Concomitant history of cancer in acute pulmonary embolism is connected with poorer outcome

Purpose: Cancer increases the risk of venous thromboembolism (VTE) substantially. VTE is connected with poorer outcome in cancer patients. The aim of our study was to investigate the impact of cancer on the severity and short-term outcome of pulmonary embolism (PE). Methods: We retrospectively analyzed the data of 182 patients with confirmed PE. PE patients were subdivided in the group with concomitant active cancer disease or history of cancer or in the group without cancer. Groups were compared with Wilcoxon–Mann–Whitney Test. Logistic regression models were calculated to investigate the association between cancer and several parameters such as age and PE severity status as well as the association between in-hospital death and the parameters age, gender, PE severity status and cancer. Results: While 20.3% PE patients reported an active cancer disease or a history of cancer (64.9% female), 79.7% of the PE patients did not (60.7% female). PE patients with cancer were 5 years older (76.0 (65.5/81.0) vs. 71.0 (58.5/80.5) years, P=0.055) and revealed a higher PE severity status in mean (1.91±0.53 vs. 1.67±0.54, P=0.069). Univariate logistic regression models showed an association between cancer and age (OR 1.04, CI 95% (1.01–1.08), P=0.017) as well as cancer and the severity status (OR 2.38 (1.05–5.26), P=0.037). In-hospital death in the early course was strongly connected with the PE severity status (OR 36.60 (2.99–448.68), P=0.0049), but not with cancer (P=0.65). Conclusions: Concomitant history of cancer in acute PE was associated with higher PE severity status and therefore poorer outcome

Evaluation of Risk Stratification Markers and Models in Acute Pulmonary Embolism: Rationale and Design of the MARS-PE (Mainz Retrospective Study of Pulmonary Embolism) Study Programme

An acute pulmonary embolism (PE) is a crucial event in patients’ life and connected with serious morbidity and mortality. Regarding a high case-fatality rate, early and accurate risk-stratification is crucial. Risk for mortality and complications are closely related to hemodynamic stability and cardiac adaptations. The currently recommended risk-stratification approach is not overall simple to use and might delay the identification of those patients, who should be monitored more closely and may treated with more aggressive treatment strategies. Additionally, some risk-stratification criteria for the imaging procedures are still imprecise. Summarized, the search for the most effective risk-stratification tools is still ongoing and some diagnostic criteria might have to be refined. In the MAinz Retrospective Study of Pulmonary Embolism (MARS-PE), overall 182 consecutive patients with confirmed PE were retrospectively included over a 5-year period. Clinical, echocardiographic, functional and laboratory parameters were assessed. The study was designed to provide answers to some of the mentioned relevant questions

Alloantigen-induced T-cell proliferation: Lyt phenotype of responding cells and blocking of proliferation by Lyt antisera

Cytotoxic T cells of the mouse express Lyt-1 as well as Lyt-2 and -3 on their surface, and T-cell cytotoxicity can be blocked by Lyt-2 and Lyt-3 (but not Lyt-1) antisera in the absence of added complement [Nakayama, E., Shiku, H., Stockert, E., Oettgen, H. F. & Old, L. J. (1979) Proc. Natl. Acad. Sci. USA 76, 1977-1981]. This analysis has now been extended to the study of the Lyt phenotype of T cells responding to alloantigens, concanavalin A (Con A), and phytohemagglutinin (PHA) and the effect of Lyt antibody on T-cell proliferation and the generation of H-2-specific killer T cells. H-2 (D/K and I), Con A, and PHA stimulation was abolished by pretreating responding cell populations with Lyt-1 antiserum and complement. Pretreatment with Lyt-2 or -3 antiserum and complement did not decrease alloantigen or Con A stimulation but did abolish PHA stimulation. Cytotoxic cells were not generated in H-2 alloantigen-primed cultures pretreated with Lyt-1, -2, or -3 antiserum and complement. When responding cells were cultured with Lyt antiserum in the absence of added complement, Lyt-2 or -3 antiserum (but not Lyt-1 antiserum) blocked alloantigen-induced proliferation and delayed generation of killer cells. Under similar conditions, Con A and PHA stimulation was not blocked by Lyt-1,-2, or -3 antiserum. Evidence from these Lyt elimination and blocking tests and from direct Lyt phenotyping of responding cells leads to the following conclusions. Two populations of Lyt(+) cells are involved: Lyt-1(+)2(-)3(-) and Lyt-1(+)2(+)3(+). Current evidence does not favor the existence of Lyt-1(-)2(+)3(+) cells but indicates that pre-killer and killer cells derive from the Lyt-1(+)2(+)3(+) population and have a Lyt-1(+)2(+)3(+) phenotype. H-2 (D/K and I) and PHA stimulation ordinarily activate the Lyt-1(+)2(+)3(+) population, whereas Con A and I region or Mls locus antigens activate the Lyt-1(+)2(-)3(-) population. However, when Lyt-1(+)2(+)3(+) cells are eliminated or blocked by Lyt-2 or -3 antiserum, H-2 alloantigen stimulation leads to proliferation of the Lyt-1(+)2(-)3(-) population. Blocking of H-2-induced proliferation by Lyt-2 or -3 antiserum adds further support to the possibility that molecules bearing Lyt-2 and -3 determinants are involved in T-cell recognition

COLOMBO: Guideline for emission optimised traffic light control

This guideline gives the traffic engineer an overview on rules to be followed and on supporting tools available to consider emission effects when developing and implementing TLC algorithms