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Biomedical subjects

T R Kramer

Publications and source records attributed to T R Kramer.

5 recordsLinked to original sources
PubMed1992

Effect of vitamin A and zinc supplementation on the nutriture of children in Northeast Thailand.

Previous surveys suggested that young children in Northeast Thailand may benefit from vitamin A and/or zinc supplementation. One hundred thirty-three children aged 6-13 y with marginal plasma retinol (less than 1.05 mumol/L) and Zn (less than 12.2 mumol/L) concentrations participated in a double-blind study. They were randomly assigned and supplemented with either zinc (25 mg/d), vitamin A (1500 RE/d), zinc plus vitamin A, or placebo for 6 mo. Biochemical indices of vitamin A (plasma vitamin A, retinol-binding protein) and zinc status (plasma zinc, alkaline phosphatase) increased significantly. The children had adequate liver stores of vitamin A (relative dose response less than 20%). Zinc supplementation resulted in an improvement in vision restoration time (VRT) in dim light (dark adaptometry). Vitamin A and zinc synergistically normalized conjunctival epithelium as measured by conjunctival impression cytology (CIC). Both functional indices, VRT and CIC, showed significant correlations with plasma zinc and vitamin A, respectively. The data suggest that functional improvements in populations with suboptimal vitamin A and zinc nutriture can be accomplished by supplementation with less than two times the recommended dietary allowance of these nutrients.

Alkaline Phosphatase↗
PubMed1992

Cytokeratin expression in corneal endothelium in the iridocorneal endothelial syndrome.

The immunocytologic characteristics of two formalin-fixed, paraffin-embedded corneas from patients with the iridocorneal endothelial (ICE) syndrome and unaffected control corneas were studied. Binding of polyclonal antisera to Factor VIII, S-100 protein, involucrin, neuron specific enolase (NSE), and the lectins peanut agglutinin and Ulex europaeus agglutinin-1 was performed using the standard peroxidase-anti-peroxidase method. We detected reactive patterns of monoclonal antibodies to cytokeratins (34BE12 is a 56-58 kD mouse IgG reactive to stratified epithelia; Pkk1 is a 44-54 kD mouse IgG reactive to simple epithelia; and KL1 is a 55-57 kD mouse IgG reactive to epidermis and simple epithelia) using the standard avidin-biotin complex method. Staining properties were similar for the polyclonal antisera, lectins, NSE, and chromogranin in corneas with ICE syndrome and in the controls. However, the cytokeratins 34BE12, Pkk1, and KL1 were detected in the endothelium of the corneas with the ICE syndrome but not in the controls. These findings suggest that various cytokeratins are expressed in the corneal endothelium in the ICE syndrome that are not expressed in unaffected corneal endothelium.

Antibodies, Monoclonal↗
PubMed1976

Nutritional deficiency, immunologic function, and disease.

Several experiments conducted by our group over a period of 6 years have shown that nutritional stress, especially protein and/or calorie deprivation, leads to many, often dramatic, changes in the immune responses of mice, rats, and guinea pigs. Chronic protein deprivation (CPD) has been shown to create an enhancing effect on the cell-mediated immune responses of these animals. Humoral responses under CPD conditions were most often found to be depressed, but sometimes were unaffected, depending on the nature of the antigen employed. Chronic protein deprivation, consistent with the pattern just mentioned, improved tumor immunity by depressing production of B-cell blocking factors, and, in at least one instance, resistance to development of mammary adenocarcinoma in C3H mice was associated with evidence of increased numbers of T suppressor cells. Profound nutritional deficits (less than 5% protein per total daily food intake) depressed both cellular and humoral immunity. Early, though temporary, protein deprivation caused a long-term depression of both cellular and humoral immunity also, with the humoral component being the first to recover. Manipulation of protein and calories was found to have a profound effect on certain autoimmune conditions. Diets high in fat and low in protein favored reproduction but shortened the life of NZB mice, whereas diets high in protein and low in fat inhibited development of autoimmunity and prolonged life. Chronic moderate protein restriction permitted NZB mice to maintain their normally waning immunologic functions much longer than mice fed a normal protein intake. Further, the low-protein diet was associated with a delay in development of manifestations of autoimmunity. Decreasing dietary calories by a reduction of fats, carbohydrates, and proteins more than doubled the average life span of (NZB X NZW)F1 mice, a strain prone to early death from autoimmune disease. Histopathologic studies using immunofluorescent microscopy revealed that the development of the renal lesions caused by the deposition of antigen-antibody complexes, which is so characteristic of these mice, was markedly delayed.

Anemia, Hemolytic↗
PubMedDate not supplied

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