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Unmyelinated axons of normal and regenerated sciatic nerve were counted in controls and vitamin E-deficient rats. No significant change in the number of unmyelinated axons of uninjured nerve was found in the vitamin E deficiency in comparison to controls (12961 +/- 1591 and 12450 +/- 1290, respectively, mean +/- SEM). In regenerated nerve of control rats the number of unmyelinated axons was higher than in uninjured nerve (16971 +/- 1854 and 20786 +/- 1574 at 1 and 2 months after crush, respectively). In vitamin E-deficient rats the increase in number of unmyelinated axons was greater than in corresponding controls (21880 +/- 662) at 1 month after lesion, but the number returned to value found in uninjured nerve at 2 months after lesion (12536 +/- 659). These results suggest that sprouting at lesion may be enhanced but some regenerated axons does not survive at long term in vitamin E-deficiency.
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PMID:Regeneration of unmyelinated peripheral axons in vitamin E-deficient rats. 774 6

Vitamin E was quantified in renal cell carcinomas (RCC) and in 'intact' renal cortex, obtained from 31 patients subjected either to unilateral nephrectomy or to partial resection of the only kidney. Histologically, 14 tumors consisted predominantly of clear cells (group 1) and 17 of other cell types (group 2). In both groups, a significant increase in vitamin E concentration, as compared to the 'intact' cortex, was observed: 167.8 +/- 27.9 and 68.2 +/- 15.2 micrograms/g wet tissue weight (mean +/- SEM) for groups 1 and 2, respectively, versus 10.1 +/- 0.53 micrograms/g wet tissue weight for the cortex. Although the total lipid content was also increased in tumors (especially in group 1), the vitamin E concentration in tumor tissue, calculated per milligram of total lipids, proved to be much higher in both groups than in 'intact' cortex. A significant positive correlation was observed between vitamin E and total lipid content in group 1 and 2 carcinomas. It was also found that vitamin E accumulation in RCC is unlikely to be attributed to an enhanced lipid deposit in the tumor cells. Thus, in 8 tumors of group 2 the vitamin E levels were markedly enhanced although these tumors did not differ from the cortex in total lipid concentrations. Vitamin A content determined in 17 carcinomas, when calculated per milligram of total lipids, was the same as in 'intact' cortex.
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PMID:Liposoluble vitamins E and A in human renal cortex and renal cell carcinomas. 777 11

Anemia of prematurity (AOP) has been conventionally treated with erythrocyte transfusions. Recent investigations have reported the use of recombinant human erythropoietin (rHuEPO) as an alternative for treating AOP. The potential of rHuEPO in increasing erythropoiesis implies its clinical usefulness. The effect of rHuEPO on reticulocyte count as well as other parameters of blood cells was examined in 14 premature babies with AOP. The average birth body weight and gestational age of these premature babies were 1533.71 +/- 61.66 g (Mean +/- SEM) and 31.36 +/- 0.49 weeks respectively. They received the first dose of rHuEPO at age 26.14 +/- 2.03 days with a hemoglobin level by 9.40 +/- 0.27 g/dL and hematocrit level of 28.20 +/- 0.81%. They were given rHuEPO 200 U/kg subcutaneously every other day for 10 doses, and iron 3 mg/kg and vitamin E 25 IU/kg per os every day. Average erythropoietin level of the patients on entry into this study was low (7.66 +/- 1.10 mu/mL). After treatment with rHuEPO for 20 days, the corrected reticulocyte count increased from 0.64 +/- 0.10% to 1.68 +/- 0.42% on Day 5 (P < 0.05), 1.96 +/- 0.41% on Day 12 (P < 0.05), 1.77 +/- 0.43% on Day 20 (P < 0.05), and hematocrit increased from 28.2 +/- 0.81% to 29.58 +/- 1.02% (p < 0.05) on Day 20. Bone marrow aspirates on Day 10 for 9 infants revealed moderate to high cellularity, mostly with erythroblasts (47.89 +/- 1.78%); the M/E ratio was low (0.57 +/- 0.05). The granulocyte series and megakaryocyte could be well visualised.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of recombinant human erythropoietin in treating the anemia of prematurity. 779 77

Vitamin E was quantified in the cortex and medulla of human, rat, canine and rabbit kidneys. For the all species investigated the vitamin concentrations, calculated both per g wet tissue weight and per mg tissue protein, was shown to be 1.4-2.2 times higher in medullary layer than in cortical one. The least vitamin E levels were observed in rabbit kidneys of which the cortical and medullary concentrations were 4.4 +/- 0.3 mkg (M +/- SEM) and 6.3 +/- 0.56 mkg per g wet tissue weight, respectively. In human renal cortex and medulla the vitamin concentrations were found to be 10.6 +/- 0.66 mkg and 16.2 +/- 1.1 mkg per g wet tissue weight, respectively. Close values were observed for other species studied as well. The increased renal medullary vitamin E concentrations are likely related to the higher phospholipid metabolism and enhanced prostaglandin synthesis in this tissue.
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PMID:[Vitamin E content in cortical and medullary layers of mammalian kidney]. 805 6

To demonstrate the role of vitamin E on cerebellar function, studies on rabbits fed low and high levels of dietary vitamin E were performed. The L-[3H]glutamate binding to cerebellar membranes of rabbits fed normal, high and low vitamin E diet showed receptor density (Bmax) values (mean +/- SEM) of 274 +/- 13, 637 +/- 37, and 265 +/- 60 pmol/mg protein, respectively, and dissociation equilibrium constant (KD) values of 257 +/- 99, 233 +/- 77, and 120 +/- 15 nM, respectively. Significant difference of Bmax from control was observed in the high dietary vitamin E group and of KD from control for the low dietary vitamin E group. These results indicate that dietary vitamin E levels have demonstrable effects on the central nervous system, especially the glutamate neurotransmitter system in rabbit cerebellum.
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PMID:Effect of dietary vitamin E on L-[3H]glutamate binding in rabbit cerebellum. 809 8

Dietary supplementation with fish oils high in the omega-3 fatty acids, eicosapentaenoic acid and docosahexaenoic acid, may have an antiinflammatory effect. We determined whether patients with cystic fibrosis (CF) could incorporate omega-3 fatty acids into their plasma and cell membrane phospholipids without adverse effects. In this double-blind study, 12 patients with pancreatic insufficiency who have CF (mean age, 12.2 +/- 5.4 (SD) years) and 13 subjects without CF (mean age, 13.4 +/- 6.3 (SD) years) were randomly assigned to ingest 8 gm daily of either encapsulated fish oil (3.2 gm of eicosapentaenoic acid and 2.2 gm of docosahexaenoic acid daily) or olive oil ethyl esters for 6 weeks. Two of seven and two of five patients with CF who received fish and olive oils, respectively, and one of eight and none of five subjects without CF discontinued taking the capsules before 6 weeks because of eructation or diarrhea. Significant incorporation of omega-3 fatty acids into plasma and erythrocyte membrane phospholipids was observed in subjects with and those without CF randomly assigned to the fish oil treatment. For example, in subjects randomly assigned to receive fish oil, the eicosapentaenoic acid/arachidonic acid ratio in plasma increased 9.8-fold, from 0.04 +/- 0.02 (mean +/- SEM) to 0.39 +/- 0.11 (p = 0.02), in the patients with CF (n = 7) and 23.0-fold, from 0.04 +/- 0.01 to 0.92 +/- 0.17 (p = 0.001), in the subjects without CF (n = 8) who received fish oil (p = 0.02, patients with CF vs subjects without CF at 6 weeks). No clinically or statistically significant changes from baseline were observed in platelet aggregation or levels of vitamin E or A in subjects who received fish oil. Future studies are indicated to determine whether omega-3 fatty acid enrichment provides a clinically beneficial antiinflammatory effect in patients with CF.
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PMID:Oral absorption of omega-3 fatty acids in patients with cystic fibrosis who have pancreatic insufficiency and in healthy control subjects. 807 70

The morphological lesions of endothelial cells in rabbits with MOF were studied by scanning (SEM) and transmission electron microscopy (TME). The edges of the cells were blurred in the MOF groups. TEM showed that the nuclei were irregular and the mitochondria were swollen. The results indicated that the vascular endothelial cells were injured in rabbits with MOF in various extent. Administration of vitamin E in the early stage seemed beneficial in protecting the endothelial cell in this event.
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PMID:[Ultrastructural changes in endothelial cells in rabbits with multiple organ failure (MOF)]. 822 93

Vitamin E is an endogenous antioxidant and is known to afford protection against lipid peroxidation. If lipid peroxidation was an important factor in the pathogenesis of reoxygenation injury in heart, then both the extent of lipid peroxidation and cell injury would be expected to be exacerbated in vitamin E-deficient hearts. To study reoxygenation injury in the present experiments, rat hearts were perfused in the Langendorff mode with a modified Krebs-Henseleit buffer under anoxic conditions for 60 min before resuming normoxic perfusion for 20 min. Creatine phosphokinase (CPK) activity and malonyldialdehyde (MDA), a product of lipid peroxidation, were assayed in the perfusate effluent from hearts during reoxygenation injury. Also, myocardial MDA and vitamin E contents were measured in extracts of freeze-clamped heart tissue obtained immediately before and 2 min after reoxygenation. Experiments were performed on hearts from groups of weanling rats fed either a vitamin E-deficient or vitamin E-supplemented diet (50 I.U. vitamin E/kg) for 5 to 6 weeks. After 5 weeks, the myocardial vitamin-E content was 103.8 +/- 5.3 (n = 5) and 11.5 +/- 1.6 (n = 4) ng/mg protein (mean +/- SEM) in the vitamin E-supplemented and vitamin E-deficient groups respectively. Perfused hearts from both dietary groups showed a peak of enzyme release 2 to 3 min after the reintroduction of oxygen, and enzyme release from vitamin E-deficient hearts was two-fold greater than enzyme release from vitamin E-supplemented hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No evidence of malonyldialdehyde formation during reoxygenation injury in vitamin E-deficient rat heart. 824 Feb 24

Wound closure with cultured skin substitutes results in epithelium that is consistently hypopigmented. Hypothetically, addition of human melanocytes to cultured skin grafts may result in normal pigmentation of healed skin. Skin substitutes were composed of human epidermal keratinocytes and melanocytes, dermal fibroblasts, and collagen-glycosaminoglycan substrates, and were incubated for 12 d in media for keratinocyte growth (KG, n = 4), for keratinocyte differentiation containing four fatty acids and vitamin E with basic fibroblast growth factor (KDF, n = 6) or epidermal growth factor (KDE, n = 6), or for melanocyte growth (MG, n = 6) with phorbol ester and 5% fetal bovine serum. Skin substitutes were grafted orthotopically to full-thickness skin wounds (2 x 2 cm) on athymic mice, and scored for percent original wound size (+/- SEM), visible pigmentation (number pigmented/n), and positive staining for human leukocyte antigens (HLA)-ABC after 6 weeks on the mice. The data show that cultured skin grafts containing human melanocytes that are incubated in KDE or MG media have statistically significant reduction in wound contraction, 1:1 correlation of expression of pigment and HLA-ABC, and increased frequency of pigmentation after healing compared to incubation in KG or KDF media. Transmission electron microscopy confirmed the presence of melanocytes, melanosomes, and pigment transfer to keratinocytes in pigmented skin. These results suggest that survival and differentiated function of cultured epithelium can support melanization of skin, and that skin analogues exposed to phorbol ester in vitro can support skin pigmentation after wound healing.
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PMID:Pigmentation and inhibition of wound contraction by cultured skin substitutes with adult melanocytes after transplantation to athymic mice. 845 98

Lung inflammation in cystic fibrosis (CF) is associated with an increased release from activated neutrophils of oxidants and proteinases. Free radical generation is not efficiently neutralized, and the major anti-proteinase, alpha 1-proteinase inhibitor (alpha 1-PI) is thought to be oxidatively inactivated. We hypothesized that enhanced antioxidant protection could represent an additional long-term strategy to attentuate the host inflammatory response. The effect on plasma neutrophil elastase/alpha 1-PI (NE/alpha 1-PI) complex levels (as a marker of lung inflammation) and plasma malondialdehyde concentrations (as a marker of lipid peroxidation) of additional oral beta-carotene supplementation was studied in 33 CF patients who had already received long-term vitamin E supplementation. In the presence of a more than 10-fold increase in plasma beta-carotene concentrations (mean +/- SEM) (0.09 +/- 0.01 to 1.07 +/- 0.19 mumol/L; p < 0.0001), a small increase in plasma alpha-tocopherol concentrations (23.8 +/- 1.31 to 28.4 +/- 1.81 mumol/L; p = 0.02), and a more than 50% decrease in plasma malondialdehyde concentrations (1.00 +/- 0.07 to 0.46 +/- 0.03 mumol/L; p < 0.0001), plasma NE/alpha 1-PI complex levels decreased from 102.2 +/- 16.0 to 83.0 +/- 10.4 micrograms/L; (p = 0.02). Plasma retinol concentrations increased (1.05 +/- 0.06 to 1.23 +/- 0.07 mumol/L; p = 0.0001) due to conversion of beta-carotene to retinol, which could have contributed to the decrease in NE/alpha 1-PI complex levels. Based on these results, we speculate that efficient antioxidant supplementation could attenuate lung inflammation in CF.
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PMID:Neutrophil elastase/alpha 1-proteinase inhibitor complex levels decrease in plasma of cystic fibrosis patients during long-term oral beta-carotene supplementation. 879 58


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