11 research outputs found

    Laparoscopic colorectal resection for a giant colonic diverticulum - video vignette

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    A giant colonic diverticulum (GCD) is a rare disease with less than 200 cases reported in the literature. By definition, a GCD is larger than 4cm in diameter with close sigmoid colon relationship in more than 90% of the cases. En bloc resection of the diverticulum with anterior sigmoid-rectal segment with primary anastomosis is the best treatment approach. The authors present a case of laparoscopic colorectal resection with partial cystectomy for a giant colonic diverticulum. A 62-years-old man with sigmoid colon diverticulosis and several episodes of diverticulitis presented at the office with a painless hypogastric/left iliac abdominal mass. CT scan showed a round 11 cm smooth walled structure filled with gas, adjacent to the sigmoid anti-mesenteric border and the urinary bladder. Four trocars were used for the laparoscopic approach. Step-by-step as follows: i. complete mobilization of colon splenic flexure. ii. Giant diverticulum dissection with partial bladder resection. iii. Bladder closure. iv. Sigmoid colon and intra-peritoneal rectum resection with primary anastomosis. The post-operative course was uneventful and the patient was discharged home on post-operative day 4. Vesical catheter was removed on post-operative day 10. Pathological specimen analysis confirmed the pre-operative diagnosis of a GCD. There is a consensus that this extremely rare diverticular disease complication should be approached with prompt standard resection due to high risk of diverticulum rupture. Laparoscopic approach seems to be feasible and safe despite of dissection higher complexity owing to the mega diverticulum. This article is protected by copyright. All rights reserved.info:eu-repo/semantics/publishedVersio

    Evaluation of appendicitis risk prediction models in adults with suspected appendicitis

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    Background Appendicitis is the most common general surgical emergency worldwide, but its diagnosis remains challenging. The aim of this study was to determine whether existing risk prediction models can reliably identify patients presenting to hospital in the UK with acute right iliac fossa (RIF) pain who are at low risk of appendicitis. Methods A systematic search was completed to identify all existing appendicitis risk prediction models. Models were validated using UK data from an international prospective cohort study that captured consecutive patients aged 16–45 years presenting to hospital with acute RIF in March to June 2017. The main outcome was best achievable model specificity (proportion of patients who did not have appendicitis correctly classified as low risk) whilst maintaining a failure rate below 5 per cent (proportion of patients identified as low risk who actually had appendicitis). Results Some 5345 patients across 154 UK hospitals were identified, of which two‐thirds (3613 of 5345, 67·6 per cent) were women. Women were more than twice as likely to undergo surgery with removal of a histologically normal appendix (272 of 964, 28·2 per cent) than men (120 of 993, 12·1 per cent) (relative risk 2·33, 95 per cent c.i. 1·92 to 2·84; P < 0·001). Of 15 validated risk prediction models, the Adult Appendicitis Score performed best (cut‐off score 8 or less, specificity 63·1 per cent, failure rate 3·7 per cent). The Appendicitis Inflammatory Response Score performed best for men (cut‐off score 2 or less, specificity 24·7 per cent, failure rate 2·4 per cent). Conclusion Women in the UK had a disproportionate risk of admission without surgical intervention and had high rates of normal appendicectomy. Risk prediction models to support shared decision‐making by identifying adults in the UK at low risk of appendicitis were identified

    Neocortex and Allocortex Respond Differentially to Cellular Stress In Vitro and Aging In Vivo

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    In Parkinson’s and Alzheimer’s diseases, the allocortex accumulates aggregated proteins such as synuclein and tau well before neocortex. We present a new high-throughput model of this topographic difference by microdissecting neocortex and allocortex from the postnatal rat and treating them in parallel fashion with toxins. Allocortical cultures were more vulnerable to low concentrations of the proteasome inhibitors MG132 and PSI but not the oxidative poison H(2)O(2). The proteasome appeared to be more impaired in allocortex because MG132 raised ubiquitin-conjugated proteins and lowered proteasome activity in allocortex more than neocortex. Allocortex cultures were more vulnerable to MG132 despite greater MG132-induced rises in heat shock protein 70, heme oxygenase 1, and catalase. Proteasome subunits PA700 and PA28 were also higher in allocortex cultures, suggesting compensatory adaptations to greater proteasome impairment. Glutathione and ceruloplasmin were not robustly MG132-responsive and were basally higher in neocortical cultures. Notably, neocortex cultures became as vulnerable to MG132 as allocortex when glutathione synthesis or autophagic defenses were inhibited. Conversely, the glutathione precursor N-acetyl cysteine rendered allocortex resilient to MG132. Glutathione and ceruloplasmin levels were then examined in vivo as a function of age because aging is a natural model of proteasome inhibition and oxidative stress. Allocortical glutathione levels rose linearly with age but were similar to neocortex in whole tissue lysates. In contrast, ceruloplasmin levels were strikingly higher in neocortex at all ages and rose linearly until middle age. PA28 levels rose with age and were higher in allocortex in vivo, also paralleling in vitro data. These neo- and allocortical differences have implications for the many studies that treat the telencephalic mantle as a single unit. Our observations suggest that the topographic progression of protein aggregations through the cerebrum may reflect differential responses to low level protein-misfolding stress but also reveal impressive compensatory adaptations in allocortex

    Critical review of the safety assessment of titanium dioxide additives in food

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    The epigenetic landscape of innate immunity

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