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| 2. |
- Glasbey, JC, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 3. |
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| 4. |
- Bravo, L, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 5. |
- Tabiri, S, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 6. |
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| 7. |
- Simpson, J, et al.
(författare)
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Prolonged elevation of galanin and tachykinin expression in mucosal and myenteric enteric nerves in trinitrobenzene sulphonic acid colitis
- 2008
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Ingår i: Neurogastroenterology and Motility. - : Wiley. - 1350-1925 .- 1365-2982. ; 20:4, s. 392-406
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Tidskriftsartikel (refereegranskat)abstract
- Diverticulitis causes recurrent abdominal pain associated with increased mucosal expression of mucosal galanin and substance P (SP). We studied changes in mucosal and myenteric plexus neuropeptides in adult rats using a model of colonic inflammation, trinitrobenzenesulphonic acid colitis. We assessed the effects on the pan-neuronal markers protein gene product 9.5 (PGP9.5) and neurofilament protein, as well as specific neuropeptides at 1, 2, 3, 4, 6, 8, 10 and 14 weeks. Following the acute injury there was macroscopic resolution of inflammation but minor microscopic abnormalities persisted. Percent area stained of mucosal PGP9.5 fell initially but average levels on days 21 and 28 levels were significantly elevated (P < 0.001), returning to normal by day 42. Percent area staining of PGP9.5 in the muscle rose immediately and remained significantly elevated at 70 days (P < 0.001). SP, neuropeptide K and galanin followed a similar overall pattern. SP to PGP9.5 ratio was significantly increased in the muscle both acutely (days 1-28) and in the long term (days 70 and 98), whereas the galanin to PGP9.5 ratio was significantly increased in the mucosa throughout the study. Low-grade chronic inflammation after an acute initial insult causes a persistent increase in the expression of galanin in the mucosa and SP in muscle layer.
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| 8. |
- Simpson, J., et al.
(författare)
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Post inflammatory damage to the enteric nervous system in diverticular disease and its relationship to symptoms
- 2009
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Ingår i: Neurogastroenterology and Motility. - : Wiley. - 1350-1925 .- 1365-2982. ; 21:8, s. 847-847
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Tidskriftsartikel (refereegranskat)abstract
- Some patients with colonic diverticula suffer recurrent abdominal pain and exhibit visceral hypersensitivity, though the mechanism is unclear. Prior diverticulitis increases the risk of being symptomatic while experimental colitis in animals increases expression of neuropeptides within the enteric nervous system (ENS) which may mediate visceral hypersensitivity. Our aim was to determine the expression of neuropeptides within the ENS in diverticulitis (study 1) and in patients with symptomatic disease (study 2). Study 1 - Nerves in colonic resection specimens with either acute diverticulitis (AD, n = 16) or chronic diverticulitis (CD, n = 16) were assessed for neuropeptide expression recording % area staining with protein gene product (PGP9.5), substance P (SP), neuropeptide K (NPK), pituitary adenylate cyclase activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP) and galanin. Study 2 - Seventeen symptomatic and 15 asymptomatic patients with colonic diverticula underwent flexible sigmoidoscopy and multiple peridiverticular mucosal biopsies. Study 1- Neural tissue, as assessed by PGP staining was increased to a similar degree in circular muscle in both AD and CD. The CD specimens showed significant increases in the immunoreactivity of SP, NPK and galanin in both mucosal and circular muscle layer compared with controls. Study 2 - Mucosal histology was normal and PGP9.5 staining was similar between groups however patients with symptomatic diverticular disease demonstrated significantly higher levels of SP, NPK, VIP, PACAP and galanin within the mucosal plexus. Patients with symptomatic diverticular disease exhibit increased neuropeptides in mucosal biopsies which may reflect resolved prior inflammation, as it parallels the changes seen in acute and chronic diverticulitis.
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| 10. |
- Humes, D. J., et al.
(författare)
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Duration and magnitude of postoperative risk of venous thromboembolism after planned inguinal hernia repair in men : a population-based cohort study
- 2018
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Ingår i: Hernia. - : Springer. - 1265-4906 .- 1248-9204. ; 22:3, s. 447-453
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Little is known regarding the magnitude and timing of the risk of VTE following inguinal hernia surgery. We aimed to determine the absolute and relative rates of venous thromboembolism (VTE) following planned inguinal hernia repair.Methods: We analysed male adults with a first inguinal hernia repair with no prior record of VTE from the Clinical Practice Research Datalink, linked to the Hospital Episode Statistics (2001-2011). Crude rates and adjusted hazard ratios (HR) of the first VTE were calculated using Cox regression analysis to compare specific time periods following the surgery compared to the general population.Results: We identified 28,782 men who underwent an inguinal hernia repair with 53 (0.18%) having a first VTE in the 90 days following surgery. The overall rate of VTE in the first 90 days following surgery was 7.61 per 1000 person years (pyrs) (95% CI 5.82-9.96). Increasing age, a body mass index > 30 kg/m(2) and an in-patient procedure were associated with an increased risk of VTE, when compared to the general population. The risk of VTE was highest in the 1st month following the surgery with a 2.3- (aHR 2.33; 95% CI 1.09-4.99) and 3.5- (aHR 3.47; 95% CI 2.07-5.83) fold increased risk compared to the general population for both day case and planned in-patient procedures, respectively.Conclusions: Reassuringly, the absolute rates of VTE following inguinal hernia repair are low. Patients should be informed that their peak risk of VTE is during the 1st month following the surgery. Further studies on the optimum duration of thromboprophylaxis following surgery are required in high-risk patients undergoing hernia repair.
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