The importance of the OHI-S for children with premature tooth loss

In spite of all the methods of prevention, there still are untreated or improperly treated caries and it’s followed by complications. This often leads to premature loss of teeth.The premature loss of the deciduous teeth depends on different factors such as oral hygiene, traumas, complicated caries. The aim of this study is to compare the OHI-S between children with premature loss and those without premature loss of deciduous teeth. Subject of the monitoring of the clinical research were 140 children between ages 6 and 9. The clinical group consisted of 90 children with prematurely extracted teeth, divided into three groups. The control group consisted of 50 children with intact denture. The oral hygiene status was examined and registered by the Greene-Vermillion index-simplified. There was a statistically significant difference in the OHI-S between the control group (1.86±0.05) and the clinical groups (1.90±0.08 and 2.01±0.05). The children with premature extraction of the primary teeth had higher OHI-S compared to the control group (children without premature extraction of teeth). The third group of children, with prematurely extracted temporary teeth and severe orthodontic deformation, have the highest OHI-S. These results demonstrate the connection between OHI, the orthodontic deformations and the need for prevention.

Jaw cysts at children and adolescence : a single-center retrospective study of 152 cases in southern Bulgaria

One hundred fifty two cysts of the upper and lower jaw were examined at patients up to 18 years old treated in the Clinics of Maxillo-Facial Surgery, University Hospital, Plovdiv, Bulgaria for the period 1998 - 2007. Patients were distributed in four age groups (up to 4 years old, from 5 to 9 years old, from 10 to 14 years old, from 15 to 18 years old). Both sexes were constantly affected (52% male, 48% female). The biggest number cystic lesions were found in the third age group (48.7%). The mandible was preferable localization of the lesions (69.7%). Dentigerous cysts predominated (61.8%) - more affected was third age group (31.6%). Radicular cysts were observed two times less (31.6%) - more affected were third (15.8%) and fourth (12.5%) age groups. The most frequently observed clinical symptom was presence of painless swelling (59.9%). The operative interventions were carried out predominantly under general anesthesia (81.6%) by intraoral approach (97.4%). The extraoral surgical approach was preferred in four cases only - three in third and one in fourth age groups. © Medicina Oral S. L

Radionuclide Contamination as a Risk Factor in Terrestrial Ecosystems: Occurrence, Biological Risk, and Strategies for Remediation and Detoxification

Radionuclide contamination poses serious hazards for terrestrial ecosystems. Beyond the readily apparent damage to the biota at high doses, low doses of ionizing radiation produce stochastic effects: mutation, carcinogenesis, and genomic instability. The proposed chapter is a review of the biological and ecological effects of radionuclides. The authors discuss, beyond the Chernobyl accident, other contamination events. The review includes the biological and ecological effects of the three principal technogenic contaminants in terrestrial ecosystems: Cs-137, Sr-90, and I-131. Ecological risks to terrestrial small mammals are assessed in detail. In addition, the chapter provides some of the lesser-known methods of remediation and detoxification, including the use of modified natural zeolites as environmental remedies and bio-sorbents. Presented herein is little-known information on environmental protection against radioactive contamination

Astrocytic 4R tau expression drives astrocyte reactivity and dysfunction

The protein tau and its isoforms are associated with several neurodegenerative diseases, many of which are characterized by greater deposition of the 4-repeat (4R) tau isoform; however, the role of 4R tau in disease pathogenesis remains unclear. We created antisense oligonucleotides (ASOs) that alter the ratio of 3R to 4R tau to investigate the role of specific tau isoforms in disease. Preferential expression of 4R tau in human tau-expressing (hTau-expressing) mice was previously shown to increase seizure severity and phosphorylated tau deposition without neuronal or synaptic loss. In this study, we observed strong colocalization of 4R tau within reactive astrocytes and increased expression of pan-reactive and neurotoxic genes following 3R to 4R tau splicing ASO treatment in hTau mice. Increasing 4R tau levels in primary astrocytes provoked a similar response, including a neurotoxic genetic profile and diminished homeostatic function, which was replicated in human induced pluripotent stem cell-derived (iPSC-derived) astrocytes harboring a mutation that exhibits greater 4R tau. Healthy neurons cultured with 4R tau-expressing human iPSC-derived astrocytes exhibited a higher firing frequency and hypersynchrony, which could be prevented by lowering tau expression. These findings support a potentially novel pathway by which astrocytic 4R tau mediates reactivity and dysfunction and suggest that astrocyte-targeted therapeutics against 4R tau may mitigate neurodegenerative disease progression

In Vivo Cytotoxicity Induced by 60 Hz Electromagnetic Fields under a High-Voltage Substation Environment

Abstract: Living beings permanently receive electromagnetic radiation, particularly from extremely low-frequency electromagnetic fields (ELF-EMFs), which may cause adverse health effects. In this work, we studied the in vivo cytotoxic effects of exposing BALB/c mice to 60 Hz and 8.8 µT EMFs during 72 h and 240 h in a switchyard area, using animals exposed to 60 Hz and 2.0 mT EMFs or treated with 5 mg/kg mitomycin C (MMC) as positive controls. Micronucleus (MN) frequency and male germ cell analyses were used as cytological endpoints. ELF-EMF exposure was observed to significantly (p < 0.05) increase MN frequency at all conditions tested, with the 2 mT/72 h treatment causing the highest response, as compared with untreated control. In addition, increased sperm counts were observed after switchyard area ELF-EMF exposure, as compared with untreated control. In contrast, low sperm counts were obtained for 72 h/2.0 mT-exposed animals and for MMC-treated mice (p < 0.05), without altering male germ cell morphological characteristics

No evidence for genotype/phenotype correlation in NPHS1 and NPHS2 mutations

Primary steroid-resistant nephrotic syndrome (SRNS) is characterized by childhood onset of proteinuria and progression to end-stage renal disease. In 26% of cases it is caused by recessive mutations in NPHS2 (podocin). Congenital nephrotic syndrome (CNS) is caused by mutations in NPHS1 (nephrin) or NPHS2 . In three families mutations in NPHS1 and NPHS2 had been reported to occur together, and these tri-allelic mutations were implicated in genotype/phenotype correlations. To further test the hypothesis of tri-allelism, we examined a group of 62 unrelated patients for NPHS1 mutations, who were previously shown to have NPHS2 mutations; 15 of 62 patients had CNS. In addition, 12 CNS patients without NPHS2 mutation were examined for NPHS1 mutations. Mutational analysis yielded three different groups. (1) In 48 patients with two recessive NPHS2 mutations (11 with CNS), no NPHS1 mutation was detected, except for 1 patient, who had one NPHS1 mutation only. This patient was indistinguishable clinically and did not have CNS. (2) In 14 patients with one NPHS2 mutation only (4 with CNS), we detected two additional recessive NPHS1 mutations in the 4 patients with CNS. They all carried the R229Q variant of NPHS2 . The CNS phenotype may be sufficiently explained by the presence of two NPHS1 mutations. (3) In 12 patients without NPHS2 mutation (all with CNS), we detected two recessive NPHS1 mutations in 11 patients, explaining their CNS phenotype. We report ten novel mutations in the nephrin gene. Our data do not suggest any genotype/phenotype correlation in the 5 patients with mutations in both the NPHS1 and the NPHS2 genes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47823/1/467_2004_Article_1629.pd

Congenital nephrotic syndrome

Congenital nephrotic syndrome (CNS) is a rare kidney disorder characterized by heavy proteinuria, hypoproteinemia, and edema starting soon after birth. The majority of cases are caused by genetic defects in the components of the glomerular filtration barrier, especially nephrin and podocin. CNS may also be a part of a more generalized syndrome or caused by a perinatal infection. Immunosuppressive medication is not helpful in the genetic forms of CNS, and kidney transplantation is the only curative therapy. Before the operation, management of these infants largely depends on the magnitude of proteinuria. In severe cases, daily albumin infusions are required to prevent life-threatening edema. The therapy also includes hypercaloric diet, thyroxin and mineral substitution, prevention of thrombotic episodes, and prompt management of infectious complications. The outcome of CNS patients without major extrarenal manifestations is comparable with other patient groups after kidney transplantation

Genetics of focal segmental glomerulosclerosis

The recent advances in understanding the pathophysiology of focal segmental glomerulosclerosis (FSGS) and molecular function of glomerular filtration barrier come directly from genetic linkage and positional cloning studies. The exact role and function of the newly discovered genes and proteins are being investigated by in vitro and in vivo mechanistic studies. Those genes and proteins interactions seem to change susceptibility to kidney disease progression. Better understanding of their exact role in the development of FSGS may influence future therapies and outcomes in this complex disease

Refining transcriptional programs in kidney development by integration of deep RNA-sequencing and array-based spatial profiling

<p>Abstract</p> <p>Background</p> <p>The developing mouse kidney is currently the best-characterized model of organogenesis at a transcriptional level. Detailed spatial maps have been generated for gene expression profiling combined with systematic <it>in situ </it>screening. These studies, however, fall short of capturing the transcriptional complexity arising from each locus due to the limited scope of microarray-based technology, which is largely based on "gene-centric" models.</p> <p>Results</p> <p>To address this, the polyadenylated RNA and microRNA transcriptomes of the 15.5 dpc mouse kidney were profiled using strand-specific RNA-sequencing (RNA-Seq) to a depth sufficient to complement spatial maps from pre-existing microarray datasets. The transcriptional complexity of RNAs arising from mouse RefSeq loci was catalogued; including 3568 alternatively spliced transcripts and 532 uncharacterized alternate 3' UTRs. Antisense expressions for 60% of RefSeq genes was also detected including uncharacterized non-coding transcripts overlapping kidney progenitor markers, Six2 and Sall1, and were validated by section <it>in situ </it>hybridization. Analysis of genes known to be involved in kidney development, particularly during mesenchymal-to-epithelial transition, showed an enrichment of non-coding antisense transcripts extended along protein-coding RNAs.</p> <p>Conclusion</p> <p>The resulting resource further refines the transcriptomic cartography of kidney organogenesis by integrating deep RNA sequencing data with locus-based information from previously published expression atlases. The added resolution of RNA-Seq has provided the basis for a transition from classical gene-centric models of kidney development towards more accurate and detailed "transcript-centric" representations, which highlights the extent of transcriptional complexity of genes that direct complex development events.</p