New Evolutionary Insights into RpoA: A Novel Quorum Sensing Reprograming Factor in Pseudomonas aeruginosa.

Quorum-sensing (QS) coordinates the expression of virulence factors in Pseudomonas aeruginosa, an opportunistic pathogen known for causing severe infections in immunocompromised patients. QS has a master regulator, the lasR gene, but in clinical settings, P. aeruginosa isolates have been found that are QS-active but LasR-null. In this study, we developed an experimental evolutionary approach to identify additional QS-reprogramming determinants. We began the study with a LasR-null mutant with an extra copy of mexT, a transcriptional regulator gene that is known to be able to reprogram QS in laboratory LasR-null strains. In this strain, spontaneous single mexT mutations are expected to have no or little phenotypic consequences. Using this novel method, which we have named "targeted gene duplication followed by mutant screening", we identified QS-active revertants with mutations in genes other than mexT. One QS-active revertant had a point mutation in rpoA, a gene encoding the α-subunit of RNA polymerase. QS activation in this mutant was found to be associated with the downregulated expression of mexEF-oprN efflux pump genes. Our study therefore uncovers a new functional role for RpoA in regulating QS activity. Our results indicate that a RpoA-dependent regulatory circuit controlling the expression of the mexEF-oprN operon is critical for QS-reprogramming. In conclusion, our study reports on the identification of non-MexT proteins associated with QS-reprogramming in a laboratory strain, shedding light on possible QS activation mechanisms in clinical P. aeruginosa isolates.

Current status of molecular rice breeding for durable and broad-spectrum resistance to major diseases and insect pests.

In the past century, there have been great achievements in identifying resistance (R) genes and quantitative trait loci (QTLs) as well as revealing the corresponding molecular mechanisms for resistance in rice to major diseases and insect pests. The introgression of R genes to develop resistant rice cultivars has become the most effective and eco-friendly method to control pathogens/insects at present. However, little attention has been paid to durable and broad-spectrum resistance, which determines the real applicability of R genes. Here, we summarize all the R genes and QTLs conferring durable and broad-spectrum resistance in rice to fungal blast, bacterial leaf blight (BLB), and the brown planthopper (BPH) in molecular breeding. We discuss the molecular mechanisms and feasible methods of improving durable and broad-spectrum resistance to blast, BLB, and BPH. We will particularly focus on pyramiding multiple R genes or QTLs as the most useful method to improve durability and broaden the disease/insect spectrum in practical breeding regardless of its uncertainty. We believe that this review provides useful information for scientists and breeders in rice breeding for multiple stress resistance in the future.

Establishment of genomic RNA reference materials for BCR-ABL1 P210 measurement.

Quantitation of BCR-ABL1 with the quantitative reverse transcriptase polymerase chain reaction (RT-PCR) is very important in monitoring chronic myeloid leukemia (CML), which relies on an RNA reference material. A genomic RNA reference material (RM) containing the BCR-ABL1 P210 fusion mutation was developed, and an absolute quantitative method based on one-step reverse transcription digital PCR (RT-dPCR) was established for characterizing the RM. The proposed dPCR method demonstrates high accuracy and excellent analytical sensitivity, as shown by the linear relationship (0.94 < slope < 1.04, R2≧0.99) between the measured and nominal values of b2a2, b3a2, and ABL1-ref within the dynamic range (104-101 copies/reaction). Homogeneity and stability assessment based on dPCR indicated that the RM was homogeneous and stable for 24 months at -80 °C. The RM was used to evaluate inter-laboratory reproducibility in eight different laboratories, demonstrating that participating laboratories could consistently produce copy concentrations of b3a2 and ABL1-ref, as well as the BCR-ABL1/ABL1 ratio (CV < 2.0%). This work suggests that the RM can be employed in establishing metrological traceability for detecting mutations in the BCR-ABL1 fusion gene, as well as in quality control for testing laboratories.

Frequent Acquisition of Glycoside Hydrolase Family 32 (GH32) Genes from Bacteria via Horizontal Gene Transfer Drives Adaptation of Invertebrates to Diverse Sources of Food and Living Habitats.

Glycoside hydrolases (GHs, also called glycosidases) catalyze the hydrolysis of glycosidic bonds in polysaccharides. Numerous GH genes have been identified from various organisms and are classified into 188 families, abbreviated GH1 to GH188. Enzymes in the GH32 family hydrolyze fructans, which are present in approximately 15% of flowering plants and are widespread across microorganisms. GH32 genes are rarely found in animals, as fructans are not a typical carbohydrate source utilized in animals. Here, we report the discovery of 242 GH32 genes identified in 84 animal species, ranging from nematodes to crabs. Genetic analyses of these genes indicated that the GH32 genes in various animals were derived from different bacteria via multiple, independent horizontal gene transfer events. The GH32 genes in animals appear functional based on the highly conserved catalytic blades and triads in the active center despite the overall low (35-60%) sequence similarities among the predicted proteins. The acquisition of GH32 genes by animals may have a profound impact on sugar metabolism for the recipient organisms. Our results together with previous reports suggest that the acquired GH32 enzymes may not only serve as digestive enzymes, but also may serve as effectors for manipulating host plants, and as metabolic enzymes in the non-digestive tissues of certain animals. Our results provide a foundation for future studies on the significance of horizontally transferred GH32 genes in animals. The information reported here enriches our knowledge of horizontal gene transfer, GH32 functions, and animal-plant interactions, which may result in practical applications. For example, developing crops via targeted engineering that inhibits GH32 enzymes could aid in the plant's resistance to animal pests.

Fabrication of 100-nm-period domain structure in lithium niobate on insulator.

Lithium niobate on insulator (LNOI) is a powerful platform for integrated photonic circuits. Recently, advanced applications in nonlinear and quantum optics require to controllably fabricate nano-resolution domain structures in LNOI. Here, we report on the fabrication of stable domain structures with sub-100 nm feature size through piezoelectric force microscopy (PFM) tip poling in a z-cut LNOI. In experiment, the domain dot with an initial diameter of 80 nm and the domain line with an initial width of 50 nm can survive after a storage of more than 3 months. Particularly, we demonstrate the successful fabrication of 1D stable domain array with a period down to 100 nm and a duty cycle of ∼50%. Our method paves the way to precisely manipulate frequency conversion and quantum entanglement on an LNOI chip.

Coordination Polymers from Biphenyl-Dicarboxylate Linkers: Synthesis, Structural Diversity, Interpenetration, and Catalytic Properties.

The present work explores two biphenyl-dicarboxylate linkers, 3,3'-dihydroxy-(1,1'-biphenyl)-4,4'-dicarboxylic (H4L1) and 4,4'-dihydroxy-(1,1'-biphenyl)-3,3'-dicarboxylic (H4L2) acids, in hydrothermal generation of nine new compounds formulated as [Co2(µ2-H2L1)2(phen)2(H2O)4] (1), [Mn2(µ4-H2L1)2(phen)2]n·4nH2O (2), [Zn(µ2-H2L1)(2,2'-bipy)(H2O)]n (3), [Cd(µ2-H2L1) (2,2'-bipy)(H2O)]n (4), [Mn2(µ2-H2L1)(µ4-H2L1)(µ2-4,4'-bipy)2]n·4nH2O (5), [Zn(µ2-H2L1)(µ2-4,4'-bipy)]n (6), [Zn(µ2-H2L2)(phen)]n (7), [Cd(µ3-H2L2)(phen)]n (8), and [Cu(µ2-H2L2) (µ2-4,4'-bipy)(H2O)]n (9). These coordination polymers (CPs) were generated by reacting a metal(II) chloride, a H4L1 or H4L2 linker, and a crystallization mediator such as 2,2'-bipy (2,2'-bipyridine), 4,4'-bipy (4,4'-bipyridine), or phen (1,10-phenanthroline). The structural types of 1-9 range from molecular dimers (1) to one-dimensional (3, 4, 7) and two-dimensional (8, 9) CPs as well as three-dimensional metal-organic frameworks (2, 5, 6). Their structural, topological, and interpenetration features were underlined, including an identification of unique two- and fivefold 3D + 3D interpenetrated nets in 5 and 6. Phase purity, thermal and luminescence behavior, as well as catalytic activity of the synthesized products were investigated. Particularly, a Zn(II)-based CP 3 acts as an effective and recyclable heterogeneous catalyst for Henry reaction between a model substrate (4-nitrobenzaldehyde) and nitroethane to give ß-nitro alcohol products. For this reaction, various parameters were optimized, followed by the investigation of the substrate scope. By reporting nine new compounds and their structural traits and functional properties, the present work further outspreads a family of CPs constructed from the biphenyl-dicarboxylate H4L1 and H4L2 linkers.

Coordination Polymers Constructed from an Adaptable Pyridine-Dicarboxylic Acid Linker: Assembly, Diversity of Structures, and Catalysis.

4,4'-(Pyridine-3,5-diyl)dibenzoic acid (H2pdba) was explored as an adaptable linker for assembling a diversity of new manganese(II), cobalt(II/III), nickel(II), and copper(II) coordination polymers (CPs): [Mn(µ4-pdba)(H2O)]n (1), {[M(µ3-pdba)(phen)]·2H2O}n (M = Co (2), Ni (3)), {[Cu2(µ3-pdba)2(bipy)]·2H2O}n (4), {[Co(µ3-pdba)(bipy)]·2H2O}n (5), [Co2(µ3-pdba)(µ-Hbiim)2(Hbiim)]n (6), and [M(µ4-pdba)(py)]n (M = Co (7), Ni (8)). The CPs were hydrothermally synthesized using metal(II) chloride precursors, H2pdba, and different coligands functioning as crystallization mediators (phen: 1,10-phenanthroline; bipy: 2,2'-bipyridine, H2biim: 2,2'-biimidazole; py: pyridine). Structural networks of 1-8 range from two-dimensional (2D) metal-organic layers (1-3, 5-8) to three-dimensional (3D) metal-organic framework (MOF) (4) and disclose several types of topologies: sql (in 1), hcb (in 2, 3, 5), tfk (in 4), 3,5L66 (in 6), and SP 2-periodic net (6,3)Ia (in 7, 8). Apart from the characterization by standard methods, catalytic potential of the obtained CPs was also screened in the Knoevenagel condensation of benzaldehyde with propanedinitrile to give 2-benzylidenemalononitrile (model reaction). Several reaction parameters were optimized, and the substrate scope was explored, revealing the best catalytic performance for a 3D MOF 4. This catalyst is recyclable and can lead to substituted dinitrile products in up to 99% product yields. The present study widens the use of H2pdba as a still poorly studied linker toward designing novel functional coordination polymers.

Reduced learning bias towards the reward context in medication-naive first-episode schizophrenia patients.

BACKGROUND: Reinforcement learning has been proposed to contribute to the development of amotivation in individuals with schizophrenia (SZ). Accumulating evidence suggests dysfunctional learning in individuals with SZ in Go/NoGo learning and expected value representation. However, previous findings might have been confounded by the effects of antipsychotic exposure. Moreover, reinforcement learning also rely on the learning context. Few studies have examined the learning performance in reward and loss-avoidance context separately in medication-naïve individuals with first-episode SZ. This study aimed to explore the behaviour profile of reinforcement learning performance in medication-naïve individuals with first-episode SZ, including the contextual performance, the Go/NoGo learning and the expected value representation performance. METHODS: Twenty-nine medication-naïve individuals with first-episode SZ and 40 healthy controls (HCs) who have no significant difference in age and gender, completed the Gain and Loss Avoidance Task, a reinforcement learning task involving stimulus pairs presented in both the reward and loss-avoidance context. We assessed the group difference in accuracy in the reward and loss-avoidance context, the Go/NoGo learning and the expected value representation. The correlations between learning performance and the negative symptom severity were examined. RESULTS: Individuals with SZ showed significantly lower accuracy when learning under the reward than the loss-avoidance context as compared to HCs. The accuracies under the reward context (90%win- 10%win) in the Acquisition phase was significantly and negatively correlated with the Scale for the Assessment of Negative Symptoms (SANS) avolition scores in individuals with SZ. On the other hand, individuals with SZ showed spared ability of Go/NoGo learning and expected value representation. CONCLUSIONS: Despite our small sample size and relatively modest findings, our results suggest possible reduced learning bias towards reward context among medication-naïve individuals with first-episode SZ. The reward learning performance was correlated with amotivation symptoms. This finding may facilitate our understanding of the underlying mechanism of negative symptoms. Reinforcement learning performance under the reward context may be important to better predict and prevent the development of schizophrenia patients' negative symptom, especially amotivation.

MiR-195-5p facilitates the proliferation, migration, and invasion of human trophoblast cells by targeting FGF2.

BACKGROUND: Preeclampsia (PE), the most significant adverse exposure to cardiovascular risk during pregnancy, is one of the three major factors contributing to maternal and fetal mortality and the leading cause of preterm birth. Recently, various miRNAs have been reported to participate in PE occurrence and development. Nevertheless, the regulatory impact of miR-195-5p in PE is still indistinct. METHODS: Quantitative realtime-PCR (qRT-PCR), western blot, and fluorescence in situ hybridization (FISH) assay were performed to examine miR-195-5p and FGF2 expressions in PE serum samples or HTR-8/SVneo and TEV-1 cells. CCK8, flow cytometry, wound scratch, and transwell assays were conducted to determine cell viability, cycle, apoptosis, migration, and invasion. Dual-luciferase reporter assay unveiled the relationship between miR-195-5p and FGF2. Migration-related and invasion-related protein expressions were measured by western blot assay. RESULTS: miR-195-5p was prominently downregulated while FGF2 was increased in serum samples from PE patients and hypoxia-treated human trophoblast cells. FGF2 was predicted as a downstream target of miR-195-5p and targeted association was verified by dual-luciferase reporter assay. Functional experiments elaborated that miR-195-5p could facilitate trophoblast cell proliferation and metastasis but hinder cell cycle and apoptosis. Inversely, overexpressing of FGF2 could reverse the effects of miR-195-5p on trophoblast cell growth. DISCUSSION: miR-195-5p was decreased in PE serum samples and cell lines, serving as a potential biomarker in protecting PE exacerbation by targeting FGF2.

Bicyclol alleviates high-fat diet-induced hepatic ER stress- and autophagy-associated non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in mice.

BACKGROUND AND OBJECTIVE: Non-alcoholic fatty liver disease (NAFLD) is a manifestation of the metabolic syndrome in the liver, and non-alcoholic steatohepatitis (NASH) represents its advanced stage. Bicyclol has protective activity against NAFLD in mice; however, the effect of bicyclol on high-fat diet (HFD)-induced NASH and its underlying molecular mechanism remains unknown particularly anti-endoplasmic reticulum (ER) stress and autophagic machinery potentials. Therefore, the present study was performed to investigate the protective effect and underlying mechanisms of bicyclol action on NAFLD/NASH. METHODS: Mice were fed an HFD to induce NAFLD/NASH, and bicyclol was administered as a treatment. Biochemistry and histopathological assays were performed to evaluate the effects of bicyclol on NAFLD/NASH. Moreover, the levels of hepatic ER stress- and autophagy-related markers were determined by western blotting. RESULTS: The present results revealed that bicyclol exerted significant protective effects against HFD-induced NAFLD/NASH. This activity was evidenced by the decrease in elevated serum transaminase and hepatic triglyceride levels, and the attenuation of negative histopathological changes. Bicyclol considerably alleviated hepatic inflammation and apoptosis. The protein expression of ER stress-related markers, including C/EBP homologous protein (CHOP) and glucose-regulated protein 78 (GRP78), was downregulated by the bicyclol treatment in HFD-induced mice. However, the protein expression of autophagy-related markers (LC3 and Beclin 1) was upregulated by the treatment with bicyclol. CONCLUSION: Bicyclol protected HFD-induced NASH, and partly due to its ability of reducing ER stress and promoting autophagy.

Mixed-lineage leukemia protein modulates the loading of let-7a onto AGO1 by recruiting RAN.

Not available.

α5-nAChR modulates melanoma growth through the Notch1 signaling pathway.

The roles of α5-nicotinic acetylcholine receptors (α5-nAChRs) in various types of solid cancer have been reported; however, its role in melanoma remains unknown. We knocked down α5-nAChR expression in melanoma cells to investigate the role of α5-nAChR in the proliferation, migration, and invasion of melanoma cells, and its effect on downstream signaling pathways. Using immunohistochemical analysis, we determined that α5-nAChR expression is significantly increased in human melanoma tissues and cell lines compared with normal human skin tissues. Knocking down α5-nAChR expression in melanoma cells in culture significantly inhibited the proliferation, migration, and invasiveness of melanoma cell lines. Specifically, knockdown of α5-nAChR inhibited PI3K-AKT and ERK1/2 signaling activity. Moreover, we confirmed that the Notch1 signaling pathway is the downstream target of α5-nAChR in melanoma. Our findings suggest that α5-nAChR plays a critical role in melanoma development and progression, and that targeting α5-nAChR may be a strategy for melanoma treatment.

Disturbance of Oxidative Stress Parameters in Treatment-Resistant Bipolar Disorder and Their Association With Electroconvulsive Therapy Response.

OBJECTIVE: Electroconvulsive therapy (ECT) is an effective option for treatment-resistant bipolar disorder (trBD). However, the mechanisms of its effect are unknown. Oxidative stress is thought to be involved in the underpinnings of BD. Our study is the first, to our knowledge, to report the association between notable oxidative stress parameters (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], catalase [CAT], and malondialdehyde [MDA]) levels and ECT response in trBD patients. METHODS: A total 28 trBD patients and 49 controls were recruited. Six-week ECT and naturalistic follow-up were conducted. SOD, GSH-Px, CAT, and MDA levels were measured by enzyme-linked immunosorbent assay, and the 17-item Hamilton Depression Rating Scale and Young Mania Rating Scale were administered at baseline and the end of the 6th week. MANCOVA, ANCOVA, 2 × 2 ANCOVA, and a multiple regression model were conducted. RESULTS: SOD levels were lower in both trBD mania and depression (P = .001; P = .001), while GSH-Px (P = .01; P = .001) and MDA (P = .001; P = .001) were higher in both trBD mania and depression compared with controls. CAT levels were positively associated with 17-item Hamilton Depression Rating Scale scores in trBD depression (radjusted = 0.83, P = .005). MDA levels in trBD decreased after 6 weeks of ECT (P = .001). Interestingly, MDA levels decreased in responders (P = .001) but not in nonresponders (P > .05). CONCLUSIONS: Our study indicates that decreased SOD could be a trait rather than a state in trBD. Oxidative stress levels are associated with illness severity and ECT response. This suggests that the mechanism of oxidative stress plays a crucial role in the pathophysiology of trBD.

miR-454 suppresses the proliferation and invasion of ovarian cancer by targeting E2F6.

BACKGROUND: The aberrant expression of microRNA-454 (miR-454) has been confirmed to be involved in the development of cancers. However, the functional role of miR-454 in the progression of ovarian cancer remains unclear. METHODS: The expression of miR-454 in ovarian cancer cells and serum of ovarian cancer patients was detected by RT-PCR. CCK8, colony formation, transwell, and flow cytometry assays were conducted to assess the effects of miR-454 on ovarian cancer cell proliferation, migration, invasion, and apoptosis, respectively. Dual-luciferase reporter assay was used to confirm the targeting relationship between miR-454 and E2F6. The expression pattern of E2F6 in ovarian cancer tissues was detected using immunohistochemistry (IHC) assay. The relative expression of related proteins was examined using western blot analysis. RESULTS: miR-454 was markedly down-regulated by hypoxia in ovarian cancer cells. Compared with normal samples, the expression of miR-454 was up-regulated in the serum of ovarian cancer patients, and correlated with the clinicopathological stages of ovarian cancer. Next, we found that miR-454 overexpression inhibited the proliferation, migration and invasion of OVCAR3 and SKOV3 cells, as well as promoted apoptosis. In addition, the Akt/mTOR and Wnt/ß-catenin signaling pathway were inhibited by miR-454 in ovarian cancer cells. Mechanically, bioinformatic analysis and dual-luciferase reporter assay confirmed that E2F6 was a direct target of miR-454 and negatively regulated by miR-454 in ovarian cancer cells. Moreover, IHC analysis showed that E2F6 was highly expressed in ovarian cancer tissues. Finally, we found that the increasing cell proliferation and migration triggered by E2F6 overexpression were abolished by miR-454 overexpression. CONCLUSION: Taken together, these results highlight the role of miR-454 as a tumor suppressor in ovarian cancer cells by targeting E2F6, indicating that miR-454 may be a potential diagnostic biomarker and therapeutic target for ovarian cancer.

The spleen may be an important target of stem cell therapy for stroke.

Stroke is the most common cerebrovascular disease, the second leading cause of death behind heart disease and is a major cause of long-term disability worldwide. Currently, systemic immunomodulatory therapy based on intravenous cells is attracting attention. The immune response to acute stroke is a major factor in cerebral ischaemia (CI) pathobiology and outcomes. Over the past decade, the significant contribution of the spleen to ischaemic stroke has gained considerable attention in stroke research. The changes in the spleen after stroke are mainly reflected in morphology, immune cells and cytokines, and these changes are closely related to the stroke outcomes. Autonomic nervous system (ANS) activation, release of central nervous system (CNS) antigens and chemokine/chemokine receptor interactions have been documented to be essential for efficient brain-spleen cross-talk after stroke. In various experimental models, human umbilical cord blood cells (hUCBs), haematopoietic stem cells (HSCs), bone marrow stem cells (BMSCs), human amnion epithelial cells (hAECs), neural stem cells (NSCs) and multipotent adult progenitor cells (MAPCs) have been shown to reduce the neurological damage caused by stroke. The different effects of these cell types on the interleukin (IL)-10, interferon (IFN), and cholinergic anti-inflammatory pathways in the spleen after stroke may promote the development of new cell therapy targets and strategies. The spleen will become a potential target of various stem cell therapies for stroke represented by MAPC treatment.

Apatinib exerts anti-tumour effects on ovarian cancer cells.

OBJECTIVE: Apatinib, a small molecule inhibitor of VEGFR-2 tyrosine kinase, shows strong anti-tumour activity against various tumours. The function of apatinib in ovarian cancer, however, remains unclear. This study was conducted to investigate the effects and potential mechanisms by which apatinib modulates the biological function of ovarian cancer cells in vitro and in vivo. METHODS: The effects of apatinib on ovarian cancer cells were determined by assessing cell viability, migration and invasion. The cell cycle distribution and apoptosis of ovarian cancer cells were analysed using flow cytometry. Western blotting was performed to determine the levels of signalling pathway markers. A mouse xenograft model was used to evaluate the efficacy of apatinib in preventing tumour growth. RESULTS: Apatinib did not appreciably affect ovarian cancer cell proliferation and vitality, but did inhibit ovarian cancer cell migration. Apatinib suppressed the epithelial-mesenchymal transition in ovarian cancer cells by inhibiting the JAK/STAT3, PI3K/AKT and Notch signalling pathways. Apatinib effectively inhibited tumour growth in vivo. CONCLUSION: Based on our findings, apatinib is a highly potent, orally active anti-angiogenic and anti-ovarian cancer agent.

Rapid detection of trace Salmonella in milk and chicken by immunomagnetic separation in combination with a chemiluminescence microparticle immunoassay.

Rapid detection of trace Salmonella is urgently needed to ensure food safety. We present an innovative pretreatment strategy, based on a two-step enrichment culture and immunomagnetic separation, combined with a chemiluminescence microparticle immunoassay to detect at least one proliferative Salmonella cell in 25 mL (25 g) food. The capture performance of immunomagnetic beads (IMBs) of sizes for Salmonella was investigated, and the IMBs of size 2.8 µm showed a high capture efficiency of 60.7% in 25 mL milk and 74.5% in 25 mL chicken culture filtrate, which ensured the successful capture of trace Salmonella after 2.5 h in situ enrichment even from only one Salmonella cell. The separated Salmonella cells, reaching an amount of 103 colony-forming units (CFU) by a secondary enrichment for 3 h, were detected by a horseradish peroxidase chemiluminescence reaction with 4-(1-imidazolyl)phenol as an enhancer, which evidenced a linear response for Salmonella concentrations ranging from 2.3 × 102 to 7.8 × 104 CFU/mL. The entire detection process was completed within 8 h, with a very low detection limit of 1 CFU/25 mL (25 g), which was verified by colony counting, and a small degree of interference of 0.17-1.06%. Trace Salmonella from five different serovars in milk and chicken was successfully detected without false negative or false positive results. Furthermore, this study provides a basis to develop a fully automated instrument based on IMBs that includes all steps from sample preparation to chemiluminescence microparticle immunoassay for high-throughput screening of foodborne pathogens. Graphical abstract.

Nanocluster-Mediated Synthesis of Diverse ZnTe Nanostructures: from Nanocrystals to 1D Nanobelts.

Liquid phase one-pot synthesis of semiconductor nanocrystals, by direct nucleation-growth crystallization, is unsuccessful for synthesis of some kinds of semiconductors. Using ZnTe as an example here, highly disperse ZnTe nanoclusters with diameters of 2-3 nm were first synthesized by a facile solvothermal method. Then the ZnTe nanoclusters were chosen as starting crystallization seeds to mediate the synthesis of flexible semiconductor nanostructures. Three-dimensional (3D) oriented assembly of ZnTe nanoclusters to monodisperse dendrimer-like nanocrystals (DLNCs), and one-dimensional (1D) ZnTe nanobelts with cubic phase, have been achieved successfully. Supported by TEM characterization of time-dependent morphology evolution, the oriented attachment assisted seed growth, based on ZnTe nanoclusters, enabled the 1D flexible ZnTe nanobelts formation, which could reach to ≈10 micrometers length.

Protective Effects of Astragaloside IV Combined with Budesonide in Bronchitis in Rats by Regulation of Nrf2/Keap1 Pathway.

BACKGROUND This study was conducted to evaluate the effects of astragaloside IV and budesonide on bronchitis in rats and to explore the mechanism involved. MATERIAL AND METHODS Eighty Sprague-Dawley (SD) rats were randomly divided into 5 groups, including a Bronchitis model group (BM), a Budesonide group (BG), an Astragaloside IV group (AG), an Astragaloside IV combined with Budesonide group (CG), and a blank control group (BC). Lung tissue was stained with hematoxylin and eosin (H&E). The activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay (ELISA). The nuclear factor erythroid 2 [NF-E2]-related factor 2 (Nrf2), Kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein 1 (Keap1), BTB and CNC homology 1 (Bach1), B-cell lymphoma-2(Bcl-2), and BCl-2-associated X protein (Bax) mRNA and protein were examined by RT-PCR and Western blot, respectively. RESULTS Compared with the Bronchitis model group, the lung tissue lesions in the Budesonide group, Astragaloside IV group, and Astragaloside IV combined with Budesonide group were effectively ameliorated and the airway resistance was significantly decreased. The activities of SOD, GSH-Px, and CAT were increased after treatment with drugs, while the content of MDA was decreased. The levels of Nrf2, Keap1, and Bcl-2 proteins were increased and the levels of Bach1 and Bax were decreased after treatment with Budesonide and Astragaloside IV. CONCLUSIONS Astragaloside IV combined with budesonide can ameliorate the lesions caused by bronchitis in rats through activating the Nrf2/Keap1 pathway, which plays a protective role on anti-oxidative stress injury.

Long Non-Coding RNA Uc.187 Is Upregulated in Preeclampsia and Modulates Proliferation, Apoptosis, and Invasion of HTR-8/SVneo Trophoblast Cells.

Among the preeclampsia-related long non-cording RNAs (lncRNAs) screened with a gene chip in our preliminary study, uc.187 attracted our attention because of its high conservation across different species and significant positive correlation with preeclampsia (PE). The literature and bioinformatics analysis suggested that lncRNA uc.187 might be associated with cell growth, invasion, and apoptosis. The expression of uc.187 in severe preeclamptic placentas (n = 31) and normal placentas (n = 18) was evaluated by real-time reverse transcription polymerase chain reaction (qRT-PCR). We constructed a silencing lentivirus vector (uc.187 siRNA) to explore the biological function of uc.187 in the development and progression of HTR-8/SVneo trophoblast cells in vitro. Furthermore, we utilized CCK8 analysis, a transwell invasion assay, and flow cytometry to determine the role of uc.187 in the proliferation, invasion, and apoptosis of HTR-8/SVneo trophoblast cells. The proteins related to proliferation (PCNA, Ki67), invasion (MMP-2/-9 and TIMP-1), and apoptosis (caspase-3, Bcl-2) were evaluated with a Western blot assay. The results showed that there was an obvious upregulation of uc.187 expression in preeclamptic placental tissues. In addition, uc.187 silencing enhanced cell proliferation and invasion and reduced the cellular apoptotic response. Taken together, our findings suggest for the first time that abnormal expression of lncRNA uc.187 may lead to the aberrant biological behavior of HTR-8/SVneo cells. Therefore, we propose uc.187 as a novel lncRNA molecule that might contribute to the development of PE and might represent a potential diagnostic and therapeutic target for this disease. J. Cell. Biochem. 118: 1462-1470, 2017. © 2016 Wiley Periodicals, Inc.