Spatiotemporal distribution and sociodemographic and socioeconomic factors associated with primary and secondary syphilis in Guangdong, China, 2005-2017.

BACKGROUND: Previous studies exploring the factors associated with the incidence of syphilis have mostly focused on individual-level factors. However, recent evidence has indicated that social-level factors, such as sociodemographic and socioeconomic factors, also affect the incidence of syphilis. Studies on the sociodemographic and socioeconomic factors associated with syphilis incidence are scarce, and they have rarely controlled for spatial effects, even though syphilis shows spatial autocorrelation. METHODOLOGY/PRINCIPAL FINDINGS: Syphilis data from 21 cities in Guangdong province between 2005 and 2017 were provided by the National Notifiable Infectious Disease Reporting Information System. The incidence time series, incidence map, and space-time scanning data were used to visualize the spatiotemporal distribution. The spatial panel data model was then applied to explore the relationship between sociodemographic factors (population density, net migration rate, male:female ratio, and the number of health institutions per 1,000 residents), socioeconomic factors (gross domestic product per capita, the proportion of secondary/tertiary industry), and the incidence of primary and secondary syphilis after controlling for spatial effects. The incidence of syphilis increased slowly from 2005 (11.91 per 100,000) to 2011 (13.42 per 100,000) and then began to decrease, reaching 6.55 per 100,000 in 2017. High-risk clusters of syphilis tended to shift from developed areas to underdeveloped areas. An inverted U-shaped relationship was found between syphilis incidence and gross domestic product per capita. Moreover, syphilis incidence was significantly associated with population density (ß = 2.844, P = 0.006), the number of health institutions per 1,000 residents (ß = -0.095, P = 0.007), and the net migration rate (ß = -0.219, P = 0.002). CONCLUSIONS/SIGNIFICANCE: Our findings suggest that the incidence of primary and secondary syphilis first increase before decreasing as economic development increases further. These results emphasize the necessity to prevent syphilis in regions at the early stages of economic growth.

1,2-Dichloroethane impairs glucose and lipid homeostasis in the livers of NIH Swiss mice.

Excessive exposure to 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to liver dysfunction. To fully explore the mechanism of 1,2-DCE-induced hepatic abnormalities, 30 male National Institutes of Health (NIH) Swiss mice were exposed to 0, 350, or 700mg/m3 of 1,2-DCE, via inhalation, 6h/day for 28days. Increased liver/body weight ratios, as well as serum AST and serum ALT activity were observed in the 350 and 700mg/m3 1,2-DCE exposure group mice, compared with the control group mice. In addition, decreased body weights were observed in mice exposed to 700mg/m3 1,2-DCE, compared with control mice. Exposure to 350 and 700mg/m3 1,2-DCE also led to significant accumulation of hepatic glycogen, free fatty acids (FFA) and triglycerides, elevation of blood triglyceride and FFA levels, and decreases in blood glucose levels. Results from microarray analysis indicated that the decreases in glucose-6-phosphatase catalytic subunit (G6PC) and liver glycogen phosphorylase (PYGL) expression, mediated by the activation of AKT serine/threonine kinase 1 (Akt1), might be responsible for the hepatic glycogen accumulation and steatosis. Further in vitro study demonstrated that 2-chloroacetic acid (1,2-DCE metabolite), rather than 1,2-DCE, up-regulated Akt1 phosphorylation and suppressed G6PC and PYGL expression, resulting in hepatocellular glycogen accumulation. These results suggest that hepatic glucose and lipid homeostasis are impaired by 1,2-DCE exposure via down-regulation of PYGL and G6PC expression, which may be primarily mediated by the 2-chloroacetic acid-activated Akt1 pathway.