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Lin Xu

Publications and source records attributed to Lin Xu.

At least 37 records · Page 2Linked to original sources

Intercalation and photophysical properties of the tetra-(8-hydroxyquinolinato) boron complex and 3,3',4,4'-benzophenone tetracarboxylic anion into Mg-Al layered double hydroxides.

The tetra-(8-hydroxyquinolinato) boron complex (Bq) and 3,3',4,4'-benzophenone tetracarboxylic anion (BPTC) were successfully intercalated into layered double hydroxides with an ion-exchange method. Elemental analyses, powder X-ray diffraction, FTIR spectra, and thermogravimetric analyses indicated that the hydrothermal treatment could efficiently improve the reaction process, the purity and crystallinity of products, and that Bq and BPTC molecules steadily arranged with C2 axis perpendicular to the layer plane, and the J-type aggregate in the host interlayer, respectively. The fluorescence studies showed that, compared with those observed in the dilute solutions of the guests, the spectra of Mg3Al-Bq and Mg3Al-BPTC evolved to the high-energy side and the low-energy side with increasing their loading, respectively, which were attributed to various arrangements of guests and the increased intermolecular interaction. Furthermore, their fluorescence intensity gradually decreased with increasing the intercalated guest content due to the concentration quenching, and Mg3Al-Bq exhibits enhanced solid-state blue luminescence due to a more rigid and constrained environment of the host.

Journal Article↗

N-glucuronidation of perfluorooctanesulfonamide by human, rat, dog, and monkey liver microsomes and by expressed rat and human UDP-glucuronosyltransferases.

N-Alkylperfluorooctanesulfonamides have been used in a range of industrial and commercial applications. Perfluorooctanesulfonamide (FOSA) is a major metabolite of N-alkylperfluorooctanesulfonamides and has a long half-life in animals and in the environment and is biotransformed to FOSA N-glucuronide. The objective of this study was to identify and characterize the human and experimental animal liver UDP-glucuronosyltransferases (UGTs) that catalyze the N-glucuronidation of FOSA. The results showed that pooled human liver and rat liver microsomes had high N-glucuronidation activities. Expressed rat UGT1.1, UGT2B1, and UGT2B12 in HK293 cells catalyzed the N-glucuronidation of FOSA but at rates that were lower than those observed in rat liver microsomes. Of the 10 expressed human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B4, 2B7, 2B15, and 2B17) studied, only hUGT2B4 and hUGT2B7 catalyzed the N-glucuronidation of FOSA. The kinetics of N-glucuronidation of FOSA by rat liver microsomes and by hUGT2B4/7 was consistent with a single-enzyme Michaelis-Menten model, whereas human liver microsomes showed sigmoidal kinetics. These data show that rat liver UGT1.1, UGT2B1, and UGT2B12 catalyze the N-glucuronidation of FOSA, albeit at low rates, and that hUGT2B4 and hUGT2B7 catalyze the N-glucuronidation of FOSA.

Animals↗

Acute behavioural stress facilitates long-term depression in temporoammonic-CA1 pathway.

Behavioural stress facilitates long-term depression in Schaffer collaterals-CA1 pathway, but it is unknown whether it influences long-term depression in temporoammonic fibres-CA1. Here, we report that low-frequency stimulation induced long-term depression and foot shock stress before slice preparation facilitated long-term depression in both pathways of young rat slices. When the field excitatory postsynaptic potentials were recorded by stimulating the two pathways alternately and low-frequency stimulation was given to the two pathways simultaneously, a reliable long-term depression was induced in Schaffer collaterals-CA1 but a reliable long-term potentiation took place in temporoammonic fibres-CA1. Interestingly, foot shock stress now enabled low-frequency stimulation to induce reliable long-term depressions in both pathways. These findings suggested that acute behavioural stress facilitated long-term depressions in both pathways and disrupted the interactions between pathways.

Animals↗

Genetic interaction between the AS1-AS2 and RDR6-SGS3-AGO7 pathways for leaf morphogenesis.

In higher plants, class I KNOTTED1-like homeobox (KNOX) gene suppression and leaf polarity establishment are two processes crucial for leaf morphogenesis. The Arabidopsis genes, ASYMMETRIC LEAVES1 and 2 (AS1 and AS2), are required for repressing the class I KNOX genes and promoting leaf adaxial cell fates. In addition, the RNA-DEPENDENT RNA POLYMERASE6 (RDR6) gene acts synergistically with AS1 and AS2 to specify the adaxial polarity and repress the KNOX genes in leaves. It is known that RDR6 is one of the key components in plant post-transcriptional gene silencing (PTGS), and is likely to function with other silencing components in a genetic pathway in regulating leaf patterning. Here we report phenotypic analyses of double mutants combining as1 or as2 with other mutations relating to different RNA silencing pathways. We show that plants carrying rdr6, suppressor of gene silencing3 (sgs3) or zippy (zip, also called ago7) in combination with as1 or as2 demonstrate severe morphological defects, and the double mutant plants are generally similar to one another. Detailed phenotypic and molecular analyses reveal that leaves of rdr6 as2(1), sgs3 as2(1) and zip as2(1) all show an abnormal adaxial identity, and contain high levels of microRNA165/166 and FILAMENTOUS FLOWER (FIL) transcripts. These results suggest that RDR6, SGS3 and AGO7 act in the same pathway, which genetically interacts with the AS1-AS2 pathway for leaf development. The RDR6-SGS3-AGO7 pathway was previously identified as regulating the plant vegetative phase change. Our results reveal a new function of the pathway, which is also required for normal leaf morphogenesis.

Arabidopsis↗

Glycine receptor activation regulates short-term plasticity in CA1 area of hippocampal slices of rats.

Functional glycine receptors (GlyRs) are enriched in the hippocampus, but their roles in synaptic transmission are unclear. In this study, we examined the effect of GlyR activation on paired-pulse stimulation of the whole-cell postsynaptic currents (PSCs) in the Schaffer-CA1 synapses in rat hippocampal slices. Bath application of glycine reduced the amplitude of PSCs, accompanied by an increase in holding current and resting conductance. Moreover, glycine application increased the paired-pulse ratio (PPR) of PSCs significantly, an effect largely abolished by the GlyR specific antagonist strychnine. Interestingly, glycine application had no significant effect on either the amplitude or the PPR of excitatory postsynaptic currents (EPSCs). Our findings suggest that GlyR activation regulates hippocampal short-term plasticity by altering GABAergic neurotransmission.

Animals↗

Average gene length is highly conserved in prokaryotes and eukaryotes and diverges only between the two kingdoms.

The average length of genes in a eukaryote is larger than in a prokaryote, implying that evolution of complexity is related to change of gene lengths. Here, we show that although the average lengths of genes in prokaryotes and eukaryotes are much different, the average lengths of genes are highly conserved within either of the two kingdoms. This suggests that natural selection has clearly set a strong limitation on gene elongation within the kingdom. Furthermore, the average gene size adds another distinct characteristic for the discrimination between the two kingdoms of organisms.

Eukaryotic Cells↗

Opiate withdrawal induces dynamic expressions of AMPA receptors and its regulatory molecule CaMKIIalpha in hippocampal synapses.

Adaptive changes in brain areas following drug withdrawal are believed to contribute to drug seeking and relapse. Cocaine withdrawal alters the expression of GluR1 and GluR2/3 subunits of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug withdrawal on hippocampus is little known. Here, we have examined the expression of GluR1 and GluR2/3 in hippocampal membrane and synaptic fractions following repeated morphine exposure and subsequent withdrawal. Repeated morphine exposure for 12 d increased GluR1 and GluR2/3 in synaptosome but not in membrane fraction. Interestingly, CaMKIIalpha, known to be able to regulate the function of AMPA receptors, was decreased in synaptosome but not in membrane fraction; pCaMKIIalpha, the phosphorylated form of CaMKIIalpha, was increased in both fractions. However, during opiate withdrawal, GluR1 was generally reduced while GluR2/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after withdrawal, but detectably increased in late phase of morphine withdrawal in both fractions. Importantly, the opiate withdrawal-induced increase in GluR2/3 was dependent on the activation of glucocorticoid receptors and NMDA receptors, as it was prevented by the glucocorticoid receptor antagonist RU38486, or intrahippocampal injection of the NMDA receptor antagonist AP-5 or the antagonist to NR2B-containing NMDA receptors, Ro25-6981. These findings indicate that opiate withdrawal induces dynamic expression of GluR1 and GluR2/3 subunits of AMPA receptors in hippocampal synapses, possibly revealing an adaptive process of the hippocampal functions following opiate withdrawal.

Analgesics, Opioid↗

Genetic variants in the MDM2 promoter and lung cancer risk in a Chinese population.

Overexpression of MDM2 may attenuate the P53 stress response pathway through direct blocking of P53 transcriptional activity and mediating P53 degradation. Two promoter polymorphisms (one is a T to G substitution at the intronic P53-response promoter, and the other is a 40-bp insertion/deletion polymorphism in the constitutive promoter) were identified, and recently the T/G substitution (SNP309) has been demonstrated to alter the levels of MDM2 gene products. In this molecular epidemiological study with 717 incident lung cancer cases and 1,083 cancer-free controls, we genotyped these 2 promoter polymorphisms of MDM2 and evaluated their associations with risk of lung cancer. We found that there were no significant associations between MDM2 SNP309 variant genotypes and lung cancer risk (adjusted OR = 1.20, 95% CI = 0.95-1.53 for TG and adjusted OR = 1.12, 95% CI = 0.85-1.48 for GG, respectively). Similarly, we did not find evidence for any association between risk of lung cancer and MDM2 insertion/deletion polymorphism. The findings suggest that these two MDM2 promoter polymorphisms may not play a major role in lung cancer susceptibility in this Chinese population.

Alleles↗

Fluoxetine reverses stress-induced fimbria-prefrontal long-term potentiation facilitation.

Stress has been reported to disrupt the induction of synaptic plasticity in different fimbria target structures. The aim of the present study was to investigate whether chronic mild stress may also affect synaptic plasticity in the medial prefrontal cortex, a fimbria target structure. Fimbria tetanus (100 Hz) did not produce any changes in medial prefrontal cortex synaptic efficacy in non-stressed rats. Rats exposed to chronic mild stress, however, developed significant long-term potentiation. Treatment with fluoxetine (10 mg/kg, intraperitoneal) suppressed long-term potentiation induction in the chronic mild stress group. These data demonstrate that stress not only inhibits long-term potentiation development, as often demonstrated, but can also facilitate long-term potentiation development in certain brain circuits.

Animals↗

Ghrelin controls hippocampal spine synapse density and memory performance.

The gut hormone and neuropeptide ghrelin affects energy balance and growth hormone release through hypothalamic action that involves synaptic plasticity in the melanocortin system. Ghrelin binding is also present in other brain areas, including the telencephalon, where its function remains elusive. Here we report that circulating ghrelin enters the hippocampus and binds to neurons of the hippocampal formation, where it promotes dendritic spine synapse formation and generation of long-term potentiation. These ghrelin-induced synaptic changes are paralleled by enhanced spatial learning and memory. Targeted disruption of the gene that encodes ghrelin resulted in decreased numbers of spine synapses in the CA1 region and impaired performance of mice in behavioral memory testing, both of which were rapidly reversed by ghrelin administration. Our observations reveal an endogenous function of ghrelin that links metabolic control with higher brain functions and suggest novel therapeutic strategies to enhance learning and memory processes.

Animals↗

White matter integrity of the whole brain is disrupted in first-episode schizophrenia.

Diffusion tensor imaging studies in schizophrenia have demonstrated lower diffusion anisotropy within white matter that provides information about brain white matter integrity. We have examined whether white matter is abnormal in first-episode schizophrenia by using diffusion tensor imaging. Twenty-one schizophrenic patients and healthy controls underwent diffusion tensor imaging scans that analyzed by using a rigorous voxel-based approach. We found that fractional anisotropy in white matter of the patients was lower than that in controls at the cerebral peduncle, frontal regions, inferior temporal gyrus, medial parietal lobes, hippocampal gyrus, insula, right anterior cingulum bundle and right corona radiata. These results suggested that white matter integrity of the whole brain was disrupted in early illness onset of schizophrenia.

Adolescent↗

Decreased regional homogeneity in schizophrenia: a resting state functional magnetic resonance imaging study.

We used a newly reported regional homogeneity approach to measure the temporal homogeneity of blood oxygen level-dependent signal for exploring the brain activity of schizophrenia in a resting state. The results showed decreased regional homogeneity in schizophrenia, which distributed over the bilateral frontal, temporal, occipital, cerebellar posterior, right parietal and left limbic lobes, similar to the findings reported in previous resting state functional studies. The brain regions that showed decreased regional homogeneity are believed to be involved in the psychopathology and pathophysiology of schizophrenia. Our results indicate that abnormal brain activity of schizophrenia may exist in a resting state and the regional homogeneity may be potentially helpful in understanding the resting state of schizophrenia.

Adult↗

[Inoculation of the cells transfected with IP10 inhibited experimental tumor metastases in vivo].

OBJECTIVE: To explore the inhibitory effects of IP10 on the experimental tumor metastases of a mammary carcinoma cell line 4T1 in vivo. METHODS: 4T1 cells were transfected with pcDNA3-IP10 plasmid and the positive clones (IP10-4T1) were screened in the presence of G418. The parental 4T1 cells and 4T1 cells transfected with pcDNA3 (pcDNA3-4T1) were used as controls. The expression of IP10 mRNA was examined with RT-PCR. The chemotactic activity of the cell-cultured supernatant for the activated lymphocytes was assessed with chemotaxis assay. All BALB/c mice were divided into 3 equal groups: IP10-4T1, parental 4T1 and pcDNA3-4T1 (6 mice in each group). Seven days after mice were inoculated with 2 x 10(6) 4T1, pcDNA3-4T1 or IP10-4T1 cells, 1 x 10(5) 4T1 cells were injected into mice in tail vein. On day 14 tumors were sectioned. On day 28 mice were sacrificed and the lung weight, metastatic forci on the lung surface, disseminated metastases in the lungs and the number of clonogenic metastases of 4T1 cells were observed. The splenocytes were isolated from tumor-bearing mice, and the cytotoxicity of the splenocytes was evaluated by CFSE/7-AAD method. RESULTS: The transcription of IP10 mRNA increased in IP10-4T1 cells compared to parental 4T1 and pcDNA3-4T1 cells (P = 0.002). Moreover, accumulated lymphocytes migrated to the supernatants of IP10-4T1 cells, which can be abrogated by anti-CXCR3 (P < 0.05). Compared to controls, inoculation of IP10-4T1 cells resulted in the decreased disseminated metastases as indicated by dramatically reduced lung metastatic forci on the surface of the lungs; the lung weight was lighter (IP10-4T1, 0.27 +/- 0.02 g v.s. 4T1, 0.48 +/- 0.08 g and pcDNA3-4T1, 0.43 +/- 0.16 g, P = 0.021); the number of clonogenic metastatic 4T1 cells enumerated in ten fields decreased greatly (IP10-4T1, 2.6 +/- 1.7 v.s. 4T1, 34 +/- 6.3 and pcDNA3-4T1, 33 +/- 2.3, P < 0.05); histological assay showed that metastasis was not found in the lungs of the 4/6 of mice in IP10-4T1 group, and was seen in all the mice of parental 4T1 and pcDNA3-4T1 groups. The splenocytes from the mice inoculated with IP10-4T1 cells exhibited stronger cytotoxic activity against 4T1 target cells at different ratios of effector versus target cells (3:1, 9:1, 27:1) than controls (P < 0.05). CONCLUSION: IP10 expressed locally could inhibit disseminated metastasis of circulating 4T1 tumor cells by enhancing anti-tumor cellular immune responses.

Animals↗

Gene therapy, cell transplantation and stroke.

The use of neuroteratocarcinoma cells for transplantation therapy in stroke has emerged as a strategy for cell replacement therapy that has begun its transition from basic science laboratories to a clinical setting. Procurement logistics and novel neuroprotective functions associated with these cells allow neuroteratocarcinoma cells to serve as efficacious alternatives to using fetal cells as donor cell grafts for stroke therapy, although the optimal transplantation regimen must still be determined. In particular, the limitations of current stroke treatments and management reveal an urgent need to examine the efficacy of experimental treatments, such as neural transplantation, in order to develop better treatment therapies. This chapter will discuss the characteristics of NT2N cells, the role of the host brain microenvironment and NT2N cell grafts, laboratory research and clinical trials for the intracerebral transplantation of NT2N cells in stroke, the mechanisms underlying the grafts' effects, and NT2N cell grafts and the need for immunosuppression. This chapter will also highlight some of the most recent findings regarding NT2N cells.

Adult↗

Production of epsilon-poly-L-lysine by newly isolated Kitasatospora sp. PL6-3.

A novel epsilon-poly-L-lysine (epsilon-PL)-producing strain PL6-3 was isolated from soil, and was identified as a strain of Kitasatospora sp. This is the first detailed report of production of epsilon-PL by a strain in the genera of Kitasatospora. By controlling the culture pH at 4.0, the yield of epsilon-PL from PL6-3 reached 13.9 g/L after 120 h of cultivation in fed-batch fermentation. The morphological characteristics of Kitasatospora sp. PL6-3 in culture broth were different from those reported from strains of Streptomycetaceae, as no mycelium pellets were observed during the course of fermentation of PL6-3, which was beneficial to the assimilation of nutrition and secretion of the products. Furthermore, the molecular mass of the purified epsilon-PL from PL6-3 was determined to be 5.01 kDa by SDS-PAGE and 5.05 kDa by gel permeation chromatography, indicating that the epsilon-PL produced by this strain might be composed of 40 lysine residues. Usually, epsilon-PL with more lysine residues showed higher antimicrobial activity; however, it was difficult to obtain epsilon-PL with more than 36 lysine residues in this study. As a result, epsilon-PL from Kitasatospora sp. PL6-3, which contains more lysine residues than that from other strains, is more promising in the field of food preservatives.

Polylysine↗

A complete protein pattern of cellulase and hemicellulase genes in the filamentous fungus Trichoderma reesei.

The complete protein pattern of cellulase and hemicellulase genes was studied through the Genome-wide analysis in Trichoderma reesei. The genome database revealed the presence of 39 ORFs encoding related proteins, including 32 enzymes with a catalysis domain related to cellulases and hemicellulases and 7 related proteins with a cellulose-binding module (CBM). Ten of these encoded yet undescribed enzymes, including six novel beta-glucosidases or xylosidases, two putative xylanases and two undescribed mannases. To better illustrate the relation of these 39 related proteins, four groups were created and analyzed by phylogenetic analysis: group A corresponding to xylanases, group B belonging to mannases and acting to degrade mannan; group C containing all known and putative cellulose-degrading proteins that have highly conserved CBMs; and group D containing beta-glucosidase and beta-xylosidase. Group D was the largest group, in which 8 beta-glucosidases appeared to be non-secreted proteins.

Cellulase↗