Genetical study of mutation in maternal-fetal ABO incompatibility.

This study looked into a family involving a rare mother-child ABO blood type inconsistency and explored its genetic and molecular basis. In the family, the mother had type AB blood and the father was blood type B and they gave birth to a baby of blood type O. Their blood types were phenotypically identified by using different techniques, including micro-column gel test, immune inhibition test, absorption and elution tests. The sequences of all 7 exons of ABO allele from the core family members were determined by using PCR and clone-based sequencing. The loci of mutated gene were compared against normal human genes. The result showed that the mother's erythrocytes were agglutinable with monoclonal anti-A antibody (2+) and had agglutination reaction with anti-B antibody (4+). The mother's serum registered agglutination action with standard blood type A cells. The findings showed an ABO inconsistency. When domestic antibodies were used, the mother's erythrocytes yielded agglutination reaction with humanized anti-B serum (4+) and anti-B monoclonal antibody but were non-agglutinable with humanized anti-A serum and anti-A monoclonal antibody. Upon absorption and elution, the titer of anit-A antibody was 128 both before and after the absorption test, with no significant difference found between pre- and post-absorption values. Our results confirmed that the mother's allelic gene was type B and contained type A. The father's blood type was type B, and son's blood type was type O. Clone-based sequencing revealed that the mother carried a heterozygous gene of B101.01 (ntA640→G)/O01, which contained an M214→V mutation that could express a weak expression of antigen A, resulting in blood type AB. However, their son did not have the M214→V mutation, which yielded a false ABO-inconsistency between him and his mother. We were led to conclude that type B gene with a M214→V mutation can encode both antigen B and weak antigen B that can lead to false ABO-inconsistencies.

Application of PET and PEt/CT imaging for cancer screening.

The aim of this study was to evaluate the potential application of 18-fluorodeoxyglucose positron emission tomography (FDG PET) and PET/CT for cancer screening in asymptomatic individuals. The subjects consisted of 3631 physical check-up examinees (1947 men, 1684 women; mean age +/- SD, 52.1 +/- 8.2 y) with non-specific medical histories. Whole-body FDG PET (or PET/CT), ultrasound and tumor markers were performed on all patients. Focal hypermetabolic areas with intensities equal to or exceeding the level of FDG uptake in the brain were considered abnormal and interpreted as neoplasia. Follow-up periods were longer than one year. Among the 3631 FDG PET (including 1687 PET/CT), ultrasound and tumor markers examinations, malignant tumors were discovered in 47 examinees (1.29%). PET findings were true-positive in 38 of the 47 cancers (80.9%). In addition, 32 of the 47 cancers were screened with the PET/CT scan. PET detected cancer lesions in 28 of the 32 examinees. However, the CT detected cancer lesions in only 15 out of 32 examinees. The sensitivity of FDG PET in the detection of a wide variety of cancers is high. Most cancer can be detected with FDG PET at a resectable stage. CT of the PET/CT for localization and characteristics of the lesion showed an increased specificity of the PET scan. The use of ultrasound and tumor markers may complement the PET scan in cancer screening for hepatic and urologic neoplasms.