should be repeated. Clumps may be due to inadequate mixing of blood or to poor
technique in obtaining the blood specimen.
F. Related Studies
Albumin decreases polymer surface affinity for platelets. When covalently linked via amino silanes, albumin decreases embolization from implanted silicone rubber rings. In
these studies, mere exposure of the surface to albumin was sufficient to prevent a decline in the circulating platelet count for up to 6 hr in membrane oxygenator circuits.
Furthermore, albumin reduced platelet release of granule contents release of LA-PF4 and largely preserved platelet reactivity to the aggregating agents ADP and epinephrine.
Preservation of platelet functional integrity was corroborated by electron microscopy, which demonstrated morphologically intact platelet granules. When an air interface was
present, albumin was less effective in preserving platelet numbers and function. Addonizio and others. 1979
The total concentrations of IgG, IgA, and albumin were all higher than normal in platelets from patients with ITP. Previous reports have interpreted increases of IgA and
albumin as abnormal plasma trapping or protein adsorption by the ITP platelets George and Saucerman 1988. Medications are sometimes used to stimulate the bone marrow to
make more platelets. The most common side effect is fluid retention, or swelling www.lungcancer.about.comodtreatmentoflungcancerathrombocyt.htm
[updated 2011]
.
Serum anti-GPIIIa-49 –66 antibody correlates with thrombocytopenia and induces
acute thrombocytopenia in mice, whose GPIIIa-49 –66 is 83 homologous with its
human GPIIIa counterpart Cientat and others 1993. The passively transferred thrombocytopenia can be prevented and reversed with an albumin conjugate of GPIIIa-
49 –66 Nardi and others 1997.
CHAPTER 3 METHODOLOGY
G. Research Design
This study aimed to determine the percent increase in the number of platelets of thrombocytopenic Mus musculus white mice after the infusions of bovine serum
albumin BSA. The white mice used were female, 6-8 weeks old, and weighed 10-20 ± 1 g each. The white mice were obtained from a private breeder.
The experiment consisted of 2 groups: the Normal Group and the Thrombocytopenic Group.
The Normal Group was composed of 4 subgroups A, B, C, and D, which had 4 white mice in each. The total number of white mice in this group was 16. The white mice
of this group were not induced with thrombocytopenia, but were still treated with BSA infusions. Subgroup B was treated with 0.2 BSA infusions, Subgroup C with 0.4
BSA infusions, and Subgroup D with 0.6 BSA infusions. The treatment of BSA infusion was administered intravenously. Subgroup A was not treated with BSA infusions
and served as the negative control. The Thrombocytopenic Group was also composed of 4 subgroups A, B, C, and D,
which had 4 white mice in each. The total number of white mice in this group was 16. The white mice of this group were induced with thrombocytopenia, and were treated with
BSA infusions. Subgroup B was treated with 0.2 BSA infusions, Subgroup C with 0.4 BSA infusions, and Subgroup D with 0.6 BSA infusions. The treatment of BSA
infusion was also administered intravenously. Subgroup A was not treated with BSA infusions and was allowed to recover from thrombocytopenia naturally.
On Day 1, all the test subjects and the needed materials and chemicals were prepared; this included the induction of thrombocytopenia to the white mice of the
Thrombocytopenic Group and the preparation of the BSA infusions. On the next day, Day 2, blood samples of all the test subjects were collected through
tail-nicking method. The blood samples were collected using a microcontainer with EDTA, were diluted in 1:100 dilution of 1 ammonium oxalate solution, were charged
into a hemacytometer, and were mounted under a 40X light microscope. The number of platelets of each blood sample was counted and was recorded as the number of platelets
before the treatment. Each subgroup then received their corresponding concentrations of BSA infusions intravenously after the blood collection.
BSA infusions were again received by the test subjects 24 hours after Day 3 and 48 hours after Day 4 the first BSA infusions. Subgroups A of both groups received no BSA
infusions. Subgroups B of both groups received 0.2 BSA infusions; subgroups C received 0.4 BSA infusions, and subgroups C received 0.6 BSA infusions.
On Day 5, blood samples of all the test subjects were collected through tail-nicking method again. The blood samples were also collected using a microcontainer with EDTA,
were also diluted in 1:100 dilution of 1 ammonium oxalate solution, were also charged into a hemacytometer, and were also mounted under a 40X light microscope. The number
of platelets of each blood sample was counted and was recorded as the number of platelets after the treatment.
The numbers of platelets of the test subjects before and after the treatment were compared. This determined if there were any significant changes in the number of
platelets of the white mice after the BSA infusions.
Figure 2. Experimental Setup
H. Preparation of Solutions
