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Biomedical subjects

J Boyce

Publications and source records attributed to J Boyce.

At least 19 recordsLinked to original sources

Marination of turkey breast fillets to control the growth of Listeria monocytogenes and improve meat quality in deli loaves.

Turkey deli loaves were evaluated using organic marinades in the raw product to control the growth of Listeria monocytogenes (LM) and improve meat quality in the cooked product. Treatments included sodium tripolyphosphate (STP; 0.45%, control), sodium lactate (3%), sodium diacetate (0.25%), sodium citrate (0.75%), and sodium lactate (3%)/sodium diacetate (0.25%) combination, all containing 1.5% salt. Data collected in the 2 trials included pH; lightness, redness, and yellowness; bind ability; cooked meat moisture; oxidation (thiobarbituric acid reactive substances); aerobic plate count (d 0 to 80); and sensory evaluation. Also, thirty-two slices from each loaf were inoculated with a 10(3) cfu/ mL surface inoculum streptomycin-resistant LM cocktail and analyzed for LM levels (d 0 to 77). The sodium lactate treatment was lower in pH (5.84) postmarination. Lactate, citrate, and the combination treatments had significantly lower lightness values; lactate, diacetate, and citrate had higher redness values; and lactate had lower yellowness values postmarination compared with premarination. Cook loss, moisture, and bind ability were higher in the STP treatment. Citrate and the combination treatments had lower thiobarbituric acid reactive substances on d 3, but there were no differences by d 15. Cohesiveness was significantly higher in the STP, lactate, and diacetate treatments, and turkey flavor was more intense in the combination treatment. The STP loaves had >10(6) cfu/cm(2) aerobic plate count by 14 d, lactate by 20 d, citrate by 40 d, diacetate by 70 d, and lactate/diacetate by 74 d. Sodium diacetate, citrate, and lactate/diacetate all extended the lag phase of LM. Therefore, acidic marinades applied in the raw product do have a negative effect on some cooked product quality attributes but do improve shelf life and decrease LM growth by extending the lag phase through 21 d postmortem.

Animals↗

Do chronic changes in nasal airflow have any physiological or pathological effect on the nose and paranasal sinuses? A systematic review.

.A reduction in nasal airflow associated with anatomical defects of the nose such as nasal septal deviation has been proposed to cause nasal pathology. . The majority of animal experiments where one nasal passage is surgically closed over several months report only minor changes in the histology of the nasal epithelium and no rhinitis or sinusitis. .Complete abolition of nasal airflow associated with laryngectomy or the treatment of atrophic rhinitis is not associated with the development of rhinitis or sinusitis. . Radiological studies have shown a lack of association between the degree of nasal septal deviation and evidence of rhinosinusitis. .Such studies provide evidence that reduced nasal airflow causes no significant nasal disease. . There is no convincing evidence that a reduction in nasal airflow is a causative factor for rhinitis or sinusitis.

Animals↗

Automated detection of diabetic retinopathy in digital retinal images: a tool for diabetic retinopathy screening.

AIMS: To develop a system to detect automatically features of diabetic retinopathy in colour digital retinal images and to evaluate its potential in diabetic retinopathy screening. METHODS: Macular centred 45 degrees colour retinal images from 1273 patients in an inner city diabetic retinopathy screening programme. A system was used involving pre-processing to standardize colour and enhance contrast, segmentation to reveal possible lesions and classification of lesions using an artificial neural network. The system was trained using a subset of images from 500 patients and evaluated by comparing its performance with a human grader on a test set of images from 773 patients. RESULTS: Maximum sensitivity for detection of any retinopathy on a per patient basis was 95.1%, accompanied by specificity of 46.3%. Specificity could be increased as far as 78.9% but was accompanied by a fall in sensitivity to 70.8%. At a setting with 94.8% sensitivity and 52.8% specificity, no cases of sight-threatening retinopathy were missed (retinopathy warranting immediate ophthalmology referral or re-examination sooner than 1 year by National Institute for Clinical Excellence criteria). If the system was implemented at 94.8% sensitivity setting over half the images with no retinopathy would be correctly identified, reducing the need for a human grader to examine images in 1/3 of patients. CONCLUSION: This system could be used when screening for diabetic retinopathy. At 94.8% sensitivity setting the number of normal images requiring examination by a human grader could be halved.

Color↗

The Audit Commission review of diabetes services in England and Wales, 1998-2001.

UNLABELLED: AIMS OF THE AUDIT COMMISSION: The Audit Commission has a statutory duty to promote the best use of public money. It does this through value for money studies, such as that reported in Testing Times[1]. This work has been followed with a review of innovative practice in commissioning. These initiatives aim to support the implementation of the diabetes national service framework. The Audit Commission also appoints external auditors to NHS organizations who assess probity and value for money in the NHS; the latter by applying national studies locally and by carrying out local studies. METHODS: Research for Testing Times consisted of structured visits to nine acute trusts, a telephone survey of 26 health authorities and a postal survey of 1400 people with diabetes and 250 general practitioners. Local audits used a subset of the original research tools. Case studies were identified through a cascade approach to contacts established during Testing Times and through self-nomination. RESULTS: Rising numbers of people with diabetes are placing increasing pressure on hospital services. Some health authorities and primary care organizations have reviewed patterns of service provision in the light of the increasing demands. These reviews show wide variations in patterns of routine care. In addition, there is a widespread lack of data on the delivery of structured care to people with diabetes. People with diabetes report delays in gaining access to services, and insufficient time with staff. There are insufficient arrangements in place for providing information and learning opportunities to support self-management. CONCLUSION: As the number of people with diabetes continues to rise, the potential for providing more care in a primary care setting needs to be explored. This will enable specialist services to focus more effectively on those with the most complex needs.

Diabetes Mellitus↗

Gastric emptying after a new, more physiological anti-obesity operation: the Magenstrasse and Mill procedure.

The Magenstrasse and Mill (M&M) procedure for obesity is designed to preserve normal gastric emptying mechanisms. The hypothesis investigated in this study was that gastric emptying would be normal after the M&M gastroplasty. Gastric emptying studies were performed using both liquid and solid test meals, in ten morbidly obese patients (MO group) and in 13 patients after the M&M procedure (MM group). Seven people of normal weight served as controls and were matched for age, sex and height to the M&M and MO groups. Three years after the M&M procedure, mean (SD) weight loss was 42 (19) kg, with a mean loss of excess weight of 58% (20%). Gastric emptying half-times (t 1/2) are expressed in minutes, as median values (25th and 75th percentiles). The t 1/2 for solids was 97 (85-110) min in the control group, 140 (86-220) min in the MO group and 79 (46-150) min in the MM group. Median gastric emptying for solids was 0.7% (0.6%-0.8%) per minute in the control group, 0.5% (0.3%-0.8%) in the MO group and 0.9% (0.4%-1.4%) in the M&M group. There were no statistically significant differences in the emptying times of the three groups. It is concluded that the M&M procedure achieves acceptable weight loss, while preserving gastric emptying mechanisms and thus minimising possible side-effects such as vomiting, dumping and diarrhoea, which are common complications of gastric bypass procedures.

Administration, Oral↗

beta(2)-Microglobulin modified with advanced glycation end products delays monocyte apoptosis.

BACKGROUND: A local inflammatory reaction to beta(2)-microglobulin (beta(2)m) amyloid deposits by monocytes/macrophages is a characteristic histologic feature of dialysis-related amyloidosis (DRA). Since beta(2)m modified with advanced glycation end products (AGE-beta(2)m) is a major constituent of amyloid in DRA, we tested the hypothesis that AGE-beta(2)m affects apoptosis and phenotype of human monocytes. METHODS: Human peripheral blood monocytes were incubated with or without in vitro-derived AGE-beta(2)m, and their viability, extent of apoptosis, morphology, and function examined over the subsequent four days. RESULTS: AGE-modified but not unmodified beta(2)m significantly delayed spontaneous apoptosis of human peripheral blood monocytes in adherent and nonadherent cultures. The effect of AGE-beta(2)m on monocytes apoptosis was time- and dose-dependent and was attenuated by a blocking antibody directed against the human AGE receptor (RAGE). There was no difference in effect between AGE-beta(2)m and that of AGE-modified human serum albumin. Culture of monocytes with AGE-beta(2)m did not alter membrane expression of Fas or Fas ligand. Monocytes cultured with AGE-beta(2)m underwent substantial changes in morphology similar to those observed when monocytes differentiate into macrophages. The cultured cells increased in size and vacuolization, and their content of beta-glucuronidase and acid phosphatase increased by 5- to 10-fold at day 4. Expression of the monocyte--macrophage membrane antigens HLA-DR, CD11b, and CD11c also increased at day 4. Although exhibiting phenotypic characteristics of macrophages, monocytes cultured with AGE-beta(2)m functioned differently than macrophages cultured with serum. Superoxide production in response to phorbol myristic acetate was maintained in monocytes cultured with AGE-beta(2)m, but declined with time in cells cultured with serum. Constitutive synthesis of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and prostaglandin E2 (PGE2) increased in monocytes cultured for four to six days with AGE-beta(2)m. CONCLUSIONS: These findings support a novel role for AGE-modified proteins such as AGE-beta(2)m that may contribute to the development of a local inflammatory response, with predominant accumulation of monocytes/macrophages, in DRA.

Antibodies↗

The transcription factor early growth-response factor 1 modulates tumor necrosis factor-alpha, immunoglobulin E, and airway responsiveness in mice.

Early growth-response factor 1 (Egr-1) is a sequence-specific transcription factor that plays a regulatory role in the expression of many genes important in inflammation, cell growth, apoptosis, and the pathogenesis of disease. In vitro studies suggest that Egr-1 is capable of regulating the expression of tumor necrosis factor-alpha (TNF-alpha) and other genes involved in airway inflammation and reactivity following allergen stimulation. On the basis of these data, we hypothesized that in the absence of Egr-1, the TNF-alpha response and subsequent downstream inflammatory events that usually follow allergen challenge would be diminished. To test our hypothesis Egr-1 knock-out (KO) mice were examined in an ovalbumin (OVA)-induced model of airway inflammation and reactivity, and compared with identically treated wild-type (WT) control mice. In response to OVA sensitization and airway challenge, KO mice had diminished TNF-alpha mRNA and protein in the lungs and mast cells compared with WT mice. Interestingly, the KO mice had elevated IgE levels at baseline and after allergen challenge compared with WT mice. Furthermore, the airways of KO mice were hyporesponsive to methacholine challenge at baseline and after allergen challenge. These data indicate that Egr-1 modulates TNF-alpha, IgE, and airway responsiveness in mice.

Animals↗

Clinical evaluation of 'local contrast enhancement' for oral fluorescein angiograms.

PURPOSE: To describe and assess the clinical impact of 'local contrast enhancement' on oral fluorescein angiograms. METHODS: Oral fluorescein angiograms (OFA) were performed on 12 patients with a range of diabetic retinopathy. The digital images were processed using two enhancement techniques: histogram equalization, a widely available method; and 'local contrast enhancement'. Twelve control images and 24 enhanced images were randomised and subjectively graded for clarity between 1 and 100 on a visual analogue scale by two masked observers. A score of 50% was chosen as the cut-off for clinically useful images. RESULTS: The mean score for the unenhanced images was 38.8% (SD 19.4); the histogram equalization performed better at 54.7% (SD 10.0) (p = 0.016) and 'local contrast enhancement' at 69.4% (SD 13.6) (p < 0.001). These results equate to a 14.7% improvement in comparison with histogram equalization and a 30.3% improvement with the 'local contrast enhancement' technique. All the 'local contrast enhancement' images were clinically useful, compared with 58.3% of the histogram equalization images (chi 2 2.08, p = 0.2), and 33.3% of the control images (chi 2 = 6.75, p = 0.01). CONCLUSION: This pilot study has demonstrated the power of 'local contrast enhancement' techniques for low-contrast fluorescein angiograms. Using 'local contrast enhancement' oral fluorescein angiograms can give high-quality images and may allow safer patient investigation.

Administration, Oral↗

Phenotypic and functional characteristics of macrophage-like cells differentiated in pro-inflammatory cytokine-containing cultures.

Previous studies have demonstrated an infiltration of monocytes and increased levels of IL-1beta and TNF-alpha in some chronic inflammatory tissues. Interleukin-1beta and TNF-alpha are capable of protecting monocytes from spontaneous apoptosis and thus maintain their viability in vitro. To study the possible effects of these cytokines on the differentiation and function of recruited monocytes, a model has been developed in which monocytes isolated from human peripheral blood were differentiated into macrophages in serum in the presence or absence of IL-1beta or TNF-alpha. Monocytes cultured with IL-1beta and TNF-alpha underwent substantial changes in morphology, similar to those observed in monocytes undergoing differentiation into macrophages. The cultured cells increased in size and vacuolization and their content of acid phosphates increased 10-fold. Although they exhibited the morphological characteristics of macrophages, monocytes matured in the cytokines differed functionally from those cultured in serum in a lower expression of HLA-DR, lower ability for triggering the proliferation of allogeneic lymphocytes, higher expression of mannose receptor and greater production of superoxide and TNF-alpha. This data suggests that IL-1beta and TNF-alpha direct monocyte differentiation into macrophages with a reduced antigen-presenting and an increased pro-inflammatory factor-releasing phenotype. Elevated levels of IL-1beta and TNF-alpha in the inflammatory tissues may therefore not only prolong the survival of recruited monocytes, but maintain them in an inflammatory state.

Acid Phosphatase↗

Cellulitis: evaluation of possible predisposing factors in hospitalized patients.

We conducted a prospective study among 62 hospitalized adults, to evaluate the factors that contribute to the development of cellulitis. The majority of patients had multiple possible predisposing factors, and the most common were: diabetes mellitus (31/62), history of cellulitis (30/62), edema (28/62), peripheral vascular disease (25/62), and skin changes suggestive of tinea pedis (20/62). A significant number of patients reported and were clinically noted to have dry skin (42/62). Large controlled studies are needed to evaluate whether aggressive control of possible risk factors can reduce the incidence of cellulitis.

Adult↗

Relationship between intraocular lens biomaterials and posterior capsule opacification.

PURPOSE: To determine whether posterior capsule opacification (PCO) is influenced by intraocular lens (IOL) material. SETTING: A British teaching hospital eye department. METHODS: Ninety eyes were prospectively randomized to receive a poly(methyl methacrylate) (PMMA), silicone, or AcrySof IOL. All lenses had 6.0 mm optics and PMMA haptics. A standardized surgical protocol was performed by a single surgeon using an extracapsular technique with capsulorhexis. Patients having surgical complications were excluded and all patients had standardized medication and follow-up. Posterior capsule opacification was assessed by a digital retroillumination camera using a dedicated software program based on the analysis of texture in the image and calculated as the percentage area of opacified capsule. Data were analyzed 2 years postoperatively. RESULTS: There was a significant difference in percentage of PCO at 2 years among the three lens types (P < .0001). The AcrySof lenses were associated with less PCO (median 11.75%) than PMMA (43.65%) and silicone (33.50%) lenses (P < .001 and P = .025, respectively). The difference between PMMA and silicone lenses was not statistically significant. CONCLUSION: Intraocular lenses made from AcrySof were associated with a significantly reduced degree of PCO.

Acrylates↗

Beta 2-microglobulin modified with advanced glycation end products modulates collagen synthesis by human fibroblasts.

Beta 2-microglobulin amyloidosis (A beta 2m) is a serious complication for patients undergoing long-term dialysis. beta 2-microglobulin modified with advanced glycation end products (beta 2m-AGE) is a major component of the amyloid in A beta 2m. It is not completely understood whether beta 2m-AGE plays an active role in the pathogenesis of A beta 2m, or if its presence is a secondary event of the disease. beta 2-microglobulin amyloid is mainly located in tendon and osteo-articular structures that are rich in collagen, and local fibroblasts constitute the principal cell population in the synthesis and metabolism of collagen. Recent identification of AGE binding proteins on human fibroblasts lead to the hypothesis that the fibroblast may be a target for the biological action of beta 2m-AGE. The present study demonstrated that two human fibroblast cell lines exhibited a decrease in procollagen type I mRNA and type I collagen synthesis after exposure to beta 2m-AGE for 72 hours. Similar results were observed using AGE-modified albumin. Antibody against the RAGE, the receptor for AGE, attenuated this decrease in synthesis, indicating that the response was partially mediated by RAGE. In addition, antibody against epidermal growth factor (EGF) attenuated the decrease in type I procollagen mRNA and type I collagen induced by beta 2m-AGE, suggesting that EGF acts as an intermediate factor. These findings support the hypothesis that beta 2m-AGE actively participates in connective tissue and bone remodeling via a pathway involving fibroblast RAGE, and at least one interposed mediator, the growth factor EGF.

Amyloidosis↗

Aminoguanidine inhibits advanced glycation end products formation on beta2-microglobulin.

Because advanced glycation end products (AGE)-modified beta2-microglobulin (AGE-beta2M) is a dominant constituent of amyloid in dialysis-related amyloidosis (DRA), AGE-beta2M may be directly involved in the pathobiology of DRA. In experimental diabetes mellitus, blocking the formation of AGE prevents AGE-mediated tissue damage. In this study, it is postulated that similar pharmacologic intervention may be beneficial in DRA. Aminoguanidine, a nucleophilic hydrazine compound that prevents AGE formation on collagen, may have a similar effect on the advanced glycation of beta2M. To test this hypothesis, beta2M was incubated in vitro with 50 or 100 mM D-glucose for 3 wk in the presence and absence of incremental concentrations of aminoguanidine. On the basis of enzyme-linked immunosorbent assay and immunoblots using anti-AGE-keyhole limpet hemocyanin antibody, aminoguanidine inhibited glucose-induced N(epsilon)-(carboxymethyl)lysine formation on beta2M. At aminoguanidine-glucose molar ratios of 1:8 to 1:1, 26 to 53% inhibition occurred. Fluorospectrometry examination showed that aminoguanidine also inhibited the formation of fluorescent AGE on beta2M in a dose-dependent manner. At aminoguanidine-glucose molar ratios of 1:8 to 1:1, fluorescent product generation was inhibited by 30 to 70%. Furthermore, aminoguanidine suppressed the AGE formation on beta2M bound to AGE-modified collagen. If aminoguanidine is similarly active in vivo, this compound may be of clinical utility for treating DRA in patients on maintenance dialysis.

Analysis of Variance↗

Interaction between beta 2-microglobulin and advanced glycation end products in the development of dialysis related-amyloidosis.

Dialysis related amyloidosis (DRA) is a progressive debilitating complication of long-term dialysis. beta 2-microglobulin (beta 2m) amyloid deposition occurs preferentially in older patients and initially is located in collagen-rich osteo-articular tissues. Since an age-dependent increase in the formation of advanced glycation end products (AGE) has been observed in collagen-containing structures, we hypothesized that AGE-modified beta 2m in the amyloid of DRA may be formed locally in osteo-articular structures as a subsequent event of its binding to collagen-AGE. Based on this hypothesis, we investigated the binding between beta 2m and AGE-modified collagen (collagen-AGE) in vitro. Significantly larger amounts of human beta 2m were bound to types I to IV of immobilized collagen-AGE than to unmodified collagens (P < 0.0001). The quantity of beta 2m bound to collagen-AGE was dependent on the concentrations of both beta 2m and of AGE contained in collagen (P < 0.01). Unmodified beta 2m was more avidly bound to collagen-AGE or collagen in comparison to AGE-modified beta 2m (P < 0.0001). beta 2m bound to collagen-AGE could be modified further by nonenzymatic glycosylation during three weeks of incubation with physiologic concentrations of glucose. Similar processes in vivo may be important in the pathobiology of DRA.

Amyloidosis↗

Molecular cloning of the gene for human leukotriene C4 synthase. Organization, nucleotide sequence, and chromosomal localization to 5q35.

Leukotriene C4 (LTC4) synthase catalyzes the conjugation of LTA4 with reduced GSH to form LTC4, the parent of the receptor active cysteinyl leukotrienes implicated in the pathobiology of bronchial asthma. Previous cloning of the cDNA for human LTC4 synthase demonstrated significant homology of its amino acid sequence to that of 5-lipoxygenase activating protein (FLAP) but none to that of the GSH S-transferase super-family. Genomic cloning from a P1 library now reveals that the gene for LTC4 synthase contains five exons (ranging from 71 to 257 nucleotides in length) and four introns, which in total span 2.52 kilobase pairs in length. The intron/exon junctions of LTC4 synthase align identically with those of FLAP; however, the small size of the LTC4 synthase gene contrasts with the > 31-kilobase pair size reported for FLAP. Confirmation of the LTC4 synthase gene size to ensure that no deletions had occurred during the cloning was obtained by two overlapping polymerase chain reactions from genomic DNA, which provided products of the predicted sizes. Primer extension analysis with poly(A)+ RNA from culture-derived human eosinophilic granulocytes or the KG-1 myelogenous cell line revealed multiple transcriptional start sites with prominent signals at 66, 69, and 96 base pairs 5' of the ATG translation start site. The 5'-flanking region revealed a GC-rich promoter sequence consistent with an SP-1 site and consensus sequences for AP-1 and AP-2 enhancer elements, 24, 807, and 877 bp, respectively, 5' from the first transcription initiation site. Southern blot analysis of a genomic DNA (with full-length cDNA as well as 5' and 3' oligonucleotide probes) confirmed the size of the gene and indicated a single copy gene in normal human genomic DNA. Fluorescent in situ hybridization mapped LTC4 synthase to chromosomal location 5q35, which is in close proximity to the cluster of genes for cytokines and receptors involved in the regulation of cells central to allergic inflammation and implicated in bronchial asthma.

5-Lipoxygenase-Activating Proteins↗