Effects of iron loading on pathogenicity in hepatitis C virus-infected chimpanzees.

Elevated iron levels have been associated with raised serum alanine transaminase (ALT) levels in hepatitis C virus (HCV)-infected humans. However, it is not clear if HCV infection causes increased iron accumulation by the liver or if the severity of HCV infection is actually worsened by higher iron levels in the host. To better understand the relationship between iron and persistent HCV infections, we examined the effect of excess dietary iron on disease severity in HCV-infected chimpanzees. Iron was supplemented in the diets of four HCV-infected and two uninfected chimpanzees for 29 weeks to achieve iron loading. Iron loading was confirmed by increases in serum iron levels, percentages of transferrin saturation, ferritin levels, elevations in hepatic iron concentration (HIC), and by histological examination. The majority of HCV-infected chimpanzees had higher iron levels before iron feeding than the uninfected animals. Although various degrees of iron loading occurred in all chimpanzees, HCV-infected animals exhibited increased loading in comparison with uninfected animals. The effects of iron loading on HCV disease expression was determined by comparing disease parameters during an extended baseline period before iron loading with the period during iron loading and immediately following iron loading. Iron loading did not influence the viral load, but did exacerbate liver injury in HCV-infected chimpanzees, as evidenced by elevated ALT and histological changes. Because all chimpanzees on high iron diets experienced iron loading, but pathological effects were only observed in HCV-infected chimpanzees, HCV infection appears to increase the susceptibility of the liver to injury following iron loading. These results confirm and extend previous observations made in human populations and serve to further validate the chimpanzee model of chronic hepatitis C.

Group play therapy. Using an interaction model with delayed regressed behaviors in children.

This article gives an overview of individual play therapy and relates the concepts of individual play therapy to group play therapy. A new model of group play therapy, an interactional model, is introduced. The article provides basic guidelines for beginning play therapists. An actual group is described and specific interventions for problems are suggested.

Dietary induction of renal mineralization in dogs.

Ten dogs were fed diets high in phosphorus and low in calcium to induce secondary hyperparathyroidism, with ten dogs fed a standard diet as controls. At the end of the feeding period, all dogs were necropsied. Because of an apparent increase in mineral deposits in the kidneys of hyperparathyroid dogs, the amount and characteristics of these mineral deposits were compared. The dogs in the test groups had larger and more widely disseminated deposits. Five additional dogs were nephrectomized unilaterally, fed the test diet and euthanized at three-month intervals. In these dogs, the amount of renal mineral increased until six months after the start of the test diet, but dit not appreciably change between six and 15 months postdiet. When compared to controls, the test dog kidneys in this second experiment had a greater amount and wider distribution of renal mineralization and tubular dilatation.

Effects of hyperparathyroidism and dietary calcium supplementation on bone healing.

Effects of nutritional secondary hyperparathyroidism and dietary calcium supplementation on bone healing were determined. Groups (n = 4) of 5 mature male dogs each were fed the following diets: group 1, control diet (0.48% Ca, 0.43% P); group 2, test diet (0.12% Ca, 1.14% P): group 3, control diet plus calcium; group 4, test diet plus calcium. The dietary calcium supplementation was calcium gluconate. Lesions were induced in the right tibial cortex by trephinization. Within the time limitations of this study, it was determined that nutritional secondary hyperparathyroidism does not inhibit bone healing and that dietary calcium supplementation does not aid bone healing.