Seasonal variation in air particulate matter (PM10) exposure-induced ischemia-like injuries in the rat brain.

Epidemiological studies imply a significantly positive association between particulate matter (PM) level and ischemic stroke hospitalization. However, considering that PM10 is highly heterogeneous and varies with season within the same location, existing experimental evidence remained low. In the present study, we first treated Wistar rats with PM10 samples collected from different seasons in Taiyuan, a typically coal-burning city of China, and determined ischemia-related markers in the cortex. The results indicated that PM10 exposure caused endothelial dysfunction, inflammatory response, and neuro-functional impairment similar to that of cerebral ischemia with season-dependent properties, and the winter sample presented the most obvious injuries. Then, we detected the chemical composition of PM10 samples followed by analysis of their correlation with the above biomarkers and found that winter PM10, characterized by higher polycyclic aromatic hydrocarbons (PAHs) and carbon load, played the major role in causing brain ischemia-like injuries among different season samples. Furthermore, by setting up an ischemic neuron model in vitro, we confirmed that winter PM10 presented the most serious aggravation on ischemia-produced injury outcome. This study provides experimental evidence for clarifying the association between season-dependent PM10 pollution in the atmospheric environment and an increased risk of ischemia-like injuries.

[Epidemiology of rheumatoid arthritis in middle-aged and elderly population in Luohe City, Henan Province].

OBJECTIVE: To explore the local prevalence of rheumatoid arthritis (RA) among the middle-aged and elderly population. METHODS: A total of 8610 residents were recruited for a two-stage cluster sampling survey through a questionnaire of RA according to 2010 ACR/EULAR classification criteria. Physical examinations and blood tests were performed. RESULTS: The responding rate was 96.10%. Joint score 0, 1, 2, 3, 5 was detected in 13.62%, 7.57%, 2.79%, 1.87% and 0.23% of subjects. The prevalence of joint score 0, 1, 2, 3, 5 was 13.62%, 7.57%, 2.79%, 1.87% and 0.23%. The rate was 17.48% and 14.27% for elevated levels of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), 6.62%, 1.96% and 5.48%, 1.55% for low titer and high titer rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) positive antibody. And 63 RA cases were confirmed. The crude prevalence was 0.76% and 0.71% for standardized prevalence. Compared to males, females had a higher prevalence of RA (1.02% vs 0.39%, P < 0.01). In the population, the awareness rate was 74.60%, cure rate 71.43% and control rate 18.57% respectively. CONCLUSION: The local prevalence of RA in elderly females is higher than that in males. And the treatment and awareness rates are also low.

Particulate matter (PM10) exposure induces endothelial dysfunction and inflammation in rat brain.

Epidemiological studies suggest that particulate matter (PM(10)) inhalation was associated with adverse effects on brain-related health, however, existing experimental data lacked relevant evidences. In this study, we treated Wistar rats with PM(10) at different concentrations (0.3, 1, 3 and 10 mg/kg body weight (bw)), and investigated endothelial dysfunction and inflammatory responses in the brain. The results indicate that mild pathological abnormal occurred after 15-day exposure (five times with 3 days each), followed by the changes of endothelial mediators (ET-1 and eNOS) and inflammatory markers (IL-1ß, TNF-α, COX-2, iNOS and ICAM-1). Also, the sample up-regulated bax/bcl-2 ratio and p53 expression, and induced neuronal apoptosis. It implicates that PM(10) exerted injuries to mammals' brain, and the mechanisms might be involved in endothelial dysfunction and inflammatory responses.

SO(2)-induced neurotoxicity is mediated by cyclooxygenases-2-derived prostaglandin E(2) and its downstream signaling pathway in rat hippocampal neurons.

Sulfur dioxide (SO(2)) pollution in atmospheric environment is involved in neurotoxicity and increased risk for hospitalization and mortality of many brain disorders; however, our understanding of the mechanisms by which SO(2) caused harmful insults on neurons remains elusive. Here, we show that SO(2) exposure produced a neuronal insult, and the neurotoxic effect was likely via stimulating cyclooxygenase-2 (COX-2) elevation by activation of nuclear factor-κB (NF-κB) activity and its acting on the promoter-distal NF-κB-binding site of COX-2 promoter. The action of SO(2) on elevating COX-2 ultimately appeared to be dependent on the increased production of arachidonic acid-derived prostaglandins, mainly prostaglandin E(2) (PGE(2)), and functioning of its EP2/4 receptors. Also, the molecular modulating process might be triggered by free radical attack from SO(2) metabolism in vivo and followed by activating cyclic adenosine monophosphate/protein kinase A pathway and enhancing probability of the release of glutamate, upregulating N-methyl-D-aspartic acid receptor expression and causing neuronal apoptosis. Our results reveal a mechanistic basis for exploring an association between SO(2) inhalation and increased risk for neurological disorders and opening up therapeutic approaches of treating, ameliorating, or preventing brain injuries resulting from SO(2) exposure in atmospheric polluting environment.

A highly efficient and selective turn-on fluorescent sensor for Cu2+ ion based on calix[4]arene bearing four iminoquinoline subunits on the upper rim.

A new fluorescent chemosensor based on calix[4]arene bearing four iminoquinoline subunits on the upper rim was conveniently synthesized, which showed a remarkable enhanced fluorescent intensity in the presence of Cu(2+) ion and a high selectivity toward Cu(2+) ion over a wide range of tested metal ions in acetonitrile.