaline in a regioregular motif in the polymer backbone significantly higher PCE can be expected versus the fully optimized high performance PhIDTT‐Q conjugated polymer.     

A diamino-functionalized silsesquioxane pillared graphene oxide for CO2 capture

In the race for viable solutions that could slow down carbon emissions and help in meeting the climate change targets a lot of effort is being made towards the development of suitable CO₂ adsorbents with high surface area, tunable pore size and surface functionalities that could enhance selective adsorption. Here, we explored the use of silsesquioxane pillared graphene oxide for CO₂ capture; we modified silsesquioxane loading and processing parameters in order to obtain pillared structures with nanopores of the tailored size and surface properties to maximize the CO₂ sorption capacity. Powder X-ray diffraction, XPS and FTIR spectroscopies, thermal analysis (DTA/TGA), surface area measurements and CO₂ adsorption measurements were employed to characterize the materials and evaluate their performance. Through this optimisation process, materials with good CO₂ storage capacities of up to 1.7/1.5 mmol g⁻¹ at 273 K/298 K in atmospheric pressure, were achieved.

Study of the CO₂ uptake performance of silsesquioxane pillared graphene oxide prepared with different pillar loading and way of drying.     

Scanning method of identify the molecular heterogeneity of δ-globin gene especially in δ-thalassemias: Detection of three novel substitutions in the promoter region of the gene

A scanning strategy for the detection of δ-globin gene mutations and polymorphisms is presented. This procedure is based on the denaturing gradient gel electrophoresis (DGGE) of four different artificially amplified DNA fragments which cover the promoter, the exons, as well as IVS I of the reported gene. To estimate the efficiency and sensitivity of the proposed procedure, we analysed the appropriate controls of δ-thalassemic carriers, uncharacterised δ-thalassemias and cases with normal hematological phenotype, but slightly increased (up to 3.5%) HbA₂. DGGE results permitted the identification of δ-globin gene mutations and the polymorphism - 199 (T→C). Three novel base substitutions inside the promoter region of the gene [−65(A→G), −55(T→C), −36(C→A)], were also revealed. These changes are either linked in cis with other mutations or are responsible for thalassemias or for positive regulatory effect in δ-globin gene expression. The proposed experimental strategy consists of an accurate, rapid, safe and inexpensive screening procedure for establishing the molecular basis of δ-globin gene defects, suitable for the application for both research and diagnostics. Hum Mutat 9:465–472, 1997 © 1997 Wiley-Liss, Inc.     

Reversion of resistance to immunosuppressive agents in three patients with psoriatic arthritis by cyclosporine A: modulation of P-glycoprotein function

Secondary resistance may be a major problem in the management of autoimmune diseases. P-glycoprotein (P-gp) over-function has been described as a mechanism of drug resistance in autoimmune patients. P-gp function can in vitro be inhibited by cyclosporine A (CSA) and verapamil; moreover, P-gp reduction by CSA in systemic lupus erythematosus and rheumatoid arthritis has been demonstrated. Here, P-gp function before and after CSA administration in three psoriatic arthritis (PsA) patients, who developed a resistance to MTX/SSA, has been evaluated. P-gp function on patient cells was analyzed by measuring the changes in rhodamine-123 (Rh-123) fluorescence after verapamil incubation. CSA treatment resulted in good clinical outcome that was related with a significant P-gp function reduction at CD3+ and CD8+ levels. In addition to its immunosuppressive activity, CSA results may also be related to MTX/SSA effect restoration through P-gp inhibition. This is the first time that CSA has been demonstrated as being able to revert MTX/SSA resistance in PsA.     

Methylation profiling in individuals with uniparental disomy identifies novel differentially methylated regions on chromosome 15

The maternal and paternal genomes possess distinct epigenetic marks that distinguish them at imprinted loci. In order to identify imprinted loci, we used a novel method, taking advantage of the fact that uniparental disomy (UPD) provides a system that allows the two parental chromosomes to be studied independently. We profiled the paternal and maternal methylation on chromosome 15 using immunoprecipitation of methylated DNA and hybridization to tiling oligonucleotide arrays. Comparison of six individuals with maternal versus paternal UPD15 revealed 12 differentially methylated regions (DMRs). Putative DMRs were validated by bisulfite sequencing, confirming the presence of parent-of-origin-specific methylation marks. We detected DMRs associated with known imprinted genes within the Prader-Willi/Angelman syndrome region, such as SNRPN and MAGEL2, validating this as a method of detecting imprinted loci. Of the 12 DMRs identified, eight were novel, some of which are associated with genes not previously thought to be imprinted. These include a site within intron 2 of IGF1R at 15q26.3, a gene that plays a fundamental role in growth, and an intergenic site upstream of GABRG3 that lies within a previously defined candidate region conferring an increased maternal risk of psychosis. These data provide a map of parent-of-origin-specific epigenetic modifications on chromosome 15, identifying DNA elements that may play a functional role in the imprinting process. Application of this methodology to other chromosomes for which UPD has been reported will allow the systematic identification of imprinted sites throughout the genome.Imprinting is a phenomenon in which the expression status of a gene is dependent on the sex of the parent from which it is inherited. Imprinted genes generally exhibit monoallelic expression accompanied by parent-of-origin-specific epigenetic marks such as differential DNA methylation and histone modifications that distinguish the maternal and paternal genomes at these loci (Reik and Walter 2001; Dindot et al. 2009). More than 60 imprinted genes have been identified in humans (http://www.geneimprint.com/), and their clustered nature suggests that many are regulated by regional control mechanisms.To date, the discovery of imprinted sites in both mouse and human has largely been driven through the use of phenotype-based approaches. The vast majority of loci subject to parent-of-origin effects were first recognized through the observation that maternal and paternal transmission of the same genetic mutation results in different phenotypes (Nicholls et al. 1989). For example, the identification of imprinted gene clusters in 15q11-q13 associated with Prader-Willi/Angelman syndrome, 11p11.5 associated with Beckwith-Wiedemann syndrome, and imprinted loci at 14q32, 6q24, and 20q13.2 were all catalyzed by the initial observation that genetic disease occurred specifically in patients with either uniparental disomy (UPD) or deletions of these regions of specific parental origin. In combination with chromosomal engineering techniques that can systematically generate defined aneuploidies, this notion has been applied to screen the mouse genome for imprinting with great success, resulting in the identification of more than 130 murine imprinted genes (Williamson et al. 2009). However, because this methodology relies on the recognition of overt phenotypic differences between individuals to detect imprinting, it is likely to miss imprinting that may cause subtle phenotype differences or those that manifest in ways that are not easily recognized by typical methods of phenotypic characterization. Further, imprinted genes will also be missed or masked by phenotypes that are lethal.In order to circumvent this limitation, a variety of genomic techniques have been developed to identify parent-of-origin effects. Several previous studies have attempted to detect imprinting based on the differential expression of parental alleles at imprinted loci. Studies using subtractive cDNA hybridization (Kaneko-Ishino et al. 1995) and high-throughput cDNA sequencing in hybrid mouse strains (Wang et al. 2008) have been used to detect imprinted expression with some success. However, these approaches are limited in that they can only assay the subset of genes expressed in the tissue(s) under investigation, and for some genes, imprinted expression is only observed in specific tissues or at certain developmental stages (Deltour et al. 1995; Rougeulle et al. 1997; Zhou et al. 2006). Furthermore, sequencing-based approaches are only able to assay allelic bias in genes containing transcribed polymorphisms (Daelemans et al. 2010).Alternative approaches to detect imprinting have used the fact that the maternal and paternal genomes have differential epigenetic marks at most imprinted loci. This approach has the advantage over expression-based methods, in that these differential methylation marks are generally conserved, even in tissues that lack imprinted expression (Dockery et al. 2009). The presence of overlapping euchromatin and heterochromatin marks has been used to highlight imprinted domains in human (Wen et al. 2008), and restriction landmark genome scanning (Hayashizaki et al. 1994) and methylation-sensitive representational difference analysis (Kelsey et al. 1999; Smith et al. 2003) have been applied as methods to detect differentially methylated regions in the mouse genome. However, the reliance of these latter techniques on restriction enzyme digestion means that they can only assay a small subset of CpGs that overlap the enzyme recognition site, and if used in outbred genomes, are liable to artifacts generated by the presence of single nucleotide variants that alter restriction patterns.Because one of the key features of imprinted genes is the presence of parent-of-origin-specific methylation, we hypothesized that the systematic comparison of DNA methylation patterns in maternal versus paternal chromosomes should represent an optimal method for the detection of imprinted loci. Based on this hypothesis, we have taken advantage of the fact that uniparental disomy provides a unique system that allows the separate study of chromosomes derived from a single parent and combined this with a methodology in which the methylation of entire chromosomes can be analyzed in an unbiased fashion. By analyzing methylation patterns in cases of maternal UPD15 (matUPD15) and paternal UPD15 (patUPD15) using immunoprecipitation of methylated DNA and high-density tiling arrays with complete coverage of human chromosome 15, we generated separate methylation profiles of the maternally and paternally derived alleles. Comparison of the two parental epigenotypes identifies numerous loci on chromosome 15 that show parent-of-origin-specific methylation differences, defining a set of DNA elements that are likely responsible for the establishment and/or maintenance of imprinting on this chromosome. We identify novel imprinted loci both within and outside of the known PWS/AS imprinted domain, suggesting candidate loci that may exert parent-of-origin effects in several human phenotypes.     

Ultrasound-assisted endocavitary HDR-Ir192 brachytherapy for unresectable locally advanced uterine cervix carcinoma: retrospective analysis focusing the efficacy and tolerability

Purpose

To evaluate the impact of uterine cavity’s ultrasound to final selected length of intracavitary tandem. The efficacy and tolerability of external beam radiation plus HDR-Ir¹⁹² brachytherapy in our cohort of patients were also estimated.

Materials and methods

48 women with locally advanced unresectable uterine cervix carcinoma were treated by HDR-Ir¹⁹² endocavitary brachytherapy between January 2007 and January 2009. The median age was 63 (range 38–74). The distribution according to Federation of Gynaecology and Obstetrics (FIGO) staging system was as follows: Stage IIB, 54.16 %; IIIA, 10.4 %; IIIB, 27.0 %; and IVA, 8.3 %. HDR intracavitary brachytherapy was given weekly, beginning at the last week of whole pelvis irradiation, with a dose of 7 Gy to point A for three to four fractions. The median overall treatment time was 50 days (range 42–73 days). The median follow-up time was 2.7 years (range 3 months to 4.9 years). Multivariate analysis was performed using the Cox regression proportional hazards model.

Results

The complete remission rate after radiotherapy was 93.75 % (45/48). The 5-year actuarial major complication rates (Grade 3 or above) were 6.3 % overall (2.1 % proctitis, 2.1 % cystitis and 2.1 % enteritis). Estimation of the length of uterine cavity by ultrasound helped decisively in the proper placement of the intrauterine tandem inserted.

Conclusions

Prior knowledge of the length of uterine cavity can facilitate the decisions regarding the proper insertion length of the tandem. Results of cervical cancer treatment with external beam radiation and HDR intracavitary brachytherapy in our hospital are encouraging.