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Biomedical subjects

W Babidge

Publications and source records attributed to W Babidge.

12 recordsLinked to original sources
PubMed2005

Predictors of success following endovascular aneurysm repair: mid-term results.

OBJECTIVE: Australian cases of endovascular aneurysm repair (EVAR) performed between 1999 and 2001 have been evaluated to determine the mid-term (6 months to 5 years) safety and efficacy of the procedure. This study looks at predictors of success, based on mid-term follow-up data. DESIGN OF STUDY: This study uses results obtained from a prospective semi-voluntary register (audit) of Australian data obtained from surgeons in the private and public sector. RESULTS: Peri-operative mortality for patients enrolled in the audit was 1.8%. Ninety-three percent of procedures were technically successful (890/961). Nearly 13% of patients have had re-interventions (mostly endoluminal) at follow-up. Analysis of audit data shows that the likelihood of experiencing post-operative complications or requiring additional procedures increases with ASA rating, increasing age, large pre-operative aneurysm size, aneurysm angle >45 degrees and number of co-morbid conditions diagnosed. CONCLUSIONS: This study confirms satisfactory mid-term results in a, national rather than unit specific, setting. Predictors of clinical failure or need for re-intervention include large aneurysm size, neck angulation >or=45 degrees and short infrarenal neck.

Aged↗
PubMed2004

Endoluminal repair of abdominal aortic aneurysm-contemporary Australian experience.

OBJECTIVE: An audit was established in November 1999 by the Australian Government Department of Health and Ageing to determine the mid- to long-term safety and efficacy of endoluminal graft repair (ELG) of abdominal aortic aneurysm (AAA). The audit has been undertaken by the Australian Safety and Efficacy Register for New Interventional Procedures-Surgical (ASERNIP-S). This study reviews contemporary Australian practice, based on audit data supplied to ASERNIP-S. DESIGN OF STUDY: This study is a prospective voluntary register (audit) of Australian data obtained from the private and public sector. Data were collected for ELG repairs performed between 1 November 1999 and 16 May 2001. Follow-up is continuing. Results. Seventy-nine vascular surgeons have contributed data on 950 patients (816 male, 134 female, of median age 75.5 (range 36-94)). The mean aneurysm size was 57.5 mm (+/-10.2) and 44% of procedures were performed on aneurysms less than 55 mm in diameter. Fifty four percent of patients were considered suitable for open repair. Most ELG procedures were performed in an angiography or endovascular suite, under general anaesthetic using an open technique via the femoral arteries. Perioperative mortality was 1.7%, mostly from cardiac causes. Prior to discharge 7.2% of patients experienced an endoleak and 18.6% had systemic complications. The average length of stay was 7.4 days (median 5 days). Unsuccessful exclusion of the aneurysm occurred in 6.7% of cases. CONCLUSIONS: Endovascular repair of AAAs is a well accepted procedure and is performed by the majority of vascular surgeons in Australia. Australian surgeons are taking a rather aggressive approach to the management of aortic aneurysms, particularly in the moderate to higher risk patient groups. Mortality rates are low, given the elderly population in question and morbidity rates acceptable. ASERNIP-S is continuing to collect follow-up data for this patient cohort.

Aged↗
PubMed2001

Ultrasound-assisted lipoplasty.

BACKGROUND: Ultrasound-assisted lipoplasty (UAL) has been associated with particular types of complications and uncertain long-term effects arising from interactions between ultrasonic energy and living tissue. The present review seeks to address these issues. METHODS: Search strategy Three search strategies were devised to retrieve literature from Medline, Current Contents, Embase and Cochrane Library databases up until April 2000. Study selection Inclusion of papers was largely determined using a predetermined protocol. English language papers were selected. Acceptable study designs included randomized controlled trials, controlled clinical trials, case series or case reports. Data collection and analysis Thirty-six papers met the inclusion criteria. They were tabulated and critically appraised in terms of methodology and design, outcomes, and the possible influence of bias, confounding and chance. Other papers were also included to provide background material. RESULTS: There was little high-level evidence available comparing UAL and suction-assisted lipoplasty (SAL), with no conclusive evidence that UAL has a safety benefit, although low-quality evidence suggests that UAL is associated with reduced surgeon fatigue as well as increased operating times, slower aspiration rates and an increased learning curve. There is inadequate evidence to determine whether the theoretical potential for DNA damage from ultrasound is realized in the clinical setting. CONCLUSIONS: The evidence base for UAL is inadequate to determine the procedure's safety and efficacy. The potential for DNA damage must be investigated with appropriate in vivo animal models. Recommendations for the safe use of UAL are discussed.

Adipose Tissue↗
PubMed2000

Evidence-based surgery at ASERNIP-S. Can this improve quality in surgical practice? Australian Safety and Efficacy Register of New Interventional Procedures-Surgical.

The Australian Safety and Efficacy Register of New Interventional Procedures-Surgical (ASERNIP-S) project has been established to form a register of new surgical procedures which have been assessed for their safety and efficacy. The ASERNIP-S project systematically reviews the evidence and produces recommendations on the future use of surgical procedures in clinical practice. Further data may be collected to provide information on the outcomes of procedures in use in Australia. Horizon Scanning of new and emerging techniques and technologies complements the ASERNIP-S process. This research identifies procedures that will impact on clinical practice in the near future. Dissemination of information from ASERNIP-S assessments, both locally and internationally, is important for quality improvement. The ultimate aim is for appropriate changes in practice to ensure the highest quality of Australian healthcare.

Australia↗
PubMed1998

Sulfides impair short chain fatty acid beta-oxidation at acyl-CoA dehydrogenase level in colonocytes: implications for ulcerative colitis.

The disease process of ulcerative colitis (UC) is associated with a block in beta-oxidation of short chain fatty acid in colonic epithelial cells which can be reproduced by exposure of cells to sulfides. The aim of the current work was to assess the level in the beta-oxidation pathway at which sulfides might be inhibitory in human colonocytes. Isolated human colonocytes from cases without colitis (n = 12) were exposed to sulfide (1.5 mM) in the presence or absence of exogenous CoA and ATP. Short chain acyl-CoA esters were measured by a high performance liquid chromatographic assay. 14CO2 generation was measured from [1-14C]butyrate and [6-14C]glucose. 14CO2 from butyrate was significantly reduced (p < 0.001) by sulfide. When colonocytes were incubated with hydrogen sulfide in the presence of CoA and ATP, butyryl-CoA concentration was increased (p < 0.01), while crotonyl-CoA (p < 0.01) and acetyl-CoA (p < 0.01) concentrations were decreased. These results show that sulfides inhibit short chain acyl-CoA dehydrogenase. As oxidation of n-butyrate governs the epithelial barrier function of colonocytes the functional activity of short chain acyl-CoA dehydrogenase may be critical in maintaining colonic mucosal integrity. Maintaining the functional activity of dehydrogenases could be an important determinant in the expression of ulcerative colitis.

Acyl Coenzyme A↗
PubMed1998

Colonic luminal hydrogen sulfide is not elevated in ulcerative colitis.

It has been proposed that the reduction in n-butyrate oxidation by colonic epithelial cells observed in ulcerative colitis may be related to exposure to reduced forms of sulfur derived from dissimilatory sulfate reduction by luminal microflora. This study aims to compare stool sulfide concentrations in control and colitic subjects. Control subjects had significant colorectal disease excluded by virtue of their selection. Patients with ulcerative colitis were stratified by disease extent and activity, and by salicylate drug use. Stool sulfide was measured using a direct spectrophotometric method on NaOH (free sulfide) and zinc acetate (total sulfide) stool slurries. Fifteen control and 19 colitic subjects were studied. There was no significant difference in stool sulfide between control and colitic patients (free sulfide, control = 0.52 (0.17), colitic = 0.45 (0.10), t = 0.36, P = 0.71, total sulfide, control = 1.33 (0.21), colitic = 0.96 (0.15), t = 1.44, P = 0.16). Disease extent or activity did not significantly influence stool sulfide. These results do not support a primary etiologic role for luminal sulfide in ulcerative colitis.

Colitis, Ulcerative↗
PubMed1997

Colonic sulfide in pathogenesis and treatment of ulcerative colitis.

A role for colonic sulfide in the pathogenesis and treatment of ulcerative colitis (UC) has emerged based on biochemical, microbiological, nutritional, toxicological, epidemiological, and therapeutic evidence. Metabolism of isolated colonic epithelial cells has indicated that the bacterial short-chain fatty acid n-butyrate maintains the epithelial barrier and that sulfides can inhibit oxidation of n-butyrate analogous to that observed in active UC. Sulfur for fermentation in the colon is essential for n-butyrate formation and sulfidogenesis aids disposal of colonic hydrogen produced by bacteria. The numbers of sulfate-reducing bacteria and sulfidogenesis is greater in UC than control cases. Sulfide is mainly detoxified by methylation in colonic epithelial cells and circulating red blood cells. The enzyme activity of sulfide methylation is higher in red blood cells of UC patients than control cases. Patients with UC ingest more protein and thereby sulfur amino acids than control subjects. Removing foods rich in sulfur amino acids (milk, eggs, cheese) has proven therapeutic benefits in UC. 5-Amino salicylic acid reduces fermentative production of hydrogen sulfide by colonic bacteria, and aminoglycosides, which inhibit sulfate-reducing bacteria, are of therapeutic benefit in active UC. Methyl-donating agents are a category of drugs of potential therapeutic use in UC. A correlation between sulfide production and mucosal immune responses in UC needs to be undertaken. Control of sulfidogenesis and sulfide detoxification may be important in the disease process of UC, although whether their roles is in an initiating or promoting capacity has yet to be determined.

Bacteria↗
PubMed1997

Hydrogen sulphide produces diminished fatty acid oxidation in the rat colon in vivo: implications for ulcerative colitis.

BACKGROUND: Several lines of evidence suggest a possible role for reduced forms of sulphur (including sulphide) in ulcerative colitis. The aims of this study were to assess the metabolic profile of colonic epithelial cells after treatment in vivo with hydrogen sulphide and correlate this with mucosal histological appearances. METHODS: Adult Sprague-Dawley rats had antegrade Roux-en-Y colostomies fashioned to allow access to the 'in-flow' bowel. Animals were treated with 2 mL sodium hydrosulphide (10, 20, 30 mmol/L) or saline control twice daily via the stoma for four (acute experiments) and 90 (chronic experiments) days. Isolated colonic epithelial cell suspensions prepared from such animals were incubated in the presence of [1-14C]-labelled n-butyrate (5 mmol/L) or [6-14C]glucose (5 mmol/L). Metabolic performance was measured radiometrically (14CO2 production) and enzymatically (ketone body production and lactogenesis). The histological appearances of treated mucosa were scored for acute inflammatory changes. RESULTS: There was a highly significant reduction in 14CO2 production from both n-butyrate and glucose in all groups compared to the control in both acute and chronic experiments. There was no difference between groups with respect to histological appearance and no evidence of acute inflammation in any specimen. CONCLUSIONS: Sodium hydrosulphide impairs rat colonic epithelial metabolic performance in vivo, but does not produce mucosal inflammation.

Animals↗
PubMed1997

Effect of sulphide on short chain acyl-CoA metabolism in rat colonocytes.

BACKGROUND: It has been proposed that the diminished n-butyrate oxidation observed in ulcerative colitis may be the result of sulphide induced inhibition of short chain acyl-coenzyme A (acyl-CoA) dehydrogenase activity. AIM: To examine the acyl-CoA ester profiles in isolated rat colonic epithelial cells treated in vitro with sodium hydrogen sulphide (NaHS). METHODS: Isolated rat colonic epithelial cell suspensions were incubated for 10 minutes in the presence of [1-14C] n-butyrate (5 mM), with and without NaHS (1.5 mM). Incubations were carried out both in the presence and the absence of exogenous CoA and ATP. Metabolic performance was assessed by 14CO2 production and by acyl-CoA ester production measured by HPLC with ultraviolet detection. RESULTS: Results are given as mean (SEM). For colonocytes incubated in the presence of exogenous CoA and ATP, treatment with NaHS significantly diminished 14CO2 production (control 0.97 (0.06) mumol/g dry weight cells/min, treated 0.26 (0.09) mumol/g dry weight cells/min, p = 0.0019), was associated with an increase in butyryl-CoA concentrations in the final reaction mixture at 10 minutes (control 2.55 (0.28) mumol/g dry weight cells, treated 3.32 (0.32) mumol/g dry weight cells, p = 0.002), and a reduction in crotonyl-CoA concentrations (control 0.274 (0.02) mumol/g dry weight cells, treated 0.120 (0.04) mumol/g dry weight cells, p = 0.008). The mean concentration of acetyl-CoA in the reaction mixture at 10 minutes was not significantly different between control and sulphide treated incubations. There were no significant differences in acyl-CoA ester profiles observed when cells were incubated in the absence of exogenous CoA and ATP. CONCLUSIONS: These results support the view that sulphides inhibit n-butyrate oxidation in colonic epithelial cells by inhibiting short chain acyl dehydrogenation of activated fatty acids.

Acyl Coenzyme A↗
PubMed1996

Methionine derivatives diminish sulphide damage to colonocytes--implications for ulcerative colitis.

BACKGROUND: Bacterial production of anionic sulphide is increased in the colon of ulcerative colitis and sulphides can cause metabolic damage to colonocytes. AIMS: To assess the reversal of the damaging effect of sulphide to isolated colonocytes by methionine and methionine derivatives. METHODS AND SUBJECTS: Isolated colonocytes were prepared from rat colons and 12 human colectomy specimens. In cell suspensions 14CO2/acetoacetate generation was measured from [1-14C]-butyrate (5.0 mmol/l) in the presence of 0-2.0 mmol/l sodium hydrogen sulphide. The effect of 5.0 mmol/l L-methionine, S-adenosylmethionine 1,4 butane disulphonate and DL-methionine-S-methylsulphonium chloride on sulphide inhibited oxidation was observed. RESULTS: In rat colonocytes sodium hydrogen sulphide dose dependently reduced oxidative metabolite formation from n-butyrate, an action reversed in order of efficacy by S-adenosylmethionine 1,4 butane disulphonate > DLmethionine-S-methyl-sulphonium chloride > L-methionine. In human colonocytes S-adenosylmethionine 1,4 butane disulphonate most significantly improved 14CO2 production (p = < 0.005) suppressed by sodium hydrogen sulphide. CONCLUSION: Sulphide toxicity in colonocytes is reversible by methyl donors. The efficiency of sulphide detoxification may be an important factor in the pathogenesis and treatment of ulcerative colitis for which S-adenosylmethionine 1,4 butane disulphonate may be of therapeutic value.

Acetamides↗