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Gliomas are the most common tumors of the central nervous system (CNS) and a frequent cause of death. The treatment of malignant gliomas is often palliative due to their high recurrence rate. A growing body of evidence suggests that glioma may arise from cancer stem cells (CSC) correlated with neural stem cells (NSC), with the capacity for self-renewal and multipotency. CSCs have been isolated from human gliomas and numerous other solid tumors. It is assumed that a number of established malignant cell lines also contain a rare subpopulation of stem cells. This study was designed to investigate the proportion of CSCs in the human glioma cell line SHG44 and to study the limitations of CD133 immunophenotyping in glioma stem cell research. SHG44 cells were cultured in both serum-containing and serum-free medium. The similar shape in growth curves (in the exponential growth phase) revealed that most cells participated in the population amplification. Time gradient BrdU labeling and monoclonal assay revealed that almost every single cell participated in the division growth (98.82%) and possessed the ability to form clones (96.19%). No significant difference was found in the proportions of CD133+ cells in the serum-containing and serum-free groups (38.25%/37.92%). In addition, no significant difference was noted in the proportions of CD133+ cells among monoclones selected randomly in the serum-containing group. These results suggested that CD133- cells generate CD133+ cells and have the ability to form clones. Thus, we concluded that most SHG44 cells were CSCs and serum-free medium was not necessary for the generation of CSCs. In this line, CD133- cells also possessed clonogenic, self-renewal capacities and were also CSCs.

In this study we report three cases of Hb Ube-1, one case of Hb Ube-2 and one case of Hb Ube-4 in mainland China. One case of Hb Ube-1 had the clinical manifestation of hemolytic anemia. Hb Ube-2 and Hb Ube-4 did not appear to be associated with clinical or hematological abnormalities. The variants were detected by Hb electrophoresis during a thalassemia screening. Genomic DNA was extracted from the peripheral blood leukocytes of Hb specimens. α1, α2 and β-globin genes were amplified by polymerase chain reaction (PCR). All variants were confirmed by DNA sequence analysis and the PCR-restriction fragment length polymorphism assay.

Hemoglobin (Hb) Ottawa [α15 (A13) Gly→Arg], also known as Hb Siam, was first described in an 82-year-old Canadian in 1974. The same year, a second case was reported in a 28-year-old Chinese male living in Thailand. A third case was found in 1986 in a Chinese female living in the Hubei province of China. Since then, there have been no reports of Hb Ottawa in mainland China in the English literature. Hb Ottawa results from a GGT→CGT mutation in codon 15 of the α1 or α2-globin gene. Hb Ottawa carriers do not present any clinical symptoms or hematological changes, and are often diagnosed during a health examination and thalassemia screening. In a hemoglobin survey of 9745 students in Chaozhou, Guangdong, China, we identified four cases of Hb Ottawa in a thalassemia screening by Hb electrophoresis, and confirmed it to be the result of a GGT→CGT mutation in codon 15 of the α2-globin gene by DNA sequence analysis.

The cellular origin of soft tissue sarcomas (STSs) is not fully understood. The cancer stem cell hypothesis presumes that tumors originate from the malignant transformation of stem cells. As a type of multipotent stem cell, adipose tissue-derived stromal/stem cells (ADSCs), which possess an unexpected degree of plasticity and often reside in other tissues, may represent a potential source of soft tissue sarcoma. To ascertain whether ADSCs are responsible for the formation of STSs, ADSCs from mice were cultured and treated with 3-methycholanthrene to derive transformed cells. These transformed ADSCs were then injected subcutaneously into immunodeficient mice to test their tumorigenic potential. We found that they generated several types of STSs, including synovial sarcoma, malignant fibrous histiocytoma and fibrosarcoma. This is the first study to report that ADSCs may be the potential initiating cells for synovial sarcoma. Our findings indicate that STSs might originate from malignantly transformed ADSCs.

Hemoglobin (Hb) G-Chinese [α30 (B11) Glu↷Gln], also known as Hb G-Honolulu, Hb G-Hongkong or Hb G-Singapore, was first identified in a Chinese woman in Singapore, and was subsequently observed in several Chinese families. This Hb variant results from a GAG↷CAG mutation at codon 30 of the α-globin gene. The aim of the present study was to identify the Hb G-Chinese mutation in three Cantonese individuals. The presence of the Hb variant was confirmed by cellulose acetate electrophoresis. DNA analysis based on the polymerase chain reaction (PCR) and sequencing were conducted to confirm the presence of the mutation in the α-globin gene. A G↷C substitution at codon 30 of the α2-globin gene was observed. According to a previous study, the G↷C substitution in Hb G-Chinese creates a PstI restriction site; we amplified the α2-globin gene, then digested the PCR products with PstI. The results indicated that only the PCR product of Hb G-Chinese α2-globin was cut by PstI. The digestive products were 120 and 730 bp, respectively. Therefore, we determined that the three cases were of the heterozygous Hb G-Chinese variant.