Fluvial carbon export from a lowland Amazonian rainforest in relation to atmospheric fluxes

We constructed a whole carbon budget for a catchment in the Western Amazon Basin, combining drainage water analyses with eddy covariance measured terrestrial CO2 fluxes. As fluvial C export can represent permanent C export it must be included in assessments of whole site C balance, but is rarely done. The footprint area of the flux tower is drained by two small streams (~5-7 km2) from which we measured the dissolved inorganic carbon (DIC), dissolved organic carbon (DOC), particulate organic carbon (POC) export and CO2 efflux. The EC measurements showed the site C balance to be +0.7 ± 9.7 Mg C ha-1 yr-1 (a source to the atmosphere) and fluvial export was 0.3 ± 0.04 Mg C ha-1 yr-1. Of the total fluvial loss 34% was DIC, 37% DOC and 29% POC. The wet season was most important for fluvial C export. There was a large uncertainty associated with the EC results and with previous biomass plot studies (-0.5 ± 4.1 Mg C ha-1 yr-1), hence it cannot be concluded with certainty whether the site is C sink or source. The fluvial export corresponds to only 3-7 % of the uncertainty related to the site C balance, thus other factors need to be considered to reduce the uncertainty and refine the estimated C balance. However, stream C export is significant, especially for almost neutral sites where fluvial loss may determine the direction of the site C balance. The fate of C downstream then dictates the overall climate impact of fluvial export

Lymph-vascular Space Involvement and Outer One-third Myometrial Invasion Are Strong Predictors of Distant Haematogeneous Failures in Patients with Stage I-II Endometrioid-type Endometrial Cancer

The aim of this retrospective study was to assess the predictive value of different clinicopathological variables (patient age, tumour size, FIGO grade, myometrial invasion, lymph-vascular space involvement [LVSI], invasion margins, peri-tumour phlogistic infiltrate and mitotic activity) for the risk of distant haematogenous recurrences in patients with endometrioid-type stage Ib-II endometrial cancer. Between August 1990 and April 2005, 259 patients had undergone laparotomy, peritoneal washing, total abdominal hysterectomy and bilateral salpingo-oophorectomy, with or without pelvic +/- para-aortic lymphadenectomy for endometrioid-type endometrial cancer. Thirty-six (13.9%) patients had developed recurrent disease after a median time of 17 months (range, 2-128 months). The relapse had been locoregional in 9, distant in 21 and both locoregional plus distant in 6 cases. This study assessed 12 patients with FIGO stage Ib-II disease who had developed distant haematogenous recurrences and 20 randomly chosen control patients with FIGO stage Ib-II disease who had remained recurrence-free after a median follow-up of 52 months (range, 37-66 months). Adjuvant therapy had been: no further treatment in 15 patients, external pelvic irradiation in 14 patients, adjuvant external pelvic irradiation plus brachytherapy in 2 patients and platinum-based chemotherapy followed by external pelvic irradiation in I patient. The site of distant failure had been the lung in 9 patients, liver in 2 patients and lung plus liver in I patient. A concomitant locoregional relapse (vagina or lymph nodes) had occurred in 3 patients. The median interval between surgery and the development of distant failure had been 16.5 months (range, 5-113 months). On univariate analysis, a higher incidence of FIGO grade 3 (50% versus 10%, p=0.0114), outer one-third myometrial invasion (91.7% versus 35.0%, p=0.0051) and LVSI (75.0.% versus 20.0%, p=0.0022) was found in the patients who had developed distant haematogeneous metastases compared to the recurrence-free women. Multivariate analysis showed that LVSI (p=0.0264) and deep myometrial invasion (p=0.0345) were independent predictive variables for the risk of distant haematogeneous failure. Patients with these pathological findings should be enrolled in randomised trials designed to assess the role of adjuvant chemotherapy alone or combined with sequential and /or concomitant external pelvic irradiation

Overview of the molecular determinants contributing to the expression of Psoriasis and Psoriatic Arthritis phenotypes

Psoriasis and psoriatic arthritis are multifactorial chronic disorders whose etiopathogenesis essentially derives from the alteration of several signalling pathways and the co-occurrence of genetic, epigenetic and non-genetic susceptibility factors that altogether affect the functional and structural property of the skin. Although shared and differential susceptibility genes and molecular pathways are known to contribute to the onset of pathological phenotypes, further research is needed to dissect the molecular causes of psoriatic disease and its progression towards Psoriatic Arthritis. This review will therefore be addressed to explore differences and similarities in the etiopathogenesis and progression of both disorders, with a particular focus on genes involved in the maintenance of the skin structure and integrity (keratins and collagens), modulation of patterns of recognition (through Toll-like receptors and dectin-1) and immuno-inflammatory response (by NLRP3-dependent inflammasome) to microbial pathogens. In addition, special emphasis will be given to the contribution of epigenetic elements (methylation pattern, non-coding RNAs, chromatin modifiers and 3D genome organization) to the etiopathogenesis and progression of psoriasis and psoriatic arthritis. The evidence discussed in this review highlights how the knowledge of patients' clinical and (epi)genomic make-up could be helpful for improving the available therapeutic strategies for psoriasis and psoriatic arthritis treatment