ObjectiveTo assess the distribution and type of nerve fibers present in human peritoneal adhesions and to relate data on location and size of nerves with estimated age and with clinical parameters such as reports of chronic pelvic pain. Summary Background DataPeritoneal adhesions are implicated in the cause of chronic abdominopelvic pain, and many patients are relieved of their symptoms after adhesiolysis. Adhesions are thought to cause pain indirectly by restricting organ motion, thus stretching and pulling smooth muscle of adjacent viscera or the abdominal wall. However, in mapping studies using microlaparoscopic techniques, 80% of patients with pelvic adhesions reported tenderness when these structures were probed, an observation suggesting that adhesions themselves are capable of generating pain stimuli. MethodsHuman peritoneal adhesions were collected from 25 patients undergoing laparotomy, 20 of whom reported chronic pelvic pain. Tissue samples were prepared for histologic, immunohistochemical, and ultrastructural analysis. Nerve fibers were characterized using antibodies against several neuronal markers, including those expressed by sensory nerve fibers. In addition, the distribution of nerve fibers, their orientation, and their association with blood vessels were investigated by acetylcholinesterase histochemistry and dual immunolocalization. ResultsNerve fibers, identified histologically, ultrastructurally, and immunohistochemically, were present in all the peritoneal adhesions examined. The location of the adhesion, its size, and its estimated age did not influence the type of nerve fibers found. Further, fibers expressing the sensory neuronal markers calcitonin gene-related protein and substance P were present in all adhesions irrespective of reports of chronic abdominopelvic pain. The nerves comprised both myelinated and nonmyelinated axons and were often, but not invariably, associated with blood vessels. ConclusionsThis study provides the first direct evidence for the presence of sensory nerve fibers in human peritoneal adhesions, suggesting that these structures may be capable of conducting pain after appropriate stimulation.Peritoneal adhesions are bands of fibrous tissue that join abdominal organs to each other or the abdominal wall. Adhesions develop rapidly after damage to the peritoneum during surgery, infection, trauma, or irradiation. Postoperative adhesion formation occurs in 93% to 100% of patients undergoing laparotomy, 1 leading to complications such as intestinal obstruction and infertility in women.2-4 Adhesions have also been implicated as a cause of chronic abdominopelvic pain, 5-8 and many patients have been relieved of their symptoms after adhesiolysis.9 -12 Chronic pelvic pain accounts for up to 25% of all gynecologic visits, 30% to 50% of all diagnostic laparoscopic procedures, and approximately 5% of hysterectomies. 13,14 In financial terms, the annual cost of resources for the diagnosis and treatment of women with chronic pelvic pain in the United Kingdom is approximately £600...

Peritoneal adhesions are a major complication of healing following surgery or infection and can lead to conditions such as intestinal obstruction, infertility, and chronic pain. Mature adhesions are the result of aberrant peritoneal healing and historically have been thought to consist of non-functional scar tissue. The aim of the present study was to analyse the cellular composition, vascularity, and extracellular matrix distribution of human peritoneal adhesions, to determine whether adhesions represent redundant scar tissue or are dynamic regenerating structures. Furthermore, the histological appearance of each adhesion was correlated with the clinical history of the patient, to determine whether maturity or intraperitoneal pathology influences adhesion structure. Human peritoneal adhesions were collected from 29 patients undergoing laparotomy for various conditions and were prepared for histology, immunocytochemistry, and transmission electron microscopy. All adhesions were highly vascularized, containing well-developed arterioles, venules, and capillaries. Nerve fibres, with both myelinated and non-myelinated axons, were present in adhesions from nearly two-thirds of the patients, with increased incidence in those with a malignancy. Approximately one-third of the adhesions contained conspicuous smooth muscle cell clusters lined by collagen fibres of heterogeneous size. Adipose tissue was a consistent feature of all the adhesions, with some areas displaying fibrosis. There appeared to be no correlation between the estimated maturity or site of each adhesion and its histological appearance. However, intraperitoneal pathology at the time of surgery did influence the incidence of some histological features, such as the presence of nerve fibres, clusters of smooth muscle cells, and inflammation. This study challenges previous concepts that adhesions represent non-functional scar tissue and clearly demonstrates that established adhesions are highly cellular, vascularized, and innervated, features more consistent with dynamic, regenerating structures.

BackgroundSilicone breast implants have been in use for breast augmentation for more than 50 years, but technological innovation has been lacking in implant design until recently.ObjectivesThis study was designed to evaluate the complication and reoperation rates following breast augmentation utilizing the Motiva silicone breast implants.MethodsThis retrospective study evaluated the safety of Motiva implants in 5813 consecutive cases of breast augmentation. Implants with two different textured surfaces were evaluated: SilkSurface (nanotextured) and VelvetSurface (micro-textured).ResultsImplants were placed between April 2013 and April 2016. A total of 44 complications were reported, with an overall complication rate of 0.76%, and the rate of reoperation was 0.76% over an interval of 3 years. There were no late complications and no cases of primary capsular contracture. No differences in complication rates were observed because of the implant date. However, among patients who received implants 300 to 499 cc in volume, complication rates were significantly lower with SilkSurface compared with VelvetSurface implants. Advanced statistical analysis supported the validity of the low complication rate reported in this study.ConclusionsOverall, these findings suggest that Motiva silicone breast implants are associated with very low rates of complication and reoperation, and that the nano-textured SilkSurface implant is associated with fewer complications than micro-textured implants.Level of Evidence: 3

Please refer to abstract number 61. This abstract was originally submitted as a poster, and on the basis of its scientific interest and merit, was chosen by the colloquium organizers to be presented as an oral communication, as well as a poster.Please refer to abstract number 52. This abstract was originally submitted as a poster, and on the basis of its scientific interest and merit, was chosen by the colloquium organizers to be presented as an oral communication, as well as a poster.

Aims: Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme that participates in base-excision repair of oxidative DNA damage and in the redox activation of transcription factors. We tested the hypothesis that APE1 upregulation protects neuronal structure and function against transient global cerebral ischemia (tGCI). Results: Upregulation of APE1 by low-dose proton irradiation (PI) or by transgene overexpression protected hippocampal CA1 neurons against tGCI-induced cell loss and reduced apurinic/apyrimidinic sites and DNA fragmentation. Conversely, APE1 knockdown attenuated the protection afforded by PI and ischemic preconditioning. APE1 overexpression inhibited the DNA damage response, as evidenced by lower phospho-histone H2A and p53-upregulated modulator of apoptosis levels. APE1 overexpression also partially rescued dendritic spines and attenuated the decrease in field excitatory postsynaptic potentials in hippocampal CA1. Presynaptic and postsynaptic markers were reduced after tGCI, and this effect was blunted in APE1 transgenics. The Morris water maze test revealed that APE1 protected against learning and memory deficits for at least 27 days post-injury. Animals expressing DNA repair-disabled mutant APE1 (D210A) exhibited more DNA damage than wild-type controls and were not protected against tGCI-induced cell loss. Innovation: This is the first study that thoroughly characterizes structural and functional protection against ischemia after APE1 upregulation by measuring synaptic markers, electrophysiological function, and long-term neurological deficits in vivo. Furthermore, disabling the DNA repair activity of APE1 was found to abrogate its protective impact. Conclusion: APE1 upregulation, either endogenously or through transgene overexpression, protects DNA, neuronal structures, synaptic function, and behavioral output from ischemic injury. Antioxid. Redox Signal. 22,[135][136][137][138][139][140][141][142][143][144][145][146][147][148]