EU-wide methodology to map and assess ecosystem condition

The EU Biodiversity Strategy for 2030 calls for developing an EU-wide methodology to map, assess and achieve good condition of ecosystems, so they can deliver benefits to society through the provision of ecosystem services. The EU-wide methodology presented in this report addresses this methodological gap. The EU-wide methodology has adopted the System of Environmental Economic Accounting - Ecosystem Accounting (SEEA EA) as reference framework. The SEEA EA is an integrated framework for organizing biophysical information about ecosystems, adopted as a global statistical standard by the United Nations. The SEEA EA is also the reference framework under the proposal for the amendment of Regulation (EU) No 691/2011 on European environmental economic accounts. Building on previous work done within the MAES initiative, the EU-wide methodology presents useful insights to operationalise the SEEA EA at EU level by integrating different EU data streams in a consistent way with this global statistical standard to consistently map and assess ecosystem condition in the EU across all ecosystem types. The adoption of the SEEA EA framework offers the flexibility to integrate different data flows, leveraging the use of available EU data, such as data reported by MS under EU legislation and EU geospatial data. The EU-wide methodology. The implementation of the EU-wide methodology, making use of available data, will provide the scientific knowledge base to support a range of policies and legal instruments

Pneumomediastinum as a complication of critical pertussis

Background and Aims: Pertussis is a common and potentially serious disease affecting mainly infants and young children. In its non-classic presentation, pertussis can be clinically indistinguishable from other respiratory illnesses. Pertussis today often remains underdiagnosed in adults. Our aims was to report a complicated cases of pertussis. Results: A case of serologically confirmed pertussis occurred in an 18-year-old man presenting with pneumomediastinum, subcutaneous emphysema in the neck and chest, and persistent attacks of coughing with apnea that required treatment in the intensive care unit. Conclusion: Pneumomediastinum and subcutaneous emphysema have never been described in adult patients with pertussis. Physicians should be aware that patients presenting with persistent cough and pneumomediastinum may have pertussis and include this in their differential diagnosis

Extra-Articular Manifestations and Comorbidities in Psoriatic Disease: A Journey Into the Immunologic Crosstalk

Psoriatic arthritis (PsA) is a chronic inflammatory disease primarily affecting peripheral and axial joints, with the possible presence of extra-articular manifestations (EAMs), such as psoriasis, uveitis, and inflammatory bowel disease. Recently, the concept of psoriatic disease (PsD) has been proposed to define a systemic condition encompassing, in addition to joints and EAMs, some comorbidities (e.g., metabolic syndrome, type II diabetes, hypertension) that can affect the disease outcome and the achievement of remission. EAMs and comorbidities in PsA share common immunopathogenic pathways linked to the systemic inflammation of this disease; these involve a broad variety of immune cells and cytokines. Currently, various therapeutics are available targeting different cytokines and molecules implicated in the inflammatory response of this condition; however, despite an improvement in the management of PsA, comprehensive disease control is often not achievable. There is, therefore, a big gap to fill especially in terms of comorbidities and EAMs management. In this review, we summarize the clinical aspects of the main comorbidities and EAMs in PsA, and we focus on the immunopathologic features they share with the articular manifestations. Moreover, we discuss the effect of a diverse immunomodulation and the current unmet needs in PsD

Clinicopathologic study of 62 acinar cell carcinomas of the pancreas: Insights into the morphology and immunophenotype and search for prognostic markers

Acinar cell carcinoma (ACC) of the pancreas is a very rare tumor that has various morphologic features, which may give rise to diagnostic difficulties. Because of its rarity, many clinicopathologic characteristics remain to be further elucidated, and prognostic factors are yet to be well established. With the aim of better characterizing this carcinoma and searching for prognostic indicators, we collected 62 ACCs and investigated the following parameters: site, size, local infiltration, node and distant metastases, architectural pattern, nuclear atypia, presence of necrosis, lymphovascular and perineural invasion, proliferation, BCL10, trypsin, carboxyl ester lipase, amylase, lipase, PDX1, cytokeratin 19 (CK19), CK7, p53, and \u3b2-catenin expression. Twelve cases showing >30% of endocrine cells were reclassified as mixed acinar-neuroendocrine carcinomas, whereas 1 tumor was reclassified as a mixed ductal-acinar carcinoma and was excluded from the statistical prognostic evaluations. BCL10 and trypsin were the most reliable immunohistochemical markers, whereas amylase and lipase were not. Surgery was statistically correlated with a better prognosis (P=0.0008). Among resected tumors there was no difference in survival between ACCs and mixed acinar-neuroendocrine carcinomas, and factors that significantly correlated with poor prognosis were size >6.5 cm (P=0.004), lymph node (P=0.0039) and distant (P=0.008) metastases, and UICC stage (P=0.009). Stage was the only independent prognostic factor at multivariable analysis, and the best prognostic discrimination was observed on grouping together stages I and II and grouping together stages III and IV, suggesting a simplification of the UICC staging for such cancers. In addition, vascular and perineural invasion and CK19 and p53 expression showed a trend for poor prognosis, not reaching statistical significance

Clinicopathologic Study of 62 Acinar Cell Carcinomas of the Pancreas: Insights Into the Morphology and Immunophenotype and Search for Prognostic Markers.

Acinar cell carcinoma (ACC) of the pancreas is a very rare tumor that has various morphologic features, which may give rise to diagnostic difficulties. Because of its rarity, many clinicopathologic characteristics remain to be further elucidated, and prognostic factors are yet to be well established. With the aim of better characterizing this carcinoma and searching for prognostic indicators, we collected 62 ACCs and investigated the following parameters: site, size, local infiltration, node and distant metastases, architectural pattern, nuclear atypia, presence of necrosis, lymphovascular and perineural invasion, proliferation, BCL10, trypsin, carboxyl ester lipase, amylase, lipase, PDX1, cytokeratin 19 (CK19), CK7, p53, and \u3b2-catenin expression. Twelve cases showing >30% of endocrine cells were reclassified as mixed acinar-neuroendocrine carcinomas, whereas 1 tumor was reclassified as a mixed ductal-acinar carcinoma and was excluded from the statistical prognostic evaluations. BCL10 and trypsin were the most reliable immunohistochemical markers, whereas amylase and lipase were not. Surgery was statistically correlated with a better prognosis (P=0.0008). Among resected tumors there was no difference in survival between ACCs and mixed acinar-neuroendocrine carcinomas, and factors that significantly correlated with poor prognosis were size >6.5 cm (P=0.004), lymph node (P=0.0039) and distant (P=0.008) metastases, and UICC stage (P=0.009). Stage was the only independent prognostic factor at multivariable analysis, and the best prognostic discrimination was observed on grouping together stages I and II and grouping together stages III and IV, suggesting a simplification of the UICC staging for such cancers. In addition, vascular and perineural invasion and CK19 and p53 expression showed a trend for poor prognosis, not reaching statistical significance

Epigenetic and Genetic Changes of APC Gene in Acinar Cell Carcinoma of the Pancreas

Background: Genetic and epigenetic alterations involved in the pathogenesis of pancreatic acinar cell carcinoma (ACC) are largely unknown. ACCs generally lack mutations of KRAS, p53, DPC4 and p16, while mutations of the APC gene have been previously described in 17.6% of ACCs. However, it is not known whether loss of function of APC gene in ACC can occur through multiple alternative genetic mechanisms. Design: We investigated promoter methylation and copy number of APC gene using MS-MLPA and FISH analysis in 14 ACCs. Droplet Digital PCR (ddPCR, Biorad Instrument) and immunohistochemistry were employed to evaluate APC mRNA and protein expression in the same tumors. Results: APC methylation was found in 10/14 (71.4%) cases and FISH analysis revealed loss of APC in 7 ACCs. Interestingly 4 ACCs (4/14 28.6% %) revealed both methylation and loss of APC. Only one case did not show any loss and methylation. Absolute quantification of APC mRNA levels demonstrated a significant reduction of the transcript in all investigated ACCs compared with normal control pancreases (10.5 \ub1 3.2 RNA copies/\u3bcl in ACCs versus 56.77 \ub1 8.1 RNA copies/\u3bcl in normal controls; p<0.0001). APC protein expression was not found in any case investigated. APC gene methylation and loss did not correlate with stage, grade and prognosis. Conclusions: APC gene inactivation is a frequent event in ACCs. Gene methylation and loss might be considered as a mechanism of APC haploinsufficiency. Moreover, our data suggest that APC gene alterations are an early event in ACC tumorigenesis

Epigenetic and Genetic Changes of APC Gene in Acinar Cell Carcinoma of the Pancreas

Background: Genetic and epigenetic alterations involved in the pathogenesis of pancreatic acinar cell carcinoma (ACC) are largely unknown. ACCs generally lack mutations of KRAS, p53, DPC4 and p16, while mutations of the APC gene have been previously described in 17.6% of ACCs. However, it is not known whether loss of function of APC gene in ACC can occur through multiple alternative genetic mechanisms. Design: We investigated promoter methylation and copy number of APC gene using MS-MLPA and FISH analysis in 14 ACCs. Droplet Digital PCR (ddPCR, Biorad Instrument) and immunohistochemistry were employed to evaluate APC mRNA and protein expression in the same tumors. Results: APC methylation was found in 10/14 (71.4%) cases and FISH analysis revealed loss of APC in 7 ACCs. Interestingly 4 ACCs (4/14 28.6% %) revealed both methylation and loss of APC. Only one case did not show any loss and methylation. Absolute quantification of APC mRNA levels demonstrated a significant reduction of the transcript in all investigated ACCs compared with normal control pancreases (10.5 \ub1 3.2 RNA copies/\u3bcl in ACCs versus 56.77 \ub1 8.1 RNA copies/\u3bcl in normal controls; p<0.0001). APC protein expression was not found in any case investigated. APC gene methylation and loss did not correlate with stage, grade and prognosis. Conclusions: APC gene inactivation is a frequent event in ACCs. Gene methylation and loss might be considered as a mechanism of APC haploinsufficiency. Moreover, our data suggest that APC gene alterations are an early event in ACC tumorigenesis