[Research on the features of DNA damage in nasopharyngeal carcinoma patients of normal constitution and abnormal constitution and in high-risk population of nasopharyngeal carcinoma].

OBJECTIVE: To explore the features of DNA damage in nasopharyngeal carcinoma (NPC) patients of normal constitution and abnormal constitution and in high-risk population of NPC. METHODS: Using single cell gel electrophoresis technique, the DNA damage of peripheral blood lymphocytes was detected in 28 healthy subjects, 27 in high-risk population of NPC, and 13 NPC patients at their first visits. The DNA damage was detected in the populations of normal constitution and of abnormal constitution. The tail length, the tail moment, and the tail DNA% were taken as the indices of DNA damage. RESULTS: The tail length was (35.77 +/- 4.22) microm, the tail moment was (8.10 +/- 1.63) microm, and the tail DNA% was 57.48% +/- 4.63% in NPC patients. They were (15.25 +/- 4.15) microm, (5.01 +/- 1.92) microm, and 31.99% +/- 4. 11% in high-risk population of NPC. They were (14.31 +/- 3.64) microm, (4. 37 +/- 1.80) microm, and 29. 89% +/- 3. 15% in healthy subjects. There was statistical difference in the three indices among the three populations (P <0.05). In all the three populations, more DNA damage existed in those of abnormal constitution than in those of normal constitution (P <0.05). CONCLUSIONS: Obvious instability of genetic materials exists in NPC patients, manifested as severe DNA damage of lymphocytes. In all the three populations, more DNA damage existed in those of abnormal constitution than in those of normal constitution.

Enhancements of skin cell proliferations and migrations via 6-dehydrogingerdione.

Human skin protects the body from mechanical and chemical damages, and skin wound healing is a costly procedure and worldwide issue. A Zingiber officinale compound, 6-dehydrogingerdione (6-DG), is presented as a novel biofunctional healing agent for human skin wound repair. The effectiveness on cell growth/migration, growth factor, collagen amount, and enzymatic activity was assessed. 6-DG treatment accelerated cellular proliferation and migration dose-dependently. Enzyme-linked immunosorbent assay (ELISA) showed that 6-DG brought about higher growth factor productions on transforming growth factor-ß (TGF-ß), platelet-derived growth factor-αß (PDGF-αß), and vascular endothelial growth factors (VEGF). Under phorbol 12-myristate 13-acetate (PMA) incubation, 6-DG increased fibroblast collagen yield obviously, reduced matrix metalloproteinase-1 (MMP-1) protein expression, and recovered tissue inhibitor of metalloproteinase-1 (TIMP-1) secretion. 6-DG also blocked the mitogen-activated protein kinase (MAPK) pathway by suppressing c-Jun protein levels and extracellular signal-regulated kinases (ERK) phosphorylation in fibroblasts. From all of the above, 6-DG has potential to be a novel agent for human skin repair.

Endothelin-1 stimulates suppressor of cytokine signaling-3 gene expression in adipocytes.

Endothelin (ET)-1 and suppressor of cytokine signaling (SOCS)-3 were respectively found to regulate energy metabolism and hormone signaling in fat cells. Although ET-1 can also regulate the expression of SOCS-3-stimulating hormones, it is still unknown whether ET-1 regulates SOCS-3 gene expression. This study investigated the pathways involved in ET-1's modulation of SOCS-3 gene expression in 3T3-L1 adipocytes. ET-1 upregulated SOCS-3 mRNA and protein expression in dose- and time-dependent manners. The concentration of ET-1 that increased SOCS-3 mRNA levels by 250-400% was ∼100nM with 2-4h of treatment. Treatment with actinomycin D prevented ET-1-stimulated SOCS-3 mRNA expression, suggesting that the effect of ET-1 requires new mRNA synthesis. Pretreatment with the ET type A receptor (ET(A)R) antagonist, BQ-610, but not the ET type B receptor (ET(B)R) antagonist, BQ-788, prevented the stimulatory effect of ET-1 on SOCS-3 gene expression. The specific inhibitors of either MEK1 (U-0126 and PD-98059), JAK (AG-490), JNK (SP-600125), or PI3K (LY-294002 and wortmannin) reduced ET-1-increased levels of SOCS-3 mRNA and respectively inhibited ET-1-stimulated activities of MEK1, JAK, JNK, and PI3K. These results imply that the ET(A)R, ERK, JAK, JNK, and PI3K are functionally necessary for ET-1's stimulation of SOCS-3 gene expression. Moreover, ET-1 was observed to upregulate expressions of SOCS-1, -2, -3, -4, -5, and -6 mRNAs, but not SOCS-7 or cytokine-inducible SH2-containing protein-1 mRNAs. This suggests that ET-1 selectively affects particular types of SOCS family members. Changes in SOCS gene expressions induced by ET-1 may help explain the mechanism by which ET-1 modulates hormone signaling of adipocytes.

Green tea epigallocatechin gallate inhibits insulin stimulation of adipocyte glucose uptake via the 67-kilodalton laminin receptor and AMP-activated protein kinase pathways.

Insulin and (-)-epigallocatechin gallate (EGCG) are reported to regulate obesity and fat accumulation, respectively. This study investigated the pathways involved in EGCG modulation of insulin-stimulated glucose uptake in 3T3-L1 and C3H10T1/2 adipocytes. EGCG inhibited insulin stimulation of adipocyte glucose uptake in a dose- and time-dependent manner. The concentration of EGCG that decreased insulin-stimulated glucose uptake by 50-60% was approximately 5-10 µM for a period of 2 h. At 10 µM, EGCG and gallic acid were more effective than (-)-epicatechin, (-)-epigallocatechin, and (-)-epicatechin 3-gallate. We identified the EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] in fat cells and extended the findings for this study to clarify whether EGCG-induced changes in insulin-stimulated glucose uptake in adipocytes could be mediated through the 67LR. Pretreatment of adipocytes with a 67LR antibody, but not normal rabbit immunoglobulin, prevented the effects of EGCG on insulin-increased glucose uptake. This suggests that the 67LR mediates the effect of EGCG on insulin-stimulated glucose uptake in adipocytes. Moreover, pretreatment with an AMP-activated protein kinase (AMPK) inhibitor, such as compound C, but not with a glutathione (GSH) activator, such as N-acetyl-L-cysteine (NAC), blocked the antiinsulin effect of EGCG on adipocyte glucose uptake. These data suggest that EGCG exerts its anti-insulin action on adipocyte glucose uptake via the AMPK, but not the GSH, pathway. The results of this study possibly support that EGCG mediates fat content.

[Cluster analysis applied in the epidemiological stratification analysis].

OBJECTIVE: To establish a new method on stratification analysis when the stratification limits of confounding factors was not clear or contradictory. METHOD: Data on a study of diabetes mellitus in Guangdong province collected in the year of 1997 and 1998 was analyzed using cluster-stratification analysis. RESULTS: The efficiency of stratification analysis was improved and the confounding bias was effectively controlled with information bias avoided when the clusters-stratification analysis was applied. CONCLUSION: The problem was logically solved using cluster analysis as an assistant stratification means.

Trends in road traffic crashes and associated injury and fatality in the People's Republic of China, 1951-1999.

The burden of road traffic injuries in the People's Republic of China is increasing as evidenced by trends since 1951. Data from the National Statistical Office, Ministry of Communications and the Traffic Administration Bureau were analyzed. Absolute numbers of crashes, fatalities, and injuries, as well as fatalities per 100,000 population and motorization (number of vehicles per 1000 population) were used as indices to measure trends. Regional variations in trends and the characteristics of people injured or killed were also analyzed. Road traffic crashes increased 68-fold, from around 6000 in 1951 to 413,000 in 1999. Excessive speed was the main reported cause of the crashes. The injuries increased 56-fold--from around 5000 to 286,000--and fatalities 97-fold--from 852 to around 84,000--over the same period. The crash, fatality and injury rates also increased after 1985, due to increased motorization spurred by rapid economic growth. The number of four-wheel motor vehicles increased from 60,000 in 1951 to just under a million four-wheel motor vehicles in 1975 and to 10 million in 1987. The number of four-wheel motor vehicles then rose to 50 million in 1999, with an additional 30 million motorcycles. The increase in motorization and fatalities affected all the provinces. Road traffic injuries are the leading cause of death for populations up to the age of 45 years and the leading cause of working-life years lost in China.