PubTransformer

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Wei Xiong - Top 30 Publications

Circulating circular RNA hsa_circ_0001785 acts as a diagnostic biomarker for breast cancer detection.

Circular RNAs (circRNAs) are a class of non-coding RNAs (ncRNAs) and characterized by covalently closed loop without 5' and 3' end. Recently, the diagnostic value of circRNAs has received more and more attention. However, the in-depth study about circRNAs diagnosis in breast cancer is still rarely reported. In present study, we try to investigate the circRNAs expression profiles in breast cancer peripheral blood and discover valuable diagnostic biomarkers.

Purification of Four Flavonoid Glycosides from Lotus (Nelumbo nucifera Gaertn) plumule by Macroporous Resin Combined with HSCCC.

High-speed counter-current chromatography (HSCCC) combined with macroporous resin (MR) column was successfully applied to the isolation and purification of four flavonoid glycosides from the medicinal herb Lotus plumule (LP). A polar two-phase solvent system composed of ethyl acetate-n-butanol-water (1:2:3, v/v/v) was selected by high-performance liquid chromatography (HPLC) and run on a preparative scale where the lower aqueous phase was used as the mobile phase with a head-to-tail elution mode. Quercetin-3-O-β-D-glucopyranoside (15 mg), isorhamnetin-3-O-β-D-glucopyranoside (13 mg), apigenin 6-C-β-D-glucopyranosyl-8-C-α-L-arabinopyranoside (18 mg) and apigenin 6,8-di-C-β-D-glucopyranoside (48 mg) were obtained in a one-step HSCCC separation from 240 mg of the sample. The purity of each compound was over 95% as determined by HPLC. Chemical structures of the isolated compounds were identified by electrospray ionization mass spectrometry (ESI-MS-MS) and nuclear magnetic resonance (NMR) methods. Moreover, the four compounds were isolated from LP for the first time.

circGFRA1 and GFRA1 act as ceRNAs in triple negative breast cancer by regulating miR-34a.

Accumulating evidences indicate that circular RNAs (circRNAs), a class of non-coding RNAs, play important roles in tumorigenesis. However, the function of circRNAs in triple negative breast cancer (TNBC) is largely unknown.

Combined Liver-kidney Perfusion Enhances Protective Effects of Normothermic Perfusion on Livers Grafts from Donation after Cardiac Death.

It has been showed that combined liver-kidney normothermic machine perfusion (NMP) is able to better maintain the circuit's biochemical milieu. Nevertheless, whether the combined perfusion is superior to liver perfusion alone in protecting livers from donation after cardiac death (DCD) is unclear. We aimed to test the hypothesis and explored the mechanisms. Livers from 15 DCD pig donors were subjected to either static cold storage group (Group A), liver alone NMP group (Group B), or combined liver-kidney NMP group (Group C). Livers were preserved for six hours and re-perfused ex vivo for two hours to simulate transplantation, or transplanted in situ. During perfusion, Group C showed improved acid-base and biochemical environment in the circuit over Group B. After re-perfusion, the architecture of liver grafts was best preserved in group C, followed by Group B, then Group A, as shown by the histology and TUNEL staining of both hepatocytes and biliary epithelium. Ki-67 staining showed substantial hepatocyte proliferation and biliary epithelial regeneration after perfusion in Group B and Group C. Group C produced more bile in reperfusion phase than those in Group A and Group B, with more physiological bile composition and less severe biliary epithelium injury. vWF positive endothelial cells and E-selectin expression decreased in both Group B and Group C. Combined liver-kidney NMP not only produced more ATP, protected the NO signaling pathway, but also diminished oxidative stress (HMGB1 and 8-OHdG levels) and inflammatory cytokine (IL-6 and IL-8) release when compared to liver alone NMP and CS. In addition, the 7-day survival rate of liver transplant recipient was higher in Group C than those in Group A and B.

Deficiency of the melanin biosynthesis genes SCD1 and THR1 affects sclerotial development and vegetative growth, but not pathogenicity in Sclerotinia sclerotiorum.

The fungus Sclerotinia sclerotiorum is a necrotrophic plant pathogen causing significant damage on a broad range of crops. This fungus produces sclerotia that serve as the long-term survival structures in the life cycle and the primary inoculum in the disease cycle. Melanin plays an important role for protecting mycelia and sclerotia from ultraviolet radiation and other adverse environmental conditions. In this study two genes, SCD1 encoding a scytalone dehydratase and THR1 encoding a trihydroxynaphthalene reductase, were disrupted by target gene replacement and their roles in mycelial growth, sclerotial development and fungal pathogenicity were investigated. Phylogenetic analyses indicated that the deduced amino acid sequences of SCD1 and THR1 were similar to the orthologs of Botrytis cinerea. Expression of SCD1 was at higher levels in sclerotia compared to mycelia. THR1 was expressed at similar levels in mycelia and sclerotia at early stages, but was up-regulated in sclerotia at the maturation stage. Disruption of SCD1 or THR1 did not change the pathogenicity of the fungus, but resulted in slower radial growth, less biomass, wider-angled hyphae branches, impaired sclerotial development and decreased resistance to ultraviolet light. This article is protected by copyright. All rights reserved.

Aldehyde dehydrogenase 1A1 increases NADH levels and promotes tumor growth via glutathione/dihydrolipoic acid-dependent NAD(+) reduction.

Aldehyde dehydrogenase 1A1 (ALDH1A1) is a member of the aldehyde dehydrogenase superfamily that oxidizes aldehydes to their corresponding acids, reactions that are coupled to the reduction of NAD(+) to NADH. We report here that ALDH1A1 can also use glutathione (GSH) and dihydrolipoic acid (DHLA) as electron donors to reduce NAD(+) to NADH. The GSH/DHLA-dependent NAD(+)-reduction activity of ALDH1A1 is not affected by the aldehyde dehydrogenase inhibitor or by mutation of the residues in its aldehyde-binding pocket. It is thus a distinct biochemical reaction from the classic aldehyde-dehydrogenase activity catalyzed by ALDH1A1. We also found that the ectopic expression of ALDH1A1 decreased the intracellular NAD(+)/NADH ratio, while knockout of ALDH1A1 increased the NAD(+)/NADH ratio. Simultaneous knockout of ALDH1A1 and its isozyme ALDH3A1 in lung cancer cell line NCI-H460 inhibited tumor growth in a xenograft model. Moreover, the ALDH1A1 mutants that retained their GSH/DHLA-dependent NAD(+) reduction activity but lost their aldehyde-dehydrogenase activity were able to decrease the NAD(+)/NADH ratio and to rescue the impaired growth of ALDH1A1/3A1 double knockout tumor cells. Collectively, these results suggest that this newly characterized GSH/DHLA-dependent NAD(+)-reduction activity of ALDH1A1 can decrease cellular NAD(+)/NADH ratio and promote tumor growth.

The plasticity of cyanobacterial carbon metabolism.

This opinion article aims to raise awareness of a fundamental issue which governs sustainable production of biofuels and bio-chemicals from photosynthetic cyanobacteria. Discussed is the plasticity of carbon metabolism, by which the cyanobacterial cells flexibly distribute intracellular carbon fluxes towards target products and adapt to environmental/genetic alterations. This intrinsic feature in cyanobacterial metabolism is being understood through recent identification of new biochemical reactions and engineering on low-throughput pathways. We focus our discussion on new insights into the nature of metabolic plasticity in cyanobacteria and its impact on hydrocarbons (e.g. ethylene and isoprene) production. We discuss approaches that need to be developed to rationally rewire photosynthetic carbon fluxes throughout primary metabolism. We outline open questions about the regulatory mechanisms of the metabolic network that remain to be answered, which might shed light on photosynthetic carbon metabolism and help optimize design principles in order to improve the production of fuels and chemicals in cyanobacteria.

Prevention of Cyanobacterial Blooms Using Nanosilica: A Biomineralization-Inspired Strategy.

Cyanobacterial blooms represent a significant threat to global water resources because blooming cyanobacteria deplete oxygen and release cyanotoxins, which cause the mass death of aquatic organisms. In nature, a large biomass volume of cyanobacteria is a precondition for a bloom, and the cyanobacteria buoyancy is a key parameter for inducing the dense accumulation of cells on the water surface. Therefore, blooms will likely be curtailed if buoyancy is inhibited. Inspired by diatoms with naturally generated silica shells, we found that silica nanoparticles can be spontaneously incorporated onto cyanobacteria in the presence of poly(diallyldimethylammonium chloride), a cationic polyelectrolyte that can simulate biosilicification proteins. The resulting cyanobacteria-SiO2 complexes can remain sedimentary in water. This strategy significantly inhibited the photoautotrophic growth of the cyanobacteria and decreased their biomass accumulation, which could effectively suppress harmful bloom events. Consequently, several of the adverse consequences of cyanobacteria blooms in water bodies, including oxygen consumption and microcystin release, were significantly alleviated. Based on the above results, we propose that the silica nanoparticle treatment has the potential for use as an efficient strategy for preventing cyanobacteria blooms.

The reverse Warburg effect is likely to be an Achilles' heel of cancer that can be exploited for cancer therapy.

Although survival outcomes of cancer patients have been improved dramatically via conventional chemotherapy and targeted therapy over the last decades, there are still some tough clinical challenges that badly needs to be overcome, such as anticancer drug resistance, inevitable recurrences, cancer progression and metastasis. Simultaneously, accumulated evidence demonstrates that aberrant glucose metabolism termed 'the Warburg effect' in cancer cell is closely associated with malignant phenotypes. In 2009, a novel 'two-compartment metabolic coupling' model, also named 'the reverse Warburg effect', was proposed and attracted lots of attention. Based on this new model, we consider whether this new viewpoint can be exploited for improving the existent anti-cancer therapeutic strategies. Our review focuses on the paradigm shift from 'the Warburg effect' to 'the reverse Warburg effect', the features and molecular mechanisms of 'the reverse Warburg effect', and then we discuss its significance in fundamental researches and clinical practice.

Radiologically Undetected Hepatocellular Carcinoma in Patients Undergoing Liver Transplantation: An Immunohistochemical Correlation With LI-RADS Score.

Orthotopic liver transplantation is the best option for patients with carefully selected unresectable disease because of underlying liver dysfunction. The 5-year survival rate after orthotopic liver transplantation for early detected hepatocellular carcinoma (HCC) is high, and a similar or even higher rate is reported in those with radiologically undetected HCC. This study evaluated and compared the histologic features of pretransplant radiologically undetected (14 patients, 25 tumors) versus detected (36 patients, 45 tumors) HCCs. Tumor size, tumor differentiation, number of unpaired arteries, mitotic count per 10 high-power fields, CD34 immunostain to assess microvessel density, and Ki67 immunostain were compared with the Liver Imaging Reporting and Data System score, which was retrospectively assigned to each tumor in both groups. The Liver Imaging Reporting and Data System score was significantly higher in the HCC detected group (P<0.001). The vast majority of the undetected HCCs (88%) was <2 cm in size. Only 12% of the undetected HCCs were ≥2 cm, whereas 51% of the detected HCCs were ≥2 cm in size. Higher rate of moderate to poor tumor differentiation was noted in the detected HCCs compared with the undetected group (89% vs. 60%; P=0.004). No statistically significant difference in the number and distribution of unpaired arteries, or mitotic count was observed in 2 groups (although fewer unpaired arteries were identified in the undetected group). The detected HCCs had a higher rate of 2+ CD34 staining compared with the undetected HCCs (68% vs. 27%; P=0.002), whereas the opposite was observed for 1+ CD34 staining (59% undetected HCCs vs. 17% detected HCCs; P=0.002). Ki67 proliferative index was not statistically different between the 2 groups (120.8/1000 cells detected HCCs vs. 81.8/1000 cells undetected HCCs; P=0.36). The factors associated with failing to detect HCCs pretransplant by radiologic studies include small tumor size (<2 cm), low-grade histologic differentiation, and low microvessel density (low CD34 staining). A significant association between the number and distribution of unpaired arteries and HCC detection has not been established by our study.

Inclusion of Highest Glasgow Coma Scale Motor Component Score in Mortality Risk Adjustment for Benchmarking of Trauma Center Performance.

The Glasgow Coma Scale (GCS) is the most widely used measure of traumatic brain injury (TBI) severity. Currently, the arrival GCS motor component (mGCS) score is used in risk-adjustment models for external benchmarking of mortality. However, there is evidence that the highest mGCS score in the first 24 hours after injury might be a better predictor of death. Our objective was to evaluate the impact of including the highest mGCS score on the performance of risk-adjustment models and subsequent external benchmarking results.

Preparation of umami octopeptide with recombined Escherichia coli: Feasibility and challenges.

The taste of umami peptide H-Lys-Gly-Asp-Glu-Glu-Ser-Leu-Ala-OH (LGAGGSLA) is controversial. One possible reason for this controversy is the use of chemically synthesized LGAGGSLA to confirm its taste. To explore other ways to further confirm the flavor of LGAGGSLA, we developed a new strategy to prepare a bio-source peptide by adopting a gene engineering method to express LGAGGSLA in recombinant Escherichia coli. In our previous work, we structured the LGAGGSLA recombinant expression system and optimized the culturing conditions for preparing a fusion protein. However, the fusion protein was not cleaved by enterokinase to obtain LGAGGSLA. Because the cleavage conditions of commercial enterokinase were not specific and recombinant engineered bacteria had the potential to be used in industrial processes, in this addendum, we calculated the mass and volume yields of key processing steps in the preparation of LGAGGSLA, and established a model of cleavage conditions with the cleavage ratio of LGAGGSLA. When the LGAGGSLA was confirmed to show umami taste, it is considered as a new umami or umami enhancer. The gene information of LGAGGSLA should have a great potential in the development of new flavor product and food product containing high umami flavor.

MicroRNA‑146a promotes the proliferation of rat vascular smooth muscle cells by downregulating p53 signaling.

The present study aimed to detect and verify gene expression profile differences for microRNA (miR)‑146a and its role in the proliferation of vascular smooth muscle cells (VSMCs). Artificially synthesized miR‑146a mimics, miR‑146 inhibitor, scramble‑miRNA or PBS was transfected into cultured primary rat VSMCs in vitro. Reverse transcription‑quantitative polymerase chain reaction confirmed that the miR‑146a expression level was significantly decreased in VSMCs treated with miR‑146a inhibitor (P<0.01). Cell Counting Kit‑8 was used to determine the proliferation ability, which demonstrated that proliferation was significantly decreased in VSMCs treated with miR‑146a inhibitor (P<0.01). Microarray expression profiling analysis revealed that the p53 signal pathway was upregulated in VSMCs treated with the miR‑146a inhibitor. Compared with untransfected VSMCs, the mRNA and protein expression levels of caspase‑3 and phosphatase and tensin homolog (PTEN) in p53 signal transduction pathway did not exhibit a significant difference (P>0.05); however, the mRNA and protein expression levels of p53 were significantly decreased in cells transfected with miR‑146a mimics and increased in miR‑146a inhibitor transfected cells (both P<0.01). The mRNA and protein expression levels of cyclin D1 significantly increased in miR‑146a mimics transfected cells and decreased in cells transfected with the miR‑146a inhibitor (both P<0.05). The present data indicated that miR‑146a may promote the proliferation of rat VSMCs by downregulating p53 and upregulating cyclin D1 expression.

Neuroscience step-down unit admission criteria for patients with intracerebral hemorrhage.

The goal of our study is to determine optimal criteria which can be used to avoid admission to neuroscience intensive care units for patients with intracerebral hemorrhage (ICH).

Tris (2-chloroethyl) phosphate induces senescence-like phenotype of hepatocytes via the p21(Waf1/Cip1)-Rb pathway in a p53-independent manner.

Tris (2-chloroethyl) phosphate (TCEP) has been widely used as a plasticizer and flame retardant. TCEP as a potential carcinogen is often detected in the occupational and nature environments. To investigate effects of TCEP on human hepatocytes, we assessed cell growth rate, cellular membrane integrity, senescence-associated β-galactosidase (SA-β-Gal) activity and analyzed expression of regulators involved in the p53-p21(Waf1/Cip1)-Rb pathway in TCEP-treated L02 cells. The results showed TCEP increased the percentage of SA-β-Gal positive cells, decreased IL-6 levels, down-regulated the regulators of p38MAPK-NF-κB pathways, but up-regulated the regulators of p21(Waf1/Cip1)-Rb pathway in L02 cells. Furthermore, we measured the SA-β-Gal activity and expression of regulators involved in the p53-p21(Waf1/Cip1)-Rb pathway in L02(-p53) cells and p53-null Hep3B cells. Similar results were found in L02(-p53) cells and Hep3B cells. The findings demonstrated that TCEP induced senescence-like growth arrest via the p21(Waf1/Cip1)-Rb pathway in a p53-independent manner, without activation of the IL-6/IL6R, p38MAPK-NF-κB pathways in hepatocytes.

Epstein-Barr Virus miR-BART6-3p Inhibits the RIG-I Pathway.

Recognition of viral pathogen-associated molecular patterns by pattern recognition receptors (PRRs) is the first step in the initiation of a host innate immune response. As a PRR, RIG-I detects either viral RNA or replication transcripts. Avoiding RIG-I recognition is a strategy employed by viruses for immune evasion. Epstein-Barr virus (EBV) infects the majority of the human population worldwide. During the latent infection period there are only a few EBV proteins expressed, whereas EBV-encoded microRNAs, such as BART microRNAs, are highly expressed. BART microRNAs regulate both EBV and the host's gene expression, modulating virus proliferation and the immune response. Here, through gene expression profiling, we found that EBV miR-BART6-3ps inhibited genes of RIG-I-like receptor signaling and the type I interferon (IFN) response. We demonstrated that miR-BART6-3p rather than other BARTs specifically suppressed RIG-I-like receptor signaling-mediated IFN-β production. RNA-seq was used to analyze the global transcriptome change upon EBV infection and miR-BART6-3p mimics transfection, which revealed that EBV infection-triggered immune response signaling can be repressed by miR-BART6-3p overexpression. Furthermore, miR-BART6-3p inhibited the EBV-triggered IFN-β response and facilitated EBV infection through targeting the 3'UTR of RIG-I mRNA. These findings provide new insights into the mechanism underlying the strategies employed by EBV to evade immune surveillance.

MDM2 Contributes to High Glucose-Induced Glomerular Mesangial Cell Proliferation and Extracellular Matrix Accumulation via Notch1.

Murine double minute 2 (MDM2) is an E3-ubiquitin ligase critical for various biological functions. Previous data have revealed an indispensable role of MDM2 in kidney homeostasis. However, its role in glomerular mesangial cell (GMC) proliferation and extracellular matrix (ECM) accumulation during hyperglycemia condition remains unclear. In our present study, we found that MDM2 protein level was significantly upregulated in high glucose-treated GMCs, while knocking down MDM2 by siRNA could attenuate high glucose-induced ECM accumulation and GMCs proliferation. Unexpectedly, Nutlin-3a, a MDM2-p53 interaction blocker, had no benefit in protecting diabetic mice from renal impairment in vivo and in alleviating high glucose-induced ECM accumulation in vitro. Intriguingly, we found that Notch1 signaling activation was obviously attenuated by MDM2 depletion in GMCs with high glucose exposure. However, Numb, a substrate of MDM2 which suppresses Notch1 signaling, was found not to be involved in the MDM2 and Notch1 association. Moreover, our findings demonstrated that MDM2 interacted with Notch1 intracellular domain (NICD1) independent of Numb and regulated the ubiquitination status of NICD1. Collectively, our data propose a pivotal role of MDM2 in high glucose-induced GMC proliferation and ECM accumulation, via modulating the activation of Notch1 signaling pathway in an ubiquitination-dependent way.

Hemostatic bioactivity of novel Pollen Typhae Carbonisata-derived carbon quantum dots.

Pollen Typhae Carbonisata (PTC) is a type of calcined herb drug that has been used as a hemostatic medicine to promote hemostasis for thousands of years. In this study, we discovered and separated novel water-soluble carbon quantum dots (CQDs, named PTC-CQDs) from aqueous extracts of PTC. These PTC-CDs were characterized using transmission electron microscopy (TEM) and high-resolution TEM, as well as Fourier transform infrared, ultraviolet-visible, and fluorescence spectroscopy. Then, we assessed the anti-hemorrhagic effects and related hemostatic mechanisms of the obtained PTC-CQDs.

Incidence of Second Malignancy after Successful Treatment of Limited-Stage Small-Cell Lung Cancer and Its Effects on Survival.

Extended survival outcomes from improved treatments for patients with cancer come with an increased risk of developing a metachronous second malignancy (MSM). We evaluated the incidence of MSM after successful treatment of SCLC and compared survival between SCLC patients who developed MSM and those who did not.

Highly Sensitive Hot-Wire Anemometry Based on Macro-Sized Double-Walled Carbon Nanotube Strands.

This paper presents a highly sensitive flow-rate sensor with carbon nanotubes (CNTs) as sensing elements. The sensor uses micro-size centimeters long double-walled CNT (DWCNT) strands as hot-wires to sense fluid velocity. In the theoretical analysis, the sensitivity of the sensor is demonstrated to be positively related to the ratio of its surface. We assemble the flow sensor by suspending the DWCNT strand directly on two tungsten prongs and dripping a small amount of silver glue onto each contact between the DWCNT and the prongs. The DWCNT exhibits a positive TCR of 1980 ppm/K. The self-heating effect on the DWCNT was observed while constant current was applied between the two prongs. This sensor can evidently respond to flow rate, and requires only several milliwatts to operate. We have, thus far, demonstrated that the CNT-based flow sensor has better sensitivity than the Pt-coated DWCNT sensor.

Molecular Interactions Control Quantum Chain Reactions toward Distinct Photoresponsive Properties of Molecular Crystals.

In this work, we fabricated four diphenylcyclopropenone (DPCP) crystals, which involved various molecular interactions encoded in individual molecular structures 1-4. On the basis of crystalline structural analysis and photoresponsive characterization of the resultant single-crystal microribbons 1-4, we demonstrated that the magnitude of molecular interactions could effectively control the quantum chain reaction and the photoresponsive property of the DPCP crystals. The microribbons 1 and 2 having weak molecular interactions exhibited an efficient chain reaction and large mechanical photoresponses (i.e., photomelting and photodeforming), whereas the microribbons 3 and 4 with strong molecular interactions exhibited no chain reaction and mechanical morphology change. Our work presented a new way to achieve molecular crystals with enhanced mechanical photoresponses.

Chemically Functionalized Phosphorene: Two-Dimensional Multiferroics with Vertical Polarization and Mobile Magnetism.

In future nanocircuits based on two-dimensional (2D) materials, the ideal nonvolatile memories (NVMs) would be based on 2D multiferroic materials that can combine both efficient ferroelectric writing and ferromagnetic reading, which remain hitherto unreported. Here we show first-principles evidence that a halogen-intercalated phosphorene bilayer can be multiferroic with most long-sought advantages: its "mobile" magnetism can be controlled by ferroelectric switching upon application of an external electric field, exhibiting either an "on" state with spin-selective and highly p-doped channels, or an "off" state, insulating against both spin and electron transport, which renders efficient electrical writing and magnetic reading. Vertical polarization can be maintained against a depolarizing field, rendering high-density data storage possible. Moreover, all those functions in the halogenated regions can be directly integrated into a 2D phosphorene wafer, similar to n/p channels formed by doping in a silicon wafer. Such formation of multiferroics with vertical polarization robust against a depolarizing field can be attributed to the unique properties of covalently bonded ferroelectrics, distinct from ionic-bonded ferroelectrics, which may be extended to other van der Waals bilayers for the design of NVM in future 2D wafers. Every intercalated adatom can be used to store one bit of data: "0" when binding to the upper layer and "1" when binding to the down layer, giving rise to a possible approach of realizing single atom memory for high-density data storage.

Vimentin is a crucial target for anti-metastasis therapy of nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is a unique subtype of head and neck cancer, with tendency to spread to regional lymph nodes and distant organs at early stage. Vimentin, a major cytoskeletal protein constituent of the intermediate filament, plays a critical role in the epithelial-mesenchymal transition. Overexpression of vimentin is considered to be a critical prerequisite for metastasis in numerous human cancers. Therefore, targeting vimentin for cancer therapy has gained a lot of interest. In the present study, we detected vimentin expression in NPC tissues and found that overexpression of vimentin is associated with poor prognosis of NPC patients. Silencing of vimentin in NPC CNE2 cells by RNAi suppresses cells migration and invasion in vitro. However, blocking vimentin did not affect cell proliferation of CNE2 cells. In addition, the in vivo metastatic potential of CNE2 cells transfected with Vimentin shRNA was suppressed in a nude mouse model of pulmonary metastasis. Silencing of Vimentin in CNE2 cells leads to a decrease of microvessel density and VEGF, CD31, MMP2, and MMP9 expressions in pulmonary metastatic tumors. Importantly, we found that it is easier for the tumor cells from the high vimentin-expressing pulmonary metastatic tumors to reinvade the microvessel and to form stable tumor plaques attached to the endothelial cells, which resemble the resource of circulating tumor cells and are very hard to eliminate. However, depletion of vimentin inhibits the formation of vascular tumor plaques. Our findings suggest that RNAi-based vimentin silencing may be a potential and promising anti-metastatic therapeutic strategy for NPC.

Role of long non-coding RNAs in glucose metabolism in cancer.

Long-noncoding RNAs (lncRNAs) are a group of transcripts that are longer than 200 nucleotides and do not code for proteins. However, this class of RNAs plays pivotal regulatory roles. The mechanism of their action is highly complex. Mounting evidence shows that lncRNAs can regulate cancer onset and progression in a variety of ways. They can not only regulate cancer cell proliferation, differentiation, invasion and metastasis, but can also regulate glucose metabolism in cancer cells through different ways, such as by directly regulating the glycolytic enzymes and glucose transporters (GLUTs), or indirectly modulating the signaling pathways. In this review, we summarized the role of lncRNAs in regulating glucose metabolism in cancer, which will help understand better the pathogenesis of malignant tumors. The understanding of the role of lncRNAs in glucose metabolism may help provide new therapeutic targets and novel diagnostic and prognosis markers for human cancer.

Melatonin increases reactive aggression in humans.

Melatonin, a hormone released preferentially by the pineal gland during the night, affects circadian rhythms and aging processes. As animal studies have shown that melatonin increases resident-intruder aggression, this study aimed to investigate the impact of melatonin treatment on human aggression.

A homozygous MYO7A mutation associated to Usher syndrome and unilateral auditory neuropathy spectrum disorder.

Usher syndrome (USH) is an autosomal recessive disorder characterized by sensorineural hearing loss, progressive visual loss and night blindness due to retinitis pigmentosa (RP), with or without vestibular dysfunction. The purpose of this study was to detect the causative gene in a consanguineous Chinese family with USH. A c.3696_3706del (p.R1232Sfs*72) variant in the myosin VIIa gene (MYO7A) was identified in the homozygous state by exome sequencing. The co‑segregation of the MYO7A c.3696_3706del variant with the phenotype of deafness and progressive visual loss in the USH family was confirmed by Sanger sequencing. The variant was absent in 200 healthy controls. Therefore, the c.3696_3706del variant may disrupt the interaction between myosin VIIa and other USH1 proteins, and impair melanosome transport in retinal pigment epithelial cells. Notably, bilateral auditory brainstem responses were absent in two patients of the USH family, while distortion product otoacoustic emissions were elicited in the right ears of the two patients, consistent with clinical diagnosis of unilateral auditory neuropathy spectrum disorder. These data suggested that the homozygous c.3696_3706del variant in the MYO7A gene may be the disease‑causing mutation for the disorder in this family. These findings broaden the phenotype spectrum of the MYO7A gene, and may facilitate understanding of the molecular pathogenesis of the disease, and genetic counseling for the family.

Inhibitory effects of tetramethylpyrazine on pain transmission of trigeminal neuralgia in CCI-ION rats.

Tetramethylpyrazine (TMP) has anti-inflammatory effects and is used to treat cerebral ischemic injury, but the mechanism of TMP on neural protection is not clear. Trigeminal neuralgia (TN) is a facial pain syndrome that is characterized by paroxysmal, shock-like pain attacks located in the somatosensory distribution of the trigeminal nerve. P2X3 receptor plays a crucial role in facilitating pain transmission. The present study investigates the effects of TMP on trigeminal neuralgia transmission mediated by P2X3 receptor of the trigeminal ganglia (TG). Chronic constriction injury of the infraorbital branch of the trigeminal nerve (CCI-ION) was used as a trigeminal neuralgia model. On day 15 after surgery, there was a significant decline in the mechanical hyperalgesia threshold in the territory of the ligated infraorbital nerve in the TN group, and an increase in expression of P2X3 receptor in the TG of the TN group compared with the Sham group. After treatment with TMP or A-317491, the mechanical hyperalgesia threshold of TN rats was significantly higher, and expression of P2X3 receptor in the TG noticeably declined compared with the TN group. Phosphorylation of p38 and ERK1/2 in the TN group was stronger than in the Sham group. However, the phosphorylation of p38 and ERK1/2 in the TN+TMP group and TN+A-317491 group was much lower than in the TN group. TMP significantly inhibited the ATP activated currents in HEK293 cells transfected with a P2X3 plasmid. Thus, TMP might have inhibitory effects on trigeminal neuralgia by suppressing the expression of P2X3 receptor in the TG and the phosphorylation of p38 and ERK1/2 in the TG.

Two-Dimensional Seeded Self-Assembly of a Complex Hierarchical Perylene-Based Heterostructure.

A complex two-dimensional (2D) hierarchical heterostructure was fabricated by a sequential two-dimensional seeded self-assembly, which consisted of laterally grown nanotubes from one perylene monomer and terminally elongated nanocoils from a similar perylene monomer on microribbon seeds from a third perylene. Because the nanotube and nanocoil monomers can form kinetically trapped off-pathway aggregates to prevent self-nucleation and have similar molecular organizations to different facets of the seeds, the nanotube and nanocoil monomers preferentially nucleate and grow on the seed sides and terminal ends, respectively, to form a complex 2D hierarchical heterostructure. The strategy used in this work can be extended to fabricate other complex nanoarchitectures from small molecules.

Inhibition of the B7-H3 immune checkpoint limits tumor growth by enhancing cytotoxic lymphocyte function.

The interaction between tumor and the immune system is still poorly understood. Significant clinical responses have been achieved in cancer patients treated with antibodies against the CTLA4 and PD-1/PD-L1 checkpoints; however, only a small portion of patients responded to the therapies, indicating a need to explore additional co-inhibitory molecules for cancer treatment. B7-H3, a member of the B7 superfamily, was previously shown by us to inhibit T-cell activation and autoimmunity. In this study, we have analyzed the function of B7-H3 in tumor immunity. Expression of B7-H3 was found in multiple tumor lines, tumor-infiltrating dendritic cells, and macrophages. B7-H3-deficient mice or mice treated with an antagonistic antibody to B7-H3 showed reduced growth of multiple tumors, which depended on NK and CD8(+) T cells. With a putative receptor expressed by cytotoxic lymphocytes, B7-H3 inhibited their activation, and its deficiency resulted in increased cytotoxic lymphocyte function in tumor-bearing mice. Combining blockades of B7-H3 and PD-1 resulted in further enhanced therapeutic control of late-stage tumors. Taken together, our results indicate that the B7-H3 checkpoint may serve as a novel target for immunotherapy against cancer.

miRNAs may regulate GABAergic transmission associated genes in aged rats with anesthetics-induced recognition and working memory dysfunction.

Isoflurane and sevoflurane are widely used anesthetics in surgery and administration of these anesthetics could lead to postoperative cognitive dysfunction (POCD). However, the mechanisms remain unclear.