Neuromuscular development following tetrodotoxin-induced inactivity in mouse embryos

Developmental aspects of the neuromuscular system in mouse embryos chronically paralyzed in utero with tetrodotoxin (TTX) between embryonic days 14 and 18 were studied using biochemical and histological methods. The number of lumbar spinal motoneurons (MNs) was higher in inactive embryos than in controls suggesting a decreased motoneuron cell death. In association with the increase in MN number, choline acetyltransferase activity was significantly increased in both spinal cord and peripheral synaptic sites. Paralyzed muscles exhibited a decreased number of mature myofibers and the nuclei were centrally located. Creatine kinase activity was greatly decreased and total acetylcholine receptor and receptor cluster numbers per myofiber were significantly increased in paralyzed muscles. A similar pattern of changes occurs in the neuromuscular system of the mutant mouse muscular dysgenesis (mdg). However, in contrast to the mdg mutant, tetrodotoxin-treated muscles were similar to controls in their innervation pattern, in the ultrastructural aspects of the excitation–contraction coupling system (i.e., dyads and triads) and in the extent of dihydropyridine binding. Thus, neuromuscular inactivity is not sufficient to impair the pattern of muscle innervation or the appearance of either the triadic junctions or dihydropyridine receptors. These results indicate that alterations of dihydropyridine binding sites and triads in muscular dysgenesis cannot be accounted for by inactivity but rather must reflect a more primary defect involving the structural gene(s) regulating the development of one or more aspects of muscle differentiation.     

Involvement of putrescine in the inductive rooting phase of poplar shoots raised in vitro

Micropropagated poplar shoots rooted 100% on a rooting medium (A) containing NAA, but they did not root in the absence of auxin (NA). Putrescine, but not spermidine and spermine, promoted rooting up to 42% when added to the NA medium. Cyclohexylamine (CHA), an inhibitor of spermine synthase, also promoted (up to 36%) rooting in the absence of auxin. The inhibitors of polyamine biosynthesis DFMA (α-difluoromethylarginine) and DFMO (α-difluoromethylomithine), aminoguanidine (AG) and methylglyoxal-bis-guanylhydrazone (MGBG), inhibited rooting when applied in the presence of auxin and had no effect in its absence.
The rooting inductive phase (in the presence of auxin) was determined by periodical transfer of shoots from A to NA medium, and by changes in peroxidase activity, to be 7 h. Putrescine (not spermidine and spermine) accumulated to a maximum during the inductive phase. Both putrescine and CHA promoted rooting on NA medium when applied during the first 7 h. In contrast DFMA and AG inhibited rooting during this period. The results point to the involvement of putrescine and its Δ¹-pyrroline pathway, in the inductive phase of rooting in poplar shoots.     

Evaluation of Probiotic Properties of Novel Brazilian Lactiplantibacillus plantarum Strains

Probiotics and Antimicrobial Proteins - Beneficial effects of Lactiplantibacillus plantarum strains have been widely reported. Knowing that the effects of probiotic bacteria are strain-dependent,...     

Discrete subaortic stenosis as part of a short stature syndrome

Summary Observations in a family point to the existence of autosomal dominant inheritance for discrete subaortic stenosis (DSS), which made up part of a multisystem disorder. Both parents, offspring of two full siblings, had short stature, obstructive lung disease (OLD), hoarseness and upturned nose. The father alone had aortic stenosis and inguinal hernia.The six offspring, aged from 13 to 28 years, were followed up for up to 8 years. While one of them was virtually normal, and one had only minor abnormalities, four siblings displayed clinical signs of progressive aortic stenosis. Of the two eldest siblings who eventually died, necropsy in one showed a discrete subaortic stenosis, which was hemodynamically proven in one and surgically corrected in another sibling.Upturned nose was present in each examined member of the family, short stature and hoarseness in five of the siblings, DSS in four, OLD, inguinal hernia and congested episcleral veins in three, kyphoscoliosis in two, while epicanthus, strabismus, microphthalmos and widely spaced teeth were noted in the deceased female. The prevalence of some of these traits in roughly three-quarters of the sibship was consistent with an underlying single gene abnormality in affected heterozygous parents. We proposed that this constitutes a new syndrome.     

Double helical arrangement of spread dinoflagellate chromosomes

Dinoflagellate chromosomes observed in thin section show regular patterns which have been shown to correspond to a liquid crystalline helicoidal arrangement of DNA. Peripheral DNA filaments form a system of loops in the surrounding nucleoplasm. When such chromosomes (studied in Prorocentrum micans) are in presence of water, they extend considerably and form a double helical bundle. At the periphery of these bundles, one observes numerous filaments, which are smooth and devoid of nucleosomes; their diameter is constant.This study, in phase contrast and in electron microscopy, allows statistical measurements. A geometrical model is proposed and shows the simplest way to pass from the intact to the extended form. The liquid crystalline character of the chromosome is probably involved in the extension mechanisms.     

Occurrence of subcutaneous zygomycosis (Entomophthoromycosis Basidiobolae) caused by Basidiobolus haptosporus with pulmonary involvement

A case of a two-year-old boy with multiple subcutaneous lesions caused by Basidiobolus haptosporus is presented.The child had also a non-toxic familial goiter and clinical and radiological features of a pulmonary illness. The pulmonary manifestations only disappeared with the treatment with potassium iodide. The authors think that the pulmonary lesions must have arisen by direct spread of the fungus from the subcutaneous lesions of the chest.