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Biomedical subjects

S McCormick

Publications and source records attributed to S McCormick.

99 records · Page 6Linked to original sources

Pigment synthesis in maize aleurone from precursors fed to anthocyanin mutants.

Aleurone tissue of c2 Pr, C2 pr, or c2 pr genotypes can utilize either of two flavanones (naringenin, homoeriodictyol) or a flavanonol (dihydroquercetin) to synthesize anthocyanin. The anthocyanins formed have substitution patterns corresponding to those of the precursors, but c2 Pr tissue can hydroxylate the 4'-OH precursor at the 3' position. The results presented suggest that C2 acts before the flavanone step and that the hydroxylation gene (Pr) can act after C2.

Anthocyanins↗

Evaluation of acellular dermal graft in sheet (AlloDerm) and injectable (micronized AlloDerm) forms for soft tissue augmentation. Clinical observations and histological analysis.

OBJECTIVES: To evaluate the histological and clinical properties of (1) subdermally implanted acellular dermal graft (AlloDerm) sheets vs intradermal bovine collagen and (2) subdermally or intradermally injected micronized AlloDerm vs type I bovine collagen cross-linked with glutaraldehyde (Zyplast). PATIENTS: Twenty-five adult patients testing nonallergic to bovine collagen. METHODS: (1) Stacked disks of AlloDerm were implanted subdermally behind one ear, and bovine collagen was injected intradermally behind the other. The soft tissue augmentation caused by the implants was measured by digital photography at 1, 4, and 12 weeks, and biopsy specimens of each implant type were examined at 3 months after implantation. (2) Micronized AlloDerm was injected intradermally and subdermally in 2 different locations behind one ear, and bovine collagen was injected in the same manner behind the other. The soft tissue augmentation caused by the implants was measured by digital photography at the time of implantation and at 1 and 4 weeks after implantation. All implants were examined 1 month after implantation. RESULTS: All patients tolerated both implants well. (1) AlloDerm implants retained a higher percentage of the original implant volume than Zyplast at 1 and 3 months after implantation. Histologically, AlloDerm implants were extensively invaded by host fibroblasts without any foreign body reaction. (2) Intradermally injected micronized AlloDerm implants retained a higher percentage of the original implant volume at 1 month after implantation than intradermal Zyplast. Histologically, micronized AlloDerm implants were extensively invaded by host fibroblasts without any foreign body reaction. No significant differences were noted between subdermally injected micronized AlloDerm and Zyplast. CONCLUSIONS: The macroscopic and microscopic behavior of subdermally implanted AlloDerm sheets and subdermally and intradermally injected micronized AlloDerm was compared with intradermally injected Zyplast. AlloDerm sheet volume persisted to a significantly (P < .001) greater degree than bovine collagen during the first 3 months after placement. Clinically, intradermally injected micronized AlloDerm volume persisted to a significantly (P = .01, .04, and .01, respectively) greater degree than intradermal Zyplast or subdermal micronized AlloDerm or Zyplast. Histologically, micronized AlloDerm and AlloDerm are well tolerated at 1 and 3 months, respectively. Host tissue incorporation with fibroblast in-growth and collagen deposition is seen in both materials. AlloDerm and micronized AlloDerm hold promise for use in facial soft tissue augmentation.

Adult↗

Serratia marcescens-a marker for an infection control program.

An infection control program was instituted at The Victoria General Hospital, an 800-bed acute care hospital, in July 1977. Serratia marcescens had infected or colonized (I/c) 225 to 232 patients yearly for each of the three previous years. Since this organism is usually acquired nosocomially, we decided to use Serratia I/C as a marker for our infection control program. During the years 1977 to 1980, we identified and eliminated several reservoirs of Serratia (contaminated urine measuring containers, urometers, diabetic urine testing equipment and in-use contamination of 2% Hibitane). Readmission of previously I/C patients proved to be an increasingly important reservoir. During 1980, only 120 patients were I/C, and gentamicin-resistant isolates of S.marcescens had dropped from 44% in 1977 to 4.4% in 1980. Use of Serratia as a marker enabled us to monitor the efficacy of our infection control program and allowed us to prove to our health care workers the usefulness of many of the measures we introduced.

Adolescent↗

Effects of copper and histidine on oxidative modification of low density lipoprotein and its subsequent binding to collagen.

It was previously shown that serum low density lipoprotein (LDL) binds to type I collagen gels and that the binding is increased after modification by cultured endothelial cells. It is now demonstrated that when LDL is incubated with cells cultured in Dulbecco's modified minimal essential medium (DMEM), the subsequent binding of LDL to collagen is considerably less than after incubation with endothelial cells cultured in Ham's F-12 medium (F12). To determine the reason for this difference, collagen gels were made with saline containing ingredients of DMEM individually or in groups, and binding of LDL to such gels was measured. Modification of LDL, manifested by a high level of binding to the collagen, by lipid peroxidation (production of thiobarbituric acid-reactive substances), and by increased electrophoretic mobility occurred on exposure to collagen gels made in saline; these changes were almost completely inhibited by the addition of histidine at a concentration equal to that in DMEM. They were also inhibited by butylated hydroxytoluene, desferrioxamine, and EDTA; penicillamine and hydroxyl-radical scavengers inhibited collagen binding but did not inhibit lipid peroxidation or the increase in electrophoretic mobility. Nominally, DMEM contains 270 microM histidine but no copper, whereas F12 contains 135 microM histidine and 10 nM copper; addition of copper (as much as 5 microM) to DMEM or of histidine (as much as 2.16 mM) to F12 did not overcome the differences between the media in supporting LDL oxidation by endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Interaction of native and cell-modified low density lipoprotein with collagen gel.

We have examined the binding of native and cell-modified low density lipoprotein (LDL) to gels of Type I collagen. Diffusion of native 125I-LDL into the collagen gel was slow, reaching equilibrium after 24 to 48 hours, while L-3H-glucose, a low molecular weight marker, equilibrated in 6 hours. Binding of 125I-LDL was measured at 48 hours as the amount associated with the collagen after extensive washing. Binding was saturable with an increasing concentration of LDL. Prior incubation with cell-free culture medium resulted in modest, but progressive, increases in electrophoretic mobility and binding to collagen. Incubation with cells produced a marked increase in electrophoretic mobility and a 5- to 10-fold increase in collagen binding; the presence of butylated hydroxytoluene during incubation prevented both effects. These changes in LDL were induced by porcine aortic endothelial cells, smooth muscle cells, human skin fibroblasts, and a variety of cell lines, as well as by acetylation. There was a curvilinear relationship between the amount of LDL protein bound and the net negative charge of the LDL; increasing net charge was associated with progressively greater increases in binding. These results suggest a potential role for collagen in trapping lipid in the extracellular matrix of arterial intima by slowing the diffusion of and by binding LDL. The data also demonstrate that binding of LDL to collagen is enhanced by modifications that increase its net negative charge.

Animals↗

Effects of porcine aortic smooth muscle cell conditioned medium on endothelial cell replication.

Previous studies suggested that arterial smooth muscle cells (SMC) may be involved in regulating the growth of capillaries into atherosclerotic plaques. In the present study, we determined the effect of SMC products on porcine aortic endothelial cell (EC) replication in vitro. Quiescent or slowly growing EC in medium without endothelial cell growth factor (ECGF) were stimulated to proliferate in the presence of porcine aortic SMC conditioned medium, while the same conditioned medium inhibited the growth of rapidly dividing EC in high serum concentrations or with ECGF. The magnitude of both activities depended on SMC conditioned medium concentration. The dose-dependent increase in EC number stimulated by ECGF was completely inhibited by SMC conditioned medium. This effect was not due to a direct interaction of conditioned medium with ECGF because SMC conditioned medium inhibited the growth of EC that were rapidly proliferating in 10% serum without ECGF. The inhibitory activity was retained by an ultrafiltration membrane with an exclusion limit of 1000 daltons; the stimulatory activity was recovered in the ultrafiltrate and remained stable after boiling, treatment with acid or base and trypsin, and repeated freezing and thawing, but was removed by activated charcoal. The growth-promoting activity could not be accounted for by release of cell contents from lysed cells or of thymidine into the medium. Conditioned medium from SMC incubated in the presence of serum contained less EC growth-stimulatory activity but more growth-inhibitory activity than that from SMC in serum-free medium.

Animals↗