Pena-Shokeir syndrome. Malformed sequence. 2 case reports

The authors report two cases of Pena-Shokeir syndrome; they emphasize its place among the numerous etiologies of hydramnios, among the different AMC, particularly the autosomal recessive entities.     

Recherches d'Histophysiologie comparée sur le pro- et le mésonéphros larvaires des anoures

Sans résumé     

The influence of fixation procedure, embedding medium and section thickness on morphometric data in thyroid gland.

In this study, the effects of fixation procedures, embedding medium and section thickness on stereological measurements of normal thyroid were analysed. The following conclusions were drawn: A) the use of a single section for the analysis of a lobe is sufficient if this section is located in the central part of the lobe. B) fixation and embedding with glutaraldehyde-Epon leads to a larger shrinkage than Bouin-paraplast, but the difference between the two procedures is not significant. C) osmium post-fixation reduces the shrinkage induced by glutaraldehyde and lowers the axial deformation produced by sectioning. D) Bouin's fixative and paraplast embedding induce considerable shrinkage of the interstitial tissue. The shrinkage obtained with glutaraldehyde-Epon is less. However, it is still not known whether this difference is due to the fixative, or to the embedding procedure or to both. E) only in glutaraldehyde and osmium-fixed material, embedded in Epon, can follicles and colloids be assumed to be spherical in shape without significant errors.     

The antigen of bile canaliculi of the mouse hepatocyte: identification and ultrastructural localization

The AgB10 antigen of bile canaliculi of the mouse hepatocyte was identified using monoclonal antibodies. The Mr value of 116000 for AgB10 was measured by immunoblotting. The tissue localization of AgB10 was studied by light and electron microscopy using the immunoperoxidase technique. AgB10 was predominantly present on the microvillus membrane of bile canaliculi, the brush border of intestinal mucosa and apical surfaces of the epithelial cells in some other organs. A small amount of AgB10 was detected on the basolateral domain of the hepatocytes. AgB10 was specific for hepatocytes and was not found in the other cell types of the liver. In primary hepatocyte culture, AgB10 was localized on the surface of cells during the first 24 h, predominantly at the sites of cell-cell and cell-substratum contacts. After 48 h of culture AgB10 gradually disappeared from contacting cell surfaces and became concentrated only in the reconstituted bile canaliculi.     

Synergistic regulation of cytosolic Ca2+ concentration by somatostatin and alpha 1-adrenergic agonists in mouse astrocytes.

The effects of somatostatin and alpha 1-adrenergic receptor agonists on cytosolic Ca2+ in striatal astrocytes from the embryonic mouse in primary culture have been investigated by microfluorimetry. Methoxamine or somatostatin induced a transitory increase in cytosolic Ca2+, but their combined addition led to a sustained increase in cytosolic Ca2+ which seems to be due to a Ca2+ influx since it was not observed in the absence of external Ca2+. Voltage-independent Ca2+ channels contribute to this process. Indeed, voltage-operated calcium channels are not involved since neither dihydropyridines nor La3+ were effective in suppressing the sustained cytosolic Ca2+ elevation. Moreover, depolarization by 50 mM KCl, which was ineffective alone, suppressed the effect of somatostatin observed in the presence of the alpha 1 agonist, methoxamine. The implication of arachidonic acid in the observed potentiation is suggested by the following observations: 1) arachidonic acid induced a sustained elevation of cytosolic Ca2+ similar to that evoked by the co-application of methoxamine and somatostatin; 2) the addition of ETYA, an inactive and non-metabolizable analogue of arachidonic acid suppressed the calcium plateau produced by the agonists. In addition, direct activation of PKC by an exogeneous diacylglycerol analogue allowed somatostatin alone to evoke a sustained elevation of cytosolic Ca2+. Therefore, methoxamine through the successive activation of PLC and PKC could allow a lipase, probably PLA2, to be stimulated by somatostatin. Since arachidonic acid has already been shown to trigger the opening of K+ channels and the formation of inositol phosphates, somatostatin, through the arachidonic acid-mediated hyperpolarization could increase the Ca2+ driving force and thus improve Ca2+ influx through the inositol phosphate gated channels.