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Based on GIS, a sediment delivery distributed (SEDD) model was established to simulate the spatial patterns of annual soil water erosion and sediment yield in two sub-watersheds at the upper reaches of Minjiang River. The model was based on the revised universal soil loss equation (RUSLE) for calculating the annual soil water erosion, and coupled with an equation for evaluating the sediment delivery ratio of each cell. The results showed that in most regions of the two sub-watersheds, erosion intensity was below high level. Similar spatial patterns of sediment delivery ratio and sediment yield were observed, i. e., being higher along river, and approached to zero in other regions. Most parts of eroded soil were deposited in the sub-watersheds during their transportation, and less than 5% of it reached the river. Shrub land and forestland were the most important sources of sediment yield, and the sum of their sediment yield occupied 70% of the total.

Objective: Multiple carboxylase deficiency (MCD) is an autosomal recessive disorder. MCD is characterized by skin rash, metabolic acidosis, vomiting and psychomotor retardation. Depending on deficiency of the enzyme, MCD includes two different forms, biotinidase deficiency (BTD, OMIM 253260) and holocarboxylase synthetase deficiency (HLCSD, OMIM 253270). In this study, we analyzed gene mutations of four Chinese MCD patients and to explore the mutation spectrum and possibility of a molecular diagnosis., Methods: All exons and their flanking introns of biotinidase gene and HLCS gene were screened by polymerase chain reaction combined with DNA direct sequencing in four Chinese MCD patients. Genomic DNA was extracted using a kit from the peripheral blood leukocytes of each patient. PCR amplification products were checked by 2% agarose gel electrophoresis and were subsequently sequenced with both the forward and reverse primers., Results: All patients showed mutations in HLCS gene, whereas no mutation was found in biotinidase gene, proving that all the four patients had HLCS deficiency. Four previously reported mutations in HLCS gene were detected (Y456C, R508W, D634N and 780delG). A missense mutation of 1522C > T in exon 11 of HLCS gene, which was a homozygotic mutation, was identified in patient 1; a mutation of 1522C > T in exon 11 combined with a mutation of 1367A > G in exon 9, which was a compound heterozygotic mutation, was identified in patient 2; a mutation of 1522C > T in exon 11 combined with a mutation of 1900G > A in exon 13, which was a compound heterozygotic mutation, was identified in patient 3; a mutation of 1522C > T in exon 11 combined with a mutation of 780delG in exon 7, which was a compound heterozygotic mutation, was identified in patient 4. All the parents were carriers of mutations. No additional carrier of this four mutations was identified from 50 samples of Chinese controls., Conclusion: The 1522C > T (R508W) mutation probably represents a mutational hot-spot in Chinese HLCS deficiency patients while the 780delG mutation which was reported only in Japanese patients was found firstly in Chinese patients.

Objective: In order to explore if power frequency magnetic field (PFMF) can act as cancer promoter or be synergistic with phorbol 12-myristate 13-acetate (TPA) in cancer promotion, the effects of 50 Hz MF on gap junction intercellular communication (GJIC) of astrocytes were observed., Methods: Fluorescence redistribution after photobleaching (FRAP) was adopted to observe the recovery of fluorescence intensity in the bleached cells thus to estimate intercellular communication by gap junction. Comparative fluorescence intensity recovery rate (CFIRR) was as evaluation index. The effects of 50 Hz MF alone or with TPA on GJIC of astrocytes were studied., Results: After 3 ng/ml TPA treatment for 1 hour, M(d) of CFIRR was 4.53%/min, whereas that in the control group was 9.74%/min (H = 12.084, P < 0.005). After exposure to 0.8 and 1.6 mT magnetic field for 24 hours respectively, M(d) of CFIRR was 8.25%/min and 6.68%/min respectively, no significant difference from that of control (H = 32.617, P > 0.05). After exposure to 0.8 and 1.6 mT magnetic field for 23 hours then combined with 3 ng/ml TPA treatment for 1 hour, M(d) of CFIRR was 3.32%/min and 2.85%/min respectively, also no significant difference from that in the group treated with 3 ng/ml TPA alone (H = 2.589, P > 0.05)., Conclusion: 50 Hz MF (within 0 - 1.6 mT) alone could not inhibit GJIC of astrocytes; with TPA, could not enhance the inhibition of TPA on GJIC of astrocytes. But with MF intensity increasing, the inhibition of MF on GJIC showed elevated tendency.