In 2014, the International Endohernia Society (IEHS) published the first international "Guidelines for laparoscopic treatment of ventral and incisional abdominal wall hernias." Guidelines reflect the currently best available evidence in diagnostics and therapy and give recommendations to help surgeons to standardize their techniques and to improve their results. However, science is a dynamic field which is continuously developing. Therefore, guidelines require regular updates to keep pace with the evolving literature. Methods For the development of the original guidelines, all relevant literature published up to year 2012 was analyzed using the ranking of the Oxford Centre for Evidence-Based Medicine. For the present update, all of the previous authors were asked to evaluate the literature published during the recent years from 2012 to 2017 and revise their statements and recommendations given in the initial guidelines accordingly. In two Consensus Conferences (October 2017 Beijing, March 2018 Cologne), the updates were presented, discussed, and confirmed. To avoid redundancy, only new statements or recommendations are included in this paper. Therefore, for full understanding both of the guidelines, the original and the current, must be read. In addition, the new developments in repair of abdominal wall hernias like surgical techniques within the abdominal wall, release operations (transversus muscle release, component separation), Botox application, and robot-assisted repair methods were included. Results Due to an increase of the number of patients and further development of surgical techniques, repair of primary and secondary abdominal wall hernias attracts increasing interests of many surgeons. Whereas up to three decades ago hernia-related publications did not exceed 20 per year, currently this number is about 10-fold higher. Recent years are characterized by the advent of new techniques-minimal invasive techniques using robotics and laparoscopy, totally extraperitoneal repairs, novel myofascial release techniques for optimal closure of large defects, and Botox for relaxing the abdominal wall. Furthermore, a concomitant rectus diastasis was recognized as a significant risk factor for recurrence. Despite insufficient evidence with respect to these new techniques, it seemed to us necessary to include them in the update to stimulate surgeons to do research in these fields. Conclusion Guidelines are recommendations based on best available evidence intended to help the surgeon to improve the quality of his daily work. However, science is a continuously evolving process, and as such guidelines should be updated about every 3 years. For a comprehensive reference, however, it is suggested to read both the initial guidelines published in 2014 together with the update. Moreover, the presented update includes also techniques which were not known 3 years before.

Background: The transcription factor BACH1 (BTB and CNC homology 1) suppressed endothelial cells (ECs) proliferation and migration and impaired angiogenesis in the ischemic hindlimbs of adult mice. However, the role and underlying mechanisms of BACH1 in atherosclerosis remain unclear. Methods: Mouse models of atherosclerosis in endothelial cell (EC)-specific-Bach1 knockout mice were used to study the role of BACH1 in the regulation of atherogenesis and the underlying mechanisms. Results: Genetic analyses revealed that coronary artery disease-associated risk variant rs2832227 was associated with BACH1 gene expression in carotid plaques from patients. BACH1 was upregulated in ECs of human and mouse atherosclerotic plaques. Endothelial Bach1 deficiency decreased turbulent blood flow- or western diet-induced atherosclerotic lesions, macrophage content in plaques, expression of endothelial adhesion molecules (ICAM1 [intercellular cell adhesion molecule-1] and VCAM1 [vascular cell adhesion molecule-1]), and reduced plasma TNF-α (tumor necrosis factor-α) and IL-1β levels in atherosclerotic mice. BACH1 deletion or knockdown inhibited monocyte–endothelial adhesion and reduced oscillatory shear stress or TNF-α-mediated induction of endothelial adhesion molecules and/or proinflammatory cytokines in mouse ECs, human umbilical vein ECs, and human aortic ECs. Mechanistic studies showed that upon oscillatory shear stress or TNF-α stimulation, BACH1 and YAP (yes-associated protein) were induced and translocated into the nucleus in ECs. BACH1 upregulated YAP expression by binding to the YAP promoter. BACH1 formed a complex with YAP inducing the transcription of adhesion molecules. YAP overexpression in ECs counteracted the antiatherosclerotic effect mediated by Bach1-deletion in mice. Rosuvastatin inhibited BACH1 expression by upregulating microRNA let-7a in ECs, and decreased Bach1 expression in the vascular endothelium of hyperlipidemic mice. BACH1 was colocalized with YAP, and the expression of BACH1 was positively correlated with YAP and proinflammatory genes, as well as adhesion molecules in human atherosclerotic plaques. Conclusions: These data identify BACH1 as a mechanosensor of hemodynamic stress and reveal that the BACH1-YAP transcriptional network is essential to vascular inflammation and atherogenesis. BACH1 shows potential as a novel therapeutic target in atherosclerosis.

BackgroundTo explore Ki67 expression in papillary thyroid carcinoma (PTC) and its clinical-pathological significance.MethodsA total of 776 consecutive PTC and benign thyroid disease patients underwent thyroidectomy at Shanghai General Hospital from January 2013 to December 2015 and were retrospectively analysed. Ki67 expression was determined in the PTC and benign thyroid disease tissues, and other clinicopathological factors were identified via statistical analyses.ResultsThe Ki67 expression intensity in the PTC group was significantly higher than that in the benign thyroid disease group. In the PTC group, a tumour size ≥ 1 cm and coexistence with thyroiditis were significantly associated with the Ki67 expression intensity. The TGAb and TPOAb plasma levels were linearly correlated with the Ki67 expression intensity. Moreover, the tumour size and Ki67 expression intensity also showed a linear correlation. Receiver operating characteristic (ROC) curve analysis suggested that the optimal cut-off value of Ki67 was 2.50%. Two groups divided by Ki67 cut-off values showed significant differences in the recurrence survival rate.ConclusionsKi67 is a suitable biomarker for distinguishing PTC from benign thyroid disease. Ki67 expression was related to the tumour size, thyroiditis and plasma levels of TGAb and TPOAb in PTC. Ki67 could be used as a prognostic indicator in PTC. Patients with high Ki67 expression are more likely to experience disease recurrence.

Background/Aims: Stanford type A and type B aortic dissections are anatomically distinct. Few animal models appropriately mimic human aortic dissection in the clinical setting. We developed animal models that mimicked uncontrollable Stanford type B aortic dissection as well as controllable dissection. Methods: Twelve female beagle dogs were randomly assigned to the uncontrollable dissection model, and 8 to the controllable. After creation of the false lumen using a self-made separator, epinephrine was injected acutely in the uncontrollable model, and a rapid injection of saline expanded the false lumen in the controllable model using a balloon catheter. Results: All models mimicked Stanford type B dissection at autopsy. Dissections formed in 9 of the 12 animals of the uncontrollable model as confirmed by digital subtraction angiography (DSA) performed 1 week after surgery. For the controllable dissection model, 6 out of 8 animals survived, and dissection was confirmed by DSA. Occlusion of the dissection developed 4 weeks after surgery in all 6 cases. Conclusions: We have developed an easy, stable animal model of Stanford type B dissection which provides a great length of false lumen and appears very similar to aortic dissection in humans.

BackgroundChronic pain as a complication following inguinal herniorrhaphy has attracted increasing attention in recent years. There is evidence that the chronic pain seriously affects patients’ quality of life. However, there are few imaging studies and diagnostic techniques of the chronic pain. The aim of this study is to explore the etiology and to analysis ultrasonographic imaging description of chronic pain following anterior open inguinal herniorrhaphy.MethodsOne hundred fifty two patients with the chronic pain following anterior open inguinal herniorrhaphy were performed by ultrasonography to identify the main causes of postoperative chronic pain. Positive ultrasonic diagnoses were confirmed to be correct by the pain relieved when the patients underwent re-operation and other clinical operations. Positive diagnoses which appeared simultaneously were grouped for pairwise comparisons.ResultsTwo hundred sixteen positive ultrasonic diagnoses, 12 categories of postoperative chronic pain were found. They were encapsulated effusion, scrotal wall edema, testitis, hydrocele testis, restricted motion of spermatic cord at the reconstructed deep inguinal ring, varicocele, scar sutured into pubic tubercle, shrinking mesh, accumulational mesh or mesh plug, recurrent hernia, cyst of spermatic cord and epididymal cyst. In the pairwise comparison groups, encapsulated effusion with scrotal wall edema, varicocele with restricted motion of spermatic cord at the reconstructed deep inguinal ring, and shrinking mesh with recurrent hernia had significant differences in each intragroup comparisons(P < 0.05).ConclusionsUltrasonography provieds important value in the diagnosis of chronic pain following anterior open inguinal herniorrhaphy. Some positive diagnoses occur simultaneously, which is necessary for doctors to consider comprehensively.

Troxipide is widely used to treat gastric ulcer (GU) in the clinic. However, a lack of systematic metabolic, pharmacokinetic and pharmacological studies limits its clinical use. This study aimed to firstly explore the metabolic, pharmacokinetic and pharmacological mechanisms of troxipide in rats with GU compared to normal control (NC) rats. First, metabolic study was perormed by a highly selective, high-resolution mass spectrometry method. A total of 45 metabolites, including 9 phase I metabolites and 36 phase II metabolites, were identified based on MS/MS spectra. Subsequently, the pharmacokinetics results suggested that the C max , K a , t 1/2 , AUC (0−t) and AUC (0−∞) of troxipide were significantly increased in rats with GU compared with NC rats. The V z , K 10 and absolute bioavailability of troxipide were obviously decreased in rats with GU compared with NC rats, and its tissue distribution (in the liver, lung and kidney) was significantly different between the two groups of rats. Additionally, the pharmacodynamic results suggested that the levels of biochemical factors (IL-17, IL-6, TNF-α, IFN-γ, AP-1, MTL, GAS, and PG-II) were significantly increased, the PG-Ӏ level was obviously decreased, and the protein expression levels of HSP-90, C-Cas-3 and C-PARP-1 were markedly increased in rats with GU compared with NC rats. The above results suggested that the therapeutic mechanisms underlying the metabolic, pharmacokinetic and pharmacological properties of troxipide in vivo in rats deserve further attention based on the importance of troxipide in the treatment of GU in this study, and these mechanisms could be targets for future studies. Gastric ulcer, (GU) a common disease in the clinic, is a peptic ulcer that affects humans of all ages. It is associated with morbidity and mortality, and has become a medical-social problem of global importance that has received increased attention 1-4. The frequent occurrence of GU between the cardia and pylorus mainly results form tissue damage caused by digestive juices decomposing the gastric mucosa, especially near the lesser curvature of the stomach and gastric antrum 5-8. Currently, GU is a widely considered multifactorial disease because it is related to gastric acid, gastric pepsin, infection, physical fitness, environment, living habits and so on 9-11. If not treated adequately, GU can lead to serious complications such as perforation and bleeding 12-15. In addition, the acetic acid-induced GU in rats is most similar to GU in humans 16-20. Here, acetic acid-induced GU is more severe than other GU models (ethanol-, ligation-and reserpine-induced models), and is the most commonly used model for experimental research on GU 21,22. Moreover,this model is reproducible and reliable. Therefore, we selected a rat model of GU to evaluate relative studies of troxipide in the paper. Troxipide (3,4,5-trimethoxy-N-3-piperidinyl, Fig. 1), a defensive factor-enhancing therapeutic agent for gastritis and GU that exerts inhibitory, therapeutic and preventive effects to specifically tho...

This study aimed to investigate the molecular mechanism of systemic vasculitis via bioinformatics analysis. Gene express profile of E-GEOD-16945 (13 Takayasu arteritis samples and 13 control samples) was downloaded from European Bioinformatics Institute (EBI) database. Differentially expressed genes (DEGs) were screened between Takayasu arteritis and normal controls (|log FC| > 1). Basic local alignment search tool (BLASTX) was used for the Clusters of Orthologous Groups (COG) classification of DEGs. Gene ontology analysis was performed for the DEGs (P < 0.05). A gene expression network was built with DEGs. Mcode in Cytoscape software was used to extract modules from the network (degree ≥ 2, K-core ≥ 2 and adjusted P-value < 0.05) followed by pathway analysis using GenMAPP (false discovery rate < 0.05). A total of 747 DEGs were identified. There were 16 significant GO function terms enriched with DEGs, of which immune and defence response was the most significant GO term. Totally, three modules were extracted from gene expression network, including one module constituted with upregulated genes and two modules constituted with downregulated genes. Furthermore, human leucocyte antigen (HLA)-DRB1, HLA-DPA1, HLA-DPB1, HLA-DOA and HLA-DRA in the downregulated modules were significantly linked to immune-related pathways (intestinal immune network for IgA production and systemic lupus erythematosus pathways), while ribosomal protein L 31 (RPL31), RPS3A and RPL9 in the upregulated module were enriched in ribosome pathway. The immune-related pathways, ribosome pathway, immune-related genes including (HLA-DRB1, HLA-DPA1, HLA-DPB1, HLA-DOA and HLA-DRA) and ribosome-related genes (RPL31, RPS3A and RPL9) might be involved in systemic vasculitis.

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