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Low-carbon economy is an emerging and inevitable pathway toward sustainable development of cold chain logistics. Low-temperature transportation is the crucial link of cold chain logistics to low-carbon economy and the industry is known to have the higher energy consumption. Prior studies are lacking in involving the carbon emission cost in the optimization process. Route optimization of low-temperature transportation is conducive to the low-carbon cold chain logistics. This study aims to introduce the low-carbon economy into the cold chain logistics. There are various costs needed to be considered in cold chain logistics, and a cold chain logistics route optimization model included the carbon emission cost was developed. Ribonucleic acid computing was combined with ant colony optimization to prevent the influence of unreasonable parameter selection on algorithm performance. This novel proposed approach was applied to solve the route optimization problem of a cold chain logistics firm located in the Xiong'an, China. The results showed this method reduced the overall cost of logistics and minimized the amount of carbon emissions. The finding shed the light on the low-carbon transformational development of cold chain logistics firms. • Low-carbon economy moves toward sustainable development of cold chain logistics. • Low-temperature transportation links cold chain logistics to low-carbon economy. • The ribonucleic acid (RNA) and the ant colony optimization (ACO) are combined. • RNA–ACO offers a better solution to the route optimization of cold chain logistics. [ABSTRACT FROM AUTHOR]

This study investigated the correlation between the level of microRNA expression in peripheral blood mononuclear cells (PBMCs) and symptomatology in patients with generalized anxiety disorder (GAD). MicroRNA array was performed in peripheral blood mononuclear cells (PBMCs) obtained from GAD patients with gender, age, ethnicity-matched healthy controls. Then real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to verify the top 7 miRNAs with the highest fold-change values in 76 GAD patients and 39 healthy controls. It demonstrated that 5 miRNAs showed significantly differences in expression levels ( P < 0.01). These 5 GAD-associated miRNAs were finally selected into our study to analyze the association between the plasma level of miRNAs expression and symptomatology scores in Hamilton Anxiety Scale (HAMA). Results showed that the level of miR-4505 and miR-663 was negatively correlated with the total HAMA scores in GAD patients ( r = 0.2228, r = 0.264 P < 0.05). MiR-663 was selected into the regression equation of HAMA total scores and psychic anxiety symptomatology scores, and it could explain 5.3% of the HAMA total scores and 15.3% of the anxiety symptomatology scores. This study analyzed preliminarily possible circulating miRNAs expression changes in GAD patients, and the expression level of miR-663 highly correlated with psychic anxiety symptoms, further molecular mechanism of which needs to be explored. [ABSTRACT FROM AUTHOR]

This study aimed to identify the difference of microRNA-7 (miR-7) expression levels between schizophrenia patients and healthy controls and to investigate the regulatory effects of miR-7 on the SHANK3 gene in schizophrenia. miR-7 levels in plasma were detected by quantitative polymerase chain reactions (qPCR) in 50 schizophrenia patients and 50 healthy controls. The hippocampal neuron cell line, HT 22 , was transfected with lentiviral vector overexpressing or knocking-down miR-7, and the expression levels of SHANK3 mRNA and Shank3 protein were measured by qPCR and immunofluorescence. A luciferase assay was carried out to analyze the regulatory effects of miR-7 on SHANK3. Circulating miR-7 level was significantly increased in schizophrenia patients ( p = 0.022). Overexpression of miR-7 suppressed the expression of SHANK3 while the levels of SHANK3 mRNA and Shank protein were significantly increased by miR-7 knockdown. We conclude that miR-7 binds to 3-prime untranslated regions of SHANK3 mRNA and causes the alteration of neuronal morphology and function, potentially playing a crucial role in the pathophysiological process of schizophrenia. [ABSTRACT FROM AUTHOR]

Findings from multiple studies on microRNA (miRNA) expression profiling in schizophrenia patients have produced conflicting results. In order to investigate miRNA as specific biomarkers in the peripheral plasma and peripheral blood mononuclear cells (PBMC) of schizophrenia patients, expression levels of the nine most frequently reported schizophrenia-associated miRNA (miR-30e, miR-34a, miR-181b, miR-195, miR-346, miR-432, miR-7, miR-132 and miR-212) were examined in the peripheral plasma and PBMC in 25 schizophrenia patients and 13 healthy controls using quantitative real-time reverse transcription polymerase chain reaction. We observed significantly increased expressions of miR-132, miR-195, miR-30e and miR-7 in plasma samples ( p < 0.05 to p < 0.001), and miR-212, miR-34a and miR-30e in PBMC samples ( p < 0.05 to p < 0.01). Receiver operating characteristic curve analysis revealed that the area under the curve (AUC) of miR-30e in plasma was 0.767 (95% confidence interval [CI] 0.608–0.926) with sensitivity and specificity of 90.90% and 60.00% respectively, and the AUC of miR-30e in PBMC was 0.756 (95% CI 0.584–0.929) with sensitivity and specificity of 81.80% and 68.00%, respectively. Logistic regression analysis demonstrated that miR-30e in plasma was more sensitive to differentiate schizophrenia patients from normal controls than miR-30e in PBMC. Our findings indicate that miRNA expression is more significant in plasma than in PBMC, and suggest that miR-30e in plasma may be a more sensitive biomarker for schizophrenia diagnosis, although its aberrant expression can be detected in both plasma and PBMC. [ABSTRACT FROM AUTHOR]

Octahedral hexanuclear ferrocenylacetylide complexes [Ag6(μ-dppm)2(μ3-η1-C&z.tbnd6;CFc)4(CH3OH)2](BF4)2 (1) and [Cu6(μ-dppm)2(μ3-η1-C&z.tbnd6;CFc)4(ClO4)2] (2) (dppm=Ph2PCH2PPh2, Fc=ferrocenyl) are synthesised and characterized structurally. [Copyright &y& Elsevier]

The reaction between [Cu2(Ph2PNHPPh2)2(MeCN)2](BF4)2 and sodium salt of mercaptoacetic acid (HSCH2COONa) at room temperature for 12 h produced a doubly μ3-SH-bridged tricopper complex [Cu3(μ-Ph2PNHPPh2)3(μ3-SH)2](BF4)·2MeOH·Et2O which affords a trigonal bipyramidal core of Cu3(μ3-SH)2 with copper ⋯ copper separations around 3.0 A˚. The complex is photoluminescent and it displays an emissive maximum at 523 nm in the solid state at 293 K. [Copyright &y& Elsevier]

Schizophrenia is a severe and debilitating psychiatric disorder of unknown etiology, and its diagnosis is essentially based on clinical symptoms. Despite growing evidence on the relation of altered expression of miRNAs and schizophrenia, most patients with schizophrenia usually had an extensive antipsychotic treatment history before miRNA expression profile analysis, and the pharmacological effects on miRNA expression are largely unknown. To overcome these impediments, miRNA microarray analysis was performed in peripheral blood mononuclear cells (PBMCs) obtained from patients with schizophrenia who were not on antipsychotic medication and healthy controls. Then, using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), we verified the top 10 miRNAs with the highest fold-change values from microarray analysis in 82 patients with schizophrenia and 43 healthy controls, and nine miRNAs demonstrated significant differences in expression levels. Finally, we compared these nine miRNA profiles before and after antipsychotic treatment. Our results revealed that serum miR-21 expression decreased strikingly in patients after antipsychotic treatment. The change of miR-21 expression was negatively correlated with improvement of positive, general psychopathology, and aggressiveness symptoms. This study preliminarily analyzed the possible changes in circulating miRNAs expression in response to antipsychotic medication for schizophrenia, and the molecular mechanisms of this needs to be further explored. [ABSTRACT FROM AUTHOR]

Currently, diagnosis and treatment of major depressive disorder (MDD) are based on the patients' description of symptoms, mental status examinations, and clinical behavioral observations, which increases the chance of misdiagnosis. There is a serious need to find a practical biomarker for the proper diagnosis of MDD. This study aimed to explore the possibility of microRNA (miRNA) in peripheral blood mononuclear cells (PBMCs) as specific blood-based biomarker for MDD patients. By using an Affymetrix array that covers 723 human miRNAs, we identified 26 miRNAs with significant changes in expression in PBMCs of MDD patients. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis in a larger cohort of 81 MDD patients and 46 healthy controls confirmed that the expression levels of 5 miRNAs (miRNA-26b, miRNA-1972, miRNA-4485, miRNA-4498, and miRNA-4743) were up-regulated. By receiver operating characteristic (ROC) curve analysis, the combining area under the ROC curve (AUC) of these five miRNAs was 0.636 [95% confidence interval (CI): 0.58-0.90]. MiRNA target gene prediction and functional annotation analysis showed that there was a significant enrichment in several pathways associated with nervous system and brain functions, supporting the hypothesis that differentially-regulated miRNAs may be involved in mechanism underlying development of MDD. We conclude that altered expression of miRNAs in PMBCs might be involved in multiple stages of MDD pathogenesis, and thus might be able to serve as specific biomarker for diagnosis of MDD. [ABSTRACT FROM AUTHOR]

Abstract: Despite the growing evidences on the relation of altered expression of miRNAs and schizophrenia, most schizophrenia subjects have an extensive antipsychotic treatment history and the pharmacological effects on miRNA expression are largely unknown. This study aimed to investigate the change of plasma microRNA-181b level and improvement of symptomatology before and after six-week antipsychotic treatment in schizophrenia patients, and explore their association. A total of 20 schizophrenia patients absent of antipsychotics and 20 age-and gender-matched normal controls were enrolled, and tested for 9 schizophrenia-associated microRNA (miR-30e, miR-34a, miR-181b, miR-195, miR-346, miR-432, miR-7, miR-132 and miR-212) expression levels in plasma using quantitative RT-PCR and for symptomatology improvement using Positive And Negative Syndrome Scale (PANSS) before and after treatment (olanzapine, quetiapine, ziprasidone and risperidone) for the patients only. Compared with the normal control group, the expression levels of miRNA-181b, miRNA-30e, miRNA-34a and miRNA-7 of the patients group were significantly higher (p < 0.05). Compared with those before treatment in the patient group, the symptomatology scores were significantly lower (p < 0.001), and the expression level of microRNA-181b was significantly down-regulated after treatment (p < 0.05). The change of miRNA-181b expression was positively correlated with the improvement of negative symptoms and lack of response symptoms (r = 0.502 and 0.557, P < 0.05, accounting for 20.2% and 26.4% respectively), and their therapeutic effects with OR being 11.283 and 5.119 respectively. We conclude that miRNA-181b, miRNA-30e, miRNA-34a and miRNA-7 are probably involved in pathogenesis of SZ, and the significant down-regulation of miRNA-181b expression predicts improvement of negative symptoms to treatment, and thus can serve as a potential plasmamolecular marker for antipsychotic responses. [Copyright &y& Elsevier]

Abstract: Sertraline is one of the most commonly used antidepressants in clinic. Although it is well accepted that sertraline exerts its action through inhibition of the reuptake of serotonin at presynaptic site in the brain, its effect on the neural stem cells (NSCs) has not been well elucidated. In this study, we utilized NSCs separated from the hippocampus of fetal rat to investigate the effect of sertraline on the proliferation and differentiation of NSCs. The study demonstrated that sertraline had no effect on NSCs proliferation but it significantly promoted NSCs to differentiate into serotoninergic neurons other than glia cells. Furthermore, we found that sertraline protected NSCs against the lipopolysaccharide-induced cellular damage. These data indicate that sertraline can promote neurogenesis and protect the viability of neural stem cells. [Copyright &y& Elsevier]

Abstract: A series of Cu(II) complexes of disubstituted 2,2′-bipyridine bearing ammonium groups [Cu(L1−4)2Br]5+ (1–4, L1 =[5,5′-(Me2NHCH2)2-bpy]2+, L2 =[5,5′-(Me3NCH2)2-bpy]2+, L3 =[4,4′-(Me2NHCH2)2-bpy]2+, L4 =[4,4′-(Me3NCH2)2-bpy]2+ and bpy=2,2′-bipyridyl) were synthesized, of which complexes 1 and 4 were structurally characterized. Both coordination configurations of Cu(II) ions can be described as distorted trigonal bipyramid. The interaction between all complexes and CT-DNA was evaluated by thermal-denaturation experiments and CD spectroscopy. Results show that the complexes interact with CT-DNA via outside electrostatic interactions and their binding ability follows the order: 1 > 2 > 3 > 4. In the absence of any reducing agents, the cleavage of plasmid pBR322 DNA by these complexes was investigated and the hydrolysis kinetics of DNA was studied in Tris buffer (pH 7.5) at 37°C. Obtained pseudo-Michaelis–Menten kinetic parameters: 15.0, 13.6, 2.01 and 1.69h−1 for 1, 2, 3 and 4, respectively, indicate that complexes 1 and 2 exhibit very high DNA cleavage activities. According to their crystal data, the high nuclease activity may be attributed to the strong interaction of the metal moiety and two ammonium groups with phosphate groups of DNA. [Copyright &y& Elsevier]