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Cystic artery pseudoaneurysm (CAP) is a rare entity, with just a few cases reported in the literature. The most common presentation of CAP is described by Quincke's triad of upper gastrointestinal bleeding, jaundice and right upper quadrant abdominal pain. We report the case of an 83-year-old male who presented to the adult emergency with a history of an acute cholecystitis 5 weeks prior for which responded to conservative management. Despite this patient not presenting with Quincke's triad, early suspicion of CAP was considered in light of his history of acute cholecystitis and a computed tomographic CT abdomen ordered promptly which showed a 6 mm cystic artery pseudoaneurysm and a thick-walled gallbladder with surrounding inflammatory changes. Management with an endovascular approach followed by an elective cholecystectomy was done.

Presents abstracts that were presented to the 14th annual meeting of the Surgical Infection Society of Europe held in Gdansk, Poland on 31 May 2, June 2001.

Background The aim of this study was to determine whether the route of administration of nutrients might affect the postoperative complication rate and to calculate costs of the treatments. Methods Two hundred and fifty-seven patients with cancer of stomach (n = 121), pancreas (n = 110) and oesophagus (n = 26), candidates for curative surgery, were randomized into two groups to receive total parenteral nutrition (TPN) (n = 131) or early enteral nutrition (EN) (n = 126) after operation. The full nutritional goal was 25 kcal kg-1 day-1. The two regimens were isocaloric and isonitrogenous and were continued until oral intake was 1000 kcal day-1. In 20 consecutive patients per group intestinal oxygen tension was evaluated by a micropolarographic implantable probe. Complications requiring either reoperation or patient transfer to the intensive care unit were defined as major. Results Groups were homogeneous for baseline and surgical variables. The nutritional goal was reached in 100 (79·4 per cent) of 126 in the EN group and 128 (97·7 per cent) of 131 in the TPN group. Alterations in glucose metabolism (4·7 versus 9·1 per cent; P < 0·05) and of plasma electrolytes (3·9 versus 13·7 per cent; P < 0·05) were significantly lower in the EN group with respect to the TPN group. Intestinal oxygen tension significantly increased in the EN group from day 5 after operation compared with that in the TPN group mean(s.d.) 43(5) versus 31(4) mmHg respectively; P < 0·05). EN was one-quarter the cost of TPN (13·2(2·0) versus 69·4(4·4) euro day-1). Conclusion Early EN was well tolerated. EN decreased metabolic complications and improved intestinal microperfusion. The route of administration of nutrients does not significantly affect postoperative outcome. EN is considerably less expensive than TPN and therefore represents a suitable alternative to TPN in this type of patient.... [ABSTRACT FROM AUTHOR]

India is one of the world's largest producers of tree nuts, yet it paradoxically remains a net importer of these commodities. This study aims to analyze the demand for imported tree nuts in India, motivated by the need to understand the factors contributing to this imbalance. The primary objective is to calculate income elasticities and own- and cross-price elasticities for five categories of imported tree nuts using the linear approximate almost ideal demand system model. Data is sourced from monthly import records from the United Nations Comtrade database covering 2014 to 2022. The tree nuts considered are almonds, cashews, pistachios, walnuts, and hazelnuts. Key findings reveal all imported tree nuts are normal goods. Cashews exhibit income elasticity (1.2), indicating a significant demand increase with rising incomes, while other nuts show income inelasticity. Cashews are price-elastic (-1.3), while other nuts are price-inelastic. Compensated cross-price elasticities indicate notable substitution effects, particularly between almonds and cashews. The study recommends enhancing domestic cashew production to meet growing demand and developing targeted marketing strategies to address competitive dynamics within the tree nut market. These strategies aim to reduce India's dependency on imports and promote a balanced, sustainable domestic market., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 The Authors.)

Background: Cardiopulmonary bypass results in ischemia/reperfusion (I/R)-induced endotoxemia. We conducted a prospective randomized trial to investigate the effect of taurolidine, an antiendotoxin agent with antioxidant and membrane-stabilizing properties, on patients undergoing coronary artery bypass grafting (CABG)., Methods: A total of 60 patients undergoing CABG were randomized into 4 groups. St Thomas' Hospital cold crystalloid cardioplegia was used in groups A and B, and cold blood cardioplegia in groups C and D. Groups A and C received a placebo infusion of normal saline, whereas groups B and D were administered intravenous taurolidine. Arrhythmias induced by pro- and anti-inflammatory cytokines (interleukin [IL]-6 and IL-10), and I/R were assessed perioperatively., Results: Administration of taurolidine in crystalloid cardioplegia patients resulted in a significant decrease in serum IL-6 and an increase in serum IL-10 at 24 hours postaortic unclamping compared to placebo (P < .0001). Although not statistically significant, this trend in serum IL-6 decrease was mirrored in the blood cardioplegia patients (P = .068). Taurolidine treatment also significantly decreased I/R-induced arrhythmias compared to placebo in the crystalloid cardioplegia patients (P < .003). There were fewer I/R-induced arrhythmias compared to placebo in the blood cardioplegia patients; the difference, however, was marginal and not statistically significant (P = .583)., Conclusion: This study demonstrates that administration of taurolidine in CABG patients induces a potent anti-inflammatory response that is associated with a significant decrease in arrhythmias., (Copyright 2010 Mosby, Inc. All rights reserved.)

Objective: To evaluate the effect of inhalation of aerosolized opsonized dead Escherichia coli on inflammatory pulmonary neutrophil (PMN) apoptosis, lung injury, and survival in a PMN-mediated lung injury model in vivo., Summary Background Data: Neutrophils that have transmigrated into an inflammatory focus display increased functional capacity and delayed apoptosis, resulting in an increased capacity to injure normal host tissue. The authors have previously shown that E. coli induces PMN apoptosis in vitro., Methods: Lung injury mediated by PMNs was established by aortic occlusion and reperfusion. Adult male Sprague-Dawley rats were randomized into four groups: sham ischemia-reperfusion (I/R) treated with intratracheal inhalation of aerosolized normal saline, I/R treated with aerosolized normal saline intratracheally, I/R treated with aerosolized opsonized dead E. coli intratracheally, and I/R treated with aerosolized opsonized dead E. coli and the caspase inhibitor zVAD-FMK intratracheally 5 minutes before reperfusion. Both systemic and bronchoalveolar lavage PMNs were isolated and apoptosis was quantified at 0, 6, 12, 18, and 24 hours. Lung injury parameters including wet/dry lung weight ratio, histology, myeloperoxidase activity, and protein content were also assessed. In addition, a survival study was performed, both in a prophylactic and in a therapeutic setting., Results: Administration of aerosolized dead E. coli before the reperfusion injury induced pulmonary PMN apoptosis and reversed the delayed apoptosis evident in the I/R plus normal saline group. There was also a significant improvement in lung injury parameters as well as in survival, both prophylactically as well as therapeutically., Conclusions: Directly modulating PMN cell death represents a novel mechanism for attenuating PMN-mediated lung injury and may ultimately benefit the outcome in patients with adult respiratory distress syndrome.

Background: The immunomodulatory effects of hypertonic saline (HTS) provide potential strategies to attenuate inappropriate inflammatory reactions. This study tested the hypothesis that administration of intratracheal aerosolized HTS modulates the development of lung injury in pancreatitis., Methods: Pancreatitis was induced in 24 male Sprague-Dawley rats by intraperitoneal injection of 20% L-arginine (500 mg/100 g body weight). At 24 and 48 h, intratracheal aerosolized HTS (7.5% NaCl, 0.5 mL) was administered to 8 rats, while a further 8 received 0.5 mL of aerosolized normal saline (NS). At 72 hours, pulmonary neutrophil infiltration (myeloperoxidase activity) and endothelial permeability (bronchoalveolar lavage and wet:dry weight ratios) were assessed. In addition, histological assessment of representative lung tissue was performed by a blinded assessor. In a separate experiment, polymorphonucleocytes (PMN) were isolated from human donors, and exposed to increments of HTS. Neutrophil transmigration across an endothelial cell layer, VEGF release, and apoptosis at 1, 6, 12, 18, and 24 h were assessed., Results: Histopathological lung injury scores were significantly reduced in the HTS group (4.78 +/- 1.43 vs. 8.64 +/- 0.86); p < 0.001). Pulmonary neutrophil sequestration (1.40 +/- 0.2) and increased endothelial permeability (6.77 +/- 1.14) were evident in the animals resuscitated with normal saline when compared with HTS (0.70 +/- 0.1 and 3.57 +/- 1.32), respectively; p < 0.04). HTS significantly reduced PMN transmigration (by 97.1, p = 0.002, and induced PMN apoptosis (p < 0.03). HTS did not impact significantly upon neutrophil VEGF release (p > 0.05)., Conclusions: Intratracheal aerosolized HTS attenuates the neutrophil-mediated pulmonary insult subsequent to pancreatitis. This may represent a novel therapeutic strategy.

Bacterial lipoprotein (BLP) is the most abundant protein in gram-negative bacterial cell walls, heavily outweighing lipopolysaccharide (LPS). Herein we present findings demonstrating the potent in vitro effects of BLP on neutrophil (PMN) activation status, function, and capacity to transmigrate an endothelial monolayer. PMNs are the principal effectors of the initial host response to injury or infection and constitute a significant threat to invading bacterial pathogens. The systemic inflammatory response syndrome (SIRS) is characterised by significant host tissue injury mediated, in part, by uncontrolled regulation of PMN cytotoxic activity. We found that BLP-activated human PMN as evidenced by increased CD11b/CD18 (Mac-1) expression. Up-regulation of PMN Mac-1 in response to BLP occurred independently of membrane-bound CD14 (mCD14). A similar up-regulation of intercellular adhesion molecule-1 (ICAM-1) on endothelial cells was observed whilst E-Selectin expression was unaffected. PMN transmigration across a human umbilical vein endothelial cell (HUVEC) monolayer was markedly increased after treating either PMN's or HUVEC independently with BLP. This increased transmigration did not occur as a result of any direct effect of BLP on HUVEC monolayer permeability, assessed objectively using the passage of FITC-labeled Dextran-70. BLP primed PMN for enhanced respiratory burst and superoxide anion production in response to PMA, but did not influence phagocytosis of opsonized Escherichia coli. BLP far exceeds LPS as a gram-negative bacterial wall component, these findings therefore implicate BLP as an additional putative mediator of SIRS arising from gram-negative infection.

Background: Taurolidine, a derivative of the amino acid taurine, exhibits antiendotoxin, antibacterial, and antiadherence activity. We hypothesized that Taurolidine may inhibit tumor cell growth, both in an in vitro and in vivo setting. Our aim was to examine the effect of Taurolidine on the growth of a rat metastatic colorectal tumor cell line (DHD/K12/TRb) in vitro and in vivo., Methods: In the in vitro experiments, DHD/K12/TRb cells were incubated with 5, 10, 15, 25, microg/ml of Taurolidine. Cells incubated in culture medium alone were used as controls. Cell proliferation, cell viability, cell death, and cell apoptosis were measured using commercially available techniques. In the in vivo experiment, BD IX rats were randomized into two groups (n = 10/group). Group A (control) underwent laparotomy and instillation of DHD/K12/TRb tumor cells intraperitoneally followed by phosphate buffered saline (PBS). Group B received Taurolidine (100 mg/kg) instead of PBS. Animals were killed after 24 days and tumor burden assessed by counting the number of tumor nodules in the peritoneal cavity., Results: Incubation of the tumor cells with Taurolidine resulted in a 4-fold decrease in proliferation rates (25+/-4% vs. 100+/-28% for controls) and a 4-fold increase in cell necrosis as demonstrated by the increase in LDH release (403+/-28% vs. 100+/-26% for controls), at a Taurolidine concentration of 25 microg/ml. A dose-dependent decrease in cell viability was also observed. In the in vivo study, local Taurolidine administration resulted in significant decreases in tumor burden (3+/-1 nodules in Group B animals vs. 649+/-101 nodules in Group A animals)., Conclusions: Taurolidine inhibits the growth of a rat metastatic colorectal tumor cell line in vitro and in vivo and thus may have potential in the prevention of peritoneal metastases.

Background: Vascular endothelial growth factor (VEGF; vascular permeability factor) is one of the most potent proangiogenic cytokines, and it plays a central role in mediating the process of angiogenesis or new blood vessel formation. Neutrophils (PMNs) recently have been shown to produce VEGF., Hypothesis: The acute inflammatory response is a potent stimulus for PMN-directed angiogenesis., Methods: Neutrophils were isolated from healthy volunteers and stimulated with lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and anti-human Fas monoclonal antibody. Culture supernatants were assayed for VEGF using enzyme-linked immunosorbent assays. Culture supernatants from LPS- and TNF-alpha-stimulated PMNs were then added to human umbilical vein endothelial cells and human microvessel endothelial cells and assessed for endothelial cell proliferation using 5-bromodeoxyuridine labeling. Tubule formation was also assessed on MATRIGEL basement membrane matrix. Neutrophils were lysed to measure total VEGF release, and VEGF expression was detected using Western blot analysis., Results: Lipopolysaccharide and TNF-alpha stimulation resulted in significantly increased release of PMN VEGF (532+/-49 and 484+/-80 pg/mL, respectively; for all, presented as mean +/- SEM) compared with control experiments (32+/-4 pg/mL). Interleukin 6 and Fas had no effect. Culture supernatants from LPS- and TNF-alpha-stimulated PMNs also resulted in significant increases (P<.005) in macrovascular and microvascular endothelial cell proliferation and tubule formation. Adding anti-human VEGF-neutralizing polyclonal antibody to stimulated PMN supernatant inhibited these effects. Total VEGF release following cell lysis and Western blot analysis suggests that the VEGF is released from an intracellular store., Conclusion: Activated human PMNs are directly angiogenic by releasing VEGF, and this has important implications for inflammation, capillary leak syndrome, wound healing, and tumor growth.