The oxidation of 2-(2-methoxyethoxy)-ethanol and 2-(2-ethoxyethoxy)-ethanol by dihydroxydiperiodato nickelate(IV): A kinetic and mechanistic study

The kinetics of oxidation of 2-(2-methoxyethoxy)-ethanol and 2-(2-ethoxyethoxy)-ethanol by dihydroxydiperiodato nickelate(IV) (DPN) had been studied spectrophotometrically in alkaline medium in the temperature range of 293.2 to 313.2 K. The reaction rate showed first order dependence on DPN, 2-(2-methoxyethoxy)-ethanol and 2-(2-ethoxyethoxy)-ethanol. It was found that the pseudo-first-order rate constant kobs increased with an increase in concentration of OH- and a decrease in concentration of IO4-. There was a positive salt effect and no free radicals were detected. A plausible mechanism is proposed and the rate equations derived from the mechanism can explain all the experimental observations

Kinetics and Mechanism of Oxidation of Diethanolamine and Triethanolamine by Potassium Ferrate

Abstract: The kinetics of oxidation of diethanolamine and triethanolamine by potassium ferrate(VI) in alkaline liquids at a constant ionic strength has been studied spectrophotometrically in the temperature range of 278.2 K-293.2 K. The reaction shows first order dependence on potassium ferrate(VI), first order dependence on each reductant, The observed rate constant (k obs ) decreases with the increase in [OH -], the reaction is negative fraction order with respect to [OH -]. A plausible mechanism is proposed and the rate equations derived from the mechanism can explain all the experimental results. The rate constants of the ratedetermining step and the thermodynamic activation parameters are calculated

Adenovirus-mediated delivery of bFGF small interfering RNA reduces STAT3 phosphorylation and induces the depolarization of mitochondria and apoptosis in glioma cells U251

Glioblastoma multiforme (GBM) carries a dismal prognosis primarily due to its aggressive proliferation in the brain regulated by complex molecular mechanisms. One promising molecular target in GBM is over-expressed basic fibroblast growth factor (bFGF), which has been correlated with growth, progression, and vascularity of human malignant gliomas. Previously, we reported significant antitumor effects of an adenovirus-vector carrying bFGF small interfering RNA (Ad-bFGF-siRNA) in glioma in vivo and in vitro. However, its mechanisms are unknown. Signal transducer and activator of transcription 3 (STAT3) is constitutively active in GBM and correlates positively with the glioma grades. In addition, as a specific transcription factor, STAT3 serves as the convergent point of various signaling pathways activated by multiple growth factors and/or cytokines. Therefore, we hypothesized that the proliferation inhibition and apoptosis induction by Ad-bFGF-siRNA may result from the interruption of STAT3 phosphorylation. In the current study, we found that in glioma cells U251, Ad-bFGF-siRNA impedes the activation of ERK1/2 and JAK2, but not Src, decreases IL-6 secretion, reduces STAT3 phosphorylation, decreases the levels of downstream molecules CyclinD1 and Bcl-xl, and ultimately results in the collapse of mitochondrial membrane potentials as well as the induction of mitochondrial-related apoptosis. Our results offer a potential mechanism for using Ad-bFGF-siRNA as a gene therapy for glioma. To our knowledge, it is the first time that the bFGF knockdown using adenovirus-mediated delivery of bFGF siRNA and its potential underlying mechanisms are reported. Therefore, this finding may open new avenues for developing novel treatments against GBM

Brain Injury Differences in Frontal Impact Crash Using Different Simulation Strategies

In the real world crashes, brain injury is one of the leading causes of deaths. Using isolated human head finite element (FE) model to study the brain injury patterns and metrics has been a simplified methodology widely adopted, since it costs significantly lower computation resources than a whole human body model does. However, the degree of precision of this simplification remains questionable. This study compared these two kinds of methods: (1) using a whole human body model carried on the sled model and (2) using an isolated head model with prescribed head motions, to study the brain injury. The distribution of the von Mises stress (VMS), maximum principal strain (MPS), and cumulative strain damage measure (CSDM) was used to compare the two methods. The results showed that the VMS of brain mainly concentrated at the lower cerebrum and occipitotemporal region close to the cerebellum. The isolated head modelling strategy predicted higher levels of MPS and CSDM 5%, while the difference is small in CSDM 10% comparison. It suggests that isolated head model may not equivalently reflect the strain levels below the 10% compared to the whole human body model

Adenovirus-mediated delivery of bFGF small interfering RNA increases levels of connexin 43 in the glioma cell line, U251

BACKGROUND: bFGF is an important growth factor for glioma cell proliferation and invasion, while connexin 43 is implicated in the suppression of glioma growth. Correspondingly, gliomas have been shown to have reduced, or compromised, connexin 43 expression. METHODS: In this study, a bFGF-targeted siRNA was delivered to the glioma cell line, U251, using adenovirus (Ad-bFGF-siRNA) and the expression of connexin 43 and its phosphorylation state were evaluated. U251 cells were infected with Ad-bFGF-siRNA (100, 50, or 25 MOI), and infection with adenovirus expressing green fluorescent protein (Ad-GFP) at 100 MOI served as a control. Western blotting and immunofluorescence were used to detect the expression levels, phosphorylation, and localization of connexin 43 in U251 cells infected, and not infected, with Ad-bFGF-siRNA. RESULTS: Significantly higher levels of connexin 43 were detected in U251 cells infected with Ad-bFGF-siRNA at 100 and 50 MOI than in cells infected with Ad-GFP, and the same amount of connexin 43 was detected in Ad-GFP-infected and uninfected U251 cells. Connexin 43 phosphorylation did not differ between Ad-bFGF-siRNA-infected and uninfected U251 cells. However, the ratio of phosphorylated to unphosphorylated connexin 43 in Ad-bFGF-siRNA cells was lower, and connexin 43 was predominantly localized to the cytoplasm. Using a scrape loading dye transfer assay, more Lucifer Yellow was transferred to neighboring cells in the Ad-bFGF-siRNA treated group than in the control group. CONCLUSION: To our knowledge, this is the first description of a role for connexin 43 in the inhibition of U251 growth using Ad-bFGF-siRNA

Multimodal magnetic resonance imaging on brain structure and function changes in subjective cognitive decline: a mini-review

Subjective cognitive decline (SCD) is the initial stage of Alzheimer’s disease (AD). Early identification of SCD and its risk factors is of great importance for targeted interventions and for delaying the onset of AD. We reviewed the relevant literature on structural magnetic resonance imaging (sMRI), diffusion tensor imaging (DTI), functional magnetic resonance imaging (fMRI), and other techniques regarding SCD research in recent years. This study applied sMRI and fMRI techniques to explore abnormal brain structures and functions, which may help provide a basis for SCD diagnosis