Biomedical subjects
C Rogers
Publications and source records attributed to C Rogers.
Physician profiling legislation.
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Regulating managed care and protecting patients' rights.
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Design-Dependent Variations in Coronary Stent Stenosis Measured as Precisely by Angiography as by Histology.
BACKGROUND: Coronary stent restenosis is a growing clinical concern which, because restenosis may vary with stent design, requires a validated, accurate, and sensitive method of evaluation as new stents are developed. Histologic analysis of arterial cross sections, a highly accurate tool in animal models, has limited applicability in humans. Quantitative coronary angiography, while commonly used in the clinical evaluation of coronary interventions, has a controversial role as an adequate measure of restenosis, and few studies have validated quantitative angiography in diseased arteries. We tested the hypothesis that in-stent stenosis could be assessed as accurately by pre-mortem angiography as by post-mortem histology, allowing angiographic discrimination of variable late luminal loss provoked by stents of different designs. METHODS AND RESULTS: Stent stenosis in porcine coronary arteries was assessed by quantitative coronary angiography and histology at 3, 28 and 56 days. Four stainless steel stent designs were studied: a slotted tube configuration with or without a polymer wrap and a corrugated ring configuration with or without a polymer coating. Although acute luminal gain (mean stent:artery ratio 1.07 +/- 0.01) and stent recoil (mean stent diameter at follow-up 2.65 +/- 0.02 mm) were similar for all designs and time points, significant differences in late luminal loss were observed and were detected as accurately by angiography as by histology. At 28 days, the polymer wrapped slotted tube design resulted in a nearly two-fold greater late loss than its bare metal counterpart (1.40 +/- 0.09 mm vs. 0.80 +/- 0.12 mm, p <.001 by angiography; 1.33 +/- 0.10 mm vs. 0.67 +/- 0.06 mm, p <.0001 by histology), while there was no significant difference in 28 day late loss between the polymer coated and bare metal corrugated ring designs (p = NS by angiography or histology). Time point differences were also observed both angiographically and histologically, with marked progression of lumen loss between 3 and 28 days and slower but persistent progression between 28 and 56 days. Overall comparison of individual lumen diameter measurements for all stented arteries independent of design or duration of follow-up demonstrated a precise correlation between angiography and histology (y = 0.96x +0.25, p <.0001, r2 = 0.82). CONCLUSIONS: Coronary stents of varied designs provoke markedly different degrees of late luminal loss, and these differences can be measured as accurately by quantitative angiography as by histologic analysis of arterial cross sections. This may be due to optimization of angiographic measurements by the concentric nature of intimal thickening in stented arteries, and to structural rigidity imparted by the stent, preserving arterial lumen size for histologic analysis. Quantitative angiography, therefore, may represent an adequate endpoint in clinical trials comparing stent designs.
Design-Dependent Variations in Coronary Stent Stenosis Measured as Precisely by Angiography as by Histology.
BACKGROUND: Coronary stent restenosis is a growing clinical concern which, because restenosis may vary with stent design, requires a validated, accurate and sensitive method of evaluation as new stents are developed. Histologic analysis of arterial cross sections, a highly accurate tool in animal models, has limited applicability in humans. Quantitative coronary angiography, while commonly used in the clinical evaluation of coronary interventions, has a controversial role as an adequate measure of restenosis, and few studies have validated quantitative angiography in diseased arteries. We tested the hypothesis that in-stent restenosis could be assessed as accurately by pre-mortem angiography as by post-mortem histology, allowing angiographic discrimination of variable late luminal loss provoked by stents of different designs. METHODS AND RESULTS: Stent stenosis in porcine coronary arteries was assessed by quantitative coronary angiography and histology at 3, 28 and 56 days. Four stainless steel stent designs were studied: a slotted tube configuration with or without a polymer wrap and a corrugated ring configuration with or without a polymer coating. Although acute luminal gain (mean stent:artery ratio of 1.07 +/- 0.01) and stent recoil (mean stent diameter at follow-up 2.65 +/- 0.02 mm) were similar for all designs and time points, significant differences in late luminal loss were observed and were detected as accurately by angiography as by histology. At 28 days, the polymer wrapped slotted tube design resulted in a nearly two-fold greater late loss than its bare metal counterpart (1.40 +/- 0.09 mm vs. 0.80 +/- 0.12 mm, p <.001 by angiography; 1.33 +/- 0.10 mm vs. 0.67 +/- 0.06 mm, p <.0001 by histology), while there was no significant difference in 28 day late loss between the polymer coated and bare metal corrugated ring designs (p = NS by angiography or histology). Time point differences were also observed both angiographically and histologically, with marked progression of lumen loss between 3 and 28 days and slower but persistent progression between 28 and 56 days. Overall comparison of individual lumen diameter measurements for all stented arteries independent of design or duration of follow-up demonstrated a precise correlation between angiography and histology (y = 0.96x +0.25, p <.0001, r2 = 0.82). CONCLUSIONS: Coronary stents of varied designs provoke markedly different degrees of late luminal loss, and these differences can be measured as accurately by quantitative angiography as by histologic analysis of arterial cross sections. This may be due to optimization of angiographic measurements by the concentric nature of intimal thickening in stented arteries, and to structural rigidity imparted by the stent, preserving arterial lumen size for histologic analysis. Quantitative angiography, therefore, may represent an adequate endpoint in clinical trials comparing stent designs.
Bath PUVA: an effective treatment for psoriasis.
At the Psoriasis Education and Research Centre, PUVA baths were introduced as an alternative therapy in 1990. Psoriatic patients soaked for 15 minutes in a solution of tap water and Ultra MOP. Forty-five patients were followed for 30 treatments. Skin types were recorded and progress was documented by PASI (Psoriasis Area and Severity Index) scores. Side effects and total amount of UVA received were documented. The purpose of this study was to record the efficacy of our protocol for PUVA baths on different skin types while evaluating all aspects of the treatment.
Structural protein 4.1 is located in mammalian centrosomes.
Structural protein 4.1 was first characterized as an important 80-kDa protein in the mature red cell membrane skeleton. It is now known to be a member of a family of protein isoforms detected at diverse intracellular sites in many nucleated mammalian cells. We recently reported that protein 4.1 isoforms are present at interphase in nuclear matrix and are rearranged during the cell cycle. Here we report that protein 4.1 epitopes are present in centrosomes of human and murine cells and are detected by using affinity-purified antibodies specific for 80-kDa red cell 4.1 and for 4.1 peptides. Immunofluorescence, by both conventional and confocal microscopy, showed that protein 4.1 epitopes localized in the pericentriolar region. Protein 4.1 epitopes remained in centrosomes after extraction of cells with detergent, salt, and DNase. Higher resolution electron microscopy of detergent-extracted cell whole mounts showed centrosomal protein 4.1 epitopes distributed along centriolar cylinders and on pericentriolar fibers, at least some of which constitute the filamentous network surrounding each centriole. Double-label electron microscopy showed that protein 4.1 epitopes were predominately localized in regions also occupied by epitopes for centrosome-specific autoimmune serum 5051 but were not found on microtubules. Our results suggest that protein 4.1 is an integral component of centrosome structure, in which it may play an important role in centrosome function during cell division and organization of cellular architecture.
Bacterial typing: storing and processing of stabilized reference bacteria for polymerase chain reaction without preparing DNA--an example of an automatable procedure.
This paper examines the use of bacteria killed on blood-storage paper as templates (ghosts) and takes, as an example, the PCR ribotyping (amplification of the intergenic spacer regions between the 16S and 23S ribosomal RNA genes) of bacteria as described by Kostman et al. (J. Infect. Dis. 171, 204-208, 1995). All procedures have been particularly designed to be compatible with automation. DNA preparation is inappropriate for routine, high-volume sequence amplification from a diversity of microorganism cultures. Blood-storage/processing media provide another way of processing samples for PCR with distinctive aspects of increased safety and ease of automatibility. Blood-storage paper can be used for killing and processing bacteria to DNA-containing ghosts for reliable PCR. From as little as a few microliters of an overnight culture or a reasonably sized, single colony, rapid processing of large sample numbers is possible. FTA blood-storage medium has additional utility in that long-term cataloguing, storage, and processing of paper, loaded with culture, for PCR, is possible via a variety of sample wash sequences. It can be performed at convenience, after collection, and can be delayed indefinitely. using this approach, the repeatability of some PCR-ribotyping methodology of the type used by Kostman et al. (J. Clin. Microbiol. 30, 2084-2087, 1992) was examined as an exercise to demonstrate the practicality of FTA blood-paper usage and to check some basic features of PCR ribotyping. Five strains of Staphylococcus and one strain Escherichia coli were stored and processed on FTA blood paper, the PCR-ribotype patterns were analyzed and found to be the equal of patterns previously seen via additional DNA preparations.
Treatment of myopic astigmatism with the Summit Apex Plus excimer laser.
PURPOSE: To assess the results of surface sequential toric photorefractive keratectomy (PRK) with the Summit Apex Plus excimer laser using an erodible mask. METHODS: A prospective study was performed on consecutive eyes having surface sequential toric PRK over a 4 month treatment period. Attempted astigmatism correction varied from 70 to 100%, depending on the power and axis of the cylinder. The myopic correction was adjusted so the combined treatment aim was emmetropia. Refraction, manual keratometry, corneal haze, and visual acuity data from preoperative and follow-up visits over 12 months were divided into various groups based on the preoperative refraction and analyzed. RESULTS: Fifty-nine eyes from 48 patients had sequential toric PRK. Preoperatively, the mean spherical equivalent at glasses plane (SEGP) was -4.88 diopters (D) +/- 3.20 (SD) and the mean refractive cylinder, 2.02 +/- 1.04 D. The mean attempted cylinder correction was 1.87 D. At 12 months the mean SEGP was -0.02 +/- 0.67 D, which was not statistically significant from plano. The mean refractive cylinder was 0.84 +/- 0.84 D, which was statistically significantly different from zero cylinder power. There was a statistically significant correlation between the preoperative and the 12 month postoperative refractive cylinder powers. At 12 months, 34 of 43 eyes (79.1%) had an uncorrected visual acuity of 6/12 or better. While 2 eyes in one patient (4.7%) lost two lines of best corrected visual acuity, with a final acuity of 6/12 in each, no patient lost more than two lines. CONCLUSION: The manifest refraction cylinder power is not fully corrected with the current treatment algorithms; however, surface sequential toric PRK using an erodible mask is capable of treating compound myopic astigmatism with moderate success.
Strategies to maintain the credibility of sham acupuncture used as a control treatment in clinical trials.
Many clinical trials concerning acupuncture are flawed by methodological problems. One of the major difficulties is the appropriate selection and use of a placebo control. This article evaluates the use of sham acupuncture as a placebo control and analyzes its credibility as a control treatment. Sixty-four subjects were assessed for their perception of whether they were receiving sham or real acupuncture while participating in a clinical trial of acupuncture. It was found that if used under specific experimental conditions, sham acupuncture can function as a credible control. Specific strategies are suggested to maintain the credibility of sham acupuncture as a placebo control.
Performance characteristics of the Gen-Probe Probe Competition Assay used as a supplementary test for the Gen-Probe PACE 2 and 2C assays for detection of Chlamydia trachomatis.
The performance characteristics of the Gen-Probe Probe Competition Assay (PCA) used in conjunction with the Gen-Probe PACE 2 and 2C direct detection assays for Chlamydia trachomatis were examined. Data collected by five public health laboratories by using the Gen-Probe PACE 2 were pooled and analyzed. Of 25,081 endocervical and male urethral specimens tested by the PACE 2 assay, 773 were tested by PCA. Of 334 specimens initially positive by the PACE 2 assay with an initial PACE 2 result of greater than 2,000 relative light units (RLU), 333 (99.7%) were positive by PCA while 242 of 339 (71.4%) specimens with an initial result between the cutoff and 2,000 RLU were positive by PCA, and 35 of 100 (35%) specimens with initial results between 200 RLU and the cutoff were positive by PCA. An additional 10,938 specimens were tested by the PACE 2C assay. Of these, positive PCA results were obtained for 187 of 188 (99.5%) specimens with initial results of greater than 2,000 RLU, 99 of 163 (60.7%) of specimens in the range of cutoff to 2,000 RLU, and 12 of 100 (12%) in the range of 200 RLU to the cutoff. These results indicate that specimens greater than 2,000 RLU do not require a supplemental test and that additional positive results can be obtained by testing specimens with an initial result below the cutoff.
7E3 monoclonal antibody directed against the platelet glycoprotein IIb/IIIa cross-reacts with the leukocyte integrin Mac-1 and blocks adhesion to fibrinogen and ICAM-1.
Recent clinical trials suggest that blockade of integrins is a promising strategy for the treatment of acute coronary syndromes. Administration of 7E3 monoclonal antibody (mAb) Fab fragment (c7E3 Fab) directed against platelet integrin IIb/IIIa (alpha IIb beta 3, CD41/CD61) reduces acute ischemic complications of coronary angioplasty and clinical restenosis at 6 months. However, 7E3 mAb is not selective for platelet IIb/IIIa but also cross-reacts with the leukocyte integrin Mac-1 (alpha M beta 2, CD11b/CD18) and the vitronectin receptor (alpha v beta 3, CD51/CD61). Information regarding how this mAb may affect other cells important in vascular repair is scant. Potential interactions of c7E3 Fab with inflammatory (i.e., monocytes and neutrophils), vascular smooth muscle, and endothelial cells may contribute to the in vivo actions of c7E3 Fab. In this study we explored the binding of 7E3 to monocytic cells and the functional effect of 7E3 and c7E3 Fab on Mac-1-mediated adhesion to fibrinogen (FGN) and intercellular adhesion molecule-1 (ICAM-1), ligands abundant in the injured vessel wall. Flow cytometry demonstrated that 7E3 bound to THP-1 monocytic cells and identified a subpopulation (approximately 10%) of Mac-1 that was qualitatively similar to that recognized by CBRM1/5, a mAb directed to an activation-specific neoepitope present on a subset of Mac-1 molecules. mAb 7E3 bound to K562 cells transfected with just the alpha subunit (CD11b) of Mac-1 but not to nontransfected cells, confirming a direct interaction between 7E3 and Mac-1. mAb 7E3 and c7E3 Fab blocked the adhesion of Mac-1-bearing cells to FGN (80 +/- 11% and 78 +/- 9% inhibition, respectively) and ICAM-1 (62 +/- 14% and 62 +/- 17%). Both 7E3 and c7E3 Fab significantly inhibited (70 +/- 6% and 62 +/- 26%) soluble FGN binding to human peripheral blood monocytes. Thus, c7E3 Fab cross-reacts with the CD11b subunit of Mac-1 and interrupts cell-extracellular matrix and cell-cell adhesive interactions and may thereby influence the recruitment of circulating monocytes to sites of vessel injury. Given the recent evidence that adherent and infiltrating monocyte number directly correlates with the extent of neointimal hyperplasia, inhibition of Mac-1-dependent adhesion and IIb/IIIa-dependent function by c7E3 Fab may jointly contribute to the regulation of vascular repair and to the sustained clinical benefits observed with c7E3 Fab after angioplasty.
Medicare CACs (Carrier Advisory Committees) and the surgical community: why surgeons should get involved.
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A child with both congenital fiber type disproportion and giant congenital melanocytic nevi with malignant melanoma.
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Endogenous cell seeding. Remnant endothelium after stenting enhances vascular repair.
BACKGROUND: Endothelial integrity is essential for maintaining vascular homeostasis, and endothelial denudation results in neointimal thickening. Balloon-expandable endovascular stents provide a luminal scaffolding within atherosclerotic arteries with minimal direct contact between balloon and endothelium. We wondered whether stents cause diminished endothelial ablation, and if so, whether the degree of endothelial damage might determine later proliferative sequelae. METHODS AND RESULTS: Stainless steel stents were expanded in normal or previously denuded iliac arteries of New Zealand White rabbits. Stented arteries were harvested 15 minutes, 1 hour, 3 days, or 14 days later. En face staining of the luminal surfaces of stented arteries demonstrated that endothelial cell loss began immediately after stent expansion and was restricted to interstices between stent struts. Remnant endothelium adjacent to struts provided the foundation for complete endothelial regeneration of the stented segment within 3 days. Both early monocyte adhesion and later intimal macrophage accumulation were reduced > 80% in nonballooned but stented arteries, in concert with a twofold reduction in intimal thickening after 14 days, compared with arteries completely denuded with a balloon before stent expansion. CONCLUSIONS: It is accepted that deep injury caused by balloon-expanded endovascular stents is a critical contributor to experimental stent-induced neointimal hyperplasia. Our data indicate that the degree of endothelial injury may also be an important component of vascular repair after stenting and an important consideration in stent and balloon design and use. The use of stents for primary endovascular intervention may allow partial retention of endothelium within treated arteries, thereby modulating vascular repair with less need for adjunctive pharmacological therapy.
Hoop dreams. Stents without restenosis.
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Expression of the alpha(1,3)fucosyltransferase Fuc-TVII in lymphoid aggregate high endothelial venules correlates with expression of L-selectin ligands.
Lymphocyte homing to lymph nodes and Peyer's patches is mediated, in part, by adhesive interactions between L-selectin expressed by lymphocytes and L-selectin ligands displayed at the surface of the cuboidal endothelial cells lining the post-capillary venules within lymphoid aggregates. Candidate terminal oligosaccharide structures thought to be essential for effective L-selectin ligand activity include a sulfated derivative of the sialyl Lewis x tetrasaccharide. Cell type-specific synthesis of this oligosaccharide is presumed to require one or more alpha(1,3)fucosyltransferases, operating upon common 3'-sialylated and/or sulfated N-acetyllactosamine-type precursors. The identity of the alpha(1,3)fucosyltransferase(s) expressed in cells that bear L-selectin ligands has not been defined. We report here the molecular cloning and characterization of a murine alpha(1,3)fucosyltransferase locus whose expression pattern correlates with expression of high affinity ligands for L-selectin. In situ hybridization and immunohistochemical analyses demonstrate that this cDNA and its cognate alpha(1,3)fucosyltransferase are expressed in endothelial cells lining the high endothelial venules of peripheral lymph nodes, mesenteric lymph nodes, and Peyer's patches. These expression patterns correlate precisely with the expression pattern of L-selectin ligands identified with a chimeric L-selectin/IgM immunohistochemical probe and by the high endothelial venule-reactive monoclonal antibody MECA-79. Transcripts corresponding to this cDNA are also detected in isolated bone marrow cells, a source rich in the surface-localized ligands for E- and P-selectins. Sequence and functional analyses indicate that this murine enzyme corresponds to the human Fuc-TVII locus. These observations suggest that Fuc-TVII participates in the generation of alpha(1,3)fucosylated ligands for L-selectin and provide further evidence for a role for this enzyme in E- and P-selectin ligand expression in leukocytes.
Lidocaine inhibits blood coagulation: implications for epidural blood patch.
Lidocaine in the epidural space, through inhibitory effects upon coagulation, may contribute to inefficacy of epidural autologous blood patch (EBP). This study was undertaken to evaluate the effect of achievable epidural concentrations of lidocaine on blood coagulation as a step in testing this hypothesis. Ex vivo blood coagulation using whole blood (n = 20) was studied with computerized thrombelastography (TEG). Each blood specimen was exposed to serial dilutions of lidocaine hydrochloride or saline to form end-concentrations of 0.0 mM, 2.3 mM, 4.6 mM, 9.2 mM, 18.5 mM, and 36.9 mM lidocaine. Statistical analysis using analysis of variance for repeated measures revealed that the three highest lidocaine concentrations tested caused hypocoagulable and/or fibrinolytic changes as compared with controls. Achievable epidural admixtures of lidocaine and whole blood will impair coagulation. Therefore, residual lidocaine in the epidural space may contribute to failures of immediate or early EBP.