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Introduction: Outcomes of long-term (5–10-year) weight loss have not been investigated thoroughly and the role of pre-operative weight loss on long-term weight loss, among other factors, are unknown. Our regional bariatric service introduced a 12 week intensive pre-operative information course (IPIC) to optimise pre-operative weight loss and provide education prior to bariatric surgery. The present study determines the effect of pre-operative weight loss and an intense pre-operative information course (IPIC), on long-term weight outcomes and sustained weight loss post-bariatric surgery. Methods: Data were collected prospectively from a bariatric center (2008–2022). Excess weight loss (EWL) ≥ 50% and ≥ 70% were considered outcome measures. Survival analysis and logistic regression identified variables associated with overall and sustained EWL ≥ 50% and ≥ 70%. Results: Three hundred thirty-nine patients (median age, 49 years; median follow-up, 7 years [0.5–11 years]; median EWL%, 49.6%.) were evaluated, including 158 gastric sleeve and 161 gastric bypass. During follow-up 273 patients (80.5%) and 196 patients (53.1%) achieved EWL ≥ 50% and ≥ 70%, respectively. In multivariate survival analyses, pre-operative weight loss through IPIC, both < 10.5% and > 10.5% EWL, were positively associated with EWL ≥ 50% (HR 2.23, p< 0.001) and EWL ≥ 70% (HR 3.24, p< 0.001), respectively. After a median of 6.5 years after achieving EWL50% or EWL70%, 56.8% (154/271) had sustained EWL50% and 50.6% (85/168) sustained EWL70%. Higher pre-operative weight loss through IPIC increased the likelihood of sustained EWL ≥ 50% (OR, 2.36; p= 0.013) and EWL ≥ 70% (OR, 2.03; p= 0.011) at the end of follow-up. Conclusions: IPIC and higher pre-operative weight loss improve weight loss post-bariatric surgery and reduce the likelihood of weight regain during long-term follow-up.

Laparoscopic fundoplication is an established treatment for refractory gastro-oesophageal reflux disease. This study aims to compare the outcome of two laparoscopic antireflux techniques in a regional specialist unit. A sequential audit was carried out on patients undergoing laparoscopic Nissen (LN: performed May 1994 to November 2000) or laparoscopic anterior (LA: performed March 2001 to December 2004) fundoplication. Patient satisfaction was assessed by postal questionnaire. The cohorts undergoing each operation were also divided into two chronological groups of 51 patients, to study the effect of possible learning curve progression on the number of nights spent in the hospital postoperatively. In all, 142/204 (70%) questionnaires were returned from patients with follow-up ranging from 5 to 40 months postoperation. Overall, 102/142 (72%) reported a good or excellent outcome. Patients who underwent LA had a higher rate of antacid medication use (LN 17.4% versus LA 34.2%, P= 0.036) but there was a higher score for inability to belch following LN (LN 2.03 versus LA 1.53, P= 0.034). When comparing the chronologically divided cohorts, LN was associated with a significantly longer hospital stay than LA (P< 0.001, Mann-Whitney Utest). There was a significant decrease in hospital stay from the first to second group of 51 LNs (P< 0.001, Mann-Whitney Utest) and a further significant reduction in hospital stay from the first 51 to second 51 LAs (P < 0.001, Mann-Whitney Utest). In conclusion, both procedures provide good symptom control. Increased requirement for acid suppression following LA and inability to belch following LN, may suggest more long-term durability of the LN wrap. The decrease in the number of nights spent in hospital may be related to the procedure performed but seems more likely to be an effect of increasing volume of surgical experience.

A series of 107 patients with cholangiocarcinoma diagnosed between January 1980 and December 1991 is reported. Changing patterns of investigation and treatment in the periods 1980–1985 and 1986–1991 are analysed. There was a decrease in the use of percutaneous transhepatic cholangiography in the second period (86 versus 51 per cent of patients) but increased use of endoscopic retrograde cholangiography (19 versus 71 per cent) and computed tomography (8 versus 59 per cent). The overall resectability rate (17 per cent) was similar to those of other reported series but greater in the second period (8 versus 21 per cent). Palliation by endoscopic and percutaneous stenting was associated with a high incidence of recurrent cholangitis (55 per cent) and jaundice (35 per cent). During the second 6-year period, more effective palliation was achieved by segment III cholangiojejunostomy with a lower incidence of recurrent cholangitis (19 per cent) and jaundice (19 per cent). Overall prognosis for patients with this condition is grim and efforts must usually be aimed at providing the most appropriate palliation.

Leucocyte activation and proinflammatory cytokine release (tumour necrosis factor (TNF) and interleukin 6 (IL-6)) are thought to contribute to the induction of a systemic inflammatory response, an acute-phase response and multiple organ failure in patients with acute pancreatitis. The serum concentration of TNF, soluble TNF receptors (sTNFR55and sTNFR75), IL-6 and Creative protein (CRP) in 58 patients with acute pancreatitis was assessed during the first 2 days of admission. Thirty patients had mild disease and 28 severe disease, of whom 18 developed local pancreatic complications alone (Atlanta classification) and ten developed organ failure (a Goris score of 1 or more). TNF was detected in only 17 patients on the first day of admission, while soluble TNF receptors were detected in all patients and IL-6 in 34. On the first and second days of admission there was a progressive and significant (P< 0·03) increase in the median concentration of sTNFR55, sTNFR75and IL-6 in patients eventually classified into those with mild disease, a local pancreatic complication alone, or organ failure. This pattern was also evident in CRP levels from the second but not the first day of admission. These findings suggest that proinflammatory cytokines or their soluble receptors may be more accurate early predictors of outcome than CRP. Moreover, markers of inflammation in the sera of patients with acute pancreatitis are highest in those who subsequently develop organ failure.

Proinflammatory cytokine release was measured from peripheral blood mononuclear cells (PBMCs) isolated from six volunteers and, on admission, from 16 patients with acute pancreatitis. Tumour necrosis factor (TNF) release in patients did not differ significantly from that of volunteers, whereas both interleukin (IL) 6 and IL-8 release in patients was raised when compared with that in the volunteer group (mean(s.e.m.) IL-6 20·7(4·6) versus9·3(1·7) ng/ml, P= 0·03; IL-8 283(40) versus128(22) ng/ml, P= 0·04). When variation in white cell count was accounted for, IL-6 and IL-8 release but not that of TNF was significantly greater in patients with severe disease than in those with mild disease. These results point to a complex upregulation of proinflammatory cytokine release from PBMCs in patients with acute pancreatitis, components of which relate to the clinical progress of the disease.

1. Neural correlates of the permanent deficits in depth perception that occur when extraocular muscle proprioceptive (EMP) afferents are interrupted unilaterally in kittens were investigated by performing extracellular recordings in the primary visual cortex (area 17) in adulthood. Unilateral section of the ophthalmic branch of the trigeminal nerve (V1 nerve) were performed in 11 cats when they were between 5 and 12 weeks of age (uni-V1 group). Electrophysiological results were compared with those obtained in 17 normal adult cats (control group). 2. Binocular interactions were assessed by testing the sensitivity of cortical neurons to dichoptic presentations of moving sine-wave gratings whose interocular positional phase relationship was randomly varied. The amplitude modulation between the minimum and the maximum binocular responses defined the dynamic range. The degree of binocular suppression or facilitation was assessed by comparing these binocular response limits with the optimal monocular responses evoked through either eye at the best spatial frequency. The variability of both monocular and binocular responses was estimated by using the variation coefficient. 3. In uni-V1 cats, both the dynamic range and the degree of binocular suppression were significantly less pronounced than in controls, whereas binocular facilitation was not affected. The variability of the binocular responses was significantly increased, unlike monocular responses, whose variability was similar to control values. 4. From Fourier analysis of the poststimulus time histograms, two clear-cut categories of cells emerged that were differentially affected in the uni-V1 group. The "modulated" cells showed significantly less binocular suppression than in controls, and the "unmodulated" cells had binocular responses that were significantly more variable than in controls. Results from "simple" cells were similar to those of modulated cells, and results from "complex" cells were similar to those of unmodulated cells. However, in the unmodulated population, which was composed of both simple and complex cells, it was shown that the increase of variability was due to that of complex cells. 5. A nonparametric statistical test was applied on the interocular phase shift tuning curves to determine the minimum stimulus change necessary to elicit a significant change in the neural response. Two categories of cells were determined: the "discriminative" cells (80% in controls but 45% in uni-V1 cats) combined pronounced binocular suppression and dynamic range with relatively low variability. The reverse was true in the case of "nondiscriminative" cells (20% in controls and 55% in uni-V1 cats). 6. In uni-V1 cats, about half of the cells were monocularly activated.(ABSTRACT TRUNCATED AT 400 WORDS)

Inflammatory mediators, such as endotoxin and tumour necrosis factor-alpha (TNF-α) have been implicated in the pathogenesis of acute pancreatitis. However, serum levels of these mediators in patients with acute pancreatitis are often not detectable on hospital admission. In contrast, their circulating antagonists (antiendotoxin antibodies and soluble TNF-α receptors) are detectable in all patients. With increasing severity of disease, patients are more likely to manifest a fall in antiendotoxin levels, suggesting exposure to endotoxin. Similarly, there is a stepwise increase in soluble TNF-a receptors with increasing severity of disease. This suggests that the degree of TNF-α-induced inflammation correlates with disease severity. The role of endotoxin, TNF-a and their relevant antagonists as markers or mediators of the systemic complications of acute pancreatitis remains under investigation.

Laparoscopic mesh repair is becoming an increasingly popular method of ventral and incisional hernia repair. Entrapment neuropathy is a recognised complication when tacks are used to fix the mesh, particularly below the inguinal ligament and laterally in the abdominal wall. We describe a novel method of ventral hernia repair, which employs transabdominal extra-peritoneal dissection to create a pocket for mesh placement with complete avoidance of tacks in the postero-lateral abdominal wall. This technique is particularly useful for incisional hernias arising through old stoma wounds or appendicectomy incisions, and for Spigelian and lumbar hernias..

In a retrospective study 84 patients aged ⩾ 50 years undergoing emergency appendicectomy were matched for age and sex with 84 randomly selected emergency admissions as controls. Of the former, 31 (37 per cent) were taking non-steroidal anti-inflammatory drugs (NSAIDs) at admission, compared with nine (11 per cent) of the controls (P< 0.01). In the study group a suppression of the white cell count was identified on admission in those taking NSAIDs (mean 11.9 × 109l−1) compared with those not (mean 14.8 × 109l−1) (P= 0.007). This is the first reported association between appendicitis and NSAIDs. The relative risk by odds ratio was substantially increased at 6.5 (95 per cent confidence interval 2.1–8.8). An NSAID-related impairment of host defences leading to failure in the resolution of inflammatory episodes may explain this association. It is further postulated that the suppression of the white cell response may be a marker of such an effect.