Prevalence and associated factors of lens opacities among Chinese type 2 diabetics in Kinmen,Taiwan

The aim of this study is to assess the prevalence and associated risk factors of lens opacities among type 2 diabetics in Kinmen, Taiwan. A community-based mass screening ascertained 971 type 2 diabetics from 1991 to 1993. From that population, a total of 578 (59.5%) patients with type 2 diabetes underwent eye screening in 1999 with a 45° thin slit-lamp biomicroscopy and ophthalmoscopy to examine the lens after dilation of the pupils. The prevalence of nuclear, cortical, and posterior subcapsular (PSC) opacity without surgery among type 2 diabetics was 22.5, 20.2, and 19.9%, respectively. The number of females affected was statistically higher than males in each type of lens opacity. The prevalence of each type of lens opacity also showed a statistically significant increase with (χ² test). Based on multiple logistic regressions, age was the most significant factor related with each type of lens opacity. Triglyceride at baseline was associated with nuclear opacity (≥200 vs. <200 mg/dl, OR = 2.35, 95% CI: 1.15–4.79) and PSC opacity (≥200 vs. <200 mg/dl, OR = 2.11, 95% CI: 1.00–4.43). In conclusion, our results show that in addition to age, higher triglyceride level may increase the risk of prevalent nuclear or PSC opacity in type 2 diabetics.     

Chemical constituents from Abutilon indicum

The investigation on the chemical constituents of the whole plant of Abutilon indicum has resulted in the isolation of two new compounds, abutilin A (1) and (R)-N-(1'-methoxycarbonyl-2'-phenylethyl)-4-hydroxybenzamide (2), as well as 28 known compounds. The structures of the two new compounds were established on the basis of the spectroscopic analysis, and the known compounds were identified by comparison of their spectroscopic and physical data with those reported in the literature.     

Paraquat inhibits postsynaptic AMPA receptors on dopaminergic neurons in the substantia nigra pars compacta

Parkinson's disease (PD) is a neurodegenerative disease that mainly affects dopaminergic (DA-ergic) neurons in the substantia nigra pars compacta (SNc). Glutamate modulates neuronal excitability, and a high concentration of glutamatergic receptors is found on DA-ergic neurons in the SNc. Paraquat (PQ) is a putative causative agent for PD. Its effects on synaptic glutamate transmission in SNc DA-ergic neurons were evaluated using whole-cell voltage-clamp recording in brain slices from 7- to 14-day-old Wistar rats. In the presence of bicuculline (BIC), strychnine, and dl-aminophosphonovaleric acid, PQ reversibly suppressed AMPA receptor-mediated evoked excitatory postsynaptic currents (eEPSCs) in a concentration-dependent manner (P < 0.05). In the presence of tetrodotoxin (1 μM), PQ (50 μM) significantly reduced the amplitudes, but not the frequencies, of miniature EPSCs in the SNc, suggesting PQ inhibited eEPSCs through a postsynaptic mechanism. Exogenous application of AMPA to induce AMPA-mediated inward currents excluded involvement of a presynaptic response. The AMPA-induced currents in the SNc were significantly reduced by PQ (50 μM) to 74% of control levels (P < 0.05), supporting that PQ acts on postsynaptic AMPA receptors. No effect of PQ on eEPSCs was seen in the LD thalamic nucleus and hippocampus, showing PQ specifically inhibited DA-ergic neurons in the SNc. Our results demonstrate a novel mechanism of action of PQ on glutamate-gated postsynaptic AMPA receptors in SNc DA-ergic neurons. This effect may attenuate the excitability and function of DA-ergic neurons in the SNc, which may contribute to the pathogenesis of PD.     

The apoptotic effect of nanosilver is mediated by a ROS- and JNK-dependent mechanism involving the mitochondrial pathway in NIH3T3 cells

Nanomaterials and nanoparticles have received considerable attention recently because of their unique properties and diverse biotechnology and life sciences applications. Nanosilver products, which have well-known antimicrobial properties, have been used extensively in a range of medical settings. Despite the widespread use of nanosilver products, relatively few studies have been undertaken to determine the biological effects of nanosilver exposure. The purpose of this study was to evaluate the toxicity of nanosilver and to elucidate possible molecular mechanisms underlying the biological effects of nanosilver. Here, we show that nanosilver is cytotoxic, inducing apoptosis in NIH3T3 fibroblast cells. Treatment with nanosilver induced the release of cytochrome c into the cytosol and translocation of Bax to mitochondria, indicating that nanosilver-mediated apoptosis is mitochondria-dependent. Nanosilver-induced apoptosis was associated with the generation of reactive oxygen species (ROS) and JNK activation, and inhibition of either ROS or JNK attenuated nanosilver-induced apoptosis. In nanosilver-resistant HCT116 cells, up-regulation of the anti-apoptotic proteins, Bcl-2 appeared to be associated with a diminished apoptotic response. Taken together, our results provide the first evidence for a molecular mechanism of nanosilver cytotoxicity, showing that nanosilver acts through ROS and JNK to induce apoptosis via the mitochondrial pathway.