Therapy of Major Ectoparasitoses in Grasscarp (Ctenopharyngodon idella) Fry and Fingerlings

Willomitzer J.: Therapy of Major Ectoparasitoses in Grasscarp (Ctenopharyn-godon idella) Fry and Fingerlings. Acta vet., 49, 1980: 279-282. Dipping, short-term and long-term baths in solutions of common substances (potassium permanganate, formaline, common salt) currently recommended for the control of ectoparasites of the genera Chilodonella, Trichodinella and Dactylogyrus in grasscarp fry and fingerlings were tested under laboratory conditions. Dipping into a 1: 1000 diluted potassium permanganate bath for 45 seconds was 100 per cent effective against Trichodinella spp. Short-term baths in a 1: 2500 formaline solution for 60 minutes was 100 per cent effective against Chilodonella spp., Trichodinella spp. and Dactylogyrus spp., but 23.3 per cent of the treated fish died. The best results in the control of Chilodonella spp. and Trichodinella spp. in grasscarp finger-lings from the 3rd week after hatching were obtained with long-term baths in a 0.7 per cent solution of common salt for 21 to 24 hours. Chilodonellosis, trichodinellosis, dactylogyrosis, intensity of infection, formaline bath

Whole-brain imaging of freely-moving zebrafish

One of the holy grails of neuroscience is to record the activity of every neuron in the brain while an animal moves freely and performs complex behavioral tasks. While important steps forward have been taken recently in large-scale neural recording in rodent models, single neuron resolution across the entire mammalian brain remains elusive. In contrast the larval zebrafish offers great promise in this regard. Zebrafish are a vertebrate model with substantial homology to the mammalian brain, but their transparency allows whole-brain recordings of genetically-encoded fluorescent indicators at single-neuron resolution using optical microscopy techniques. Furthermore zebrafish begin to show a complex repertoire of natural behavior from an early age, including hunting small, fast-moving prey using visual cues. Until recently work to address the neural bases of these behaviors mostly relied on assays where the fish was immobilized under the microscope objective, and stimuli such as prey were presented virtually. However significant progress has recently been made in developing brain imaging techniques for zebrafish which are not immobilized. Here we discuss recent advances, focusing particularly on techniques based on light-field microscopy. We also draw attention to several important outstanding issues which remain to be addressed to increase the ecological validity of the results obtained

Dihydropyrimidine Dehydrogenase Deficiency: Metabolic Disease or Biochemical Phenotype?

Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disorder of pyrimidine metabolism that impairs the first step of uracil und thymine degradation. The spectrum of clinical presentations in subjects with the full biochemical phenotype of DPD deficiency ranges from asymptomatic individuals to severely affected patients suffering from seizures, microcephaly, muscular hypotonia, developmental delay and eye abnormalities.We report on a boy with intellectual disability, significant impairment of speech development, highly active epileptiform discharges on EEG, microcephaly and impaired gross-motor development. This clinical presentation triggered metabolic workup that demonstrated the biochemical phenotype of DPD deficiency, which was confirmed by enzymatic and molecular genetic studies. The patient proved to be homozygous for a novel c.2059-22T>G mutation which resulted in an in-frame insertion of 21 base pairs (c.2059-21_c.2059-1) of intron 16 of DPYD. Family investigation showed that the asymptomatic father was also homozygous for the same mutation and enzymatic and biochemical findings were similar to his severely affected son. When the child deteriorated clinically, exome sequencing was initiated under the hypothesis that DPD deficiency did not explain the phenotype completely. A deletion of the maternal allele on chromosome 15q11.2-13-1 was identified allowing the diagnosis of Angelman syndrome (AS). This diagnosis explains the patient's clinical presentation sufficiently; the influence of DPD deficiency on the phenotype, however, remains uncertain