Sialic acid (SA) is overexpressed on cell membranes of
tumor cells,
and increased serum SA concentration has been observed in tumor-bearing
patients. Herein, a series of lanthanide-containing bimetallic complexes
(TDA–M–Lns) for targeting SA were prepared via coordination
among luminescent lanthanide ions (Ln3+ = Tb3+, Eu3+, Dy3+, or Sm3+), metal ion
quenchers (M2+ = Cu2+ or Co2+), and
the organic ligand 2,2′-thiodiacetic acid (TDA). SA can competitively
coordinate with Ln3+, resulting in the “signal-on”
of the Ln3+. Therefore, the TDA–M–Lns can
be simply used for cost-saving detection of SA in the blood samples.
Among the TDA–M–Lns, TDA–Co–Eu showed
the highest sensitivity to detect SA in the blood of tumor-bearing
mice. Furthermore, the TDA–Co–Eu was successfully used
to target SA and deposit Eu3+ on the surfaces of tumor
cells for the inhibition of tumor cell growth and migration. The therapeutic
effect of TDA–Co–Eu on a Balb/c mouse liver tumor model
was evaluated. It was proved that TDA–Co–Eu can be applied
for SA detection as well as for inhibiting tumor growth.
Crude extract from Escherichia coli which expressed a recombinant protein containing amino acids 2 to 127 of the hepatitis C virus (HCV) core protein was used to detect the antibody against HCV core protein (anti-HCc). After electrophoretic separation of proteins from the extract, Western blot (immunoblot) analysis was performed with the serum samples. This method was compared with a commercially available secondgeneration enzyme immunoassay (EIA) which employed synthetic peptides corresponding to highly antigenic segments of both structural and nonstructural portions of HCV. Also, reverse transcription PCR for HCV RNA was used for comparison. Seventy-two serum samples from three groups of patients were tested. Groups I and II represented healthy subjects and subjects with acute hepatitis A or B, respectively. Group III included patients with newly acquired acute hepatitis C. By Western blot analysis, 31 of 31 (100%) samples from group I were negative for anti-HCc antibody, whereas 4 of 22 (18%) samples from group II were positive for anti-HCc. One of these four samples was also positive for anti-HCV antibody by the second-generation EIA (1 of 22 [4.5%]). Among 19 patients diagnosed with newly acquired acute hepatitis C, 4 (21%) were positive for anti-HCV by the second-generation EIA, whereas 12 of 19 (63%) were positive for anti-HCc by Western blot analysis. Of EIA-positive subjects, 4 of 4 (100%) were also positive for anti-HCc by Western blot analysis, whereas among EIA-negative subjects, 8 of 15 (53%) were positive. For HCV RNA detected by reverse transcription PCR, 15 of 19 (80%) of this group of samples were positive. Strikingly, the peak bilirubin level for patients with EIA-negative and Western blot-positive results is significantly higher than that for patients with consistent EIA and Western blot results (22.7 versus 7.2 mg/dl). A series of serum samples from a patient with concurrent hepatitis B and C viral infection was also studied by both tests. Although anti-HCc persisted throughout the course of infection, anti-HCV by EIA converted from negative to positive 20 days after admission and then converted back to negative 30 days later.
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