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Biomedical subjects

R M Price

Publications and source records attributed to R M Price.

12 recordsLinked to original sources
PubMed1997

Skin perfusion pressure measurement is valuable in the diagnosis of critical limb ischemia.

PURPOSE: Critical limb ischemia (CLI) is equated with a need for limb salvage. Arterial reconstruction and major amputation are the therapies ultimately available to such patients. We studied whether measurements of skin perfusion pressure (SPP) can be used to accurately identify those patients with CLI who require vascular reconstruction or major amputation and distinguish them from patients whose foot ulcer would heal with local wound care or minor amputation. METHODS: Fifty-three patients with a total of 61 limbs with a nonhealing foot ulcer (age range, 47 to 88 years; mean, 70.8 +/- 9.8 years; 33 men, 20 women) who were referred to the Vascular Laboratory at Morristown Memorial Hospital for evaluation of arterial insufficiency were studied in a prospective, double-blinded fashion. Patients were included in the study if informed consent was obtained, and patients were excluded if there was uncontrolled sepsis or if they required guillotine amputation. The size and site of the foot ulcer was recorded. If gangrene was present, the location and extent was also noted. The pulses were examined and recorded, and the ankle-brachial index was determined for each limb. Measurements of SPP were made at the proximal margin of the ulcer in viable tissue (not in the bed of the ulcer). SPP measurements were made independent of the vascular surgeon's evaluation of the limb and were not part of his clinical decision regarding management of the foot ulcer. The SPP measurements were compared (Fischer's exact test) with the clinical decision for therapy (group I, arterial reconstruction or major amputation; or group II, wound debridement, minor amputation, or both). SPP was also compared with the outcome (ulcer healed or failed to heal) of therapy in group II. From contingency tables we calculated the sensitivity, specificity, positive and negative predictive values (PPV, NPV), and the overall accuracy of SPP measurement as a diagnostic test for critical limb ischemia. RESULTS: There was no difference in the size or location of foot ulcers between groups I and II, nor was there a difference in ulcer size or location between limbs that healed and did not heal in group II. The prevalence of diabetes was similar in all groups and subgroups. The ABI was not predictive of the need for reconstruction or major amputation nor the outcome of local therapy. SPP measurements identified 31 of 32 limbs diagnosed as having CLI by clinical evaluation (i.e., group I, those limbs that required vascular reconstruction or major amputation). Of those patients who were clinically assessed as not having CLI (group II), SPP measurements diagnosed 12 of the 14 limbs that did not heal as having CLI (PPV, 75%) and 11 of 15 limbs that did heal as not having CLI (NPV, 85%). The sensitivity of SPP less than 30 mm Hg as a diagnostic test of CLI was 85%, and the specificity was 73%. The overall diagnostic accuracy of SPP less than 30 mm Hg as a diagnostic test of critical limb ischemia was 79.3% (p < 0.002, Fischer's exact test). CONCLUSIONS: We conclude that SPP measurement is an objective, noninvasive method that can be used to diagnose critical limb ischemia with approximately 80% accuracy.

Aged↗
PubMed1992

Use of o-phthalaldehyde to detect O-phosphorylethanolamine in bacterial lipopolysaccharide.

We have developed a method to measure O-phosphorylethanolamine groups in bacterial lipopolysaccharide using a fluorescent reagent, o-phthalaldehyde. The optimal excitation and emission wavelengths were 335 nm and 450 nm, respectively. The reaction was pH-dependent with an optimum at pH 10.5. The maximum fluorescence intensity occurred two min after mixing lipopolysaccharide with the reagent at pH 10.5. The assay was linear over a range of 1 microgram to 100 micrograms of lipopolysaccharide. When we compared the amount of primary amine (as O-phosphorylethanolamine) in native and p-hydroxyphenylacetic acid-derivatized lipopolysaccharide, we found that 97% of amine groups in native lipopolysaccharide were derivatized by p-hydroxyphenylacetic acid in the presence of 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide.

Ethanolamines↗
PubMed1991

Periodontal regeneration: myth or reality?

Recent scientific advances have enabled scientists to understand some of the basic biological events leading both to an accelerated and improved healing of many tissues. These advances are now being applied to periodontal wound healing. Previous studies have indicated that various oncogenes are sequences related to growth factors and, that when these sequences are altered, cellular phenotype and especially cellular proliferation is altered. Data are presented using various human cell lines, including a c-myc-transfected periodontal ligament (PDL) cell line, which delineate the relationship between oncogenes, mRNA oncogene transcripts and polypeptide growth factors as inducers of cell phenotypic alterations, including adhesion, migration and proliferation. The polypeptide growth factors are a unique class of molecules that regulate cell phenotype both in vitro and in vivo. These demonstrable phenotypic conversions have indicated that such factors will play an important role in hard-soft tissue repair. Additionally, new data suggest that older PDL cells are not responsive to polypeptide stimulation; both the migratory and proliferative responses are diminished. A unique growth factor has been isolated and sequenced, which when applied to older PDL cells will reverse this refractory phenotype. These recent studies are extensively reviewed with emphasis and conclusions based on growth factor-induced periodontal regeneration. These studies stress the undeniable role that these novel approaches will have in future chairside periodontal practice.

Biological Factors↗
PubMed1990

Fluorescent detection of lipopolysaccharide interactions with model membranes.

The critical importance of the lipid A moiety of LPS in resistance and pathogenesis in gram negative infections has led to the assumption that LPS interaction with target cells is due to hydrophobic interaction with plasma membranes. However, work from several laboratories, including our own, is consistent with the presence of a cell membrane structure with characteristics of a "receptor". We have proposed a two-step model for LPS-membrane interaction which resolves the two views, and have developed a model system to control the first step (binding to membrane protein) and study the second step (intercalation into lipid bilayer). We examined the interaction of LPS with small unilamellar phosphatidylcholine vesicles labeled in the hydrophobic portion of the bilayer with the fluorescent probe diphenylhexatrine (DPH) and detected changes in the physical properties of the bilayer by measuring DPH fluorescence anisotropy (delta r). We have found that purified, phenol-extracted S. typhimurium LPS interacts with the bilayer as measured by an increase in delta r and conclude that the LPS aggregate coalesced with the lipid bilayer. The greatest change in delta r was achieved with lipid A, Ra-Re glycolipids and diphosphoryl lipid A. Monophosphoryl lipid A and lipid X were less effective. Preparations of wild-type LPS fractionated according to the length of the O-antigen side chain and unfractionated LPS had least effect on delta r. Thus other factors such as serum components or membrane proteins may be necessary to enhance the interaction of LPS with target cells.

Carbohydrates↗
PubMed1990

Relationships between tumour necrosis factor, eicosanoids and platelet-activating factor as mediators of endotoxin-induced shock in mice.

1. The toxicity of intravenous recombinant human tumour necrosis factor (rhTNF), a TNF fragment (TNF114-130), endotoxin and combinations of rhTNF or TNF114-130 were tested in mice. Neither rhTNF nor TNF114-130 was lethal alone, but when combined with a non-lethal dose of endotoxin, rhTNF provoked dose-dependent mortality, as did higher doses of endotoxin alone. 2. Both the toxicity and the vasopermeability changes induced by endotoxin alone were blocked by the platelet-activating factor (PAF) antagonist BN52021, indomethacin or the dual cyclo-oxygenase/lipoxygenase inhibitor BW755C. 3. The lethality of the combined low dose endotoxin/rhTNF challenge was unaffected by pretreatment with BN52021, indomethacin or BW755C, or by treatment at 6 h intervals with BN52021 or BW755C. 4. The results of these studies suggest that TNF, a putative, early mediator of septic or endotoxin shock, cannot by itself mimic all of the effects of bacterial endotoxin in the model used in this study. Apparently, TNF works synergistically with other mediators whose release is stimulated by endotoxin. 5. The results also suggest that the mechanism of shock production by the rhTNF/endotoxin combination in mice is not dependent on the early stimulation of eicosanoid or PAF synthesis by rhTNF.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1986

Fluorescent detection of lipopolysaccharide interactions with model membranes.

We have modeled the initial interaction of bacterial lipopolysaccharide (endotoxin) with mammalian cells as consisting of two steps. The first step, adherence, we have previously shown to be ionic in nature and contains the necessary elements to determine the observed cell specificity of lipopolysaccharide interactions. The second step, coalescence, is the hypothetical insertion of the Lipid A component of lipopolysaccharide into the cell membrane lipid bilayer. Using small, unilamellar vesicles composed of phosphatidylcholine to model the cell membrane lipid bilayer, we found that lipopolysaccharide interacted with these vesicles to change the fluidity of the lipid bilayer, as measured by an increase in the fluorescence anisotropy of diphenylhexatriene in the vesicles. Since this increase in diphenylhexatriene anisotropy could not be attributed to a transfer of diphenylhexatriene between non-interacting lipopolysaccharide aggregates and vesicles, we concluded that the lipopolysaccharide aggregate coalesced with the lipid bilayer.

Cell Membrane↗
PubMed1985

Macromolecules mediate prostacyclin release from human umbilical artery.

Previous reports regarding the modulation of prostaglandin release from tissues by serum components did not identify these components. We have found that inhibition of prostacyclin release from human umbilical artery by human serum is attributable to serum macromolecules. We demonstrate that such inhibitory activity depends on macromolecular size and may result from macromolecule/cell surface interactions.

Arteries↗
PubMed1984

Methods for extracting phospholipids from human amniotic fluid compared.

Phospholipids were extracted from human amniotic fluid by various procedures, including the two most commonly applied to amniotic fluid for evaluation of fetal lung maturity. We find that the yield of phospholipid is greatly procedure dependent. This should be taken into account when one is considering the various reported methods of evaluating fetal lung maturity, because in some of them phospholipid data are expressed in terms of absolute concentration in the amniotic fluid. There were also significant differences in phospholipid composition in extracts prepared by the various procedures, but in general these were not large enough to influence evaluation of fetal lung maturity by methods in which phospholipid data are expressed in relative terms, as ratios or percentages--e.g., in the lecithin/sphingomyelin ratio and "lung profile" procedures. In the extraction method originally recommended for determination of the lecithin/sphingomyelin ratio, both the yield and composition of phospholipid depend on the extent of mixing.

Amniotic Fluid↗