Conversely, 212 out of 543 initially seropositive animals became seronegative for their second serum sample.
Besides the clinical symptoms and initial serum beta-hCG level, the second serum beta-hCG measurement (i.e., rising or declining) and trend in serum beta-hCG concentration are also very indicative for the management choice.
As depicted in Figure 2a, all recipient mice had high levels of anti-J8 IgG antibodies when tested on day 0 after the second serum administration.
After 6 or 12 months, treatment was discontinued since viral load did not decrease more than 2 logs and a second serum sample was obtained for analysis (T1 and T2 samples for 6 and 12 months, respectively).
The results, presented in Figure 5A, demonstrate that the serum usually used in this study (FBS) induced CYP1A1, unlike the second serum characterized by a naturally low FA content (FBSLess).
For non-responder patients from the HCV T group a second serum sample taken after interruption of treatment (6 or 12 months after its start) was available and included in the study.
For the second serum (anti-GAD65 9%TC; anti-GAD67 17%TC), GAD65 did not inhibit anti-GAD67, although competition with each of the homologous antigens caused complete inhibition, indicating that the two antibody populations were not cross-reactive.
A second round of analysis was performed 86 days after the first analytical round, on the 104 antigens, using a second serum aliquot that had been subjected to an identical freeze/thaw history as the samples used in round one.
A second serum sample was not available.
A second serum sample was obtained from nine patients.
Second, serum cortisol concentrations were not measured at baseline.
