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The transportation of container trucks in urban areas not only frequently causes traffic jams but also produces severe air pollution. With regard to this consideration, measurements of particle concentrations and traffic volume on different polluted days were carried out to discover the varied characteristics of particles from container truck transportation in the port area. Based on the original data, descriptive statistics were performed firstly to reveal the statistical characteristics of particle number concentrations (PNC). The Kolmogorov-Smirnov test as well as the Anderson-Darling test was adopted to identify the "best-fit" distributions on PNC data while the corresponding maximum likelihood estimation was conducted to estimate the parameters of the identified distribution. Additionally, the Pearson correlation analysis and principal component analysis were performed respectively to reveal the relationships between traffic volume and PNC. The results showed that on a hazy day, PNC levels in the morning were generally higher than those in the afternoon, while on a non-hazy day, the results were opposite. Particles in all sizes on a non-hazy day and larger than 0.5 μm on a hazy day were verified to fit the lognormal distribution. In contrast to the particles below 2 μm, the particles above 2 μm exhibited higher correlations with the traffic flow of a container truck in the morning on a hazy day. These results indicate the importance of reducing air pollution from a container truck and provide policymakers with a foundation for possible measures in a port city.

Vohwinkel syndrome (VS) is a rare autosomal dominant condition, also known as mutilating palmoplantar keratoderma accompanied by sensorineural deafness. The LOR and GJB2 genes are reported to be responsible for VS. The GJB2 gene encodes connexin 26, a component of intercellular gap junctions expressed in various tissues. We report the case of a 31-year-old Chinese woman with classic VS characterized by sensorineural deafness and mutilating palmoplantar keratoderma. Further genetic studies demonstrated a nucleotide change (c.175G>A) in the GJB2 gene, leading to an amino acid alteration (G59S). This identical missense mutation (G59S) has also been reported in a patient with Bart-Pumphrey syndrome. Together with our findings and previous studies, we conclude that the identical mutation (G59S) in the GJB2 gene contributes to various manifestations.

In this paper, a coupled map car-following model is extended to two-lane traffic system. Based on it, the numerical simulations for one stop and series stops situations are performed respectively under the open boundary condition. The evolution of traffic jam and corresponding energy consumption are then explored and compared each other. Additionally, the influences of the lane changing rule and control scheme on traffic jam and energy consumption are investigated separately. The results show that lane changing rule and control scheme are found not only to suppress the traffic jam but also to reduce the energy consumption. The control scheme exhibit better behavior than lane changing rule does in suppressing traffic jam and reducing energy consumption in two-lane traffic system. The outputs of these findings demonstrate the potential of the proposed model to be applicable to evaluate the control schemes for suppressing traffic jam and reducing energy consumption in real traffic condition.

Reduction of protein phosphatase-2A (PP2A) activity is a common clinical feature of Alzheimer's disease and vascular dementia. In this study, we observed that chronic brain hypoperfusion induced by bilateral common carotid artery occlusion of rats led to PP2A inactivation based on the increase in tyrosine-307 phosphorylation and leucine-309 demethylation of PP2AC and the depression in PP2ABα. Knockdown of miR-195 using overexpression of its antisense molecule oligonucleotide (pre-AMO-miR-195) delivered by a lentivirus (lenti-pre-AMO-miR-195) increased tyrosine-307 phosphorylation and decreased both PP2ABα expression and leucine-309 methylation; these effects were prevented by the overexpression of miR-195 using lenti-pre-miR-195 and controlled by an increase in methylesterase (PME-1) and a decrease in leucine carboxyl methyltransferase-1. In vitro studies demonstrated that miR-195 regulated PME-1 expression by binding to the Ppme1 gene 3'-untranslated region (3'UTR) domain. Masking the miR-195 binding sites in the amyloid precursor protein (APP) and β-site APP cleaving enzyme 1 genes prevented miR-195-induced leucine carboxyl methyltransferase-1 elevation. We concluded that the miR-195 downregulation in chronic brain hypoperfusion involved PP2A inactivity, which was mediated by the post-transcriptional regulation PME-1, APP, and β-site APP cleaving enzyme 1 expression.

Impaired synaptic plasticity and neuron loss are hallmarks of Alzheimer’s disease and vascular dementia. Here, we found that chronic brain hypoperfusion (CBH) by bilateral common carotid artery occlusion (2VO) decreased the total length, numbers and crossings of dendrites and caused neuron death in rat hippocampi and cortices. It also led to increase in N-terminalβ-amyloid precursor protein (N-APP) and death receptor-6 (DR6) protein levels and in the activation of caspase-3 and caspase-6. Further study showed that DR6 protein was downregulated bymiR-195overexpression, upregulated bymiR-195inhibition, and unchanged by binding-site mutation and miR-masks. Knockdown of endogenousmiR-195by lentiviral vector-mediated overexpression of its antisense molecule (lenti-pre-AMO-miR-195) decreased the total length, numbers and crossings of dendrites and neuron death, upregulated N-APP and DR6 levels, and elevated cleaved caspase-3 and caspase-6 levels. Overexpression ofmiR-195using lenti-pre-miR-195prevented these changes triggered by 2VO. We conclude thatmiR-195is involved in CBH-induced dendritic degeneration and neuron death through activation of the N-APP/DR6/caspase pathway.