RESULTS: Questionnaires were obtained on 234 of 284 fatalities. 55% of deaths were attributed directly to SSc and 41% to non-SSc causes; in 4% the cause of death was not assigned. Of the SSc-related deaths, 35% were attributed to pulmonary fibrosis, 26% to pulmonary arterial hypertension (PAH) and 26% to cardiac causes (mainly heart failure and arrhythmias). Among the non-SSc-related causes, infections (33%) and malignancies (31%) were followed by cardiovascular causes (29% ABSTRACT ObjectivesTo determine the causes and predictors of mortality in systemic sclerosis (SSc). Methods Patients with SSc (n=5860) fulfi lling the American College of Rheumatology criteria and prospectively followed in the EULAR Scleroderma Trials and Research (EUSTAR) cohort were analysed. EUSTAR centres completed a structured questionnaire on cause of death and comorbidities. Kaplan-Meier and Cox proportional hazards models were used to analyse survival in SSc subgroups and to identify predictors of mortality. Results Questionnaires were obtained on 234 of 284 fatalities. 55% of deaths were attributed directly to SSc and 41% to non-SSc causes; in 4% the cause of death was not assigned. Of the SSc-related deaths, 35% were attributed to pulmonary fi brosis, 26% to pulmonary arterial hypertension (PAH) and 26% to cardiac causes (mainly heart failure and arrhythmias). Among the nonSSc-related causes, infections (33%) and malignancies (31%) were followed by cardiovascular causes (29%).Of the non-SSc-related fatalities, 25% died of causes in which SSc-related complications may have participated (pneumonia, sepsis and gastrointestinal haemorrhage). Independent risk factors for mortality and their HR were: proteinuria (HR 3.34), the presence of PAH based on echocardiography (HR 2.02), pulmonary restriction (forced vital capacity below 80% of normal, HR 1.64), dyspnoea above New York Heart Association class II (HR 1.61), diffusing capacity of the lung (HR 1.20 per 10% decrease), patient age at onset of Raynaud's phenomenon (HR 1.30 per 10 years) and the modifi ed Rodnan skin score (HR 1.20 per 10 score points). Conclusion Disease-related causes, in particular pulmonary fi brosis, PAH and cardiac causes, accounted for the majority of deaths in SSc.Systemic sclerosis (SSc) is a multisystem disease with vascular, infl ammatory and fi brotic components.

Results from the application of Persistent Scatterers Interferometry in Lisbon Metropolitan Area revealed two previously unknown subsiding urban areas: one (Laranjeiras) is located in the center of Lisbon; another (Vialonga) is to be found toward the North, in an industrial region crossed by Lisbon's main highway and railway lines. The two subsiding sectors are bordered by sharp velocity gradients, and the subsidence pattern appears partially delimited by mapped geologic faults. Surface geology and urbanization alone are unable to explain the phenomena. In the Vialonga area, the historical record of water pore pressure shows a clear decline of the levels (up to 65 m in 27 years), providing evidence of over-exploitation of groundwater resources. Limited information from wells drilled inside and outside the subsidence area points to a spatial correlation between the subsidence and the water pressure levels, and suggests that faults could be acting as hydraulic barriers in the aquifer system. The surface subsidence detected is probably caused by compaction of a clay-rich Oligocene-aged aquitard, led by over-exploitation of adjacent aquifers. The same Oligocene aquitard layer is present in the Laranjeiras area, immediately bellow a multi-layered sand-clay-limestone Miocene aquifer, but further work is needed to diagnose the possibility of over-exploitation of groundwater here. In this work we were able to independently confirm the PSI results, by comparing autonomous PSI results processed for the same geographical areas, and by comparing PSI with leveling and continuous GPS derived subsidence velocities, whose close match provided further ground validation of the space-borne PSI technique.

Two cases of fatal infection caused by parvovirus in a white tiger (Panthera tigris) and an African lion (Panthera leo) at the Lisbon Zoo (Portugal) are described. Gross findings at necropsy were catharral enteritis in the tiger and severe hemorrhagic enteritis in the lion. Histopathologic examination revealed, in both animals, intestinal crypt necrosis and lymphocyte depletion in the germinal centers of the mesenteric lymph nodes. Bacteriologic examination was negative for common bacterial pathogens, including Salmonella. Amplification of the parvovirus VP2 complete gene was achieved in both cases and sequencing analysis identified these isolates as feline panleukopenia virus (FPLV). The nucleotide sequences obtained from these two viruses were genetically indistinguishable. The phylogenetic analysis of FPLV strains from domestic cats obtained in the Lisbon area revealed the circulation of FPLV strains highly similar to those isolated from the tiger and lion, which strongly suggests that stray cats may have been the source of infection.

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 To evaluate the applicability of NS3-ELISA in field scenario, a total of 562 serum 39 samples collected from uninfected, BTV infected and vaccinated animals were tested 40 for NS3 antibodies. Taken together, the results confirm that NS3 antibodies were 41 induced to the greatest levels in animals infected with BTV in comparison to the levels 42 induced in animals immunized with inactivated BTV vaccines, implying that antibody 43 response to NS3 allows the differentiation between infected and vaccinated animals. 44 45