No abstract

Cryopreservation would potentially very much facilitate the inventory control and distribution of laboratory-produced organs and tissues. Although simple freezing methods are effective for many simple tissues, bioartificial organs and complex tissue constructs may be unacceptably altered by ice formation and dissolution. Vitrification, in which the liquids in a living system are converted into the glassy state at low temperatures, provides a potential alternative to freezing that can in principle avoid ice formation altogether. The present report provides a brief overview of the problem of renal vitrification. We report here the detailed case history of a rabbit kidney that survived vitrification and subsequent transplantation, a case that demonstrates both the fundamental feasibility of complex system vitrification and the obstacles that must still be overcome, of which the chief one in the case of the kidney is adequate distribution of cryoprotectant to the renal medulla. Medullary equilibration can be monitored by monitoring urine concentrations of cryoprotectant, and urine flow rate correlates with vitrification solution viscosity and the speed of equilibration. By taking these factors into account and by using higher perfusion pressures as per the case of the kidney that survived vitrification, it is becoming possible to design protocols for equilibrating kidneys that protect against both devitrification and excessive cryoprotectant toxicity.

PURPOSE-To determine the incidence of new chorioretinal lesions in children with toxoplasmosis diagnosed after, and therefore not treated during, their first year. RESULTS-Twenty-eight of 38 children had one of the following: diagnosis with serum antibody to T. gondii indicative of chronic infection at age 24 months, central nervous system calcifications, hydrocephalus, illness compatible with congenital toxoplasmosis perinatally but not diagnosed at that time. Twenty-five returned for follow-up during 1981 to 2005. Their mean (range) age at last exam was 10.9 ± 5.7 (range, 3.5 to 27.2) years and mean follow-up was 5.7 ± 2.9 years. Eighteen (72%) children developed at least one new lesion. Thirteen (52%) had new central lesions, 11 (44%) had new peripheral lesions, and six (24%) had both. Thirteen (52%) had new lesions diagnosed at age ≥ 10 years. New lesions were found at more than one visit in four (22%), and bilateral new lesions developed in seven (39%) of 18 children who developed new lesions. Of 10 additional children with eye findings and serologic tests indicative of chronic infection, six returned for follow-up, four (67%) developing new lesions at ≥ 10 years of age. CONGENITAL TOXOPLASMOSIS THAT WAS UNTREATED or treated only for one month has been described in small series of patients as a relapsing, recrudescent disease causing significant visual impairment. 1,2 However, the prospective follow-up into adolescence of chorioretinal lesions in children with congenital toxoplasmosis, other than a small group of those with congenital toxoplasmosis diagnosed at birth and treated during the first year of life, has not been rigorously defined. Herein we describe a cohort of 38 children with toxoplasmosis presenting after one year of age, who were followed prospectively in a single center according to a standardized protocol. DESIGN-Prospective longitudinal cohort study. METHODS-Thirty-eight CONCLUSIONS-More METHODS DESIGN OF STUDYThe children in this study and their mothers were referred by their physicians and evaluated at the University of Chicago by a group of specialists at the onset of enrollment into the study and later at prespecified times: 1, 3.5, 5, 7.5, 10, 15, 20, 25, 30, 35, 40, and 45 years of age. 3, 4 Written informed consent was obtained from all parents or legal guardians of participating minor-age children and/or directly from the patient (if of legal adult age). PATIENT COHORTThis cohort consists of 38 persons who were children at the time of diagnosis of their ocular toxoplasmosis, who, with their mothers, had nonacute serologic tests for Toxoplasma gondii infection at the time their contact with the Chicago Toxoplasmosis Center was initiated. They were not diagnosed until after their first year of life. Patients in this cohort were not treated during their first year of life. All children with active chorioretinitis were treated when this occurred and was detected. It appears that children in the present cohort seem to have much more frequent new lesions than we report in a co...