Suppressive Effects of 24,25-Dihydroxycholecalciferol on Bone Resorption Induced by Acute Bilateral Nephrectomy in Rats

The possible suppressive effects of 24,25-dihydroxycholecalciferol on secondary hyperparathyroidism and increased bone resorption were investigated in adult rats raised on a diet normal in calcium, phosphorus, and vitamin D, and subjected to acute bilateral nephrectomy. The animals had received subcutaneous radiocalcium 4 wk before the experiment. 5 h after nephrectomy an increase in serum total calcium, ⁴⁵Ca-specific activity, citrate, phosphorus, and magnesium concentrations were observed. Serum immunoreactive parathyroid hormone increased, while serum calcitonin decreased. The osteoclast count in the tibial metaphyses was augmented. The biochemical and histological changes observed were partly parathyroid hormone and calcitonin independent, as they also occurred in parathyroidectomized hypocalcemic rats. Pretreatment with 650 pmol of 24,25-dihydroxycholecalciferol 16 h before nephrectomy prevented bone calcium mobilization and diminished the rise in serum total calcium and citrate both in parathyroid-intact and in parathyroidectomized animals. In parathyroid-intact rats, serum immunoreactive parathyroid hormone and calcitonin remained normal in spite of the fall in serum-ionized calcium, and the number of osteoclasts did not increase. In parathyroidectomized rats, 24,25-dihydroxycholecalciferol did not prevent the postnephrectomy rise in the osteoclast count. This latter observation suggests that this metabolite exerts its effect on bone either by acting on cells other than osteoclasts, i.e., the osteocytes, or by inhibiting cell activity. At equimolar dosage 1,25-dihydroxycholecalciferol had a potent stimulatory effect on bone resorption. This effect of 1,25-dihydroxycholecalciferol was partly blocked by the simultaneous administration of 24,25-dihydroxycholecalciferol.     

Chromosomal aadD2 encodes an aminoglycoside nucleotidyltransferase in Bacillus clausii

Bacillus clausii SIN is one of the four strains of B. clausii composing a probiotic administered to humans for the prevention of gastrointestinal side effects due to oral antibiotic therapy. The strain is resistant to kanamycin, tobramycin, and amikacin. A gene conferring aminoglycoside resistance was cloned into Escherichia coli and sequenced. The gene, called aadD2, encoding a putative 246-amino acid protein, shared 47% identity with ant(4')-Ia from Staphylococcus aureus, which encodes an aminoglycoside 4'-O-nucleotidyltransferase. Phosphocellulose paper-binding assays indicated that the gene product was responsible for nucleotidylation of kanamycin, tobramycin, and amikacin. The aadD2 gene was detected by DNA-DNA hybridization in the three other strains of the probiotic mixture and in the reference strain B. clausii DSM8716, although it did not confer resistance in these strains. Mutations in the sequence of the putative promoter for aadD2 from B. clausii SIN resulted in higher identity with consensus promoter sequences and may account for aminoglycoside resistance in that strain. The aadD2 gene was chromosomally located in all strains and was not transferable by conjugation. These data indicate that chromosomal aadD2 is specific to B. clausii.     

La pancréatectomie totale chez l'oie

Résumé Très peu d'auteurs se sont intéressés aux effets de la pancréatectomie chez l'Oie.Paton (1905) ne constata aucun changement de la glycémie chez des Oies pancréatectomisées, alors queKausch (1896) etMirsky etGitelson (1958) notèrent le développement d'un syndrome diabétique après la même expérience ou après éviscération. — Depuis, comme d'autres auteurs sur d'autres espèces, nous avons obtenu des résultats différents, en étudiant l'évolution de la glycémie et de la tolérance au glucose, chez des animaux normaux ou totalement pancréatomisés, à jeun. — La glycémie de l'Oie normale à jeun est relativement stable, mais la tolérance au glucose diminue pour des jeûnes de 15 à 30 heures, puis se stabilise. Les Oies totalement pancréateetomisées développent une hypoglycémie persistante, accompagnée de convulsions pouvant entraîner la mort. Mais on peut les maintenir en vie par des injections intraveineuses de glucose qui permettent de révéler une diminution de la tolérance au glucose. Ces faits peuvent être interprétés de la façon suivante: 1. l'hypoglycémie semble être due à un manque de glucagon. 2. la diminution de la tolérance au glucose résulterait de la suppression de l'insuline. 3. les résultats des auteurs cités ci-dessus sont probablement dus à des pancréatectomies partielles ou au choc opératoire. — Nos résultats sont en accord avec les travaux deMialhe (1955) sur le Canard et ceux deMikami etKazuyuki (1962) sur le Coq.

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Total Pancreatectomy in the Goose.

Summary Very few authors have been interested in the effects of pancreatectomy in goose;Paton (1905) found no change in the blood glucose level after pancreatectomy, whereasKausch (1896) andMirsky andGitelson (1958) noted a diabetic syndrome after the same procedure or after evisceration. — Since in other avian species some authors have obtained results that were different from those already mentioned, we have studied the glycaemia and glucose tolerance curve in normal and totally pancreatectomized geese in the fasting state. In the normal goose, there was no change in the blood glucose level during a fasting period of 15 to 70 hours; however, there was a slight decrease of the glucose tolerance between 15 and 30 hours, but no further change there-after. — After total pancreatectomy, a severe hypoglycaemia developed, leading to hypoglycaemic convulsions and death. This hypoglycaemia was persistent. If the animals were given glucose intravenously, they survived and a pronounced decrease of the glucose tolerance was noted. — e interpret these facts as follows: 1. the hypoglycaemia seems to be due to a lack of glucagon; 2. the decreased glucose tolerance appears to result from the suppression of insulin; 3. the results reported by the authors cited above may have been due to incomplete pancreatectomy or to surgical stress. Our results are in accordance with those reported byMialhe (1955) in the duck, andMikami andKazuyuki (1962) in the fowl.

Travail présenté comme Diplôme d'Etudes Supérieures, Faculté des Sciences de Strasbourg.     

ALS: Recent Developments from Genetics Studies

Amyotrophic lateral sclerosis (ALS) is a fatal disorder that is characterized by a progressive degeneration of the upper and lower motor neurons. Most cases appear to be sporadic, but 5–10 % of cases have a family history of the disease. High-throughput DNA sequencing and related genomic capture tools are methodological advances which have rapidly contributed to an acceleration in the discovery of genetic risk factors for both familial and sporadic ALS. It is interesting to note that as the number of ALS genes grows, many of the proteins they encode are in shared intracellular processes. This review will summarize some of the recent advances and gene discovery made in ALS.     

Evaluation of the necessity of hospitalization in children with an isolated linear skull fracture (ISF)

Objective

The prevalence of skull fractures after mild head trauma is 2 % in children of all ages and 11 % in children younger than 2 years. The current standard management for a child diagnosed with an isolated skull fracture (ISF), in our institute, is hospitalization for a 24-h observation period. Based on data from the literature, less than 1 % of all minor head injuries require neurosurgical intervention. The main objective of this study was to evaluate the risk of neurological deterioration of ISF cases, in order to assess the need for hospitalization.

Methods

We reviewed the medical charts of 222 children who were hospitalized from 2006 to 2012 with ISF and Glascow Coma Scale—15 at the time of arrival. We collected data regarding demographic characteristics, mechanism of injury, fracture location, clinical symptoms and signs, need for hospitalization, and need for repeated imaging. Data was collected at three time points: at presentation to the emergency room, during hospitalization, and 1 month after admission, when the patients’ parents were asked about the course of the month following discharge.

Results

None of the 222 children included in the study needed neurosurgical intervention. All were asymptomatic 1 month after the injury. Two children underwent repeated head CT due to persistence or worsening of symptoms; these CT scans did not reveal any new findings and did not lead to any intervention whatsoever.

Conclusion

Children arriving at the emergency room with a minor head injury and isolated skull fracture on imaging studies may be considered for discharge after a short period of observation. Discharge should be considered in these cases provided the child has a reliable social environment and responsible caregivers who are able to return to the hospital if necessary. Hospital admission should be reserved for children with neurologic deficits, persistent symptoms, suspected child abuse, or when the parent is unreliable or is unable to return to the hospital if necessary. Reducing unnecessary hospitalizations can prevent emotional stress, in addition to saving costs for the child’s family and the health care system.

     

Regional expression and ultrastructural localization of EphA7 in the hippocampus and cerebellum of adult rat

EphA7 is expressed in the adult central nervous system (CNS), where its roles are yet poorly defined. We mapped its distribution using in situ hybridization (ISH) and immunohistochemistry (IHC) combined with light (LM) and electron microscopy (EM) in adult rat and mouse brain. The strongest ISH signal was in the hippocampal pyramidal and granule cell layers. Moderate levels were detected in habenula, striatum, amygdala, the cingulate, piriform and entorhinal cortex, and in cerebellum, notably the Purkinje cell layer. The IHC signal distribution was consistent with ISH results, with transport of the protein to processes, as exemplified in the hippocampal neuropil layers and weakly stained pyramidal cell layers. In contrast, in the cerebellum, the Purkinje cell bodies were the most strongly immunolabeled elements. EM localized the cell surface‐expression of EphA7 essentially in postsynaptic densities (PSDs) of dendritic spines and shafts, and on some astrocytic leaflets, in both hippocampus and cerebellum. Perikaryal and dendritic labeling was mostly intracellular, associated with the synthetic and trafficking machineries. Immunopositive vesicles were also observed in axons and axon terminals. Quantitative analysis in EM showed significant differences in the frequency of labeled elements between regions. Notably, labeled dendrites were ～3–5 times less frequent in cerebellum than in hippocampus, but they were individually endowed with ～10–40 times higher frequencies of PSDs, on their shafts and spines. The cell surface localization of EphA7, being preferentially in PSDs, and in perisynaptic astrocytic leaflets, provides morphologic evidence that EphA7 plays key roles in adult CNS synaptic maintenance, plasticity, or function. J. Comp. Neurol. 524:2462–2478, 2016. © 2016 Wiley Periodicals, Inc.