One-Component Multichannel Sensor Array for Rapid Identification of Bacteria.

Bacterial infections routinely cause serious problems to public health. To mitigate the impact of bacterial infections, sensing systems are urgently required for the detection and subsequent epidemiological control of pathogenic organisms. Most conventional approaches are time-consuming and highly instrument- and professional operator-dependent. Here, we developed a novel one-component multichannel array constructed with complex systems made from three modified polyethyleneimine as well as negatively charged graphene oxide, which provided an information-rich multimode response to successfully identify 10 bacteria within minutes via electrostatic interactions and hydrophobic interactions. Furthermore, the concentration of bacteria (from OD600 = 0.025 to 1) and the ratio of mixed bacteria were successfully achieved with our smart sensing system. Our designed sensor array also exhibited huge potential in biological samples, such as in urine (OD600 = 0.125, 94% accuracy). The way to construct a sensor array with minimal sensor element with abundant signal outputs tremendously saves cost and time, providing a powerful tool for the diagnosis and assessment of bacterial infections in the clinic.

A simple array integrating machine learning for identification of flavonoids in red wines.

Bioactive flavonoids, the major ingredients of red wines, have been proven to prevent atherosclerosis and cardiovascular disease due to their anti-inflammatory and anti-oxidant activity. However, flavonoids have proven challenging to identify, even when multiple approaches are combined. Hereby, a simple array was constructed to detect flavonoids by employing phenylboronic acid modified perylene diimide derivatives (PDIs). Through multiple non-specific interactions (hydrophilic, hydrophobic, charged, aromatic, hydrogen-bonded and reversible covalent interactions) with flavonoids, the fluorescence of PDIs can be modulated, and variations in intensity can be used to create fingerprints of flavonoids. This array successfully discriminated 14 flavonoids of diverse structures and concentrations with 100% accuracy, based on patterns in fluorescence intensity modulation, via optimized machine learning algorithms. As a result, this array demonstrated the parallel detection of 8 different types and origins of red wines with a high accuracy, revealing the excellent potential of the sensor array in food mixtures detection.

Effect of hydrodynamics on the transformation of nitrogen in river water by regulating the mass transfer performance of dissolved oxygen in biofilm.

Biofilms drive crucial ecosystem processes in rivers. This study provided the basis for overall quantitative calculations about the contribution of biofilms to the nitrogen cycle. At the early stage of biofilm formation, dissolved oxygen (DO) could penetrate the biofilms. As the biofilm grew and the thickness increased, then the mass transfer of DO was restricted. The microaerobic layer firstly appeared in biofilm under the turbulent flow conditions, with the appearance of the microaerobic and anaerobic layer, the nitrification and denitrification reaction could proceed smoothly in biofilm. And the removal efficiency of total nitrogen (TN) increased as the biofilm matured. Under the turbulent flow conditions, mature biofilms had the smallest thickness, but the highest proportion the anaerobic layer to the biofilm thickness, the highest density, and the highest nitrogen removal efficiency. However, the nitrogen removal efficiency of biofilm was the lowest under laminar flow conditions. The difference of layered structure of biofilm and the DO flux in biofilm explained the difference of nitrogen migration and transformation in river water under different hydrodynamic conditions. This study would help control the growth of biofilm and improve the nitrogen removal capacity of biofilm by regulating hydrodynamic conditions.

Pretreatment with Salvia miltiorrhiza Polysaccharides Protects from Lipopolysaccharides/d-Galactosamine-Induced Liver Injury in Mice Through Inhibiting TLR4/MyD88 Signaling Pathway.

The study was conducted to investigate the protective effects of Salvia miltiorrhiza polysaccharides (SMPs) on lipopolysaccharides (LPS)/d-galactosamine (d-GalN)-induced liver injury in mice and its mechanism. Seventy-two mice were allocated to 6 groups of 12 each, that is, the untreated control group, the liver injury model group, the Bifendate group (Bifendate 200 mg/kg/day), and 3 SMP-treated groups at low (250 mg/kg/day), medium (500 mg/kg/day), and high doses (750 mg/kg/day). After 12 days oral treatment, liver injury was induced with LPS/d-GalN, and 1 h later the mice were sacrificed for a series of analyses. The results showed that SMPs significantly alleviated pathological changes in the hepatic tissue. Compared with the untreated control group, the messenger RNA (mRNA) levels of lipopolysaccharide-binding protein (LBP), cluster of differentiation 14 (CD14), myeloid differentiation factor 2 (MD-2), toll-like receptor 4 (TLR4), and myeloid differentiation primary response protein 88 (MyD88) detected by quantitative real-time polymerase chain reaction (qRT-PCR), the protein levels of TLR4, MyD88, phosphorylated inhibitor of nuclear factor kappa-B kinase alpha/beta (P-IKK-α/ß), phosphorylated inhibitor of NF-κB alpha (P-IκB-α) and phosphorylated P65 (P-P65) detected by Western blot, the levels of C-X-C motif chemokine 10 (CXCL-10) and Intercellular Adhesion Molecule 1 (ICAM-1) detected by immunohistochemistry, and the concentrations of tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1ß) detected by enzyme-linked immunosorbent assay of liver injury model group were increased significantly (P < 0.01). Compared with liver injury model group, the mRNA levels of LBP, CD14, MD-2, TLR4, and MyD88; protein levels of TLR4, MyD88, P-IKK-α/ß, P-IκB-α, and P-P65; levels of CXCL-10 and ICAM-1; and the concentrations of TNF-α and IL-1ß of SMP groups and Bifendate group were decreased significantly (P < 0.01 or P < 0.05). In conclusion, SMPs can effectively inhibit TLR4/MyD88 inflammatory signaling pathway of LPS/d-GalN-induced liver injury in mice, and it may be part of the mechanism by which SMPs relieve excessive inflammation in the liver of mice.

Neuroprotective effects of pyrroloquinoline quinone against rotenone injury in primary cultured midbrain neurons and in a rat model of Parkinson's disease.

Mitochondrial dysfunction and oxidative stress have been implicated in the pathogenesis of Parkinson's disease (PD). Pyrroloquinoline quinone (PQQ), a redox cofactor in the mitochondrial respiratory chain, has been reported to protect SH-SY5Y cells from cytotoxicity induced by rotenone, a mitochondrial complex I inhibitor. In this study, we aimed to investigate the neuroprotective effects of PQQ against rotenone injury in primary cultured midbrain neurons and in a rat model of Parkinson's disease. Pre-treatment with PQQ prevented cultured midbrain neurons from rotenone-induced apoptosis, restored mitochondrial membrane potential, inhibited intracellular reactive oxygen species (ROS) production, and affected microtubule depolymerization. On the other hand, intraperitoneal administration of PQQ exerted protective effects on rats that had received rotenone injection into the medial forebrain bundle through decreasing the apomorphine-evoked rotation, inhibiting neuronal loss and TH down-regulation in SNc, increasing the antioxidative ability, and regulating intracellular expressions of Ndufs1 and Ndufs 4. Silencing of Ndufs1 or Ndufs4 in cultured SH-SY5Y cells or midbrain neurons reduced the neuroprotective effects of PQQ. Overall, our results suggest that PQQ neuroprotection may be mediated by the inhibition of mitochondrial dysfunction and oxidative stress as well as by the gene modulation of Ndufs1 and Ndufs4.

Pyrroloquinoline quinone-conferred neuroprotection in rotenone models of Parkinson's disease.

Pyrroloquinoline quinone (PQQ), a redox cofactor in the mitochondrial respiratory chain, has proven to protect neurons against glutamate-induced damage both in vitro and in vivo. This study was aimed to investigate the possible neuroprotective effects of PQQ in rotenone-induced Parkinson's disease (PD) model. Pre-treatment with PQQ prevented cultured SH-SY5Y cells from rotenone-induced apoptosis, accompanied by modulation of apoptosis-related proteins (Bcl-2, Bax and Smac), restoration of the mitochondrial membrane potential, inhibition of intracellular reactive oxygen species (ROS) production, suppression of tyrosine residues nitration, and dopamine redistribution. PQQ also exerted protective effects in an in vivo PD model, which was created by rotenone injection into the medial forebrain bundle of rats. Co-injection with PQQ and rotenone improved the apomorphine-evoked rotation, decreased neuronal loss, increased the ROS-scavenging ability, regulated intracellular expressions of mitochondrial complex subunits (Ndufs1-4), tyrosine hydroxylase, and vesicular monoamine transporter 2. Taken together, our results collectively suggest that PQQ confers neuroprotection in rotenone-induced PD model probably through complex and multifaceted mechanisms, at least involving oxidative stress, mitochondrial integrity, and dopamine functions.