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Biomedical subjects

G Wild

Publications and source records attributed to G Wild.

At least 19 recordsLinked to original sources

Direct fitness or inclusive fitness: how shall we model kin selection?

Two standard mathematical formulations of kin-selection models can be found. Inclusive fitness is an actor-centred approach, which calculates the fitness effect on a number of recipients of the behaviour of a single actor. Direct fitness is a recipient-centred approach, which calculates the fitness effect on the recipient of the behaviour of a number of actors. Inclusive fitness offers us a powerful heuristic, of choosing behaviour to maximize fitness, but direct fitness can be mathematically easier to work with and has recently emerged as the preferred approach of theoreticians. In this paper, we explore the fundamental connection between these two approaches in both homogeneous and class-structured populations, and we show that under simple assumptions (mainly fair meiosis and weak selection) they provide equivalent formulations, which correspond to the predictions of Price's equation for allele frequency change. We use a couple of examples to highlight differences in their conception and formulation, and we briefly discuss a two-species example in which we have a class of 'actor' that is never a 'recipient', which the standard direct fitness method can handle but the usual inclusive fitness cannot.

Biological Evolution↗

Cutaneous myiasis with Dermatobia hominis (human bot fly) larvae treated both conservatively and surgically.

A case is presented of infestation with the larvae of Dermatobia hominis (human bot fly). This case is unusual in that it provides an example of three different outcomes for separate lesions in the same patient; spontaneous resolution, conservative treatment and surgical intervention. It also illustrates that myiasis should be included in the differential diagnosis of any skin lesion of a patient returning from the tropics.

Adult↗

Do serum levels of eosinophil granule-derived protein change in patients undergoing pelvic radiotherapy?

AIMS: Eosinophils have an important role in the pathogenesis of inflammatory bowel disease, with faecal levels of the eosinophil granule proteins, eosinophil cationic protein (ECP) and eosinophil protein X (EPX) reflecting disease activity. Eosinophil crypt abscesses are a characteristic histological finding in acute gastrointestinal radiation-induced mucosal damage. This pilot study aimed to investigate changes in serum levels of ECP/EPX during pelvic radiotherapy. MATERIALS AND METHODS: Patients with no history of inflammatory bowel disease, starting a 5-week course of pelvic radiotherapy, had serum ECP/EPX levels measured before radiotherapy and during the fourth week of treatment. Bowel toxicity was graded at week 4 using the Common Toxicity Criteria Scale. RESULTS: Fifteen patients who were to undergo adjuvant radiotherapy for gynaecological cancer were recruited. The mean serum levels of ECP and EPX before treatment were 17.3 microg/l (range 2.0-49.3 microg/l) and 37.3 microg/l (range 12.0-94.0 microg/l), respectively. The mean serum levels during week 4 of radiotherapy for ECP and EPX were 43.0 microg/l (range 2.4-164.0 microg/l) and 38.7 microg/l (range 9.0-79.0 microg/l), respectively. Serum ECP levels increased at week 4 compared with levels before radiotherapy (P = 0.02). Acute bowel toxicity was seen in 12 patients (80%) at week 4: Grade 1 in 25% patients and Grade 2 in 75%. In this small study, no correlation was seen between acute bowel toxicity at week 4 and serum ECP or EPX levels. CONCLUSIONS: Serum ECP levels increase in response to pelvic irradiation. This may reflect the known involvement of eosinophils in the acute response to radiotherapy. Further study is required to determine when levels start to rise and their relationship to the degree of acute bowel toxicity.

Aged↗

Dietary lipids modify intestinal lipid-binding protein RNA abundance in diabetic and control rats.

BACKGROUND: Lipid-binding proteins have been identified in the enterocyte, including the cytosolic intestinal and liver fatty acid binding proteins (I-FABP and L-FABP, respectively) as well as the brush border membrane fatty acid transporter (FAT). It is unclear whether variations in the type of dietary lipids or diabetes modify the RNA abundance of these proteins. Diabetes is associated with an increased intestinal lipid uptake, and the lipid uptake is greater in rats fed a semisynthetic saturated fatty acid (SFA) as compared with a polyunsaturated fatty acid (PUFA) diet. METHODS: Male Sprague-Dawley rats were injected with streptozotocin or control vehicle and fed chow or either SFA or PUFA for 2 weeks. Northern blotting was performed on RNA isolated from jejunal and ileal tissues. RESULTS: In controls, feeding SFA as compared with PUFA reduced the jejunal abundance of I-FABP and L-FABP RNA. In diabetic rats, feeding SFA increased the ileal FAT RNA. Feeding PUFA reduced jejunal L-FABP and ileal FAT RNA in diabetic rats as compared with controls. CONCLUSIONS: The enhanced lipid uptakes reported with feeding an SFA diet or with diabetes were not associated with parallel alterations in lipid-binding proteins. We speculate that these lipid-binding proteins act as a storage mechanism for lipids in enterocytes and are not directly involved in lipid uptake.

Animals↗

Dietary lipids modify the age-associated changes in intestinal uptake of fructose in rats.

Because reduced nutrient absorption may contribute to malnourishment in the elderly, age and diet modulate fructose uptake in mice, and alterations in fructose uptake may be paralleled by changes in the abundance of fructose transporters, the objectives of this study were to determine 1) the effects of aging on fructose absorption in rats, 2) the effect of feeding diets enriched with saturated fatty acids (SFA) vs. polyunsaturated fatty acids (PUFA), and 3) the mechanisms of these age-and diet-associated changes. Male Fischer 344 rats aged 1, 9, and 24 mo received isocaloric diets enriched with SFA or PUFA. The uptake of (14)C-labeled D-fructose was determined in vitro using the intestinal sheet method. Northern and Western blot analyses and immunohistochemistry were used to determine the abundance of sodium-independent glucose and fructose transporters (GLUT)2 and GLUT5. When expressed on the basis of mucosal surface area, jejunal fructose uptake was increased in 9 and 24 mo compared with 1-mo-old animals fed SFA. PUFA-fed animals demonstrated increased fructose uptake at 24 mo compared with younger animals. Ileal fructose uptake was increased with SFA vs. PUFA in 9-mo-old rats but was reduced with SFA in 1- and 24-mo-old rats. Variations in GLUT2 and GLUT5 abundance did not parallel changes in uptake. These results indicate that 1) age increases fructose uptake when expressed on the basis of mucosal surface area, 2) age influences the adaptive response to dietary lipid modifications, and 3) alterations in fructose uptake are not explained by variations in GLUT2 or GLUT5.

Absorption↗

Elevated epsilon-(gamma-glutamyl)lysine in human diabetic nephropathy results from increased expression and cellular release of tissue transglutaminase.

INTRODUCTION: Diabetic nephropathy (DN) is the leading cause of chronic kidney failure, however the mechanisms underlying the characteristic expansion of the extracellular matrix (ECM) in diabetic kidneys remain controversial and unclear. In non-diabetic kidney scarring the protein crosslinking enzyme tissue transglutaminase (tTg) has been implicated in this process by the formation of increased epsilon-(gamma-glutamyl)lysine bonds between ECM components in both experimental and human disease. Studies in db+/db+ diabetic mice and in streptozotocin-treated rats have suggested a similar mechanism, although the relevance of this to human disease has not been addressed. METHODS: We have undertaken a retrospective analysis of renal biopsies from 16 DN patients with type 2 diabetes mellitus using an immunohistochemical and immunofluorescence approach, with tTg and epsilon-(gamma-glutamyl)lysine crosslink quantified by confocal microscopy. RESULTS: Immunofluorescent analysis of human biopsies (confocal microscopy) showed increases in levels of tTg (+1,266%, p < 0.001) and epsilon-(gamma-glutamyl)lysine (+486%, p < 0.001) in kidneys with DN compared to normal. Changes were predominantly in the extracellular periglomerular and peritubular areas. tTg staining correlated with epsilon-(gamma-glutamyl)lysine (r = 0.615, p < 0.01) and renal scarring (Masson's trichrome, r = 0.728, p < 0.001). Significant changes in epsilon-(gamma-glutamyl)lysine were also noted intracellularly in some (< or =5%) tubular epithelial cells. This is consistent with cells undergoing a novel transglutaminase-mediated cell death process in response to Ca2+ influx and subsequent activation of intracellular tTg. CONCLUSION: Changes in tTg and epsilon-(gamma-glutamyl)lysine occur in human DN. Cellular export of tTg may therefore be a factor in the perpetuation of DN by crosslinking and stabilisation of the ECM, while intracellular activation may lead to cell death contributing towards tubular atrophy.

Adolescent↗

The age-associated decline in the intestinal uptake of glucose is not accompanied by changes in the mRNA or protein abundance of SGLT1.

Studies performed using human and animal models offer conflicting results regarding the effect of age on nutrient absorption. The objectives of this study were to determine (1) the effects of aging on the in vitro uptake of glucose in rats; and (2) the molecular mechanisms of these age-associated changes. Male Fischer 344 rats aged 1, 9 and 24 months were fed a standard laboratory diet (PMI # 5001). The uptake of 14C-labelled D-glucose was determined in vitro using the intestinal sheet method. Northern blotting, Western blotting and immunohistochemistry were used to determine the effects of age on the BBM sodium-dependent glucose transporter, SGLT1, and the BLM Na+K(+)-ATPase. When expressed on the basis of intestinal weight, mucosal weight or surface area, there was a reduction in glucose uptake in the 24-month-old animals. SGLT1, GLUT2 and Na+K(+)-ATPase mRNA and protein abundance did not parallel the changes seen in glucose uptake. These results indicate that (1) age reduces in vitro intestinal glucose uptake in the rat; and (2) this age-associated decline in glucose uptake was not explained by alterations in SGLT1, GLUT2 or Na+K(+)-ATPase.

Aging↗

Feeding a polyunsaturated fatty acid diet prevents the age-associated decline in glucose uptake observed in rats fed a saturated diet.

The ability of the intestine to adapt to changes in environmental stimuli may be compromised with aging. Young animals fed saturated fatty acids (SFA) versus polyunsaturated fatty acids (PUFA) have an increased intestinal uptake of glucose. The objectives of this study were to determine (1) the effects of age on glucose uptake in rats; (2) the influence of feeding SFA versus PUFA; and (3) the mechanisms of these age- and diet-associated changes. Male Fischer 344 rats aged 1, 9 and 24 months received semi-purified isocaloric diets enriched with either SFA or PUFA. The uptake of 14C-labelled D-glucose was determined in vitro using the intestinal sheet method. Northern blotting, Western blotting and immunohistochemistry were used to determine the effects of age and diet on SGLT1, GLUT2 and Na(+)K(+)-ATPase. The mucosal surface area of the jejunum was reduced in 9 and 24 as compared with 1-month-old rats fed SFA. PUFA delayed this age-associated reduction in surface area. In SFA, the ileal uptake of glucose fell with age when expressed on the basis of intestinal or mucosal weight. Feeding PUFA prevented this decline. Alterations in glucose uptake were not paralleled by the changes in SGLT1, GLUT2 or Na(+)K(+)-ATPase abundance.

Aging↗

Adaptation following intestinal resection: mechanisms and signals.

The intestine has an inherent ability to adapt morphologically and functionally in response to internal and external environmental changes. The functional adaptations encompass modifications of the brush border membrane fluidity and permeability, as well as up- or down-regulation of carrier-mediated transport. Intestinal adaptation improves the nutritional status following the loss of a major portion of the small intestine, following chronic ingestion of ethanol, following sublethal doses of abdominal irradiation, in diabetes, in pregnancy and lactation, with ageing, and with fasting and malnutrition. Following intestinal resection, morphological and functional changes occur depending upon the extent of the intestine removed, the site studied, and the lipid content of the diet. Therefore, intestinal adaptation has important implications in the survival potential and welfare of the host. An understanding of the mechanisms of, and signals for, intestinal adaptation in the experimental setting forms the basis for the use of management strategies in humans with the short-bowel syndrome.

Animals↗

Dietary lipids alter the effect of steroids on the uptake of lipids following intestinal resection in rats.

Steroids alter the transport function of the intestine. This study was undertaken to assess the effect of glucocorticosteroids on lipid uptake in rats fed either a saturated (SFA) or a polyunsaturated fatty acid (PUFA) diet. Sprague-Dawley rats underwent transection or 50% resection of the small intestine. The steroids had no effect on the uptake of lipids. However, resection decreased the jejunal uptake of palmitic acid in animals fed SFA and increased the jejunal uptake of palmitic and linoleic acids in those fed PUFA. In animals undergoing intestinal resection, fed SFA, and given control vehicle, there was a reduction in jejunal proglucagon mRNA expression as compared to those fed chow or PUFA. Ornithine decarboxylase (ODC) mRNA expression in the jejunum of resected animals was reduced. In summary, dietary lipids modify the uptake of lipids in resected animals and ODC and proglucagon may be involved in this adaptive response.

Adaptation, Physiological↗

Early human renal allograft fibrosis: cellular mediators.

BACKGROUND: The development of early renal interstitial fibrosis (IF) in renal allografts is likely to depend on multiple factors. We studied retrospectively renal biopsies from cadaveric human renal allografts, transplanted from 1996 to 1998, with the intention of detecting early fibrotic changes and determining the underlying cellular mediators. We studied 23 transplant patients whose 46 renal biopsies were analysed, including a donor biopsy taken routinely at implantation from each patient and 23 follow-up biopsies, taken as clinically indicated over a period of 3 months following transplantation. METHODS: Histological evaluation of induction and progression of fibrosis relied on point count analysis of conventional (Masson's trichrome/MT) and immunohistochemical staining for collagen III and IV, and alpha-smooth muscle actin (alpha-SMA) as a marker of myofibroblast differentiation. Mast cells (MC) were counted in sections stained with an anti-human mast cells tryptase monoclonal antibody. Activated macrophages as well as total, helper and cytotoxic T-lymphocytes were identified on frozen sections by direct immunofluorescence using mouse anti-CD71, CD3, CD4 and CD8 antibodies respectively. Eosinophils (E) were counted in hematoxylin and eosin (HE)-stained sections. Changes in interstitial fibrosis (IF) scores were evaluated and correlated with myofibroblasts, MC, E and lympho-monocytic cells. RESULTS: We noted a significant increase in IF over a 3 months period following transplantation. There was also a significant increase in alpha-SMA+ cells, MC and E counts from implantation to follow-up biopsies. Similarly, there was a significant increase in interstitial infiltration by T-lymphocytes (modal category = 2 versus 0, p = 0.012) but not by macrophages. MC at implantation and follow-up were found to be predictive of IF (immunostainable collagen III) at follow-up (R(2) = 0.510, p = 0.023 and p = 0.030). Further, the predictive value for total T-lymphocyte infiltration at follow-up was also significant (R(2) = 0.617, p = 0.036). A strong correlation was found between alpha-SMA+ cells and MC counts at implantation (r = 0.7259, p < 0.001) and in follow-up biopsies (r = 0.5183, p < 0.01). However, there was no correlation between E counts and either alpha-SMA+ cells or MC either at implantation or in follow-up biopsies. Based on changes in interstitial immunostainable alpha-SMA, our patients were divided arbitrarily into 2 groups; group 1 (n = 12) with >100% increase in alpha-SMA and group 2 (n = 11) with <100% increase. Group 1 patients differed significantly from group 2 regarding the degree of MC infiltration at follow-up (t = 0.4519, p < 0.05) with the mean increase in MC count from implantation to follow-up biopsies being +5.1 cells/high power field (HPF) in group 1 and +0.8 cell/HPF in group 2 (p = 0.0237). MC counts in group 1 were associated with a higher modal category (greater than one) of cytotoxic: helper T-lymphocytes ratio compared to group 2 (2:1 versus 1:1 respectively). CONCLUSION: Multiple cells may contribute to early interstitial fibrosis in a subgroup of human renal allograft recipients with MC playing a major role.

Adult↗

Detection of serum M2 anti-mitochondrial antibodies by enzyme-linked immunosorbent assay is potentially less specific than by immunofluorescence.

AIM: To compare the predictive values of enzyme-linked immunosorbent assays (ELISAs) and indirect immunofluorescence (IIF) techniques for the detection of M2 anti-mitochondrial antibodies. METHODS: Commercial ELISAs are widely available for the detection of anti-mitochondrial antibody subtypes in primary biliary cirrhosis (PBC). We compared the results from two ELISAs (one recombinant, one purified antigen) with those from two IIF methods in a well-defined cohort of PBC patients and in patients with systemic lupus erythematosus, Sjögren's syndrome, sicca syndrome, systemic sclerosis, rheumatoid arthritis and blood donor controls. RESULTS: There was good correlation between a rodent substrate IIF and ELISA A (r=0.9134), but poor correlation with ELISA B (r=0.5999), which produced many false-positive results in the control population. We show that rodent IIF alone or human epithelial cell (HEp-2000) screening with confirmation by ELISA produce similar predictive values for PBC and require lesser degrees of skilled interpretation of IIF patterns. CONCLUSIONS: We conclude that the specificities of IIF are greater than the ELISA methods (99% versus 85-97%), although the ELISAs are slightly more sensitive in biopsy-proven PBC. Careful in-house validation of all new ELISA technologies is mandatory for good laboratory practice, but IIF in experienced hands remains an effective and specific assay.

Animals↗

Early progressive interstitial fibrosis in human renal allografts.

BACKGROUND: Early fibrosis has been described in renal allografts and implicated in the progression of chronic allograft nephropathy (CAN). The precise factors implicated in the initiation and progression of early allograft fibrosis remain uncertain. PATIENTS AND METHODS: We studied retrospectively 23 cadaveric renal allograft recipients over a 3-year period, who had paired renal biopsies (Bx) (at implantation and as clinically indicated) within 3 months of transplantation (Tx). Eight of them have progressed over an average period of 3.16 +/- 0.83 years to CAN. Histological evaluation of interstitial fibrosis (IF) relied on point count analysis of Masson's trichrome (MT) staining as well as immunostainable collagens III (iCol III) and IV (iCol IV). The severity of the IF scores was correlated with the clinical, biochemical and histological parameters. The nature and severity of the interstitial inflammatory infiltrate were also evaluated by immunofluorescence. In addition, patients were subdivided into those whose fibrosis progressed (> 50% increase in IF/iCol IlI; Group 1) and non-progressors (< 50% increase in fibrosis score; Group 2) in an attempt to determine discriminatory features. RESULTS: In the whole group, there was a significant increase in the IF score, as estimated by MT staining and iCol III, from implantation to follow-up Bx (p = 0.0027 and p = 0.0088, respectively). The changes in iCol IV were not significant. Further, the increase in interstitial inflammatory infiltrate of total T lymphocytes, and not of macrophages, from implantation (modal category = 2) to follow-up (modal category = 0) was significant (p = 0.0121). The predictive value of such increase was significant (R2 = 0.617, p = 0.03). The donor's age (R2 = 0.892, p = < 0.0001), death from cerebrovascular accident (CVA) (R2 = 0.822, p = 0.047), as well as recipient's body weight (R2 = 0.892, p = 0.001), male gender (R2 = 0.687, p = 0.041) and elevated mean arterial pressure (MAP) (R2 = 0.892, p = < 0.0001) were all significant risk factors for early IF. Delayed graft function (DGF) proved to be a significant predictor of early IF (R2 = 0.822, p = 0.003) and became more significant in the presence of superimposed acute rejection (AR) (p = 0.0001). Proteinuria > 1 g/day (R2 = 0.882, p = 0.004) and hypertriglyceridemia > 2.25 mmol/l (R2 = 0.808, p = < 0.0001) were also associated with early IF. Of the implantation histological parameters, iCol III proved to be a highly significant predictor of early IF (R2 = 0.892, p = < 0.0001). Interestingly, the predictive value of iCol III for graft survival in terms of CAN was significant (Cox p = 0.088). Group 1 progressor patients (n = 10) were all males (p = 0.038) and received their kidneys from donors who died from CVAs in 90% of cases (p = 0.011). They had, compared to non-progressors, a lower cyclosporin A level (p = 0.047), a higher incidence of AR episodes (80% versus 54%), a higher serum creatinine at 10 days post-Tx (p = 0.005), a higher proteinuria (2.07 +/- 3.89 g/l vs 0.96 +/- 0.97 g/l, p = 0.041) and a higher serum triglyceride (2.48 +/- 1.37 mmol/l vs 1.69 +/- 0.81 mmol/l, p = 0.039) level. 8% of Group 1 patients had DGF compared to 30% in Group 2 (p = 0.023). Of note, the modal category of cytotoxic: helper T lymphocytes ratio was greater than 1 in Group 1 (2:1) patients and not in Group 2 (1:1). CONCLUSION: Implantation histology, and in particular iCol III, is a predictor of early IF in a subgroup of patients with DGF and AR. Additional risk factors include hypertension, proteinuria and hypertriglyceridemia especially in patients receiving kidneys from older donors who died of CVAs.

Adult↗

Clinical, biological, and histologic parameters as predictors of relapse in ulcerative colitis.

BACKGROUND & AIMS: Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease. We aimed to assess whether clinical, biological, and histologic parameters in quiescent UC predict time to clinical relapse. METHODS: Seventy-four patients with clinically and endoscopically determined inactive UC were followed up for 1 year or for a shorter period if they had a relapse. Serum erythrocyte sedimentation rate; C-reactive protein, interleukin (IL)-1beta, IL-6, and IL-15 values; anti-neutrophil cytoplasmic antibody titers; and rectal biopsy specimens were obtained at baseline, at 6 and 12 months, and/or at relapse. Multivariate survival analysis was performed to determine independent predictors of clinical relapse. RESULTS: Twenty-seven patients relapsed (19/42 women; 8/32 men). Multivariate Cox regression analysis retained younger age (P = 0.003; hazard ratio, 0.4 per decade), greater number of prior relapses in women (P < 0.001; hazard ratio, 1.6 per prior relapse), and basal plasmacytosis (P = 0.003; hazard ratio, 4.5) on rectal biopsy specimens as predictors of shorter time to clinical relapse. Kaplan-Meier survival curves showed the 20-30-year-old age group and women with more than 5 prior relapses to be groups with shorter times to relapse. CONCLUSIONS: Younger age, multiple previous relapses (for women), and basal plasmacytosis on rectal biopsy specimens were independent predictors of earlier relapse. These findings may help identify patients with inactive UC who will require optimal maintenance medical therapy.

Adult↗

Small bowel review: Part II.

In the past year, there have been many advances in the area of small bowel physiology and pathology. In preparation for this review, over 1500 papers were assessed. Some have been selected and reviewed, with a particular focus on presenting clinically useful information for the practising gastroenterologist. Relevant review articles have been highlighted, and important clinical learning points have been stressed. The topics are varied in scope and wherever possible show a logical progression from basic physiology to pathophysiology to clinical disorders and management.

Adaptation, Physiological↗

Infliximab for the treatment of Crohn's disease: efficacy, safety and pharmacoeconomics.

Crohn's disease is a chronic inflammatory disorder of the gastrointestinal tract. From the perspective of the patient, symptoms of the disease significantly impair quality of life and interfere with activities of daily living. Conventional medical treatment of Crohn's disease includes the use of nonspecific anti-inflammatory drugs, immunosuppressives and antibiotics. These therapies are characterized by a delayed onset of action, incomplete response rates and a substantial risk of adverse effects. Although surgery is frequently used to treat complications, postoperative recurrence is an important problem. Infliximab, a chimeric monoclonal antibody directed toward tumour necrosis factor alpha, is highly effective for the treatment of active Crohn's disease. In randomized, placebo-controlled clinical trials, 82% of patients who received 5 mg/kg of infliximab had a clinically significant response, compared with 17% of those given placebo (P<0.001). Moreover, infliximab is the only medical therapy that has been shown to be effective for the treatment of fistulizing Crohn's disease. Infusion reactions are the most common adverse effect. Whether treatment with infliximab is associated with an increased risk of neoplasia, infection or autoimmune disease is unknown. Therefore, further long term safety studies are required. Despite the relatively high cost of drug acquisition, preliminary pharmacoeconomic analysis indicates that infliximab is cost effective compared with existing treatments. Infliximab is recommended for the treatment of active Crohn's disease refractory to conventional drugs, and is the treatment of choice for fistulizing Crohn's disease.

Antibodies, Monoclonal↗