A case of dispermic chimerism with normal phenotype identified during ABO blood grouping.

BACKGROUND: Human chimerism with normal phenotype derived from the fusion of two different zygotes is a rare phenomenon. We describe a case of a phenotypically normal 17-year-old diagnosed with dispermic chimerism during routine ABO blood grouping. METHODS: ABO grouping, ABO genotyping, karyotyping, human leukocyte antigen (HLA) typing, and short tandem repeat (STR) analysis were performed. RESULTS: Forward typing with anti-A and anti-B sera resulted in mixed-field agglutination of red blood cells. The mother and father were blood group O and AB, respectively. The proposita had O1, A201 and B alleles in the ABO locus; O1 was a maternal allele, while A201 and B were the paternal alleles. The proposita karyotype was 46,XX/46,XY. HLA typing revealed that the proposita had three alleles (46, 51, 54) at the HLA-B locus, with the additional allele of paternal origin. STR analysis identified three alleles for five of the 15 markers (D2S1338, TPOX, D8S1179, D19S433, and D21S11) analyzed in the proposita's blood- and skin fibroblast-derived DNA. The additional alleles of TPOX, D8S1179, and D21S11 were of paternal origin. CONCLUSIONS: The genetic findings suggest that this proposita was produced by dispermic fertilization of two identical haploid ova formed by parthenogenetic activation.

[Effect of highway transportation on the quality of red blood cells].

This study was purposed to investigate the effect of highway transportation on the quality of blood components so as to provide experimental basis to meet the needs of military operations. The transport condition was simulated by random vibration test. The red blood cells, leukocyte-reduced red blood cells, washed red blood cells were randomly vibrated (C Road) for 4 hours. Then, these blood components were stored in refrigerator for 15 days (4 degrees C). Six milliliters of blood were collected before vibration, after vibration, and at day 15 days of storage after vibration, respectively. The suspension was isolated. The free hemoglobin (FHb), routine hematological parameters, and biochemical indexes were determined. The results showed that FHb, lactate dehydrogenase (LDH), K(+) of red blood cells and leukocyte-reduced red blood cells did not significantly change after vibration and storage. However, FHb, LDH and K(+) of washed red blood cells increased significantly after simulated transportation (p < 0.05). The levels of these parameters at day 15 of storage after vibration were also significantly higher than those after vibration (p < 0.01). The changes of other hematological parameters were not significant in three blood components after vibration (C Road) and storage for 15 day. In conclusion, red blood cells and leukocyte-reduced red blood cells were qualified for clinic transfusion even after transportation within 4 hours for 15 day storage later, if they were kept in proper blood container and protected from damping. However, the washed red blood cells could not be used for clinic after similar transport in the military operations.

[Effects of triptolide on proliferation and apoptosis of Jurkat cell line in acute T lymphocytic leukemia].

The aim of this study was to investigate the anti-proliferation and pro-apoptosis of triptolide on Jurkat cell line in acute T lymphocytic leukemia. The Jurkat cells were treated with various concentrations of triptolide (0, 1, 2, 4, 8, 16 microg/L) for 12 hours. The inhibitory ratio was measured by Cell Counting Kit-8 assay. The effects of triptolide on apoptosis of Jurkat cells were determined by DNA fragmentation (DNA ladder), Hoechst 33258, PI and Annexin V-FITC/PI double staining. The results demonstrated that triptolide inhibited the proliferation of Jurket cells. The 50% inhibitory concentration (IC(50)) was 4.0 microg/L. Chromatin condensation in the cells treated with triptolide could be seen by light microscopy. DNA electrophoresis showed evidence of nuclear fragmentation (DNA ladder). The hypoploid (sub-G(1)) population was increased after treatment with triptolide. The translocation of phosphatidylserine at the outer surface of the cell plasma membrane could be induced by triptolide. After treatment with triptolide for 12 hours, the rates of apoptotic cells were significantly increased. Moreover, these pro-apoptosis effects were in time-dependent manner. It is concluded that triptolide can inhibit the proliferation and induce the apoptosis of Jurkat cells. This study provides experimental basis for clinical use of triptolide in leukemia therapy.