Uniparental Genetic Analyses Reveal the Major Origin of Fujian Tanka from Ancient Indigenous Daic Populations.

The Fujian Tanka people are officially classified as a southern Han ethnic group, whereas they have customs similar to Daic and Austronesion people. Whether they originated in Han or Daic people, there is no consensus. Three hypotheses have been proposed to explain the origin of this group: (1) the Han Chinese origin, (2) the ancient Daic origin, (3) and the admixture between Daic and Han. This study addressed this issue by analyzing the paternal Y chromosome and maternal mtDNA variation of 62 Fujian Tanka and 25 neighboring Han in Fujian. The southern East Asian predominant haplogroups (e.g., Y-chromosome O1a1a-P203 and O1b1a1a-M95, and mtDNA F2a, M7c1, and F1a1) had relatively high frequencies in Tanka. The interpopulation comparison revealed that the Tanka have a closer affinity with Daic populations than with Han Chinese in paternal lineages but are closely clustered with southern Han populations such as Hakka and Chaoshanese in maternal lineages. Network and haplotype-sharing analyses also support the admixture hypothesis. The Fujian Tanka mainly originate from the ancient indigenous Daic people and have only limited gene flows from Han Chinese populations. Notably, the divergence time inferred by the Tanka-specific haplotypes indicates that the formation of Fujian Tanka was a least 1033.8-1050.6 years before present (the early Northern Song dynasty), indicating that they are an indigenous population, not late Daic migrants from southwestern China.

Heijiangdan ointment relieves oxidative stress from radiation dermatitis induced by (60)Co γ-ray in mice.

OBJECTIVE: To investigate the effects of Heijiangdan Ointment ( HJD) on oxidative stress in (60)Co γ-ray radiation-induced dermatitis in mice. METHODS: Female Wistar mice with grade 4 radiation dermatitis induced by (60)Co γ-rays were randomly divided into four groups (n=12 per group); the HJD-treated, recombinant human epidermal growth factor (rhEGF)-treated, Trolox-treated, and untreated groups, along with a negative control group. On the 11th and 21st days after treatment, 6 mice in each group were chosen for evaluation. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and lactate dehydrogenase (LDH) were detected using spectrophotometric methods. The fibroblast mitochondria were observed by transmission electron microscopy (TEM). The expressions of fibroblast growth factor 2 (FGF-2) and transforming growth factor ß1 (TGF-ß1) were analyzed by western blot. RESULTS: Compared with the untreated group, the levels of SOD, MDA and LDH, on the 11th and 21st days after treatment showed significant difference (P<0.05). TEM analysis indicated that fibroblast mitochondria in the untreated group exhibited swelling and the cristae appeared fractured, while in the HJD group, the swelling of mitochondria was limited and the rough endoplasmic reticulum appeared more relaxed. The expressions of FGF-2 and TGF-ß1 increased in the untreated group compared with the negative control group (P<0.05). After treatment, the expression of FGF-2, rhEGF and Trolox in the HJD group were significantly increased compared with the untreated group (P<0.05), or compared with the negative control group (P<0.05). The expression of TGF-ß1 showed significant difference between untreated and negative control groups (P<0.05). HJD and Trolox increased the level of TGF-ß1 and the difference was marked as compared with the untreated and negative control groups (P<0.05). CONCLUSION: HJD relieves oxidative stress-induced injury, increases the antioxidant activity, mitigates the fibroblast mitochondrial damage, up-regulates the expression of growth factor, and promotes mitochondrial repair in mice.

[Pathological basis of qi-deficiency and blood stasis syndrome in patients with non-small cell lung cancer viewing from tumor metastasis related factors].

OBJECTIVE: To observe the expressions of tumor metastasis related factors (TMRF) in peripheral blood of patients with non-small cell lung cancer (NSCLC) for exploring the molecular mechanism for genesis of qi-deficiency and blood stasis (QDBS) syndrome in patients. METHODS: Eighty selected NSCLC patients of stage II B/III were differentiated into the QDBS group and the non-QDBS group according to the Chinese medicine syndrome differentiation criteria, 40 in each group. The serum levels of vascular endothelial growth factor (VEGF), endostatin (ES) and soluble intercellular adhesive molecule-1 (slCAM-1) in patients were detected by ELISA, and the expression of adhesive molecule CD44 in peripheral blood was determined using flow cytometry. RESULTS: Serum levels of VEGF (1002.78 +/- 312.08 ng/L), ES (120.88 +/- 20.00 microg/L), slCAM-1 (531.78 +/- 213.37 microg/L) and CD44 (136.65 +/- 29.60) were significantly higher in patients of QDBS group than in patients of non-QDBS group (653.18 +/- 318.99 ng/L, 98.29 +/- 23.92 microg/L, 409.36 +/- 167.65 microg/L and 98.46 +/- 20.64, respectively, P<0.01). CONCLUSION: Objective inner links are found between the QDBS syndrome and TMRF in NSCLC patients; serum levels of VEGF, ES, slCAM-1 and CD44 can be served as the microcosmic basis for QDBS syndrome differentiation.