The tapeworm Raillietina trapezoides was studied in a Tunisian population of the fat sand rat Psammomys obesus. Seasonal changes in the abundance of parasite and host were monitored in a longitudinal field survey lasting 20 months. In total 582 intestinal samples were collected during 10 trapping sessions between May 1995 and January 1997 and examined. The impact of abiotic and biotic factors on the prevalence and parasite burden were explored, using generalized linear models. R. trapezoides showed a seasonal pattern with most transmission occurring in summer and autumn. In August-September when the rodents were at low density and most adult (90-100 %) were infected. In winter, infections with R. trapezoides were highly prevalent in the cohort of adults only. The worm burden by number was also high in late summer and autumn. Prevalence and parasite burden by number or by biomass were highly age dependent. Season and age act in synergy so that the rodents were highly infected in late summer and autumn. Unusually dry conditions in winter seemed to increase prevalence and to reduce the number of worms. There was no difference between males and females in prevalence or parasite burden (by number or by biomass). Prevalence was not correlated with the relative density of the hosts whereas parasite burden depended upon their densities. The more numerous the worms were, the smaller they were individually, reflecting a crowding effect. The possibility of an immune response regulating P. obesus is discussed, in regard to the very high natural prevalence and the variation in worm burden, and compared with other parasite-host systems.

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Background: Phelan-McDermid syndrome is a rare genetic disorder resulting from heterozygous deletion of 22q13.3 with the involvement of at least part of SHANK3 or a heterozygous pathogenic variant in SHANK3. We would like to explore the possible pathogenesis and therapeutic direction of PMS.Methods: We identified a child who harbored a de novo SHANK3 gene mutation and had a speech delay and mental retardation. This pathogenic mutation (c.3679dup, p.A1227Gfs*69) may lead to early termination of protein transcription and is speculated to cause changes in protein function. The gene expression profiles of family members were evaluated by RT-PCR, which showed that SHANK3 expression was significantly lower in the child than in the other family members. The sites of pathogenic and likely pathogenic mutations in the SHANK3 gene reported by ClinVar were searched, and the mutation sites were summarized and marked. Results: The relevant literature was reviewed to understand the current state of research progress and possible future treatment directions. Researchers have found that CDPPB is a potent and selective positive allosteric modulator of mGluR5. In addition, it is important to further study whether NMD is involved in the expression of SHANK3 and to further investigate PTCs.Conclusions: Genetic testing is essential for children with development delay. It’s necessary to do further research about the therapeutic direction.