Alveolar hydatid disease of the liver: Brief review and spectrum of adjacent organ invasion

The purpose of this study is to show the spectrum of adjacent organ invasion and to make a brief review of hepatic alveolar hydatid disease (AHD), using CT and MR imaging. We retrospectively reviewed CT and MR images of three patients with various adjacent organ invasions surgically and histologically proven to be AHD. Local invasion to right kidney and adrenal, right hemidiaphragm and lung were detected in one patient, right adrenal in another patient and gall bladder, duodenum, gastric wall and pancreas invasion in the other. AHD may rarely extend to the gall bladder, stomach, duodenum, pancreas, right adrenal and kidney, diaphragm, pleura and lung. The extension of the disease outside the liver is usually encountered in patients with large, peripherally located masses in the advanced stage of the disease.     

Deprivation of form vision suppresses diurnal cycling of retinal levels of leu-enkephalin

Deprivation of form vision by the fitting of translucent occluders suppressed the diurnal cycling of enkephalinergic amacrine cells (the ENSLI amacrine cells), in the chicken. Daily periods of normal vision or enforcing temporal contrast using strobe lighting appeared to restore normal functioning of the ENSLI cells. These results suggest that the ENSLI cells are involved in retinal circuits that assess the quality of the visual image and control eye growth.     

Ultrasound-guided Lumbar Facet Nerve Block: Accuracy of a New Technique Confirmed by Computed Tomography

Background: Lumbar facet nerve (medial branch) blocks are often used to diagnose facet joint-mediated pain. The authors recently described a new ultrasound-guided methodology. The current study determines its accuracy using computed tomography scan controls.

Methods: Fifty bilateral ultrasound-guided approaches to the lumbar facet nerves were performed in five embalmed cadavers. The target point was the groove at the cephalad margin of the transverse (or costal) process L1-L5 (medial branch T12-L4) adjacent to the superior articular process. Axial transverse computed tomography scans, with and without 1 ml contrast dye, followed to evaluate needle positions and spread of contrast medium.

Results: Forty-five of 50 needle tips were located at the exact target point. The remaining 5 were within 5 mm of the target. In 47 of 50 cases, the applied contrast dye reached the groove where the nerve is located, corresponding to a simulated block success rate of 94% (95% confidence interval, 84-98%). Seven of 50 cases showed paraforaminal spread, 5 of 50 showed epidural spread, and 2 of 50 showed intravascular spread. Despite the aberrant distribution, all of these approaches were successful, as indicated by contrast dye at the target point. Abnormal contrast spread was equally distributed among all lumbar levels. Contrast traces along the needle channels were frequently observed.     

Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP)

Mutations in the PEX gene at Xp22.1 (phosphate-regulating gene with homologies to endopeptidases, on the X-chromosome), are responsible for X-linked hypophosphataemic rickets (HYP). Homology of PEX to the M13 family of Zn2+ metallopeptidases which include neprilysin (NEP) as prototype, has raised important questions regarding PEX function at the molecular level. The aim of this study was to analyse 99 HYP families for PEX gene mutations, and to correlate predicted changes in the protein structure with Zn2+ metallopeptidase gene function. Primers flanking 22 characterised exons were used to amplify DNA by PCR, and SSCP was then used to screen for mutations. Deletions, insertions, nonsense mutations, stop codons and splice mutations occurred in 83% of families screened for in all 22 exons, and 51% of a separate set of families screened in 17 PEX gene exons. Missense mutations in four regions of the gene were informative regarding function, with one mutation in the Zn2+-binding site predicted to alter substrate enzyme interaction and catalysis. Computer analysis of the remaining mutations predicted changes in secondary structure, N-glycosylation, protein phosphorylation and catalytic site molecular structure. The wide range of mutations that align with regions required for protease activity in NEP suggests that PEX also functions as a protease, and may act by processing factor(s) involved in bone mineral metabolism.