Search PubMed⌕ Search

Biomedical subjects

E Seifter

Publications and source records attributed to E Seifter.

At least 19 recordsLinked to original sources
PubMed1995

Time-dependent effect of glutaraldehyde on the tendency to calcify of both autografts and xenografts.

To determine mechanisms responsible for the reduced calcification in short-term glutaraldehyde (Glu)-treated autologous pericardial bioprostheses, we studied the time effect of Glu on subsequent calcification and differences in calcification of autograft and xenograft implants in a rat subcutaneous implantation model. In experiment 1, four groups of bovine pericardial pieces (1 cm2) were prepared: (A) fresh bovine pericardium without Glu, (B) with 15-minute Glu, (C) with 60-minute Glu, and (D) with 120-minute Glu. Seven young male Sprague-Dawley rats were used; each received four bovine pericardial pieces from group A, B, C, or D for subcutaneous implantation. Calcium content of the implants (microgram/mg dry weight) 45 days later was 4.8 +/- 2.9, 29.8 +/- 13.6, 106.3 +/- 13.7, and 176.3 +/- 85.5 in groups A, B, C, and D, respectively (p < 0.05 between any two groups). Experiment 2 used 8 young male Sprague-Dawley rats from different mothers. Each received five subcutaneous skin implants. The five skin implants were prepared as follows: (1) fresh self skin, (2) self skin with 30-minute Glu, (3) self skin with 48-hour Glu, (4) fresh skin of others, and (5) skin of others with 48-hour Glu. After 45 days of implantation, the calcium content of the implants was 1.4 +/- 1.1, 57.9 +/- 35.4, 142.7 +/- 61.4, 1.5 +/- 1.1, and 94.9 +/- 24.1 micrograms/mg dry weight in groups 1, 2, 3, 4, and 5, respectively (p < 0.05 for 1 versus 2, 3, or 5; 2 versus 3, 4, or 5; 3 versus 4; and 4 versus 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Bioprosthetic cardiac valve degeneration: role of inflammatory and immune reactions.

Inflammatory and immune reactions are thought to mediate both calcification and biodegradation of bioprosthetic cardiac valve implants. To investigate the mechanisms of implant degeneration, we evaluated the role of inflammatory and immune reactions and the effects of tissue preservative treatment in three series of experiments. In the first experiment, three kinds of implants, i.e. glutaraldehyde-treated autograft Sprague-Dawley (SD) rat skin, xenograft Swiss-Webster (SW) mouse skin, and saline-treated autograft (control) were subcutaneously implanted in ten weanling SD rats, and retrieved after 70 days. There was no significant difference in the level of calcification in the autograft (113.13 +/- 27.09 micrograms/mg dry weight) and xenograft (78.27 +/- 31.53 micrograms/mg dry weight) (p > 0.05), but both differed significantly from the control specimens (1.55 +/- 0.87 micrograms/mg dry weight). In the second experiment, the immunological response to glutaraldehyde-treated bovine pericardium (glut tBP) and glycerol treated bovine pericardium (glyc tBP) implants were tested in vivo and in vitro. A Gore-Tex implant was used as a control. Sections of these materials were implanted to the abdominal muscle wall of Lewis rats, with each group composed of twelve animals. Lymphocytes and sera from the animals were isolated, and histological examination was performed at two or four weeks post-implantation. Collagen type 1 (calf skin) was used as antigen. Tritiated thymidine incorporation was used to measure lymphocyte response to antigen collagen type 1 (calf skin), and an Enzyme Linked Immunosorbent Assay (ELISA) was used to test antibodies. The results showed that lymphocytes from both the glut tBP and the glyc tBP groups responded to collagen type 1. The ELISA results showed that the glyc tBP group produced more antibodies than did the glut tBP group, with the difference being significant at a level of p < 0.02. Histology revealed that the glyc tBP had greater inflammatory changes and collagen degeneration than did the glut tBP. In the third experiment, sections of glut tBP and glyc tBP were implanted subcutaneously in two groups of ten weanling SD rats, and retrieved after 70 days. The results showed that glut tBP caused more calcification (197.04 +/- 83.56 micrograms/mg dry weight) than did the glyc tBP (6.74 +/- 0.55 microgram/mg dry weight), with the difference being significant at a level of p < 0.05. From these investigations it is concluded that tissue treatment prior to implantation was very important in determining the tendency of tissue to calcify, and that there was no obvious relationship between bioprosthetic calcification and immunogenicity.

Animals↗
PubMed1992

Diphenylhydantoin inhibits calcification of bovine pericardial implants and myocardium: a preliminary study.

Calcification is a major cause of glutaraldehyde-fixed bioprosthetic valve failure. Recent studies have shown that dystrophic calcification shares basic features with normal bone mineralization, including crystal initiation through the mediation of cell membranes, usually in the form of extracellular vesicles. In this study, we observed that calcification of the myocardium of DBA/2J mice was inhibited or reversed by diets supplemented with 100 mg/kg diet diphenylhydantoin (dilantin) for 70 days, with a calcification incidence of 25% in the dilantin group versus 58% in control. We further studied the effects of dilantin on bioprosthetic valve calcification. Three groups of young male Sprague-Dawley rats (100 g, 9/group) were implanted subcutaneously with 1-cm2 pieces of glutaraldehyde-fixed bovine pericardium. Controls were fed a ground chow for 45 or 90 days postimplantation; experimentals received the same chow for the first 45 days postimplantation and then were fed the same diet supplemented with 1000 mg dilantin/kg for the succeeding 45 days. Calcium content (microgram/mg dry weight) of the implants in the dilantin group was 137 +/- 18.6 versus 214 +/- 34.3 in 90 days control and 79.9 +/- 41.5 in 45 days control (mean +/- SD, P < 0.01 and P < 0.05 respectively, t test). The tibia calcium content of the dilantin group was not significantly different from 90 days control. We conclude that orally administered dilantin inhibits calcification of glutaraldehyde-fixed bovine pericardial implants preferentially. It does not cause decalcification either of implants that have already calcified or of the bones. The anti-calcification effect of dilantin may be associated with its anti-vitamin D effect.

Animals↗
PubMed1992

The role of aromatic hydrocarbons in the genesis of breast cancer.

The incidence of breast cancer in women has increased dramatically over the last decade. Epidemiological markers of this increased incidence include: endocrine related phenomena (early menarche, age of first parity and age of menopause); exposure of the breast to X-radiation; and a group of seemingly disparate factors--urban residence, dietary selection and alcohol consumption. Although experimental breast cancer may be induced by estrogenic hormones, X-radiation and aromatic hydrocarbons, only aromatic hydrocarbons have not been previously implicated in human mammary carcinogenesis. The seemingly unrelated human factors can best be understood by examining the role of breast tissue in aromatic hydrocarbon metabolism. Aromatic hydrocarbons are important environmental chemicals produced by the incomplete combustion of hydrocarbons for use in energy production. Benzene, benz(a)pyrene, dibenz(ah)anthracene and 1-nitropyrene, known experimental breast carcinogens, are produced in this way. Human exposure to aromatic hydrocarbon metabolites induces and promotes altered DNA by mechanisms described as increased intracellular pro-oxidant production as well as direct adduction to DNA. The breast is anatomically embedded in a major fat depot which stores and concentrates aromatic hydrocarbons and can metabolize these hydrocarbons to carcinogenic metabolites. Ductal cells concentrate these metabolites and themselves become target cells for carcinogenesis. Some lifestyle factors increase the amount of carcinogens produced or enhance their activity. A unitary model for mammary carcinogenesis in humans as well as in experimental carcinogenesis is hypothesized. If correct, the hypothesis would account for some of the increase in breast cancer incidence in industrial countries--and would suggest environmental and dietary modifications that would inhibit hydrocarbon induced mammary carcinogenesis.

Animals↗
PubMed1991

Aldehyde tanning: the villain in bioprosthetic calcification.

Preservation of bioprosthetic valves may play a role in valvular calcification. Subcutaneous implants in rats were used to test the effect of different preservation solutions. Fifty male Sprague-Dawley rats were divided into five groups. Fresh bovine pericardium was treated in one of five ways: group A: 99.5% glycerol for 1 week; group B: as group A, then normal saline wash and 0.25% formaldehyde storage for 24 h; group C: as group A, then normal saline wash and 4% formaldehyde storage for 24 h; group D: as group A, then normal saline wash and 0.625% glutaraldehyde storage for 24 h; group E: 0.625% glutaraldehyde and 4% buffered formaldehyde storage. Treated bovine pericardium was cut into 1-cm2 pieces and washed for 30 min with normal saline before implantation. In each animal, three pieces were implanted in the subcutaneous tissue of the back. After 70 days, retrieved specimens were examined grossly, and X-ray densitometry, calcium analysis, and histological examinations were carried out. The results showed that glycerol-treated tissue (group A) had less calcification (calcium 6.92 +/- 4.46 micrograms/mg dry weight) than other groups: group B (calcium 323.12 + 63.56 micrograms/mg dry weight); group C (calcium 240.65 + 13.47 micrograms/mg dry weight); group D (calcium 232.29 + 13.01 micrograms/mg dry weight). These differences were markedly significant (p less than 0.0001). It appears that aldehydes play an important role in the calcification of bioprosthetic valves. Experience with glutaraldehyde- and glycerol-treated pericardium in valvular applications in sheep support these observations.

Animals↗
PubMed1990

Zone II flexor tendon repair: effects of vitamins A, E, beta-carotene.

Ninety-six adult Leghorn chickens each had the flexor profundus tendon in each middle toe sharply divided in Zone II with immediate repair (pentobarbital, ketamine anesthesia). Animals were then randomly assigned to receive unsupplemented standard chick chow or the chow supplemented with vitamin A (150,000 IU/kg chow), Vitamin E (1000 IU/kg chow), or beta-carotene (90 mg/kg chow). Eight animals from each of the four groups were examined at 7, 30, or 45 days post repair. After sacrifice, in situ composite wound breaking strength was measured in the amputated toe by constant speed tensiometry. Vitamin A-supplemented animals demonstrated breaking strength more than double that of control at each postoperative test day, while those animals receiving supplemental Vitamin E had breaking strength less than half that of control at Day 7 and Day 45. These results are statistically significant. Tensiometry curves differed markedly at all time points among the groups: Vitamin A curves being broader, higher, and having more spikes. These differences in the tensiometry curves, both qualitative and quantitative, may be due to differences in intrinsic tendon healing or to differences in adhesion formation or a combination of both. beta-Carotene supplementation had modest effect. We conclude that supplemental dietary vitamin A increases the breaking strength of composite tendon wounds and that supplemental dietary vitamin E decreases it.

Animals↗
PubMed1990

Supplemental vitamin A prevents the tumor-induced defect in wound healing.

To test our hypothesis that supplemental vitamin A would mitigate the impaired healing that occurs in tumor-bearing animals, six groups of C3H mice, eight per group, eating a standard commercial mouse chow ad libitum that supports normal growth, reproduction, and longevity were innoculated with 200,000 C3HBA cells. When tumors measured approximately 6 mm in diameter, the mice were anesthesized and wounded (dorsal skin incisions and subcutaneous polyvinyl alcohol sponges). Twenty-four hours later, two groups (one continued on the chow and the other started on the chow supplemented with 150,000 IU vitamin A/kg chow) underwent local tumor irradiation; two groups, one ingesting the chow, the other the vitamin A supplemented chow, were started on cyclophosphamide therapy; two groups, one ingesting the chow, the other the vitamin A supplemented chow, received neither local tumor irradiation nor cyclophosphamide therapy. An additional two groups ingesting the chow, one group neither innoculated with tumor nor wounded, the other wounded by not innoculated, served as controls. Wound breaking strength and sponge reparative collagen accumulation (assessed by hydroxyproline proline measurement) were used as indicators of wound healing. The mice were killed 12 days after wounding. Tumor presence decreased wound breaking strength and sponge hydroxyproline content; these effects were largely negated by supplemental vitamin A. Local tumor irradiation diminished the adverse effect of tumor on sponge reparative collagen content but to a lesser extent than the supplemental vitamin A. Supplemental vitamin A added to the irradiation effect on healing but irradiation did not add to the vitamin A effect. Cyclophosphamide, a systemic radiomimetic anti-tumor agent, did not alter the impaired wound healing of the tumor-bearing mice. Supplemental vitamin A mitigated the impaired wound healing in the cyclophosphamide-treated tumor-bearing mice. Supplemental vitamin A also moderated the effects of wounding, tumor, and tumor therapies (local irradiation and cyclophosphamide) on the increase in adrenal size, leukopenia, thrombocytopenia, and thymic involution (except the last was not moderated in the cyclophosphamide-treated tumor-bearing rats). The splenic enlargement in the untreated tumor-bearing wounded rats and in those treated with cyclophosphamide was lessened by supplemental vitamin A. We hypothesize that these anti-stress effects of vitamin A underlie, in part, its action in mitigating the impaired wound healing of tumor-bearing mice, including those treated by local irradiation or cyclophosphamide. These findings have implications for the care of patients with malignant tumors.

Animals↗
PubMed1988

Structure and expression of the human L-myc gene reveal a complex pattern of alternative mRNA processing.

We analyzed in detail the structure of the L-myc gene isolated from human placental DNA and characterized its expression in several small-cell lung cancer cell lines. The gene is composed of three exons and two introns spanning 6.6 kilobases in human DNA. Several distinct mRNA species are produced in all small-cell lung cancer cell lines that express L-myc. These transcripts are generated from a single gene by alternative splicing of introns 1 and 2 and by use of alternative polyadenylation signals. In some mRNAs there is a long open reading frame with a predicted translated protein of 364 residues. Amino acid sequence comparison with c-myc and N-myc demonstrated multiple discrete regions with extensive homology. In contrast, other mRNA transcripts, generated by alternative processing, could encode a truncated protein with a novel carboxy-terminal end.

Amino Acid Sequence↗
PubMed1987

Effect of supplemental vitamin A on colon anastomotic healing in rats given preoperative irradiation.

We studied the effect of dietary supplementation with vitamin A on the healing of colon anastomoses in irradiated bowel. Rats were divided into two groups. Those in the first group were fed a standard chow diet and those in the second group were fed the same diet supplemented with 150 IU vitamin A/g of chow. The rats were maintained on their respective diets throughout the experiment. After 7 days, half the rats in each group underwent abdominal irradiation (200 rads). Seven days later, all of the rats underwent distal colon division and anastomosis under pentobarbital anesthesia. All rats were killed 7 days postoperatively, the colons excised, and bursting strength and hydroxyproline determinations performed on both the anastomotic segment and a normal proximal segment of adjacent colon. There was a significant decrease in the bursting strength at the colon anastomosis (p less than 0.02) and in the collagen content (p less than 0.02) after preoperative irradiation. This effect was mitigated by dietary vitamin A supplementation.

Animals↗
PubMed1985

The effect of vitamin E on experimentally induced peritoneal adhesions in mice.

Previous studies in our laboratory demonstrated that dietary supplementation with vitamin A enhances peritoneal adhesion formation in mice. Other researchers have shown that vitamin E antagonizes some effects of vitamin A in various systems, eg, wound healing. We investigated our hypothesis that dietary supplementation with vitamin E would decrease peritoneal adhesion formation. Adult mice were divided into the following groups: group 1, which ate a standard chow containing 65 IU of vitamin E per kilogram diet (twice the National Research Council's recommended daily allowance for normal mice); and group 2, which ate the same chow supplemented with vitamin E at 300 IU/kg diet (a nontoxic level). Following peritoneal ligation, all mice were killed on the tenth postoperative day and their peritoneal cavities examined for the presence and extent of adhesions. There was a statistically significant decrease in the incidence and degree of adhesions in the vitamin E-supplemented animals; these data supported our hypothesis.

Animals↗
PubMed1985

Effect of dimethyl sulfoxide and glycerol on acute bowel ischemia in the rat.

After a 30 minute period of superior mesenteric artery occlusion in adult rats, there was a significant decrease in peritoneal inflammatory reaction, ileus, peritoneal adhesion formation, and histologically proved bowel wall necrosis in animals given intravenous dimethyl sulfoxide at the end of the ischemic period. In contrast, control rats given normal saline solution intravenously demonstrated severe inflammatory reaction, ileus, hemorrhagic peritoneal fluid, extensive adhesion formation, and areas of bowel wall necrosis. Intravenous glycerol did not have the beneficial effect seen with dimethyl sulfoxide. Neither compound was effective when given intraperitoneally. We conclude that intravenous dimethyl sulfoxide has a significant protective effect in rats with acute intestinal ischemia due to the superior mesenteric artery occlusion in the rat.

Animals↗
PubMed1985

Vitamin A and retinoic acid: induced fibroblast differentiation in vitro.

The role of vitamin A in wound healing and fibroplasia has been studied extensively in vivo but the mechanism(s) of its action has not been established. In this study the effect of vitamin A and retinoic acid on fibroblast growth and collagen accumulation in vitro was examined. Vitamin A and retinoic acid added to Balb 3T3 mouse fibroblasts in tissue culture resulted in induction of cell differentiation as manifested by a decrease in cell growth rate, enhanced collagen accumulation, and morphologic differentiation. The results of this in vitro study suggest that the stimulatory in vivo effect of vitamin A and retinoic acid on collagen accumulation and fibroplasia in healing wounds is due in a major way to fibroblast differentiation and enhanced collagen synthesis.

Animals↗
PubMed1984

Carnitine biosynthesis from gamma-butyrobetaine and from exogenous protein-bound 6-N-trimethyl-L-lysine by the perfused guinea pig liver. Effect of ascorbate deficiency on the in situ activity of gamma-butyrobetaine hydroxylase.

The production of carnitine from peptide-bound 6-N-trimethyl-L-lysine (Lys(Me3)) or 4-N-trimethyl-aminobutyrate(gamma-butyrobetaine) perfused through isolated guinea pig livers was investigated. [Methyl-3H] Lys(Me3)-labeled agalacto-orosomucoid (AGOR) and asialofetuin were rapidly taken up and degraded by the perfused liver. Most of the free Lys(Me3) derived from Lys(Me3)-AGOR was released unmodified into the perfusion medium. However, Lys(Me3), arising from Lys(Me3)-asialofetuin was converted mostly to gamma-butyrobetaine and carnitine. gamma-Butyrobetaine added to the perfusion medium was hydroxylated to carnitine by the liver at a rate of 2.3 mumol/h. Guinea pigs maintained on an ascorbate-free diet for 17-60 days showed lowered ascorbate contents in all tissues measured and, coincidentally, a sharp reduction in carnitine levels in kidney, liver, and cardiac, and skeletal muscle. Carnitine production from [1,2,3,4-14C]gamma-butyrobetaine and [methyl-3H]Lys(Me3)-asialofetuin was reduced in perfused livers obtained from ascorbate-deficient guinea pigs. Although hydroxylation of gamma-butyrobetaine to carnitine was effectively depressed in the perfused isolated livers from ascorbate-deficient animals, hydroxylation of [methyl-3H]Lys(Me3) (derived from asialofetuin) to [methyl-3H]3-hydroxy-6-N-trimethyl-L-lysine was unaffected. Prior administration of ascorbate to the medium perfusing the isolated livers caused carnitine biosynthesis from all precursors examined to return to control values.

Animals↗
PubMed1984

Effects of vitamin A and beta carotene on intra-abdominal sepsis.

Vitamin A may play a role systemically and locally in controlling intra-abdominal sepsis. Adult male rats were divided into three groups. Group 1 ate a standard rat laboratory chow (not vitamin A deficient), group 2 ate the same chow supplemented with vitamin A, and group 3 ate the chow supplemented with beta carotene. All animals underwent cecal ligation, and the cecum was perforated either with a 27-gauge or an 18-gauge needle. Vitamin A dietary supplementation had a significant protective effect, which was manifested by improved survival in the animals whose cecum was perforated with an 18-gauge needle, prevention of postoperative hypothermia, maintenance of peripheral WBC counts at normal or above-normal values, and better localization of the intra-abdominal inflammatory process. Dietary supplementation with beta carotene had a lesser protective effect.

Abdomen↗
PubMed1984

Compound 48/80 and the healing of wounds in rats. The effect of timing of drug injections.

Wound breaking strength was measured in Long-Evans rats in two settings: in one experiment animals received Compound 48/80 i.p. for 8 consecutive days, starting 1 day before infliction of wound and in the second experiment 48/80 was given for 6 days before wounding. Wound breaking strength was always measured on the seventh day after wounding. There was a significant increase in wound breaking strength in animals treated before incision was made, as compared to controls, saline-treated animals (p less than 0.01). When 48/80 was given one day before incision was made, the breaking strength was significantly decreased (p less than 0.0002). Possible explanation for these opposite results is discussed.

Animals↗