Clinical features of selenium deficiency in infants receiving long-term nutritional support.

OBJECTIVE: Selenium deficiency is a known complication in patients requiring long-term nutritional support; however, the clinical features of selenium deficiency in infants have not been completely described. We describe the clinical features of selenium deficiency in infants. METHODS: Six infants with selenium deficiency were studied retrospectively, with a focus on the period of nutritional support, the clinical symptoms, and the chronologic changes in serum selenium concentrations before and after the administration of selenite. RESULTS: The onset of selenium deficiency in five patients occurred at <6 mo of age; selenium deficiency occurred in one patient 14 mo after birth. One patient received parenteral nutrition for 15 mo after birth; the other five patients primarily received an elemental diet for 2-6 mo. In all patients, growth retardation and alopecia with pseudoalbinism were the characteristic symptoms of selenium deficiency. At the time of diagnosis, the serum selenium level in four patients was <2.0 microg/dL and serum selenium levels in two patients were 3.2 and 3.3 microg/dL, respectively. The resolution of hair symptoms corresponded to the level of serum selenium after 1-2 mo and a rapid improvement in growth occurred in all patients after the administration of selenite. CONCLUSION: The early clinical symptoms of selenium deficiency in infants include growth retardation and alopecia with pseudoalbinism, which are reversible if the patients are treated with adequate amounts of selenite. Clinicians who manage infants receiving long-term nutritional support, including an elemental diet, should be aware of the symptoms associated with selenium deficiency.

Biphasic and directed translocation of protein kinase Cα inside cultured endothelial cells before migration.

Mechanical wounding of an endothelial monolayer induces an immediate Ca2+ wave. Several hours later, the denuded area is covered by endothelial cells (ECs) that migrate to the wound. This migration process is closely related to protein kinase Cα (PKCα), a Ca2+-dependent protein that translocates from the cytosol to the cell membrane. Because the cells adjacent to the wounded area are the first to migrate into the wound, we investigated whether a mechanical wound immediately induces PKCα translocation in adjacent cells. We monitored Ca2+ dynamics and PKCα translocation simultaneously using fluorescent microscopy. For this simultaneous observation, we used Fura-2-acetoxymethyl ester to visualize Ca2+ and constructed a green fluorescent protein-tagged fusion protein to visualize PKCα. Mechanical wounding of the endothelial monolayer induced an immediate Ca2+ wave in cells adjacent to the wounded cells before their migration. Almost concurrently, PKCα in the neighboring cells translocated to the cell membrane, then accumulated at the periphery near the wounded cell. This report is the first description of this biphasic and directed translocation of PKCα in cells before cell migration. Our results may provide new insights into the directed migration of ECs.

The Effect of Nitric Oxide on Ammonia Decomposition in Co-cultures of Hepatocytes and Hepatic Stellate Cells.

Hepatic functions, such as albumin secretion and ammonia metabolism, are upregulated in response to hepatocyte growth factor (HGF) produced by hepatic stellate cells (HSC), as well as nitric oxide (NO) produced by endothelial cells under shear stress. However, the simultaneous effect of HSC and NO has not been previously investigated in a tri-co-culture model containing hepatocytes with HSC and endothelial cells under shear stress. We hypothesized that NO inhibits HGF production from HSC. To test this idea, we constructed a mono-culture model of hepatocytes and a co-culture model of hepatocytes and HSC and measured ammonia decomposition and HGF production in each model under NO load. Ammonia decomposition was significantly higher in the co-culture model under 0 ppm NO load, but no significant increase was observed under NO load. In the co-culture model, HGF was produced at 1.0 ng/mL under 0 ppm NO load and 0.3 ng/mL under NO load. Ammonia decomposition was increased by 1.0 ng/mL HGF, but not by 0.3 ng/mL HGF. These results indicated that NO inhibits HGF production from HSC; consequently, the effects of NO and co-culture with HSC cannot improve hepatic function simultaneously. Instead, the simultaneous effect of 1.0 ng/mL HGF and NO may further enhance hepatic function in vitro.

Biphasic and boundary lubrication mechanisms in artificial hydrogel cartilage: A review.

Various studies on the application of artificial hydrogel cartilage to cartilage substitutes and artificial joints have been conducted. It is expected in clinical application of artificial hydrogel cartilage that not only soft-elastohydrodynamic lubrication but biphasic, hydration, gel-film and boundary lubrication mechanisms will be effective to sustain extremely low friction and minimal wear in daily activities similar to healthy natural synovial joints with adaptive multimode lubrication. In this review article, the effectiveness of biphasic lubrication and boundary lubrication in hydrogels in thin film condition is focused in relation to the structures and properties of hydrogels. As examples, the tribological behaviors in three kinds of poly(vinyl alcohol) hydrogels with high water content are compared, and the importance of lubrication mechanism in biomimetic artificial hydrogel cartilage is discussed to extend the durability of cartilage substitute.