French reconnection: A conservative pancreato-enteric reconnection for disconnected pancreatic duct syndrome

Background/objectivesDisconnectedpancreatic duct syndrome (DPDS), a severe complication of acute necrotizing pancreatitis (ANP), may require surgery, usually by distal splenopancreatectomy, thus increasing the risk of diabetes. We describe a new technique reconnecting the distal pancreas to the digestive tract.MethodsThis technique was proposed after failure of non-surgical treatment and at least 3 months after the onset of ANP in non-diabetic or non-insulin dependent diabetic patients with a distal pancreas of at least 5 cm. The ruptured zone was identified and the distal side was anastomosed to the stomach or the jejunum.ResultsFrom 2013 to June 2019, 36 patients (median age = 49 years) with DPDS underwent a “French reconnection” procedure, indicated for chronic pain/recurrent pancreatitis (n = 35; 97%), persistent pancreatic fistula (n = 33; 91%), or digestive compression/fistulisation (n = 9; 25%). Median preoperative weight loss was 10 kg (4-27), the median number of hospitalisations per patient was 5(1–8) and 24(67%) patients had received endoscopic/percutaneous treatment. Surgery was performed in median 279(90–2000) days after ANP, laparoscopically in 9(25%) patients. The remnant pancreas (median length = 70 mm; range = 50–130) was anastomosed to the stomach (n = 30) or the jejunum (n = 6). There were 13(36%) postoperative grade B/C pancreatic fistulas and 3(10%) bleedings including one death (mortality = 3%). The median hospital stay was 18 (7–121) days. After a median follow-up of 24 (4–53) months, all pancreatic fistulas had healed and the clinical success rate was 91%. Median BMI increased from 22 to 25 kg/m². In patients with normal pancreatic function, postoperative de novo endocrine and severe exocrine insufficiencies were observed in 4/27 (15%) and 7/22 (32%), respectively.ConclusionsThe “French reconnection” procedure, as an alternative to distal splenopancreatectomy for the treatment of DPDS, provides good control of symptoms and decreases the risk of pancreatic insufficiency.     

Program of cell survival underlying human and experimental hibernating myocardium

Hibernating myocardium refers to chronically dysfunctional myocardium in patients with coronary artery disease in which cardiac viability is maintained and whose function improves after coronary revascularization. It is our hypothesis that long-term adaptive genomic mechanisms subtend the survival capacity of this ischemic myocardium. Therefore, the goal of this study was to determine whether chronic repetitive ischemia elicits a gene program of survival protecting hibernating myocardium against cell death. Accordingly, we measured the expression of survival genes in hibernating myocardium, both in patients surgically treated for hibernation and in a chronic swine model of repetitive ischemia reproducing the features of hibernation. Human hibernating myocardium was characterized by an upregulation of genes and corresponding proteins involved in anti-apoptosis (IAP), growth (VEGF, H11 kinase), and cytoprotection (HSP70, HIF-1alpha, GLUT1). In the swine model, the same genes and proteins were upregulated after repetitive ischemia, which was accompanied by a concomitant decrease in myocyte apoptosis. These changes characterize viable tissue, because they were not found in irreversibly injured myocardium. Our report demonstrates a novel mechanism by which the activation of an endogenous gene program of cell survival underlies the sustained viability of the hibernating heart. Potentially, promoting such a program offers a novel opportunity to salvage postmitotic tissues in conditions of ischemia.     

Colon cancer: comprehensive evaluation with 64-section CT colonography using water enema as intraluminal contrast agent-a pictorial review

Sixty-four-section CT colonography with water enema combines intracolonic neutral contrast agent with high-resolution CT images of the abdomen. Owing to submillimeter isotropic voxels, high-quality reformatted images are obtained. High-resolution images offer added value for the detection and localization of colonic lesions, evaluation of the local extent of the disease, and depiction, if any, of synchronous colorectal lesions and distant metastases. Sixty-four-section CT colonography with water enema has a major role in the evaluation of patients with colon cancer before planning therapy. It can be used to complement failed or incomplete colonoscopy and investigate the colon in elderly patients.     

Cognitive demand does not influence the responsiveness of homonymous Ia afferents pathway during postural dual task in young and elderly adults

Purpose

This study was designed to investigate the influence of a cognitive task on the responsiveness of the homonymous Ia afferents pathway during upright standing in young and elderly adults.

Methods

Twelve young and twelve elderly adults stood upright on a foam surface positioned over a force platform, and performed a colour-naming test (cognitive task) with two cognitive loads: congruent and incongruent colour conditions. The rate of correct response in naming colour (accuracy) and associated reaction time (RT) were recorded for the cognitive task. The excursion of the centre of pressure and surface electromyogramme (EMG) of leg muscles were measured. Modulation in the efficacy of homonymous Ia afferents to discharge spinal motor neurones was assessed by means of the Hoffmann (H) reflex method.

Results

The accuracy and RT were similar in the congruent condition between young and elderly adults (p > 0.05), and increased for both age groups in the incongruent condition, but more so for elderly adults (p = 0.014). In contrast, the H reflex amplitude did not change with the cognitive load. The excursions of the centre of pressure in the sagittal plane and muscle EMG did not vary with colour conditions in both groups (p > 0.05).

Conclusion

This study indicates a lack of modulation in the efficacy of group Ia afferent to activate soleus motor neurones with the cognitive demand of a concurrent task during upright standing in young and elderly adults.     

OSBPL10, a novel candidate gene for high triglyceride trait in dyslipidemic Finnish subjects, regulates cellular lipid metabolism

Analysis of variants in three genes encoding oxysterol-binding protein (OSBP) homologues (OSBPL2, OSBPL9, OSBPL10) in Finnish families with familial low high-density lipoprotein (HDL) levels (N?=?426) or familial combined hyperlipidemia (N?=?684) revealed suggestive linkage of OSBPL10 single-nucleotide polymorphisms (SNPs) with extreme end high triglyceride (TG; >90th percentile) trait. Prompted by this initial finding, we carried out association analysis in a metabolic syndrome subcohort (Genmets) of Health2000 examination survey (N?=?2,138), revealing association of multiple OSBPL10 SNPs with high serum TG levels (>95th percentile). To investigate whether OSBPL10 could be the gene underlying the observed linkage and association, we carried out functional experiments in the human hepatoma cell line Huh7. Silencing of OSBPL10 increased the incorporation of [³H]acetate into cholesterol and both [³H]acetate and [³H]oleate into triglycerides and enhanced the accumulation of secreted apolipoprotein B100 in growth medium, suggesting that the encoded protein ORP10 suppresses hepatic lipogenesis and very-low-density lipoprotein production. ORP10 was shown to associate dynamically with microtubules, consistent with its involvement in intracellular transport or organelle positioning. The data introduces OSBPL10 as a gene whose variation may contribute to high triglyceride levels in dyslipidemic Finnish subjects and provides evidence for ORP10 as a regulator of cellular lipid metabolism.     

The expression of BIRC5 is correlated with loss of specific chromosomal regions in breast carcinomas

Expression of BIRC5 (survivin), a member of the inhibitor of apoptosis protein (IAP) family, is elevated in fetal tissues and in various human cancers. Mechanisms up-regulating BIRC5 in cancer are poorly understood. Here, we show that overexpression of BIRC5 induces a high proliferation level in MCF-7 breast tumor cells. In a population of 191 breast carcinomas, BIRC5 expression is not affected by BIRC5 promoter polymorphism at -31, or BIRC5 gene copy number. However, a significant correlation was found between expression of demethylase (dMTase) and expression of BIRC5. In addition, among 13 chromosomal regions tested for allelic loss [loss of heterozygosity (LOH)], two regions close to D3S1478 and D6S264 were related to BIRC5 expression. In tumors with LOH at D3S1478 and/or D6S264, BIRC5 expression was significantly increased. These regions have been suggested to harbor tumor suppressor genes and/or common fragile sites that may play a role in increasing genetic instability. These results suggest that genes located near D3S1478 and D6S264 might work by inhibiting, directly or indirectly, BIRC5 expression and thus their loss leads to its up-regulation. In addition, BIRC5 expression may induce breast tumor proliferation by promoting genetic instability. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat.