SGK1-dependent salt appetite in pregnant mice

Aim: Pregnancy is typically paralleled by substantial increase in maternal extracellular fluid volume, requiring net accumulation of water and NaCl. The positive water and salt balance is accomplished at least in part by increased uptake of salt secondary to enhanced salt appetite. Little is known about the underlying cellular mechanisms. Stimulation of salt appetite by mineralocorticoids, however, is known to be dependent on the serum‐ and glucocorticoid‐inducible kinase SGK1. Methods: To test for a role of SGK1 in the stimulation of salt appetite during pregnancy, fluid intake was recorded in pregnant SGK1 knockout mice (sgk1^?/?) and their wild type littermates (sgk1^+/+). The mice were offered two bottles, one with plain water and the other with isotonic saline. Results: In early pregnancy, i.e. up to 10 days prior to parturition, the sgk1^+/+ mice displayed a significant preference for saline, whereas the sgk1^?/? mice preferred water. Accordingly, the water intake was significantly smaller and saline intake was significantly larger in sgk1^+/+ mice than in sgk1^?/? mice and the preference for water was significantly stronger in sgk1^?/? mice than in sgk1^+/+ mice. Plasma aldosterone levels were higher in sgk1^?/? mice than in sgk1^+/+ mice, a difference contrasting the enhanced salt appetite of sgk1^+/+ mice. Conclusions: SGK1 participates in the stimulation of salt appetite during pregnancy.     

Expression and structure of CD22 in acute leukemia

The purpose of this study was to examine the expression and structure of CD22 in B cell precursor acute lymphoblastic leukemia (BCP-ALL), acute myeloid leukemia (AML), and T cell acute lymphoblastic leukemia (T-ALL). By using immunofluorescence microscopy and flow cytometry we observed that CD22 is expressed not only in the cytoplasm (as previously reported) but also on the cell surface of virtually all (15/16) BCP-ALL examined. CD22 that was biosynthetically labeled with 35S-cysteine and immunoprecipitated from the uncommon cytoplasmic CD22- positive/surface CD22-negative BCP-ALL cells was analyzed by single- dimension sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Our results indicated that the cytoplasmic form of CD22 comigrated with 125I/lactoperoxidase-labeled surface CD22. Therefore, cytoplasmic CD22 is probably a pool of fully processed glycoprotein. We also observed unusual cases of AML (approximately 20%) that expressed cytoplasmic CD22 based on immunofluorescent staining; however, biosynthetic labeling and immunoprecipitation revealed an apparently cross-reactive protein(s) of approximately 250 to 300 kd in AML cells. No T-ALL cell lines examined expressed either cytoplasmic or surface CD22. Thus, cytoplasmic and surface expression of bona fide CD22 appears restricted to B cells, which suggests that this molecule subserves a function unique to B cells.     

Des-gamma-carboxyprothrombin (PIVKA II) and plasma vitamin K1 in newborns and their mothers.

Assessments of the vitamin K status in newborns and their mothers by means of des-gamma-carboxy-prothrombin (PIVKA II) measurement have given equivocal results. Part of the variability could be attributed to differences in sensitivity (i.e. the ability to detect small concentrations) and validity (i.e. ability to detect vitamin K deficiency) of the methods applied. None of these methods have yet been validated with respect to plasma vitamin K1. In 22 healthy mother/infant pairs PIVKA II was determined using three different assays including ratio Xa/ecarin (Xa/ec), crossed immunoelectrophoresis (CIE), and an ELISA with a monoclonal antibody (MAB). The results were compared with conventional clotting tests and plasma vitamin K1. The following results were obtained: Cord blood: Clotting tests within age-related normal ranges; PIVKA II detection rates: 0/22 (Xa/ec), 1/22 (CIE), 4/22 (MAB); plasma vitamin K1: undetectable in 20/22. Mothers: Clotting tests all within normal range; PIVKA II detection rates: 1/22 (Xa/ec), 0/22 (CIE), 5/22 (MAB); plasma vitamin K1 (pg/ml) for all mothers (median; range): 186; 55-833; for PIVKA II positive mothers: 213; 59-699. PIVKA II detectability in newborns and mothers was not correlated. The results show an increase in sensitivity for PIVKA II detection in the order of MAB > CIE > Xa/ec. Due to the very low plasma vitamin K1 at birth, no correlation was possible between cord PIVKA II detectability and plasma vitamin K1. However, in mothers at term PIVKA II MAB appears to be unrelated to the vitamin K status.     

Mercuric ions are potent noncompetitive antagonists of human brain kainate receptors expressed in Xenopus oocytes

Kainate receptors are one of the major subtypes of excitatory amino acid receptors in the vertebrate central nervous system. Using Xenopus oocytes injected with RNA from human temporal cortex, it is possible to detect electrophysiologically the expression of this receptor subtype in these cells. Ions of the group IIb elements, particularly mercuric ions, are highly potent, noncompetitive inhibitors of these human brain kainate receptors. Mercury-containing sulfhydryl reagents are also very effective, irreversible blockers of the kainate-gated currents of these oocytes. The recovery of kainate-activated currents after washout of Hg2+ is slow and incomplete relative to that seen after treatment either with Cd2+ or Zn2+. Cysteine or dithiothreitol can accelerate this recovery of kainate-inducible currents after Hg2+ inhibition. Besides the toxicological implications of these results, mercury compounds may be useful for future studies of the structure and physiology of the kainate receptor-channel complex.     

Pseudoaneurysm detection with Tc-99m-labeled red blood cells

A technique for the noninvasive diagnosis of pseudoaneurysms is described. This method employs in vivo labeling of red blood cells with Tc-99m to allow better delineation of the vascular anatomy than standard radionuclide angiography. Four cases are illustrated.     

Evolution of post-traumatic cervical syringomyelia: case report

A patient with complete post-traumatic paraplegia below T6 developed urinary problems and late secondary syringolmyelia. The concordance between the appearance of micturition difficulties and the first sensory symptoms leads us to discuss the r?le of important and repeated efforts to obtain reflex micturition, during the development of post-traumatic syringomyelia.     

Intraoperative arteriography: comparison of conventional screen-film with photostimulable imaging plate radiographs

This prospective study compared images obtained with a photostimulable imaging plate with matched images obtained with a conventional screen-film combination in 26 patients undergoing intraoperative arteriography. Diagnostic accuracy of the two techniques was assessed objectively, and image quality was assessed subjectively. In 16 patients (62%), the radiation exposure was reduced by 50% for the imaging plate technique by decreasing the mAs level generally used for the screen-film combination. Because of the dynamic range of the imaging plate system, no repeat examinations were necessary, while 12% of the screen-film studies had to be repeated because of over- or under-penetration. Imaging plate studies required 6% more time for processing than screen-film studies. Receiver-operating-characteristic analysis indicated no difference in diagnostic accuracy between the two imaging techniques. Subjective evaluation also revealed no difference in observer preference for imaging plate or screen-film studies. The imaging plate technique is an excellent alternative to screen-film studies in the operating room.     

An 11 base pair duplication in exon 6 of the SMN gene produces a type I spinal muscular atrophy (SMA) phenotype: further evidence for SMN as the primary SMA-determining gene

The gene for autosomal recessive spinal muscular atrophy (SMA) has been mapped to 5q12 in a region that contains repeated markers and genes. Three cDNAs that detect deletions in SMA patients have been reported. One of these, the survival motor neuron (SMN) cDNA, is encoded by two genes (SMNT and SMNC) which are distinguished by base changes in exons 7 and 8. Exon 7 of the SMNT gene is not detectable in approximately 95% of SMA cases, due either to deletion or sequence conversion. There is limited information on the mutations in SMA patients that have detectable SMNT, these are critical for confirmation of SMNT as the SMA gene. Using SSCP analysis of the SMN exons we screened our SMA patients that possess at least one intact SMNT allele for mutations in SMNT. We identified one type I SMA patient with an 11 bp duplication in exon 6 which causes a frameshift and premature termination of the deduced SMNT protein. Dosage and SSCP analysis of SMNT in this family indicated that the father contributed a SMNT-deleted allele to the affected child whereas the mother passed on the 11 bp exon 6 duplication SMNT allele. Analysis of RNA by RT-PCR conclusively demonstrated that the 11 bp duplication is associated with the SMNT locus and not SMNC. This mutation provides strong support for SMN as the SMA-determining gene and indicates that disruption of SMNT on its own is sufficient to produce a severe type I SMA phenotype.