First report of Pandora neoaphidis resting spore formation in vivo in aphid hosts

2012 ◽  
Vol 116 (2) ◽  
pp. 196-203 ◽  
Author(s):  
Ana Clara Scorsetti ◽  
Annette Bruun Jensen ◽  
Claudia López Lastra ◽  
Richard A. Humber
2001 ◽  
Vol 79 (9) ◽  
pp. 1076-1082 ◽  
Author(s):  
Lene Thomsen ◽  
José Bresciani ◽  
Jørgen Eilenberg

Three species within the Entomophthora muscae (Cohn) Fresenius complex (Entomophthora schizophorae Keller & Wilding, E. muscae s.str., and E. muscae "group B") were investigated for resting spore formation in vivo in the house fly (Musca domestica L.). Resting spores of E. muscae group B were experimentally induced from August to the beginning of February, while no resting spores were ever observed in E. schizophorae infected M. domestica or in flies infected by E. muscae s.str. originating from M. domestica. When newly dead fly cadavers containing E. muscae group B resting spores were kept moist, cystidia emerged from the abdomen; this is the first report of cystidia in the genus Entomophthora. Resting spore production was significantly affected by both temperature and E. muscae group B strain. More infected flies formed resting spores when kept 1 week at 10°C compared with constant exposure at 22°C, but the tendency of the different E. muscae group B strains to form resting spores persisted with shifting temperatures. After 4 months of incubation under natural winter conditions in Denmark, E. muscae group B resting spores germinated on water agar at 20°C with a 16 h light : 8 h dark photoperiod within 1 week, but no germ conidia were observed.Key words: Entomophthorales, Entomophthora muscae complex, Diptera, Musca domestica, resting spore formation, resting spore germination.


Blood ◽  
2009 ◽  
Vol 114 (8) ◽  
pp. 1655-1657 ◽  
Author(s):  
Claudio Graziano ◽  
Simona Carone ◽  
Emanuele Panza ◽  
Flora Marino ◽  
Pamela Magini ◽  
...  

Abstract Hereditary thrombocythemia is a rare autosomal dominant disorder caused by mutations in either the thrombopoietin gene (TPO) or its receptor c-MPL. TPO mutations described so far lead to thrombopoietin overproduction through increased translation of m-RNA. Unilateral transverse reduction limb defects are usually sporadic and generally thought to be caused by vascular disruptions. Reports of inherited unilateral limb defects are extremely rare. In the present study, we describe a family with segregation of G185T TPO mutation in the 5′ UTR region in 4 subjects with thrombocythemia. Three of these patients also present congenital transverse limb defects. Association of these events gives a strong hint of the in vivo involvement of thrombopoietin in vasculogenesis, confirming the role of TPO in human development of the hemangioblast, the embryonic progenitor of the hematopoietic and endothelial lineages. This is the first report showing that vascular disruptions could be secondary to specific gene derangements.


JTCVS Open ◽  
2020 ◽  
Vol 3 ◽  
pp. 140-148
Author(s):  
Takuma Miyamoto ◽  
Yuichiro Kado ◽  
David J. Horvath ◽  
Barry D. Kuban ◽  
Shiva Sale ◽  
...  

2002 ◽  
Vol 46 (11) ◽  
pp. 3648-3649 ◽  
Author(s):  
Amanda J. Leach ◽  
Peter S. Morris ◽  
Heidi Smith-Vaughan ◽  
John D. Mathews

ABSTRACT This is the first report of in vivo pneumococcal penicillin MIC drift from 4.0 to 16.0 mg/liter, possibly associated with alterations in the pbp1a gene. The case presented here is of an infant with early onset recurrent pneumonia and chronic bronchitis requiring repeated antibiotics.


1994 ◽  
Vol 47 (11) ◽  
pp. 978-981 ◽  
Author(s):  
T F McCaul ◽  
A J Dare ◽  
J P Gannon ◽  
A J Galbraith

Blood ◽  
2011 ◽  
Vol 117 (17) ◽  
pp. 4615-4622 ◽  
Author(s):  
Ellen Vercauteren ◽  
Jan Emmerechts ◽  
Miet Peeters ◽  
Marc F. Hoylaerts ◽  
Paul J. Declerck ◽  
...  

Abstract The enhancement of fibrinolysis constitutes a promising approach to treat thrombotic diseases. Activated thrombin activatable fibrinolysis inhibitor (TAFIa) attenuates fibrinolysis and is an attractive target to develop profibrinolytic drugs. TAFI can be activated by thrombin, thrombin/thrombomodulin, or plasmin, but the in vivo physiologic TAFI activator(s) are unknown. Here, we generated and characterized MA-TCK26D6, a monoclonal antibody raised against human TAFI, and examined its profibrinolytic properties in vitro and in vivo. In vitro, MA-TCK26D6 showed a strong profibrinolytic effect caused by inhibition of the plasmin-mediated TAFI activation. In vivo, MA-TCK26D6 significantly decreased fibrin deposition in the lungs of thromboembolism-induced mice. Moreover, in the presence of MA-TCK26D6, plasmin-α2-antiplasmin complexes in plasma of thromboembolism-induced mice were significantly increased compared with a control antibody, indicative of an acceleration of fibrinolysis through MA-TCK26D6. In this study, we show that plasmin is an important TAFI activator that hampers in vitro clot lysis. Furthermore, this is the first report on an anti-TAFI monoclonal antibody that demonstrates a strong profibrinolytic effect in a mouse thromboembolism model.


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