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T R Kramer

Publications and source records attributed to T R Kramer.

32 records · Page 2Linked to original sources
PubMed1991

Increased vitamin E intake restores fish-oil-induced suppressed blastogenesis of mitogen-stimulated T lymphocytes.

We sought to determine whether fish-oil supplementation would suppress blastogenesis in vitro of concanavalin A (ConA)-stimulated peripheral blood mononuclear cells (PBMCs) and, if so, whether it could be reversed with increased intake of vitamin E. Healthy males ate a controlled basal diet providing a total of 40% of energy from fat when fed in conjunction with 15 g/d of either placebo oil (PO) or fish-oil concentrate (FOC) fortified with 15 mg alpha-tocopherol/d for three periods. The subjects were supplemented with PO for 10 wk (PO), with FOC for 10 wk (FOC), and with FOC plus an additional 200 mg alpha-tocopherol/d for 8 wk (FOC+E). During FOC supplementation mitogenic responsiveness of PBMCs to ConA was suppressed, but this effect was reversed by concurrent supplementation with all-rac-alpha-tocopherol (FOC+E). There was a significant positive relationship (P less than 0.001) between plasma alpha-tocopherol concentrations and responsiveness of T lymphocytes to ConA.

Cells, Cultured↗
PubMed1989

Fatty acid pattern of tissue phospholipids in copper and iron deficiencies.

Because copper and iron have been reported to be essential cofactors in delta 9 desaturation of fatty acids, the effects of different dietary intakes of copper and iron on tissue fatty acids were studied. Male Long-Evans rats (ten per group) were fed diets containing adequate, deficient or excess copper or iron. On day 42 of the dietary regimen, the animals were killed and tissues and blood were removed for analysis of metals and fatty acids of phospholipids. Compared with the copper-adequate rats, the copper-deficient rats showed increased 18:0 in liver and decreased 16:1 omega 7 in liver, heart and serum. There were no differences for 16:0 or 18:1 omega 9. Intake of excess copper did not cause an increase in products of delta 9 desaturation. Comparisons between iron-deficient and iron-adequate rats showed that iron deficiency increased 18:2 omega 6 in liver and serum and decreased 20:4 omega 6 in serum only. Relative percentages of 16:0, 18:0, 16:1 omega 7 and 18:1 omega 9 in liver and serum phospholipids were similar for both groups. Intake of excess iron caused a decrease in 18:2 omega 6; and 16:0 and 18:1 omega 9 were higher in the liver of the iron-excess group than the iron-deficient group. This study did not support the requirement for copper or iron in the delta 9 desaturation of fatty acids as expressed in phospholipids of liver, heart and serum.

Animals↗
PubMed1988

Influence of iron and the sex of rats on hematological, biochemical and immunological changes during copper deficiency.

The influence of dietary iron and the sex of rats on suppressed lymphocyte functions caused by copper deficiency was examined. Male and female weanling Lewis rats were fed two concentrations of copper (0.6 or 5.6 micrograms Cu/g diet) and iron (50 or 300 micrograms Fe/g diet) for 42 d. Regardless of dietary iron concentrations, male and female rats consuming low copper diets had lower serum ceruloplasmin activity and serum and liver copper concentrations than those fed the high copper diet. However, hemoglobin and hematocrit levels were higher in copper-deficient females than in copper-deficient males and were unaffected by copper deficiency in females fed the high iron diet. Copper-deficient females also had higher serum and liver iron concentrations than copper-deficient males. Proliferation of concanavalin A (Con A)-stimulated spleen lymphoid cells (SLC) was suppressed in copper-deficient males and females, but the suppression was less in the females. Thus, the primary cause of suppressed SLC proliferation in copper-deficient rats is poor copper status; poor iron status induced by copper deficiency had little influence on proliferation.

Animals↗
PubMed1987

Effect of copper deficiency on erythrocyte membrane proteins of rats.

The effects of copper deficiency on the proteins of rat erythrocyte membranes were assessed by electrophoretic analysis. For 42 d, rats were fed diets containing less than 1 ppm Cu with 35 or 250 ppm Fe or 5 ppm Cu with 35 or 250 ppm Fe. Electrophoresis of erythrocyte membrane proteins indicated a significant increase in the amount of a 170,000-dalton protein in rats fed copper-deficient diets. High dietary iron reduced the amount of the 170,000-dalton protein in erythrocyte membranes from rats in both the copper-deficient and copper-adequate groups. However, feeding high dietary iron to copper-deficient rats did not reduce the amount of the protein to the level found in rats fed the copper-adequate diet containing 35 ppm Fe. Triton X-100 extraction of erythrocyte membranes demonstrated that the 170,000-dalton protein was associated with the membrane cytoskeleton. Thus, copper deficiency possibly alters the cell's mechanical properties and consequently decreases erythrocyte survivability by modifying the membrane cytoskeleton.

Animals↗
PubMed1984

Effects of biotin deficiency on polyunsaturated fatty acid metabolism in rats.

The effects of biotin and protein-calorie deficiency on metabolism of liver phospholipids in rats were determined. Weanling male Long-Evans rats were fed ad libitum a biotin-deficient (0.4 micrograms biotin/g diet) or a biotin-adequate (2.4 micrograms biotin/g diet) diet for 49 days. A pair-fed group was fed biotin-adequate diet but restricted to the amount consumed by biotin-deficient rats. The effects of these diets on food intake, weight gain, biotin content of serum and fatty acid composition of liver phospholipid were determined. Growth and food intake were significantly depressed in biotin-deficient and pair-fed rats. Biotin concentration in serum was significantly reduced in biotin-deficient and in pair-fed rats. Biotin deficiency caused significantly increased concentrations of 15:0, 17:0 and total odd-chain fatty acids in liver phospholipids. Combined biotin and protein-calorie deficiency and protein-calorie deficiency alone caused significantly increased concentrations of 18:2 omega 6 in liver phospholipids. Biotin deficiency caused significant reduction in liver phospholipid 20:3 omega 6. Reduced arachidonic acid (20:4 omega 6) level was due to combined biotin protein-calorie deficiency. Protein-calorie deficiency alone was primarily responsible for reduced levels of 22:5 omega 6. Biotin deficiency alone caused significant increases in liver phospholipids 18:3 omega 3 and 22:6 omega 3.

Animals↗
PubMed1984

Reevaluation of zinc deficiency on concanavalin-A-induced rat spleen lymphocyte proliferation.

Zinc concentrations of serum, nonlymphoid and lymphoid tissues, and the responsiveness of concanavalin-A (Con-A)-stimulated spleen lymphocytes (SL) and cervical lymph node cells ( CLNC ) from ad libitum-fed zinc-deficient (ZD), pair-fed (PF) and ad libitum-fed zinc-adequate rats (AL) were determined. In vitro effects of serum from ZD, PF and AL rats on responsiveness of Con-A-stimulated SL and CLNC were determined. Weanling male Long-Evans rats were fed ad libitum zinc-deficient (less than 1.0 microgram Zn/g diet) and zinc-adequate (20 micrograms Zn/g diet) diets for 7-42 days. Effects of undernutrition on test parameters were determined on PF rats, which received a restricted zinc-adequate diet (restricted in amount to that consumed by ZD rats). Growth, food intake and zinc concentrations in serum, liver and pancreas were significantly depressed in ZD and PF rats. Zinc per gram of thymus tissue and per number of SL was elevated in ZD and PF rats. Spleen lymphocytes from ZD and PF rats displayed equivalent to significantly increased levels of proliferation following stimulation with Con-A. [3H]Thymidine incorporation by Con-A-stimulated SL and CLNC from ZD, PF and AL rats was not significantly different when cultured in medium containing serum from ZD, PF and AL rats. The present study shows that zinc deficiency causes major changes in total-body and organ growth but minor changes in zinc content and mitogen-induced proliferation of lymphocytes.

Animals↗
PubMed1984

Influence of reduced food intake on polyunsaturated fatty acid metabolism in zinc-deficient rats.

The influence of reduced food intake on metabolism of liver phospholipids (PL) in zinc-deficient (ZD) rats was measured. Wealing male Long-Evans rats were fed ad libitum zinc-deficient (2 micrograms Zn/g diet) and zinc-adequate (20 micrograms Zn/g diet) diets for 21 days. A pair-fed (PF) group was included. ZD and PF rats displayed significantly increased levels of linoleic (18:2 omega 6) and dihomo-gamma-linolenic acid (20:3 omega 6). Both ZD and PF rats displayed increased levels of gamma-linolenic acid (18:3 omega 6), but the increase was significant only in PF rats. ZD and PF rats displayed decreased levels of arachidonic acid (20:4 omega 6), but the decrease was significant only in PF rats. Both ZD and PF rats displayed significantly reduced levels of 22:5 omega 6. Both ZD and PF rats displayed increased products of delta 6 desaturation and decreased products of delta 5 and delta 4 desaturation. Significantly increased products of delta 9 desaturation were noted in both ZD and PF rats. ZD and PF rats displayed significant increases in C20 elongation products. ZD and PF rats displayed significantly decreased levels of omega 6 metabolites but not total omega 6 acids. ZD rats showed significantly increased levels of total omega 3 acids and omega 3 metabolites. ZD and PF rats showed significant increases in omega 9 acids but not significant changes in omega 9 metabolites. This study does not indicate that zinc affects the delta 6 desaturase in the metabolism of essential fatty acids. The aberrations previously attributed to zinc deficiency are probably due to the accompanying decreased food intake.

Animals↗
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

Optic nerve enlargement and chronic visual loss.

We present four patients with sarcoidosis of the anterior visual pathways. The first patient presented with unilateral visual loss, a mass lesion at the optic nerve head, and an enlarged orbital optic nerve. The second patient presented with bilateral progressive painless visual loss, associated with optic nerve pallor and visual field loss. In these two patients, optic nerve biopsy was diagnostic of sarcoidosis. The third patient developed optic nerve and chiasmal involvement after sarcoidosis was established by lacrimal gland biopsy. The fourth patient had optic nerve, pulmonary, and lymph node involvement with sarcoidosis. A conjunctival and lung biopsy were diagnostic. Computed tomography and magnetic resonance imaging have greatly facilitated diagnosis of sarcoidosis of the anterior visual pathways. Sarcoidosis of the anterior visual pathways may occur alone or in association with other ocular or systemic manifestations. A conjunctival or lacrimal gland biopsy may be preferable as the initial diagnostic approach. Treatment of patients with this condition may require systemic immunosuppression, in addition to corticosteroids, to prevent permanent visual loss.

Adult↗
PubMedDate not supplied

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