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use of an advanced electronic cell counter/flow cytometer (ADVIA 120) allowed us to screen other parameters as well despite of the limited murine blood volume. We analysed leukocytes, red blood cells, haemoglobin content, haematocrit, mean cellular volume, mean cellular haemoglobin, mean cellular haemoglobin concentration, platelets, neutrophiles, lymphocytes, monocytes, eosinophiles and basophiles. In these tests of whole blood we found only a change in the platelet numbers, whereas all other haematological parameters were not affected. The mean platelet counts from wild type and anxA7-/- mutant mice are determined as 674 × 103/μl and 774 × 103/μl, respectively. The platelet counts in knock out mice are significantly higher (p = 0.0275; n knock out = 11, n wild type = 14). An increase in platelet counts is a rather uncommon disorder. In humans, platelet counts normally increase only transiently as in reactive thrombocytosis and under postoperative conditions or are largely increased in neoplastic diseases. By contrast, the anxA7-/-mice are healthy and viable. Therefore we tested the platelet function and performed aggregometry measurements with platelet rich plasma. Platelet activation is observed as a morphological change from the resting discoid state to activated spherical cells with pseudopods. The morphological changes are due to cytoskeletal rearrangements. In vitro the activated cells form aggregates recruiting additional cells in the solution thereby reducing its cloudiness. Analysis of the transmission values of aggregation curves after platelet activation by ristocetin addition (von Willebrand cofactor) showed that both curves differed significantly at the time point of seven seconds after platelet initiation (p = 0.0287, n knock out = 16, n wild type = 15; Fig. 6). Annexin A7 deficient platelets showed a slightly lowered aggregation velocity. When we compared the aggregation curves of human platelets from a healthy donor with the ones obtained from an individual with a von Willebrand factor type 1 defect, we found that the difference in the curves was much more pronounced as observed in our studies of healthy mouse platelets and anxA7-/-platelets. Furthermore we found that murine platelets responded immediately to the initiating chemical whereas human platelets have a lag phase [23]."}

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Therefore we tested the platelet function and performed aggregometry measurements with platelet rich plasma. Platelet activation is observed as a morphological change from the resting discoid state to activated spherical cells with pseudopods. The morphological changes are due to cytoskeletal rearrangements. In vitro the activated cells form aggregates recruiting additional cells in the solution thereby reducing its cloudiness. Analysis of the transmission values of aggregation curves after platelet activation by ristocetin addition (von Willebrand cofactor) showed that both curves differed significantly at the time point of seven seconds after platelet initiation (p = 0.0287, n knock out = 16, n wild type = 15; Fig. 6). Annexin A7 deficient platelets showed a slightly lowered aggregation velocity. When we compared the aggregation curves of human platelets from a healthy donor with the ones obtained from an individual with a von Willebrand factor type 1 defect, we found that the difference in the curves was much more pronounced as observed in our studies of healthy mouse platelets and anxA7-/-platelets. Furthermore we found that murine platelets responded immediately to the initiating chemical whereas human platelets have a lag phase [23]."}

{"project":"2_test","denotations":[{"id":"12925238-11798399-8102399","span":{"begin":2336,"end":2338},"obj":"11798399"}],"text":"The use of an advanced electronic cell counter/flow cytometer (ADVIA 120) allowed us to screen other parameters as well despite of the limited murine blood volume. We analysed leukocytes, red blood cells, haemoglobin content, haematocrit, mean cellular volume, mean cellular haemoglobin, mean cellular haemoglobin concentration, platelets, neutrophiles, lymphocytes, monocytes, eosinophiles and basophiles. In these tests of whole blood we found only a change in the platelet numbers, whereas all other haematological parameters were not affected. The mean platelet counts from wild type and anxA7-/- mutant mice are determined as 674 × 103/μl and 774 × 103/μl, respectively. The platelet counts in knock out mice are significantly higher (p = 0.0275; n knock out = 11, n wild type = 14). An increase in platelet counts is a rather uncommon disorder. In humans, platelet counts normally increase only transiently as in reactive thrombocytosis and under postoperative conditions or are largely increased in neoplastic diseases. By contrast, the anxA7-/-mice are healthy and viable. Therefore we tested the platelet function and performed aggregometry measurements with platelet rich plasma. Platelet activation is observed as a morphological change from the resting discoid state to activated spherical cells with pseudopods. The morphological changes are due to cytoskeletal rearrangements. In vitro the activated cells form aggregates recruiting additional cells in the solution thereby reducing its cloudiness. Analysis of the transmission values of aggregation curves after platelet activation by ristocetin addition (von Willebrand cofactor) showed that both curves differed significantly at the time point of seven seconds after platelet initiation (p = 0.0287, n knock out = 16, n wild type = 15; Fig. 6). Annexin A7 deficient platelets showed a slightly lowered aggregation velocity. When we compared the aggregation curves of human platelets from a healthy donor with the ones obtained from an individual with a von Willebrand factor type 1 defect, we found that the difference in the curves was much more pronounced as observed in our studies of healthy mouse platelets and anxA7-/-platelets. Furthermore we found that murine platelets responded immediately to the initiating chemical whereas human platelets have a lag phase [23]."}

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Therefore we tested the platelet function and performed aggregometry measurements with platelet rich plasma. Platelet activation is observed as a morphological change from the resting discoid state to activated spherical cells with pseudopods. The morphological changes are due to cytoskeletal rearrangements. In vitro the activated cells form aggregates recruiting additional cells in the solution thereby reducing its cloudiness. Analysis of the transmission values of aggregation curves after platelet activation by ristocetin addition (von Willebrand cofactor) showed that both curves differed significantly at the time point of seven seconds after platelet initiation (p = 0.0287, n knock out = 16, n wild type = 15; Fig. 6). Annexin A7 deficient platelets showed a slightly lowered aggregation velocity. When we compared the aggregation curves of human platelets from a healthy donor with the ones obtained from an individual with a von Willebrand factor type 1 defect, we found that the difference in the curves was much more pronounced as observed in our studies of healthy mouse platelets and anxA7-/-platelets. Furthermore we found that murine platelets responded immediately to the initiating chemical whereas human platelets have a lag phase [23]."}