Toothbrushing in children with autism spectrum disorders: qualitative analysis of parental difficulties and solutions in France.

PURPOSE: The oral care of a child with autism spectrum disorders (ASD) is a challenge, not only for dentists, but also for parents. The objective of this study was to evaluate the difficulties encountered by parents in maintaining oral hygiene in autistic children and the solutions they found to facilitate this daily act. METHODS: A questionnaire with closed and open questions about characteristics of the child and oral health at home, conducted via Google Form, was sent to French families through 301 associations of parents with autistic children. For the quantitative analysis, logistic regression was used. The open answers were analysed by theme. RESULTS: This study included 756 offspring aged 14.4 (± 8.1) years. Girls were 1.7 (95% CI: 1.1-2.8) times more likely to have toothbrushing difficulty than boys. Nonverbal patients (OR:3.2; 95% CI: 2.2-4.9), autistic patients (OR:2.8; 95% CI: 1.4-5.2), patients using pictograms (OR:1.6; 95% CI: 1.1-2.4), and younger children (OR:0.9; 95% CI: 0.9-0.9) were significantly more likely to encounter difficulties in tolerating toothbrushing. The qualitative analysis showed that parents used three main ways to facilitate toothbrushing: planning, modelling and making it enjoyable. Seventy-nine percent of parents did not feel sufficiently informed about the different oral hygiene prevention tools and techniques for their ASD children and would like to be educated in the daily management of oral hygiene. CONCLUSION: The role of parents remains essential and professionals should work in collaboration with them.

Combinatorial control by the protein kinases PKA, PHO85 and SNF1 of transcriptional induction of the Saccharomyces cerevisiae GSY2 gene at the diauxic shift.

Genes involved in storage carbohydrate metabolism are coordinately induced when yeast cells are subjected to conditions of stress, or when they exit the exponential growth phase on glucose. We show that the STress Responsive Elements (STREs) present in the promoter of GSY2 are essential for gene activation under conditions of stress, but dispensable for gene induction and glycogen accumulation at the diauxic shift on glucose. Using serial promoter deletion, we found that the latter induction could not be attributed to a single cis -regulatory sequence, and present evidence that this mechanism depends on combinatorial transcriptional control by signalling pathways involving the protein kinases Pho85, Snf1 and PKA. Two contiguous regions upstream of the GSY2 coding region are necessary for negative control by the cyclin-dependent protein kinase Pho85, one of which is a 14-bp G/C-rich sequence. Positive control by Snf1 is mediated by Mig1p, which acts indirectly on the distal part of the GSY2 promoter. The PKA pathway has the most pronounced effect on GSY2, since transcription of this gene is almost completely abolished in an ira1ira2 mutant strain in which PKA is hyperactive. The potent negative effect of PKA is dependent upon a branched pathway involving the transcription factors Msn2/Msn4p and Sok2p. The SOK2 branch was found to be effective only under conditions of high PKA activity, as in a ira1ira2 mutant, and this effect was independent of Msn2/4p. The Msn2/4p branch, on the other hand, positively controls GSY2 expression directly through the STREs, and indirectly via a factor that still remains to be discovered. In summary, this study shows that the transcription of GSY2 is regulated by several different signalling pathways which reflect the numerous factors that influence glycogen synthesis in yeast, and suggests that the PKA pathway must be deactivated to allow gene induction at the diauxic shift.

The Saccharomyces cerevisiae YPR184w gene encodes the glycogen debranching enzyme.

The YPR184w gene encodes a 1536-amino acid protein that is 34-39% identical to the mammal, Drosophila melanogaster and Caenorhabditis elegans glycogen debranching enzyme. The N-terminal part of the protein possesses the four conserved sequences of the alpha-amylase superfamily, while the C-terminal part displays 50% similarity with the C-terminal of other eukaryotic glycogen debranching enzymes. Reliable measurement of alpha-1,4-glucanotransferase and alpha-1, 6-glucosidase activity of the yeast debranching enzyme was determined in strains overexpressing YPR184w. The alpha-1, 4-glucanotransferase activity of a partially purified preparation of debranching enzyme preferentially transferred maltosyl units than maltotriosyl. Deletion of YPR184w prevents glycogen degradation, whereas overexpression had no effect on the rate of glycogen breakdown. In response to stress and growth conditions, the transcriptional control of YPR184w gene, renamed GDB1 (for Glycogen DeBranching gene), is strictly identical to that of other genes involved in glycogen metabolism.

MRG1-1, a dominant allele that confers methomyl resistance in yeast expressing the cytoplasmic male sterility T-urf13 gene from maize.

We have previously described a eukaryotic heterologous expression system, with the urf13TW gene in yeast, which mimics the disease susceptibility associated with the Texas cytoplasmic male sterility in maize. This yeast model was used to isolate yeast nuclear mutants conferring methomyl resistance. The genetic strategy we have developed focused on screening for nuclear dominant yeast mutations which restore methomyl resistance. MRG1-1, a yeast nuclear dominant allele, was identified as a methomyl-resistance restorer. We have shown that methomyl resistance co-segregated with a pleiotropic phenotype in the heterozygous MRG1-1/MRG1 diploids, detectable even in the absence of the maize-derived mitochondrial protein and/or methomyl. We observed an increase in oxygen uptake, a significant decrease of the levels of cytochrome aa3, and a decrease in the growth yield. This phenotype is influenced by the carbon source and the results suggest a defect in the adaptation to the respiratory pathway in MRG1-1 yeast cells.

Sensory and motor maximum nerve conduction velocity in the peripheral and central nervous system of the beagle dog.

Sensory maximum nerve conduction velocity (MNCV) and motor MNCV were monitored in altogether 14 beagle dogs anaesthetized with pentobarbital. Sensory MNCV was determined by averaging cortically evoked potentials from somatosensory area I (SS I) in response to repeated electrical stimulation of digital paw pads, tibial nerve at calcaneus or sciatic nerve at trochanter. Sensory MNCV determined from paw to tibial nerve at calcaneus was 53 m/sec, from tibial nerve at calcaneus to sciatic nerve at trochanter 64 m/sec and from sciatic nerve at trochanter to crotex SS I 53 m/sec. Motor peripheral MNCV determined in the customary way from sciatic nerve at trochanter to tibial nerve at calcaneus was 68 m/sec and distal latency 3.6 msec. Motor central MNCV from motor cortex to the sciatic nerve at the trochanter in 5 unanaesthetized dogs was 57 m/sec. These testing procedures serve for quantitative assessment of possible impairment of impulse transmission in the central and peripheral sensory and motor pathway of beagle dogs used in routine toxicity studies.

Single fiber electromyography. A method for the evaluation of motor axonopathy during toxicity studies in dogs.

In man, single fiber electromyography is used as a very sensitive indicator for the assessment of functional changes in motor nerves. The purpose of the present study was to adapt the above testing procedure to allow repeated investigations of dogs used in subchronic toxicity tests. Experiments were performed on anesthetized pure-bred beagle dogs. Action potentials from single muscle fibers in response to electrical stimulation of motor nerves were recorded with Medelec microelectrodes, amplified with a Medelec system and monitored on a Tektronic oscilloscope. Repeated electrical stimulation with pulses of 0.03 msec and 1 p.p.s. produced characteristic action potentials of single muscle fibers consisting of a positive, followed by a negative, deflection having a duration of from 500 to 800 microseconds altogether. Successive potentials occurred with a variable latency (the jitter) ranging from +/- 5 to 15 microseconds. Quantitative evaluation of the jitter will allow the clinical evaluation of motor axonopathies in dogs.