bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bacterial lipoprotein delays neutrophil apoptosis via a CD14-independent pathway
Authors: Power C , Wang J H , Blankson S , Kirwan W O , Redmond H P 
Published: December 2004

Abstract

Background
Lipopolysaccharide (LPS) is considered the most potent exogenous mediator of the systemic inflammatory response syndrome (SIRS) which results, in part, from delayed neutrophil (PMN) apoptosis. The effects of another ubiquitous bacterial component, bacterial lipoprotein (BLP), the most abundant protein in the cell wall of all bacteria, on PMN apoptosis are unknown. The potential role of BLP in the regulation of PMN apoptosis was investigated and these effects were compared with those of LPS.

Methods
PMNs from healthy volunteers were isolated and exposed to identical concentrations of LPS and BLP in the presence or absence of recombinant antihuman CD14 monoclonal antibody. PMN apoptosis was assessed 6 hourly using Annexin V–propidium iodide staining and confirmed on cell morphology. PNM activation was assessed flow cytometrically using expression of functional markers CD11b and CD18.

Results
BLP significantly delayed PMN apoptosis and upregulated PMN adhesion receptor expression compared with control values. The effects seen were markedly similar to those of LPS.

Conclusion
BLP is capable of upregulating PMN adhesion receptor expression and delaying PMN apoptosis in a time- and dose-dependent manner independent of CD14. The potency, and the effects mediated by, BLP are very similar to those of LPS. This identifies BLP as a putative mediator of SIRS and demands that due attention be paid to other bacterial products in the investigation and treatment of septic states.
Requirement for fungal prophylaxis in high-risk surgical patients: a randomized trial
Authors: Emparan C , Diaz-Aguirregoitia J , Iturburu I , Perdigo L F 
Published: December 2004

Abstract

Background
In previous studies the authors have selected patients and surgical procedures with a high risk of fungal infection. Whether these patients and procedures require fungal prophylaxis was studied.

Methods
From June to December 1999, 850 surgical patients from two university hospitals were enrolled in a prospective open randomized study. Fifty were selected according to demographics (age, sex, co-morbidity) and surgical procedures (defined by GDRs and ICD9-CM) as at high risk of fungal infection according to a previously defined algorithm (presented to the Surgical Infection Society of Europe 1999). In these 50 patients the CD lymphocyte population was recollected, and urine, blood, sputum and wound (if infected) cultures were performed. Then, 25 were treated with nystatin wash and swallow, and the others with placebo. Fungal infection and fungal colonization were defined and used as the endpoint of the study.

Results
Patients not selected for the study did not develop fungal infection. Of the high-risk patients, 20 presented with fungal colonization (12 urine, seven wound and five bloodstream cultures) and 12 presented with subsequent fungal infections. Of these 20 colonized patients, only those with nystatin prophylaxis did not require fungal treatment, whereas controls required treatment. CD4 lymphocyte recount (below 300) was uniformly decreased in all patients with fungal infection.

Conclusion
Immunodepressed patients at high risk with concomitant fungal colonization develop fungal infections 2–5 days after high-risk surgical procedures. Nystatin prophylaxis in such patients may reduce the degree and severity of fungal infection. If fungal colonization is present and the CD4 lymphocyte count is below 300, fungal treatment might be advisable.
Antivascular endothelial growth factor therapy prevents peritoneal adhesion formation without adversely affecting wound strength or anastomotic integrity
Authors: Sookhai S , Wang J , Austin K , Maguire D , Blankson S , Kirwan W O , Redmond H P 
Published: December 2004

Abstract

Background
Postoperative intra-abdominal adhesion formation remains a significant cause of complications in surgical patients. To date, no agent has been shown consistently to block adhesion formation; preliminary evidence has shown that intra-abdominal adhesion formation is angiogenesis dependent. Vascular endothelial growth factor (VEGF) is a potent stimulator of angiogenesis and promotes vascular leakage. This study determined whether a specific VEGF monoclonal antibody (mAb) could prevent postoperative adhesion formation without affecting wound and anastomotic integrity.

Methods
After developing a standardized peritoneal injury which resulted in a reproducible adhesion model, 40 CD-1 mice were randomized and treated intraperitoneally with either VEGF mAb (n = 20) or immunoglobulin (Ig) G isotype control mAb (n = 20) at the time of abdominal closure. Animals (n = 10 per group) were killed on postoperative day 14, and the development of intra-abdominal adhesions was determined and graded blindly using well established criteria. Animals (n = 10 per group) were also killed 10 days after operation, and laparotomy wounds and gastrointestinal anastomoses were assessed by tensiometry. Statistical analyses were performed using the Mann–Whitney and Fisher's exact tests.

Results
Treatment with VEGF mAb resulted in a significantly lower incidence of adhesion formation compared with control animals (P &lt; 0·001). Furthermore, intergroup analysis for the presence of marked adhesions (grade 2 or 3) demonstrated that mice treated with VEGF mAb had a significantly lower incidence of advanced adhesions compared with controls (10 versus 90 per cent). Laparotomy wound and gastrointestinal anastomotic strength were similar between groups.

Conclusion
This study demonstrates that the formation of postoperative intra-abdominal adhesions is attenuated following the administration of VEGF mAb without adversely affecting wound strength or anastomotic integrity.
Standardized infection ratio: the next generation of risk-adjusted wound infection measures
Authors: Gustafson T L , Haley R W 
Published: December 2004

Abstract

Background
The scientific literature overwhelmingly supports the value of surgical site infection (SSI) surveillance with feedback of infection rates to surgeons. Recognizing that feedback has little value without some form of adjustment for patient factors, surgeons long ago developed the four-level wound classification system. In the 1980s the SENIC multivariate risk index was introduced, followed by the National Nosocomial Infection Surveillance multivariate risk index which is the currently recommended US standard.

Methods
To address recent advances in surgical technology, ambulatory surgery, and differences between the USA and other countries, newer risk-adjustment methods were explored. The ideal approach would overcome the following common practical problems encountered in generating SSI rates such as: (1) new patient-level risk factors, (2) technology-specific factors, (3) small monthly denominators and (4) postdischarge surveillance. Despite increased mathematical complexity, an acceptable risk-adjustment technique must still provide easily interpretable results.

Results
The standardized infection ratio (SIR) is proposed as the next generation in epidemiological approaches for monitoring and feeding back risk-adjusted SSI rates to surgeons. The SIR is a single monthly number for each surgeon, calculated by dividing the observed number of SSIs by the expected number predicted from a complex statistical model of patient-level and technology-specific risk factors. Like the well known standardized mortality ratio, the SIR offers the advantage of providing one generalizable quality index regardless of the mix of operations performed. In addition, the SIR is well suited to control chart techniques and for providing valid interhospital comparisons.

Conclusion
The SIR model offers simple data input and easily interpretable output suitable for application in all healthcare settings worldwide.
Renal arginine synthesis is impaired after experimental ischaemia–reperfusion
Authors: Prins H A , Nijveldt R J , Rauwerda J A , van Lambalgen A A , Teerlink T , van Leeuwen P A M 
Published: December 2004

Abstract

Background
Endogenous arginine synthesis is important for maintaining normal plasma levels of arginine. Recently it was shown that low plasma levels of arginine are the drive for renal arginine synthesis. In chronic renal insufficiency low plasma levels of arginine are common. To evaluate renal arginine synthesis in acute renal injury, as seen after periods of ischaemia during major vascular surgery, ischaemia–reperfusion of one kidney was performed in a rat model.

Methods
In this model of unilateral renal ischaemia–reperfusion male Wistar rats were used. Arginase infusion (ASE) was used to lower arginine plasma levels to 50 per cent of normal and control rats received saline infusion (SAL). After an ischaemic period of 90 min, the kidney was perfused for 150 min (IR kidney). The contralateral kidney was left in situ and served as a control (CL kidney). Blood flow measurement was performed at the end of the experiment using radiolabelled microspheres. Blood samples were taken for amino acid analysis (high-pressure liquid chromatography). Uptake or release of arginine (flux) was calculated from flow and the arteriovenous concentration difference.

Results
Infusion of arginase efficiently decreased arginine plasma levels (ASE: mean(s.d.) 45·3(4·8) μmol/dm3 versus SAL: 107·5(6·0); P &lt; 0·0001). In SAL rats, in both IR and CL kidneys a net uptake of arginine was observed (arginine flux CL kidney: + 12·5(4·9), IR kidney: + 23·6(5·8) μmol/dm3; P not significant). Lowering arginine plasma levels by arginase resulted in production of arginine in the (non-ischaemic) CL kidney. In contrast, in the IR kidney a net uptake of arginine was seen (arginine flux CL kidney: − 5·3(2·2) μmol/dm3, IR kidney: + 10·3(3·7) μmol/dm3; P &lt; 0·01).

Conclusion
Synthesis of arginine by the kidney was impaired after a period of acute ischaemia–reperfusion. Ischaemia–reperfusion injury of the kidney is a condition often seen after major vascular reconstruction and impaired arginine synthesis might limit substrate for the l-arginine nitric oxide pathway.
Tumour necrosis factor α and interleukin 1β mediate lipopolysaccharide-induced endothelial monolayer permeability in whole blood
Authors: Nooteboom A , Hendriks T , van der Linden C J 
Published: December 2004

Abstract

Background
Overproduction of cytokines may be responsible for irreversible and systemic vascular damage observed among patients suffering from the sepsis syndrome. The resultant excessive fluid loss from the circulation may cause tissue hypoperfusion, organ failure and death. A whole blood assay and an in vitro endothelial model have been used to simulate permeability changes during the acute phase of Gram-negative infection.

Methods
Freshly drawn heparinized human blood from healthy volunteers was treated with bacterial lipopolysaccharide (LPS; Escherichia coli B55: 05). Plasma was then collected and incubated on human umbilical vein endothelial cell (HUVEC) monolayers cultured on semipermeable Transwell COL membranes. The permeability of the monolayers was determined using fluorescein isothiocyanate (FITC) albumin and rhodamine-β-isothiocyanate (RITC) dextran. The production of tumour necrosis factor (TNF) α and interleukin (IL) 1β in whole blood was measured using radioimmunossay.

Results
Incubation of whole blood with as little as 10 pg ml−1 LPS was sufficient to yield plasma that significantly increased endothelial permeability. This effect was dose dependent up to 10 ng ml−1 LPS, at which the permeability exceeded about seven times the permeability of control monolayers. In contrast, significant stimulation of endothelial permeability by LPS alone (i.e. without prior incubation in blood) required more than 50 ng ml−1 LPS. The effect of LPS pretreatment on endothelial permeability was also time dependent: at least 2–4 h of LPS preincubation was required, while maximum permeability was reached at longer preincubations (8–24 h). At these amounts and incubation times LPS was also capable of inducing TNF-α and IL-1β in whole blood. When antibodies directed against TNF-α and IL-1β were added to LPS-conditioned plasma before incubation on HUVEC monolayers the permeability increase was partly inhibited. However, almost complete inhibition was achieved when anti-TNF-α and anti-IL-1β were both added to LPS-conditioned plasma. Similar effects of LPS-conditioned plasma and anti-TNF-α and anti-IL-1β treatment were observed on the expression of E-selectin and intracellular adhesion molecule 1 by endothelial cells.

Conclusion
Whole blood potentiates the inflammatory response of endothelial cells to physiologically relevant doses of LPS. This potentiation is achieved by the production of both TNF-α and IL-1β. If this in vitro endothelial model represents the events observed in patients suffering from Gram-negative sepsis, these data indicate that protection requires simultaneous administration of inhibitors to TNF-α and IL-1β.
Determination of 2-keto-3-deoxyoctanate: a simple method for the quantitative comparison of cytokine induction by meningococcal lipopolysaccharide and that of other bacteria
Authors: Sprong T , van der Ley P , van der Meer J W M , van Deuren M 
Published: December 2004

Abstract

Background
Lipopolysaccharide (LPS), or endotoxin, is considered to be the toxic element in Gram-negative septic shock. There is increasing evidence that the pathogenic properties of LPS differ from species to species but, to date, exact comparison between the biological activities of LPS has been difficult.

Methods
With the aim of quantitatively comparing the cytokine-inducing capacities of Neisseria meningitidis LPS and Escherichia coli LPS in human peripheral blood mononuclear cells on a molar basis, 2-keto-3-deoxyoctanate (KDO) spectrophotometry was used.

Results
Since the KDO region of LPS is a preserved part of the LPS molecule, unlike the saccharide tail, and the molecular weight of this region is known, KDO measurement can provide accurate information about the molarity of an LPS suspension. On a molar basis, the cytokine-inducing capacity of meningococcal LPS was at least ten times higher than that of E. coli LPS.

Conclusion
KDO spectrophotometry is a simple method of making a quantitative comparison between the biological effects of different endotoxins. N. meningitidis LPS is a more potent inducer of cytokine production than E. coli LPS. This may, in part, explain the more fulminant course of meningococcal sepsis compared with E. coli sepsis.
Aneurysm-related mortality during late follow-up after endovascular aneurysm repair of infrarenal aorta
Authors: Vallabhaneni S R , Harris P L , Gilling-Smith G L , Laheij R 
Published: December 2004

Abstract

Background
Aneurysm-related mortality (ARM) accounts for around 1·5 per cent of all deaths following open aneurysm repair. The incidence of ARM following endovascular aneurysm repair (EVAR) is unknown. The aim was to examine all causes of death, including ARM, during late follow-up after EVAR. ARM was defined as death resulting directly from rupture of the repaired aneurysm or another complication of the aneurysm, more than 30 days after repair, or death within 30 days of a secondary intervention undertaken solely to rectify a complication of repair.

Methods
Preoperative and follow-up data on 2194 patients from 88 European centres were collected prospectively on to a database. Survival up to 48 months after EVAR was analysed by means of Kaplan–Meier survival analysis. The causes of death during this period were noted.

Results
There were 161 deaths between 1 and 48 months after EVAR. The cumulative rate of secondary intervention for this cohort at 4 years was 33 per cent. The causes of death were: cardiac 28·6 per cent, malignancy 18·6 per cent, cerebrovascular 6·8 per cent, respiratory 3·1 per cent, renal 1·8 per cent, other 22·3 per cent and ARM 11·8 per cent. There were 19 deaths from aneurysm-related causes. Nine patients died following proven rupture of the aneurysm, three died from presumed rupture of the aneurysm and a further seven died following late conversion (three patients), graft sepsis (two) and secondary intervention (two). Sudden death of uncertain cause occurred in ten patients in whom rupture of AAA was a possibility.

Conclusion
Non-aneurysm-related causes of death were comparable to those in published reports of survival after open repair. However, the proportion of aneurysm-related deaths (11·8 per cent) was appreciably higher than that reported after open repair. These results may reflect the learning curve experience of the teams involved in the study, but continued caution is advisable regarding expectations of outcome following EVAR.
Chronic venous insufficiency in the general population: clinical and duplex correlations
Authors: Ruckley C V , Evans C J , Allan P L , Lee A J , Fowkes F G R 
Published: December 2004

Abstract

Background
If operations for chronic venous insufficiency (CVI) are to be rational and cost effective, the natural history needs to be understood and patients with early disease who will progress to advanced CVI and leg ulcer need to be identified. Published data have derived largely from selected referred hospital patients. The pattern of venous disease in the general population is unknown. The aim was to determine the prevalence of CVI in the general population and to correlate clinical features with the findings on duplex ultrasonography.

Methods
A cross-section of men and women aged 18–64 years randomly selected from 12 general practices were surveyed. Subjects were screened by questionnaire, examination, photography, blood tests and continuous-wave Doppler ultrasonography. Eight segments of the deep and superficial veins were assessed for reflux by means of duplex ultrasonography.

Results
Some 1566 patients were screened (867 women of mean age 44·8 years and 699 men of mean age 45·8 years), of whom 134 were diagnosed as having CVI (Basle classification): grade 1, 95; grade 2, 19; grade 3, ten. The age-adjusted prevalence for the whole series was 3·1 per cent (2·6 per cent in men, 3·4 per cent in women). The prevalence of CVI correlated closely with age, being 15·2 per cent in men aged over 50 years and 9·0 per cent in women aged above 50 years. Heaviness, tension, swelling, aching and itching were significantly commoner in patients with CVI than in the general population. CVI was significantly associated with reflux in all deep and superficial segments. The frequency of reflux in both superficial and deep segments increased with the clinical severity of disease (P = 0·01). In 48·1 per cent reflux was limited to the superficial system and was thus potentially remediable.

Conclusion
CVI was common in this relatively young population. Having established the frequency of CVI and its related pattern of reflux in the general population, this cohort provides a benchmark for clinical studies and will form the basis of further longitudinal epidemiological studies.
Jugular venous neurone-specific enolase and s-100 levels after carotid endarterectomy under local or general anaesthesia
Authors: Wijeyaratne S M , Cruickshank J , Collins M , Barth J , Homer Vanniasinkam S , Mavor A I D , Gough M J 
Published: December 2004

Abstract

Background
Previous studies using near infrared spectroscopy have indicated that carotid endarterectomy (CEA) performed under local anaesthesia (LA) preserves cerebral cytochrome oxidase and autoregulation compared with surgery under general anaesthesia (GA). The hypothesis that LA offers a degree of protection against ischaemic cerebral injury has thus been investigated by measuring ipsilateral jugular venous neurone-specific enolase (NSE; a glycolytic enzyme released from injured neurones) and s-100 (a protein released from glial cells) during and after CEA.

Methods
Sixteen patients with symptomatic 70–99 per cent carotid stenosis were randomized (with ethics committee approval) to CEA with either LA (n = 7; mean stump pressure 48·5 (range 37–80) mmHg; none of seven shunted) or GA (n = 9; mean stump pressure 49·1 mmHg; five of nine shunted). Jugular venous samples were assayed for NSE and s-100 concentration (immunoluminometric assay) before carotid clamping, 5 min before and 5 min, 2, 4, 6, 8, 12 and 24 h after clamp release.

Results
There were no neurological complications. Median (range) levels of s-100 were low and did not increase from baseline levels (GA 0·10 (0·08–0·11) μg l−1, LA 0·13 (0·12–0·17) μg l−1) in either group. Preclamp NSE levels were similar in both groups (LA 17·6 (15·2–20·7) μg l−1versus GA 21·5 (11·3–26·2) μg l−1; P = 0·37). Peak levels occurred at 2 h and were significantly higher in patients having GA (48·2 (31·4–61·3) versus 25·5 (16·6–27·8) μg l−1; P = 0·05, Mann–Whitney U test). Furthermore, the increase from baseline in patients having GA was also significant (P = 0·04) and NSE levels were higher at all time points up to 12 h, returning to baseline at 24 h.

Conclusion
These results suggest that CEA performed under LA is associated with reduced cerebral ischaemic injury compared with GA, and are consistent with niroscopic data indicating improved cerebral oxygenation in these patients. Furthermore, NSE would seem to be a more sensitive marker of cerebral injury than s-100.
Outcome after septic complications in J pouch procedures
Authors: Heuschen U A , Allemeyer E H , Hinz U , Lucas M , Herfarth C , Heuschen G 
Published: December 2004

AbstractBackgroundDespite the wide range of surgical approaches for pouch salvage, septic complications are among the main causes of pouch failure.MethodsThis study analysed the mode and outcome of various therapeutic approaches for pouch salvage and the impact of time of diagnosis, localization and form of septic complications on the risk of pouch failure in 131 patients with septic complications of a total of 706 patients undergoing a J pouch procedure.ResultsSeptic complications consisted of 76·3 per cent fistulas, 15·3 per cent anastomotic breakdowns and 8·4 per cent pelvic abscesses. A total of 107 patients (81·7 per cent) with septic complications required a mean of 2·2 surgical procedures. The frequency of permanent defunctioning and excision of the pouch in the 131 patients with septic complications was 23·7 and 6·1 per cent respectively. The estimated cumulative 3-, 5- and 10-year rate of pouch failure in patients with septic complications was 19·6, 31·1 and 39·2 per cent respectively. The risk of pouch failure was significantly affected by the site of origin of septic complications (P = 0·02). The 5-year pouch failure rate increased in a subgroup of patients with septic complications at the pouch–anal anastomosis when the anal sphincter was involved (50·1 versus 29·2 per cent; P = 0·18).ConclusionPouch failure as a result of septic complications may occur several years after ileal pouch–anal anastomosis. For prevention of pouch failure, surgery for septic complications is required in a high percentage of patients and repeated attempts are justified. Follow-up studies are required for further analysis of pouch failure.