Clinical and hand-held Doppler examination of primary varicose veins.
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Biomedical subjects
Publications and source records attributed to B Campbell.
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In this work we propose a theoretical description of the process of creaming of batch emulsions when a sharp boundary exists between a clear serum phase and the sedimenting drops. The creaming is represented as a continuous consolidation of partially aggregated network. The treatment reproduces correctly the trend for gradually decreasing rate of sedimentation as time goes on. The theoretical results are compared quantitatively with experimental measurements of the creaming rate. Oil-in-water systems, stabilized by proteins (beta-lactoglobulin (BLG), bovine serum albumin, and mixtures BLG+beta-casein) were investigated. Faster creaming is attributed to larger size of the sedimenting objects (flocs of emulsion droplets). In systems obeying the creaming mechanism with sharp boundary (SB) the flocs are smaller when the protein concentration is higher. This supports the hypothesis for the stabilizing role of the excess amount of protein (forming lumps and multilayers on the interface). Theoretical analysis demonstrates that the formation of flocs by gravitational coagulation is a much faster process than the consolidation of the cream. Hence, the dispersions first flocculate and then cream. With increasing beta-casein content in mixtures BLG+beta-casein the emulsions depart from the SB-type behavior and are characterized by the presence of small nonflocculated droplets, which do not sediment (the serum is turbid and the boundary with the concentrated dispersion is diffuse, DB behavior). This is connected with hindered flocculation, perhaps due to beta-casein's augmented ability to prevent droplet aggregation. Copyright 2000 Academic Press.
Coronary heart disease (CHD) accounts for half of the 1 million deaths annually ascribed to cardiovascular disease and for almost all of the 1.5 million acute myocardial infarctions. Within families affected by early and apparently heritable CHD, dyslipidemias have a much higher prevalence than in the general population; 20%-30% of early familial CHD has been ascribed to primary hypoalphalipoproteinemia (low HDL-C). This study assesses the evidence for linkage of low HDL-C to chromosomal region 11q23 in 105 large Utah pedigrees ascertained with closely related clusters of early CHD and expanded on the basis of dyslipidemia. Linkage analysis was performed by use of 22 STRP markers in a 55-cM region of chromosome 11. Two-point analysis based on a general, dominant-phenotype model yielded LODs of 2.9 for full pedigrees and 3.5 for 167 four-generation split pedigrees. To define a localization region, model optimization was performed using the heterogeneity, multipoint LOD score (mpHLOD). This linkage defines a region on 11q23.3 that is approximately 10 cM distal to-and apparently distinct from-the ApoAI/CIII/AIV gene cluster and thus represents a putative novel localization for the low HDL-C phenotype.
Endothelial dysfunction and loss of nitric oxide (NO) is an integral part of the initiation and maintenance of the inflammatory process such as that occurring in traumatic shock, and is considered responsible for much of the trauma induced microvascular injury. We investigated the effects of a vascular endothelial growth factor (VEGF) in a rat model of traumatic shock. Pentobarbital-anaesthetized rats subjected to Noble-Collip drum trauma developed a shock state characterized by marked hypotension and a 93% mortality rate with a mean survival time of 108+/-10 min in 14 rats. Accompanying these effects was a significant degree of endothelial dysfunction and a markedly elevated intestinal myeloperoxidase (MPO) activity. Treatment with 125 microg kg(-1) VEGF administered intravenously 18 h pre-trauma, increased survival rate to 67% (P<0.01), and prolonged survival time to 252+/-24 min in 12 rats (P<0.01). VEGF also significantly preserved the endothelium-dependent relaxation to ACh indicating a preservation of endothelium-derived NO. Our results indicate that endothelial dysfunction with its accompanying loss of NO plays an important role in tissue injury associated with trauma, and that preservation of NO is beneficial in traumatic shock. The mechanisms of the protective effect of VEGF in trauma involves preservation of eNOS function and diminished neutrophil accumulation resulting in reduced neutrophil-mediated tissue injury. British Journal of Pharmacology (2000) 129, 71 - 76
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Advanced trauma life support (ATLS) has become a desirable or even essential part of training for many surgeons and anaesthetists, but aspects of the ATLS course have attracted criticism. In the absence of published data on the views of trainees, this study sought their opinions in a structured questionnaire, which was completed by trainees in accident and emergency (A & E) (26), anaesthetic (82), general surgical (26), orthopaedic (42) and other (5) posts in different hospitals (response rate 66%). Of the trainees, 78% had done an ATLS course and, of these, 83% considered ATLS a 'major advantage' or 'essential' for practising their proposed specialty--100% for A & E, 94% for orthopaedics, 92% for general surgery, and 75% for anaesthetics. ATLS was considered a major curriculum vitae (CV) advantage by 94%, 85%, 50%, and 45%, respectively. Over 90% had positive attitudes towards ATLS, and 74% selected 'genuine improvement of management of trauma patients' as the most important reason for doing the course: 93% thought ATLS saved lives. Of the respondents, 83% thought that all existing consultants dealing with trauma patients should have done the course, and 41% thought it offered major advantages to doctors not involved in trauma. Funding problems for ATLS courses had been experienced by 14% trainees. This survey has shown that most trainees view ATLS positively. They believe that it provides genuine practical benefit for patients, and very few regard ATLS primarily as a career advantage or mandate.
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Bovine splenic nerve was used as a source of axolemma-enriched fractions derived from mammalian unmyelinated axons. By electron microscopy, splenic nerve consisted entirely of fascicles of unmyelinated axons and associated Schwann cells. The epineurium and blood vessels were stripped from the dissected nerve, which was then homogenized followed by preparation of a microsomal fraction by differential centrifugation. The microsomes were fractionated on a 10% to 40% continuous sucrose gradient. The individual fractions were combined into six fractions based on sucrose concentration and each fraction was analyzed for membrane markers. The 20% to 23% region of the sucrose gradient was enriched approximately sevenfold in acetylcholinesterase activity and twofold enrichment in saxitoxin binding activity was noted in the same fraction. Relative to other microsomal fractions, this same fraction was less enriched in a microsomal marker (cytochrome c reductase) and only moderately enriched in the activity of a myelin membrane marker (2',3' cyclic nucleotide 3' phosphohydrolase, CNPase). Polyacrylamide electrophoresis of the axolemma-enriched fraction revealed five prominent peptides ranging in molecular weight from 40 kDa to 130 kDa. Lipids, comprising 59.4% of the dry weight, were enriched in cholesterol and sphingomyelin, consistent with the origin from a peripheral nervous system (PNS) plasma membrane. On a molar basis, the major gangliosides were G(T1b), G(D1a), and G(M1). As a whole, these molecular characteristics are consistent with the origin of the axolemma-enriched fraction in the unmyelinated splenic nerve axons. This membrane preparation should prove useful in future studies of the myelinogenic potential of mammalian unmyelinated axolemma.
BACKGROUND: Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac contractile dysfunction as well as cardiomyocyte injury. These deleterious effects are due in large part to endothelial dysfunction leading to the upregulation of cell adhesion molecules and subsequent neutrophil-endothelium interaction. At clinically relevant doses, simvastatin, an HMG-CoA reductase inhibitor, has been shown to lower serum cholesterol levels and normalize endothelial cell function. We wanted to test the effects of simvastatin on neutrophil-mediated cardiac dysfunction in a controlled model of myocardial ischemia-reperfusion. METHODS AND RESULTS: This study examines the effects of simvastatin in a neutrophil-dependent isolated perfused rat heart model of ischemia (I) (20 minutes) and reperfusion (R) (45 minutes) injury. Administration of simvastatin 25 micrograms/rat improved coronary flow and preserved left ventricular developed pressure (LVDP) and dP/dtmax, indexes of cardiac contractile function. Final LVDP was 95+/-5 mm Hg in I/R hearts perfused with PMNs and simvastatin, compared with 49+/-4 mm Hg in PMN-perfused I/R hearts receiving only vehicle (P<0.001). In addition, simvastatin significantly reduced PMN accumulation in the ischemic myocardium (P<0.01). In PMN-perfused rat hearts after I/R, simvastatin also significantly attenuated P-selectin expression, CD18 upregulation in rat PMNs, and PMN adherence to rat vascular endothelium. Significant, although less potent, effects were obtained with pravastatin. CONCLUSIONS: These results provide evidence that HMG-CoA reductase inhibitors are potent and effective cardioprotective agents that inhibit leukocyte-endothelial cell interactions and preserve cardiac contractile function and coronary perfusion after myocardial ischemia and reperfusion. Moreover, these effects are unrelated to the cholesterol-lowering action of this agent and appear to be mediated by enhanced endothelial release of NO.
HYPOTHESIS: Despite successful efforts in California to increase the number of graduating medical students entering primary care residencies, general surgery remains a popular career choice. DESIGN: Retrospective survey of annual graduating medical student residency selections from allopathic medical schools in California between 1993 and 1998. METHODS: Each medical school in California was sent a survey of its graduates' specialty choices from 1993 to 1998. Once quantified, comparisons using t tests, chi2 analyses, and analyses of variance were performed to assess differences in graduating medical student career choices. RESULTS: Surveys were received from 7 of 8 allopathic medical schools in California representing 5154 students (3645 from University of California medical schools). In the study period, the number entering primary care residencies rose from 45.5% in 1993 to 54.3% in 1998. Despite this overall trend, statistically significant increases were seen only for pediatrics between 1993 and 1994. The number of students entering general surgery did not change significantly. Significant decreases were seen in emergency medicine and obstetrics and gynecology between 1997 and 1998 and in anesthesiology between 1994 and 1995 and again between 1995 and 1996. When considering only University of California graduates, the number choosing primary care residencies rose from 46.6% in 1993 to 54.2% in 1998. As before, the number entering general surgery did not change (6.1% in 1993 and 6.3% in 1998). CONCLUSION: Owing to institutional, legislative, and market pressures, more graduates of California medical schools (both public and private institutions) are choosing to become primary care practitioners. A corresponding decrease in medical students entering general surgery has not resulted, which points to an optimistic future and continuing demand for surgeons.
Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac contractile dysfunction as well as myocardial injury. These effects are due in large part to endothelial dysfunction leading to an upregulation of cell adhesion molecules and subsequent neutrophil induced cardiac injury. The proteasome inhibitor, PS-519, has been shown to attenuate leukocyte-endothelial cell interactions. We tested the effects of PS-519 on neutrophil mediated cardiac dysfunction in ischemia/reperfusion. This study examines the effects of PS-519 in a neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of PS-519 (0.01, 0.1, 0.3, 1.0 mg/kg) to I/R hearts perfused with PMNs improved coronary flow, and preserved left ventricular developed pressure (LVDP) and + dP/dt max as indices of cardiac contractile function. At 1.0 mg/kg, PS-519 treated hearts exhibited a final LVDP of 98 +/- 3% of initial compared to 52 +/- 8% in I/R hearts receiving only vehicle (P < 0.001). In addition, PS-519 significantly reduced PMN accumulation in the ischemic myocardium from 25.1 +/- 2.1 PMNs/mm2 in untreated hearts to 7.3 PMNs/mm2, and attenuated P-selectin surface expression on coronary vascular endothelium from 7.1 +/- 0.3% to 1.4 +/- 0.2% (P < 0.01). These results provide evidence that PS-519 is a potent and effective cardioprotective agent that inhibits P-selectin leukocyte-endothelial cell interactions and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.
OBJECTIVE: Neutrophils (PMNs) contribute importantly to the tissue injury associated with ischemia and subsequent reperfusion of a vascular bed. The effects of a recombinant soluble human form of P-selectin glycoprotein ligand-1 (rsPSGL.Ig) on PMN-endothelial cell interactions were investigated in a well established model of feline myocardial-ischemia reperfusion injury. METHODS: Cats were subjected to 90 min of myocardial ischemia followed by 270 min of reperfusion. RESULTS: Administration of rsPSGL.Ig (1 mg/kg) just prior to reperfusion resulted in a significant reduction in myocardial necrosis compared to that in cats administered a low affinity mutant form of rsPSGL.Ig (1 mg/kg) (16 +/- 3 vs. 42 +/- 7% of area-at-risk, P < 0.01). Cardioprotective effects were confirmed by significant (P < 0.05) reductions in plasma creatine kinase activity in cats treated with rsPSGL.Ig. Inhibition of PMN-endothelial cell interactions was evidenced by a significant attenuation in cardiac myeloperoxidase activity (P < 0.01) and reduced PMN adherence to ischemic-reperfused coronary endothelium (P < 0.001). In addition, rsPSGL.Ig treatment significantly (P < 0.01) preserved endothelium-dependent vasorelaxation in ischemic-reperfused coronary arteries. CONCLUSION: These results demonstrate that the administration of a recombinant soluble PSGL-1 reduces myocardial reperfusion injury and preserves vascular endothelial function, which is largely the result of reduced PMN-endothelial cell interactions.
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PURPOSE: This study was undertaken to evaluate simplified methods of human embryo coculture using either attached or nonattached autologous cumulus tissue. METHODS: Eight hundred one zygotes were cultured for 48 hr in a prospective, randomized trial comparing culture of embryos either with intact cumulus tissue, with cumulus tissue added to the droplet of culture medium, or without any cumulus tissue. In a follow-up study, embryo quality, pregnancy rates, and implantation rates were compared in 120 consecutive patients undergoing in vitro fertilization with a coculture system using cumulus tissue compared to a cohort of 127 patients undergoing IVF immediately preceding the institution of the coculture protocol. RESULTS: Embryo morphology was significantly improved (P < 0.05) following culture with attached cumulus tissue (5.61 +/- 0.29) and culture with added cumulus tissue (4.72 +/- 0.31) compared to that of embryos grown in culture medium without cumulus tissue (3.95 +/- 0.26). The clinical pregnancy rate improved from 39.4% (50/127) to 49.2% (59/120) following institution of a system of coculture with attached cumulus tissue. CONCLUSIONS: These data indicate that a simple coculture system using autologous cumulus tissue can result in improved embryo morphology, implantation rates, and clinical pregnancy rates during in vitro fertilization. This coculture system is simple, is non-labor intensive, and eliminates many of the risks which may be present in other embryo coculture systems.
Using data from a 2-year longitudinal study of 200 Black and White adolescent girls (mean age was 13.8 years at study entry), the authors investigated the implications of differences in body fat for dating and sexual activity and the implications of heterosexual activity for dieting and weight concerns. Among White girls, and Black girls with college-educated mothers, more body fat was associated with a lower probability of dating, even among nonobese girls. However, dating and sexual experience were unrelated to subsequent dieting and weight concerns. For both Blacks and Whites, body fat was the key determinant of dieting, weight dissatisfaction, and eating concerns. These findings indicate that adolescent girls' concerns about weight have a basis in real experiential differences, and efforts to promote healthy attitudes and eating habits may be more effective if the experiential implications of weight differences are taken into account.