Combined adenocarcinoid and mucinous cystadenoma of the appendix: a case report

<p>Abstract</p> <p>Introduction</p> <p>Adenocarcinoid of the appendix is a rare malignant tumour with features of both adenocarcinoma and carcinoid, showing both epithelial and endocrine differentiation. Mucinous cystadenoma is the commonest of the benign neoplasms of the appendix, with an incidence of 0.6% in appendicectomy specimens. We report a rare combination of these tumours and discuss the latest treatment options. To the best of our knowledge, only six cases have been reported in the literature to date.</p> <p>Case presentation</p> <p>A 71-year-old Caucasian man presented to our department with a right iliac fossa mass associated with pain. Laparoscopy revealed an adenocarcinoid of the appendix in combination with mucinous cystadenoma. He underwent a radical right hemicolectomy with clear margins and lymph nodes.</p> <p>Conclusion</p> <p>Adenocarcinoids account for 2% of primary appendiceal malignancies. Most tumours are less than 2 cm in diameter and 20% of them metastasize to the ovaries. The mean age for presentation is 59 years and the 5-year survival rate ranges from 60% to 84%. Right hemicolectomy is generally advised if any of the following features are present: tumours greater than 2 cm, involvement of resection margins, greater than 2 mitoses/10 high-power fields on histology, extension of tumour beyond serosa. Chemotherapy mostly with 5-Fluorouracil and Leucovorin is advised for remnant disease after surgery. Cytoreductive surgery with intraperitoneal chemotherapy can offer improved survival for advanced peritoneal dissemination.</p

Patient and public involvement in patient safety research: a workshop to review patient information, minimise psychological risk and inform research

Background Patient safety has attracted increasing attention in recent years. This paper explores patients’ contributions to informing patient safety research at an early stage, within a project on intravenous infusion errors. Currently, there is little or no guidance on how best to involve patients and the wider public in shaping patient safety research, and indeed, whether such efforts are worthwhile. Method We ran a 3-hour workshop involving nine patients with experience of intravenous therapy in the hospital setting. The first part explored patients’ experiences of intravenous therapy. We derived research questions from the resulting discussion through qualitative analysis. In the second part, patients were asked for feedback on patient information sheets considering both content and clarity, and on two potential approaches to framing our patient information: one that focused on research on safety and error, the other on quality improvement. Results The workshop led to a thorough review of how we should engage with patients. Importantly, there was a clear steer away from terms such as ‘error’ and ‘safety’ that could worry patients. The experiences that patients revealed were also richer than we had anticipated, revealing different conceptions of how patients related to their treatment and care, their role in safety and use of medical devices, the different levels of information they preferred, and broader factors impacting perceptions of their care. Conclusion Involving patients at an early stage in patient safety research can be of great value. Our workshop highlighted sensitivities around potentially worrying patients about risks that they might not have considered previously, and how to address these. Patient representatives also emphasised a need to expand the focus of patient safety research beyond clinicians and error, to include factors affecting perceptions of quality and safety for patients more broadly

Elevated c-Src is linked to altered cell–matrix adhesion rather than proliferation in KM12C human colorectal cancer cells

Elevated expression and/or activity of c-Src, the prototype of the Src family of protein tyrosine kinases, is associated with the development of human colon cancer. However, despite the known pleiotropic effects of these kinases in promoting (a) cell growth downstream of growth factor receptors, and (b) the dynamic regulation of integrin adhesions in fibroblast model systems, their precise role in epithelial cancer cells is unknown. Here we addressed whether elevated expression and activity of cellular Src alters cell proliferation and/or cell–matrix adhesion in cancer cells from the Fidler model of colorectal metastasis. Although elevated Src correlates with ability to metastasise to the liver after intrasplenic injection, we found that this was not linked to enhanced growth, either in vitro or in vivo as sub-cutaneous tumours. However, elevated Src was associated with enhanced attachment to extracellular matrix. In addition, adhesion to fibronectin, was suppressed by agents that inhibited Src activity, while enforced elevation of Src in non-metastatic cells was sufficient to stimulate adhesion to fibronectin and enhanced assembly of adhesion complexes, without influencing cell growth. Thus, we conclude that one role of elevated Src in human colon cancer cells is to modulate integrin-dependent cell–matrix attachment and formation of adhesion structures, which may, in turn, influence cell motility and integrin-dependent cellular responses

Mutations in SLC12A5 in epilepsy of infancy with migrating focal seizures

The potassium-chloride co-transporter KCC2, encoded by SLC12A5, plays a fundamental role in fast synaptic inhibition by maintaining a hyperpolarizing gradient for chloride ions. KCC2 dysfunction has been implicated in human epilepsy, but to date, no monogenic KCC2-related epilepsy disorders have been described. Here we show recessive loss-of-function SLC12A5 mutations in patients with a severe infantile-onset pharmacoresistant epilepsy syndrome, epilepsy of infancy with migrating focal seizures (EIMFS). Decreased KCC2 surface expression, reduced protein glycosylation and impaired chloride extrusion contribute to loss of KCC2 activity, thereby impairing normal synaptic inhibition and promoting neuronal excitability in this early-onset epileptic encephalopathy

Sub region-specific modulation of synchronous neuronal burst firing after a kainic acid insult in organotypic hippocampal cultures

<p>Abstract</p> <p>Background</p> <p>Excitotoxicity occurs in a number of pathogenic states including stroke and epilepsy. The adaptations of neuronal circuits in response to such insults may be expected to play an underlying role in pathogenesis. Synchronous neuronal firing can be induced in isolated hippocampal slices and involves all regions of this structure, thereby providing a measure of circuit activity. The effect of an excitotoxic insult (kainic acid, KA) on Mg²⁺-free-induced synchronized neuronal firing was tested in organotypic hippocampal culture by measuring extracellular field activity in CA1 and CA3.</p> <p>Results</p> <p>Within 24 hrs of the insult regional specific changes in neuronal firing patterns were evident as: (i) a dramatic <it>reduction </it>in the ability of CA3 to generate firing; and (ii) a contrasting <it>increase </it>in the frequency and duration of synchronized neuronal firing events in CA1. Two distinct processes underlie the increased propensity of CA1 to generate synchronized burst firing; a lack of ability of the CA3 region to 'pace' CA1 resulting in an increased frequency of synchronized events; and a change in the 'intrinsic' properties limited to the CA1 region, which is responsible for increased event duration. Neuronal quantification using NeuN immunoflurescent staining and stereological confocal microscopy revealed no significant cell loss in hippocampal sub regions, suggesting that changes in the properties of neurons within this region were responsible for the KA-mediated excitability changes.</p> <p>Conclusion</p> <p>These results provide novel insight into adaptation of hippocampal circuits following excitotoxic injury. KA-mediated disruption of the interplay between CA3 and CA1 clearly increases the propensity to synchronized firing in CA1.</p

Production of phi mesons at mid-rapidity in sqrt(s_NN) = 200 GeV Au+Au collisions at RHIC

We present the first results of meson production in the K^+K^- decay channel from Au+Au collisions at sqrt(s_NN) = 200 GeV as measured at mid-rapidity by the PHENIX detector at RHIC. Precision resonance centroid and width values are extracted as a function of collision centrality. No significant variation from the PDG accepted values is observed. The transverse mass spectra are fitted with a linear exponential function for which the derived inverse slope parameter is seen to be constant as a function of centrality. These data are also fitted by a hydrodynamic model with the result that the freeze-out temperature and the expansion velocity values are consistent with the values previously derived from fitting single hadron inclusive data. As a function of transverse momentum the collisions scaled peripheral.to.central yield ratio RCP for the is comparable to that of pions rather than that of protons. This result lends support to theoretical models which distinguish between baryons and mesons instead of particle mass for explaining the anomalous proton yield.Comment: 326 authors, 24 pages text, 23 figures, 6 tables, RevTeX 4. To be submitted to Physical Review C as a regular article. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm

Resectable adenocarcinomas in the pancreatic head: the retroperitoneal resection margin is an independent prognostic factor

Pancreatic cancer is a lethal disease, and even after assumed margin-free pancreatoduodenectomy, most patients die within few years. The aims were to evaluate the importance of standardised histopathologic assessment for adequacy of reporting and survival estimates, and to report on prognostic factors in a setting of standardised histopathologic assessment. We performed immunohistochemical evaluation, slide review, and review of histopathologic reports from all pancreatoduodenectomies at Rikshospitalet University Hospital in 1980–2004. Reports from 1998-2004 at this institution were compared with reports from all other Norwegian institutions in the same period. Standardised histopathologic assessment and reporting was found necessary to avoid underestimation of poor prognostic factors, and to avoid misdiagnosis of tumours originating from non-pancreatic tissue (ampulla, distal bile duct, duodenum). Standardised histopathology was more important than surgical volume for completeness of reporting and for reliability of survival estimates, particularly with respect to lymph node evaluation. Immunostaining for MUC1 and MUC4 identified a subgroup of patients with particularly poor prognosis. Standardised histopathologic evaluation should be a first prerequisite to assure adequate histopathology after pancreatoduodenectomy. Immunostaining may identify tumour markers potentially targetable in future adjuvant treatments for pancreatic cancer

Anticipated impact of the 2009 Four Corners raid and arrests

Archaeological looting on United States federal land has been illegal for over a century. Regardless, the activity has continued in the Four Corners region. This paper discusses how the 1979 Archaeological Resources Protection Act (ARPA) can be viewed as sumptuary law, and within a sumptuary context, subversion can be anticipated. An analysis of 1986 and June 2009 federal raids in the Four Corners will exemplify this point by identifying local discourses found in newspapers both before and after each raid, which demonstrate a sumptuary effect. Ultimately, this paper concludes that looting just adapted, rather than halted, after each federal raid and that understanding this social context of continued local justification and validation of illegal digging is a potential asset for cultural resource protection