Hepatic reticuloendothelial function during parenteral nutrition including an MCT/LCT or LCT emulsion after liver transplantation – a double-blind study

It has been demonstrated that total parenteral nutrition (TPN) modulates the function of the hepatic reticuloendothelial system (RES). The objective of this study was to evaluate the impact of two different TPN lipid emulsions on the recovery of allograft RES function after orthotopic liver transplantation (OLTx). In a prospective, double-blind study, OLTx patients were randomly assigned to two treatment groups. Group I ( n=13) received a TPN regimen that included long-chain triglycerides (LCT). Group II ( n=9) received a TPN regimen that included a fat emulsion consisting of both medium-chain triglycerides (MCT) and LCT. At baseline, i.e., on days 2 or 3 after OLTx ( t1), before lipids for TPN were started, hepatic RES function was determined using the human serum albumin millimicrosphere technique (K-value, 1/min). A second measurement ( t2) was obtained after 7 days of TPN, including one of the study's two fat emulsions. The mean (+/- SD) K-value (1/min) was 0.48+/-0.16 in the LCT group and 0.55+/-0.28 in the MCT/LCT group at t1, and it improved to 0.62+/-0.21 in the LCT group and to 0.86+/-0.32 in the MCT/LCT group at t2. RES function recovery was significantly better in the MCT/LCT group ( P< or = 0.05). MCT/LCT emulsion appears to be the TPN fat emulsion of choice after OLTx as it seems to have less impact on hepatic RES recovery.     

The photoionization-reduced energy in LSC.

The atomic rearrangement cascade that follows the electron-capture decay process in low-Z radionuclides involves X-rays which have high photoelectric interaction probabilities. When the K-shell binding energy of the ionized atom (e.g., hydrogen) is significantly lower than the energy of the X-ray photon, the detector response to a photon-equivalent energy electron and the whole photoionization process are very similar. This is not the case when the scintillator cocktail contains larger atoms (e.g., oxygen and phosphorus in Ultima Gold). For larger Z atoms, the reduced energy of the whole photoionization process is less than the reduced energy of the interacting photon due to the nonlinear effects of ionization quenching. This paper shows the convenience of including a more detailed simulation of the photoionization process in the atomic rearrangement detection model for electron-capture nuclides such as (55)Fe, (51)Cr and (54)Mn. The need for more elaborate atomic rearrangement models is a consequence of the analysis of (125)I data.     

Evidence for frequent divergence impairment in French dyslexic children: deficit of convergence relaxation or of divergence per se?

Aim There is a controversy as to whether dyslexic children present visuo-motor disabilities such as vergence and accommodative problems assessed with orthoptic tests. The purpose of this study is to re-examine this issue in a large population of children. Methods Extensive orthoptic evaluation was made in 57 dyslexic and 46 non-dyslexic (“normal”) age-matched children. Convergence and divergence capacities were evaluated at two distances (30 cm and 400 cm). Results Binocular vision measured with stereo-acuity tests was normal in dyslexics. In contrast, the near point of convergence was significantly more remote in dyslexics; most importantly, divergence at both far and near distance was significantly more reduced in dyslexics (median value 4 pD and 10 pD, respectively, at far and near) than in “normals” (median value 6 pD and 12 pD, at far and near). Conclusion The existence of the divergence deficit at far distance indicates the presence of deficit of divergence per se, independently from convergence and accommodation relaxation. This result is novel and corroborated by physiological studies indicating distinct control of convergence and divergence, both at the cortical and subcortical premotor level. We conclude that vergence deficits are frequently present in dyslexics, and that dyslexics should be re-educated; training should address distinctively convergence and divergence subsystems.     

Medizinische Beurteilungskriterien zu bandscheibenbedingten Berufskrankheiten der Lendenwirbelsäule (I)

Occupational diseases Nos. 2108 and 2110 correspond to intervertebral disc-related diseases of the lumbar spine from many years of carrying or lifting heavy loads, occupations in extreme postures of full flexion or oscillation of the whole body when seated, and which compel the cessation of all activities which are or could be the cause for the origin, exacerbation or recurrence of the disease. These occupational diseases came into force at the start of 1993, but there have been considerable problems in their implementation. The present Part I of the contribution is the result of the work of an interdisciplinary study group and contains medical criteria for the assessment of possibly strain-related clinical characteristics and the evaluation of other possible causes. Part II is to be published in Volume 4/2005 and will deal with questions related to forced cessation and to the assessment of the loss of earning ability. Agreement was reached in many areas related to the assessment of occupational claims. This should allow for evidence-based decision making in the future for the occupational diseases Nos. 2108 and 2110.     

Localization of Apaf1 gene expression in the early development of the mouse by means of in situ reverse transcriptase-polymerase chain reaction.

Apoptosis is an essential ubiquitous process that controls the duration of the life span of cells, thus playing a crucial role in morphogenetic, histogenetic, and phylogenetic developmental processes. Apaf1 (apoptosis protease activating factor 1) is one of the central mediators of the intrinsic apoptotic pathway and a part of the apoptosome, which activates procaspase-3 and promotes cell death. Gene knockout of Apaf1 in mice leads to late embryonic lethality with malformations such as the persistence of interdigital webs and hyperplasia of brain and retina. Therefore, Apaf1 is generally believed to play a crucial role in developmental apoptosis and have a widespread expression. However, its pattern of expression in early development remains unknown. To specify whether Apaf1 indeed plays this key role, we investigated the pattern of gene expression for Apaf1 in mouse embryos on day 7, 9, and 12 of development. Our results show, that gene expression for Apaf1 first occurs within the embryo between day 7 and 9 of development, becoming more widespread toward day 12 and then includes structures, such as yolk sac, mesenchyme, cartilage, heart anlage, otic vesicle, peridermis, and anlagen of the spinal ganglia and vertebral bodies. Our results also show that gene expression for Apaf1 is not ubiquitous in early mouse development. This finding indicates that cell death processes are independent of or less dependent on Apaf1 during this time. Of interest, an active gene expression for Apaf1 is also present in organ anlagen such as heart or intestine, in which no obvious phenotype is seen after Apaf1 deletion. This finding suggests a possible role for Apaf1 in such anlagen as a putative alternative compensatory pathway, which could be switched on in the case of defects in the mediators that are normally involved in such organs.