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Title:

Hu W, Liu J, Hu Y, Xu Q, Deng T, Wei M, Lu L, Mi J, Bergquist J and Tian G <1 more author(s)>

Hu W, Liu J, Hu Y, Xu Q, Deng T, Wei M, Lu L, Mi J, Bergquist J, Xu F, Tian G (- 1)

Ref:

PubMed

ESTHER: Hu_2022_Front.Mol.Neurosci_15_1044022
PubMedSearch: Hu 2022 Front.Mol.Neurosci 15 1044022
PubMedID: 36590920

Abstract

Cholesterol metabolism in the brain plays a crucial role in normal physiological function, and its aberrations are associated with cognitive dysfunction. The present study aimed to determine which cholesterol-related genes play a vital role in cognitive dysfunction and to dissect its underlying molecular mechanisms using a systems genetics approach in the BXD mice family. We first systematically analyzed the association of expression of 280 hippocampal genes related to cholesterol metabolism with cognition-related traits and identified lipoprotein lipase (Lpl) as a critical regulator. This was further confirmed by phenome-wide association studies that indicate Lpl associated with hippocampus volume residuals and anxiety-related traits. By performing expression quantitative trait locus mapping, we demonstrate that Lpl is strongly cis-regulated in the BXD hippocampus. We also identified -3,300 genes significantly (p < 0.05) correlated with the Lpl expression. Those genes are mainly involved in the regulation of neuron-related traits through the MAPK signaling pathway, axon guidance, synaptic vesicle cycle, and NF-kappa B signaling pathway. Furthermore, a protein-protein interaction network analysis identified several direct interactors of Lpl, including Rab3a, Akt1, Igf1, Crp, and Lrp1, which indicates that Lpl involves in the regulation of cognitive dysfunction through Rab3a-mediated synaptic vesicle cycle and Akt1/Igf1/Crp/Lrp1-mediated MAPK signaling pathway. Our findings demonstrate the importance of the Lpl, among the cholesterol-related genes, in regulating cognitive dysfunction and highlighting the potential signaling pathways, which may serve as novel therapeutic targets for the treatment of cognitive dysfunction.

Title:

Wei M, Xie X, Yu X, Lu Y, Ke L, Ye B, Zhou J, Li G, Li B and Li J <3 more author(s)>

Wei M, Xie X, Yu X, Lu Y, Ke L, Ye B, Zhou J, Li G, Li B, Tong Z, Lu G, Li W, Li J (- 3)

Ref:

PubMed

ESTHER: Wei_2022_Eur.J.Clin.Invest__e13741
PubMedSearch: Wei 2022 Eur.J.Clin.Invest e13741
PubMedID: 34981831

Abstract

BACKGROUND: Severe acute pancreatitis has a high mortality of 20-40%, but there is lack of optimal prognostic biomarker for the severity of acute pancreatitis (AP) or mortality. This study is designed to investigate the relationship between serum cholinesterase (ChE) level and poor outcomes of AP. METHODS: A total of 1904 AP patients were screened in the study, and we finally got 692 patients eligible for analysis. Patients were divided into 2 groups based on serum ChE. The primary outcome was mortality, and multivariable logistic regression analysis for mortality was completed. Additionally, we used receiver operator characteristic (ROC) curve analysis to clarify the predictive value of serum ChE for mortality and organ failure. RESULTS: 378 patients and 314 patients were included in ChE low and normal group, respectively. Patients in ChE low group were older (46.68+/-12.70 vs 43.56+/-12.13 years old, p=0.001) and had a lower percentage of male (62.4% vs 71.0%, p=0.017) when compared with the ChE normal group. Mortality was significantly different in two groups (10.3% vs 0.0%, p<0.001). Moreover, organ failure also differed significantly in two groups (46.6% vs 8.6%, p<0.001). Decreased ChE level was independently associated with mortality in acute pancreatitis (odds ratio: 0.440; 95% confidence interval, 0.231, 0.838, p=0.013). The area under the curve of serum ChE was 0.875 and 0.803 for mortality and organ failure, respectively. CONCLUSIONS: Lower level of serum ChE was independently associated with the severity and mortality of AP.

Title:

Lu Y, Wei M, Wang C, Wei W, Liu Y

Ref:

PubMed

ESTHER: Lu_2020_Nanoscale__
PubMedSearch: Lu 2020 Nanoscale
PubMedID: 32053129

Abstract

Organophosphorus pesticides (OPs) are harmful to people's health and d-amino acids (d-AAs) in the human body are closely related to various diseases. So, detection of OPs in foods and d-AAs in serum is important for food safety and clinical diagnosis. Herein, a long-lasting chemiluminescence (CL) imaging sensor was constructed for the detection of OPs and d-AAs. The method was based on N-(4-aminobutyl)-N-ethylisoluminol/Co2+/chitosan (ABEI/Co2+/CS) hydrogels, where metal organic framework materials (MOF-Pt) were selected as catalysts to improve the sensitivity greatly. Under the catalysis of acetylcholinesterase (AChE) and choline oxidase (CHO), H2O2 was produced by using acetylcholine chloride (ACh) as a substrate, which was sensitive to the proposed CL system. OPs inhibited the activity of AChE and decreased the production of H2O2, reducing CL intensity. The linear range of the method for chlorpyrifos was 0.5 ng mL-1-1.0 mug mL-1, with a limit of detection (LOD) of 0.21 ng mL-1. Seventeen kinds of OPs can be visually and simultaneously discerned by the CL imager. On the other hand, d-AAs were catalyzed and oxidized by d-alpha-amino oxidase (DAAO) to produce H2O2. Thus, d-Ala in serum was used as a model to be detected by the proposed method. The linear range for d-Ala was 1.0 muM-10 mM, with an LOD of 0.12 muM.

Title:

Liu Y, Liu Z, Wei M, Hu M, Yue K, Bi R, Zhai S, Pi Z, Song F

Ref:

PubMed

ESTHER: Liu_2019_Food.Funct_10_432
PubMedSearch: Liu 2019 Food.Funct 10 432
PubMedID: 30623955

Abstract

Schisandra chinensis (Turcz.) Baill is produced mainly in northeast China, Korea and Japan. Its fruit has been used in food as a nutritional and functional ingredient for centuries. Polysaccharide is an important chemical component in Schisandra. Previous studies have shown that Schisandra polysaccharide (SCP) could be used to improve cognitive function clinically and treat age-related neurodegenerative disorders. In this study, a urinary metabolomics method based on ultra-high-performance liquid chromatography combined with quadrupole-time-of-flight mass spectrometry (UHPLC-Q-TOF-MS) was established to investigate the change of endogenous metabolites in an amyloid beta-protein (Abeta) 25-35-induced Alzheimer's disease (AD) rat model. Meanwhile, levels of 9 neurotransmitters were evaluated with ultrahigh-performance liquid chromatography-triple-quadrupole mass spectrometry (UHPLC-TQ-MS) to explore the therapeutic mechanisms of SCP on the AD rat model. Additionally, the synthesis of phosphorylated tau protein (p-tau), acetylcholinesterase (AchE) activity and oxidative damage in the brain of the AD rats were assessed using glycogen synthase kinase-3beta (GSK3beta), AchE and antioxidant assays, NOS (nitric oxide synthase) and SOD (superoxide dismutase), respectively. The results indicated that the AD model was established successfully and the inducement of Abeta25-35 caused the phosphorylation of tau protein and the deposition of Abeta. In the AD model rats, the levels of AchE, GSK-3beta and NOS were significantly elevated and SOD activity was reduced. In the hippocampus of the model rats, the contents of gamma-aminobutyric acid, acetylcholine, glycine, norepinephrine, taurine, serotonin and dopamine were significantly decreased and the contents of glutamate and aspartic acid were increased significantly. However, SCP could reduce the degree of phosphorylation of tau protein, the deposition of Abeta and oxidative damage and reverse these changes of neurotransmitters in the AD rats. In a metabolomics study, a total of 38 metabolites were finally identified as potential biomarkers of AD and all of them had a significant recovery compared with the AD model after SCP administration. Metabolomics studies have shown that SCP plays a role in protecting the central nervous system, regulating intestinal microbial metabolism, regulating energy metabolism, and promoting antioxidant effects by regulating the levels of endogenous metabolites in related pathways. This is first report of the use of urine metabolomics combined with the evaluation of 9 neurotransmitter levels to investigate the mechanism of SCP on the treatment of AD.

Title:

Yao T, Liu A, Liu Y, Wei M, Wei W, Liu S

Ref:

145

PubMed

ESTHER: Yao_2019_Biosens.Bioelectron_145_111705
PubMedSearch: Yao 2019 Biosens.Bioelectron 145 111705
PubMedID: 31550630
Inhibitor(s) related to this paper: Scopoletin

Abstract

The detection of organophosphorus pesticides (OPs) has received considerable attention for their great harm to human beings. Herein, a novel ratiometric fluorescence biosensor was constructed for the determination of OPs by using Scopoletin (SC) and Amplex Red (AR) as probe pairs that have opposite responses to MnO2 nanosheets (MnO2 NS). MnO2 NS possess peroxidase-like catalytic activity, which could quench the fluorescence of SC as well as enhance the fluorescence of the non-fluorescent substance AR by oxidation. In the absence of OPs, acetylcholinesterase (AChE) hydrolyzed acetylcholine chloride (ATCh) into choline (TCh) and acetate. TCh led the decomposition of MnO2 NS to manganese ions (Mn(2+)), increasing signal of SC and decreasing signal of AR. In the presence of OPs, the activity of AChE was inhibited and the decomposition of MnO2 NS was hindered, therefore the fluorescence intensity of SC was weak and the fluorescence intensity of AR had an obvious increase. Moreover, under the optimal conditions, the ratio of fluorescence intensity response recorded on the AR/SC increases with increasing the concentration of DDVP. The method has wider linear range of 5.0pg/mL approximately 500ng/mL with a detection limit of 1.6pg/mL, which is superior to previously reported methods. This strategy has also been applied to a visual observation based on the color change of the solution under UV light.

Title:

Zhu T, Sun X, Wei M, Yi B, Zhao X, Wang W, Feng J

Ref:

PubMed

ESTHER: Zhu_2019_Int.J.Colorectal.Dis_34_255
PubMedSearch: Zhu 2019 Int.J.Colorectal.Dis 34 255
PubMedID: 30368570

Abstract

OBJECTIVE: Short-segment Hirschsprung disease (HSCR) is the predominant type of HSCR that affects approximately 75% of patients. Whether single-stage endorectal pull-through (ERPT) surgery is appropriate for neonatal patients with HSCR has not been definitively determined. This retrospective cohort study concerning infants with short-segment HSCR investigated the optimal age for single-stage ERPT surgery, regardless of the operative approach. METHODS: The 198 patients were stratified by operative age <= 3 or > 3 months (groups A or B, respectively, n = 62 and 136, respectively). Diagnoses of short-segment HSCR were conducted by preoperative contrast enema and rectal suction biopsy with acetylcholinesterase immunohistochemical staining. The perioperative clinical course for all patients was reviewed and the accuracy rate of the preoperative diagnoses and postoperative short- and midterm outcomes were assessed. RESULTS: The rates of diagnostic accuracy, according to the results of the preoperative contrast enema or rectal suction biopsy, were lower in group A (67.2 and 93.5%, respectively) than in group B (81.4 and 94.9%, respectively). In groups A and B, 49 (79.1%) and 108 (79.4%) infants, respectively, completed follow-up examinations. The short-term outcomes were postoperative HSCR-associated enterocolitis, adhesive bowel obstruction, anastomosis leakage, and anal stenosis during the first 12 months after surgery. The midterm outcomes were incontinence and constipation at ~24 months after surgery. Compared with group B, group A experienced more incidences of anastomotic leakage in the short-term and more soiling in the midterm. In groups A and B, the rates of constipation recurrence were nil and 1.9%, respectively. CONCLUSION: Infants with HSCR <=3 months old at the time of single-stage ERPT surgery showed lower rates of accurate and conclusive diagnostic results and poorer postoperative outcomes. Waiting to perform this surgery until infants are older might be more beneficial.

Title:

Wei M, Jia M, Zhang J, Yu L, Zhao Y, Chen Y, Ma Y, Zhang W, Shi YS, Zhang C

Ref:

PubMed

ESTHER: Wei_2017_Front.Mol.Neurosci_10_55
PubMedSearch: Wei 2017 Front.Mol.Neurosci 10 55
PubMedID: 28303090

Abstract

The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPARs) are major excitatory receptors that mediate fast neurotransmission in the mammalian brain. The surface expression of functional AMPARs is crucial for synaptic transmission and plasticity. AMPAR auxiliary subunits control the biosynthesis, membrane trafficking, and synaptic targeting of AMPARs. Our previous report showed that alpha/beta-hydrolase domain-containing 6 (ABHD6), an auxiliary subunit for AMPARs, suppresses the membrane delivery and function of GluA1-containing receptors in both heterologous cells and neurons. However, it remained unclear whether ABHD6 affects the membrane trafficking of glutamate receptor subunits, GluA2 and GluA3. Here, we examine the effects of ABHD6 overexpression in HEK293T cells expressing GluA1, GluA2, GluA3, and stargazin, either alone or in combination. The results show that ABHD6 suppresses the glutamate-induced currents and the membrane expression of AMPARs when expressing GluA2 or GluA3 in the HEK293T cells. We generated a series of GluA2 and GluA3 C-terminal deletion constructs and confirm that the C-terminus of GluAs is required for ABHD6's inhibitory effects on glutamate-induced currents and surface expression of GluAs. Meanwhile, our pull-down experiments reveal that ABHD6 binds to GluA1-3, and deletion of the C-terminal domain of GluAs abolishes this binding. These findings demonstrate that ABHD6 inhibits the AMPAR-mediated currents and its surface expression, independent of the type of AMPAR subunits, and this inhibitor's effects are mediated through the binding with the GluAs C-terminal regions.

Title:

Wei M, Zhang J, Jia M, Yang C, Pan Y, Li S, Luo Y, Zheng J, Ji J and Zhang C <4 more author(s)>

Wei M, Zhang J, Jia M, Yang C, Pan Y, Li S, Luo Y, Zheng J, Ji J, Chen J, Hu X, Xiong J, Shi Y, Zhang C (- 4)

Ref:

113

PubMed

ESTHER: Wei_2016_Proc.Natl.Acad.Sci.U.S.A_113_E2695
PubMedSearch: Wei 2016 Proc.Natl.Acad.Sci.U.S.A 113 E2695
PubMedID: 27114538
Gene_locus related to this paper: human-ABHD6

Abstract

In the brain, AMPA-type glutamate receptors are major postsynaptic receptors at excitatory synapses that mediate fast neurotransmission and synaptic plasticity. alpha/beta-Hydrolase domain-containing 6 (ABHD6), a monoacylglycerol lipase, was previously found to be a component of AMPA receptor macromolecular complexes, but its physiological significance in the function of AMPA receptors (AMPARs) has remained unclear. The present study shows that overexpression of ABHD6 in neurons drastically reduced excitatory neurotransmission mediated by AMPA but not by NMDA receptors at excitatory synapses. Inactivation of ABHD6 expression in neurons by either CRISPR/Cas9 or shRNA knockdown methods significantly increased excitatory neurotransmission at excitatory synapses. Interestingly, overexpression of ABHD6 reduced glutamate-induced currents and the surface expression of GluA1 in HEK293T cells expressing GluA1 and stargazin, suggesting a direct functional interaction between these two proteins. The C-terminal tail of GluA1 was required for the binding between of ABHD6 and GluA1. Mutagenesis analysis revealed a GFCLIPQ sequence in the GluA1 C terminus that was essential for the inhibitory effect of ABHD6. The hydrolase activity of ABHD6 was not required for the effects of ABHD6 on AMPAR function in either neurons or transfected HEK293T cells. Thus, these findings reveal a novel and unexpected mechanism governing AMPAR trafficking at synapses through ABHD6.

Title:

Wei M, Lu YS, Li PP

Ref:

PubMed

ESTHER: Wei_2009_Zhonghua.Yi.Xue.Yi.Chuan.Xue.Za.Zhi_26_219
PubMedSearch: Wei 2009 Zhonghua.Yi.Xue.Yi.Chuan.Xue.Za.Zhi 26 219
PubMedID: 19350521
Gene_locus related to this paper: human-LIPC

Abstract

OBJECTIVE: To investigate the association of hepatic lipase -250G/A gene promoter polymorphism with type 2 diabetes mellitus combining with coronary heart disease. METHODS: Using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), we detected the genotypes of the hepatic lipase gene promoter -250G/A, the effect of this polymorphism on plasma lipids, lipoproteins and apolipoproteins in 364 patients with type 2 diabetes mellitus and coronary heart disease(T2DM+CHD), 357 patients with type 2 diabetes mellitus alone(T2DM) and 356 healthy controls. RESULTS: The frequencies of alleles and genotypes in the T2DM group were not significantly different from that of controls. However, the AA and GA genotypes in the T2DM+CHD group were lower than those in controls (0.431vs 0.618, P=0.031). The frequencies of both allele and genotype were not related to gender, family history, smoking and BMI. When adjusted by factors such as gender, age, BMI, history of smoking, family history of coronary atherosclerosis and systemic hypertension, Spearmanos correlation and linear regression analyses showed that the A allele is related positively to the levels of HDL-C and apoA1 in T2DM and T2DM+CHD patients. However, logistic regression analysis showed that the A allele is one risk factor for the presence of coronary heart disease. CONCLUSION: The hepatic lipase gene promoter -250G/A polymorphisms is associated with type 2 diabetes mellitus with coronary heart disease, its polymorphisms may affect the levels of HDL-C and apoA1.

Title:

McMinn J, Wei M, Sadovsky Y, Thaker HM, Tycko B

Ref:

PubMed

ESTHER: McMinn_2006_Placenta_27_119
PubMedSearch: McMinn 2006 Placenta 27 119
PubMedID: 16338457

Abstract

The PEG1 gene (a.k.a. MEST) is expressed in human placental trophoblast and endothelium, and data from knockout mice show that this gene regulates placental and fetal growth. Isoform 1 of PEG1 mRNA initiates from exon 1c and produces the long form of the MEST protein. This isoform is imprinted, with expression only from the paternal allele in many human and mouse organs, including placenta. In contrast, PEG1 isoform 2, initiating from exon 1a and producing the short form of MEST protein, is biallelically expressed (non-imprinted) in several non-placental organs. Here we show that PEG1 isoform 2 is in fact imprinted in a large subset of human placentae. A CpG island overlapping PEG1 exon 1a is unmethylated in various fetal and adult non-placental tissues, but is often substantially methylated in the placenta, with the extent of methylation in a large series approximating a normal distribution. Bisulfite conversion/sequencing indicates that the inter-individual differences reflect the relative representation of heavily methylated vs. unmethylated alleles, and RT-PCR/RFLP analysis shows strongly biased allelic expression of PEG1 isoform 2 mRNA in a majority of placentae with a high proportion of methylated alleles. These data highlight PEG1 isoform 2 as a marker for future studies of inter-individual epigenetic variation and its relation to placental and fetal growth in humans.

Title:

Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG, Smith HO, Yandell M, Evans CA and Zhu X <264 more author(s)>

Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG, Smith HO, Yandell M, Evans CA, Holt RA, Gocayne JD, Amanatides P, Ballew RM, Huson DH, Wortman JR, Zhang Q, Kodira CD, Zheng XH, Chen L, Skupski M, Subramanian G, Thomas PD, Zhang J, Gabor Miklos GL, Nelson C, Broder S, Clark AG, Nadeau J, McKusick VA, Zinder N, Levine AJ, Roberts RJ, Simon M, Slayman C, Hunkapiller M, Bolanos R, Delcher A, Dew I, Fasulo D, Flanigan M, Florea L, Halpern A, Hannenhalli S, Kravitz S, Levy S, Mobarry C, Reinert K, Remington K, Abu-Threideh J, Beasley E, Biddick K, Bonazzi V, Brandon R, Cargill M, Chandramouliswaran I, Charlab R, Chaturvedi K, Deng Z, Di Francesco V, Dunn P, Eilbeck K, Evangelista C, Gabrielian AE, Gan W, Ge W, Gong F, Gu Z, Guan P, Heiman TJ, Higgins ME, Ji RR, Ke Z, Ketchum KA, Lai Z, Lei Y, Li Z, Li J, Liang Y, Lin X, Lu F, Merkulov GV, Milshina N, Moore HM, Naik AK, Narayan VA, Neelam B, Nusskern D, Rusch DB, Salzberg S, Shao W, Shue B, Sun J, Wang Z, Wang A, Wang X, Wang J, Wei M, Wides R, Xiao C, Yan C, Yao A, Ye J, Zhan M, Zhang W, Zhang H, Zhao Q, Zheng L, Zhong F, Zhong W, Zhu S, Zhao S, Gilbert D, Baumhueter S, Spier G, Carter C, Cravchik A, Woodage T, Ali F, An H, Awe A, Baldwin D, Baden H, Barnstead M, Barrow I, Beeson K, Busam D, Carver A, Center A, Cheng ML, Curry L, Danaher S, Davenport L, Desilets R, Dietz S, Dodson K, Doup L, Ferriera S, Garg N, Gluecksmann A, Hart B, Haynes J, Haynes C, Heiner C, Hladun S, Hostin D, Houck J, Howland T, Ibegwam C, Johnson J, Kalush F, Kline L, Koduru S, Love A, Mann F, May D, McCawley S, McIntosh T, McMullen I, Moy M, Moy L, Murphy B, Nelson K, Pfannkoch C, Pratts E, Puri V, Qureshi H, Reardon M, Rodriguez R, Rogers YH, Romblad D, Ruhfel B, Scott R, Sitter C, Smallwood M, Stewart E, Strong R, Suh E, Thomas R, Tint NN, Tse S, Vech C, Wang G, Wetter J, Williams S, Williams M, Windsor S, Winn-Deen E, Wolfe K, Zaveri J, Zaveri K, Abril JF, Guigo R, Campbell MJ, Sjolander KV, Karlak B, Kejariwal A, Mi H, Lazareva B, Hatton T, Narechania A, Diemer K, Muruganujan A, Guo N, Sato S, Bafna V, Istrail S, Lippert R, Schwartz R, Walenz B, Yooseph S, Allen D, Basu A, Baxendale J, Blick L, Caminha M, Carnes-Stine J, Caulk P, Chiang YH, Coyne M, Dahlke C, Mays A, Dombroski M, Donnelly M, Ely D, Esparham S, Fosler C, Gire H, Glanowski S, Glasser K, Glodek A, Gorokhov M, Graham K, Gropman B, Harris M, Heil J, Henderson S, Hoover J, Jennings D, Jordan C, Jordan J, Kasha J, Kagan L, Kraft C, Levitsky A, Lewis M, Liu X, Lopez J, Ma D, Majoros W, McDaniel J, Murphy S, Newman M, Nguyen T, Nguyen N, Nodell M, Pan S, Peck J, Peterson M, Rowe W, Sanders R, Scott J, Simpson M, Smith T, Sprague A, Stockwell T, Turner R, Venter E, Wang M, Wen M, Wu D, Wu M, Xia A, Zandieh A, Zhu X (- 264)

Ref:

291

PubMed

ESTHER: Venter_2001_Science_291_1304
PubMedSearch: Venter 2001 Science 291 1304
PubMedID: 11181995
Gene_locus related to this paper: human-AADAC, human-ABHD1, human-ABHD10, human-ABHD11, human-ACHE, human-BCHE, human-LDAH, human-ABHD18, human-CMBL, human-ABHD17A, human-KANSL3, human-LIPA, human-LYPLAL1, human-NDRG2, human-NLGN3, human-NLGN4X, human-NLGN4Y, human-PAFAH2, human-PREPL, human-RBBP9, human-SPG21

Abstract

A 2.91-billion base pair (bp) consensus sequence of the euchromatic portion of the human genome was generated by the whole-genome shotgun sequencing method. The 14.8-billion bp DNA sequence was generated over 9 months from 27,271,853 high-quality sequence reads (5.11-fold coverage of the genome) from both ends of plasmid clones made from the DNA of five individuals. Two assembly strategies-a whole-genome assembly and a regional chromosome assembly-were used, each combining sequence data from Celera and the publicly funded genome effort. The public data were shredded into 550-bp segments to create a 2.9-fold coverage of those genome regions that had been sequenced, without including biases inherent in the cloning and assembly procedure used by the publicly funded group. This brought the effective coverage in the assemblies to eightfold, reducing the number and size of gaps in the final assembly over what would be obtained with 5.11-fold coverage. The two assembly strategies yielded very similar results that largely agree with independent mapping data. The assemblies effectively cover the euchromatic regions of the human chromosomes. More than 90% of the genome is in scaffold assemblies of 100,000 bp or more, and 25% of the genome is in scaffolds of 10 million bp or larger. Analysis of the genome sequence revealed 26,588 protein-encoding transcripts for which there was strong corroborating evidence and an additional approximately 12,000 computationally derived genes with mouse matches or other weak supporting evidence. Although gene-dense clusters are obvious, almost half the genes are dispersed in low G+C sequence separated by large tracts of apparently noncoding sequence. Only 1.1% of the genome is spanned by exons, whereas 24% is in introns, with 75% of the genome being intergenic DNA. Duplications of segmental blocks, ranging in size up to chromosomal lengths, are abundant throughout the genome and reveal a complex evolutionary history. Comparative genomic analysis indicates vertebrate expansions of genes associated with neuronal function, with tissue-specific developmental regulation, and with the hemostasis and immune systems. DNA sequence comparisons between the consensus sequence and publicly funded genome data provided locations of 2.1 million single-nucleotide polymorphisms (SNPs). A random pair of human haploid genomes differed at a rate of 1 bp per 1250 on average, but there was marked heterogeneity in the level of polymorphism across the genome. Less than 1% of all SNPs resulted in variation in proteins, but the task of determining which SNPs have functional consequences remains an open challenge.

Title:

Yang Q, Wei M, Sun F, Tian J, Chen X, Lu C

Ref:

166

PubMed

ESTHER: Yang_2000_Exp.Neurol_166_166
PubMedSearch: Yang 2000 Exp.Neurol 166 166
PubMedID: 11031092

Abstract

Optokinetic nystagmus (OKN) eye movements of myasthenia gravis (MG) and nonmyasthenic ocular palsies, and normal subjects were examined under closed-loop and open-loop conditions. The open-loop OKN condition was achieved by adding the signal of eye-movement velocity of OKN to the computer-generated signal controlling the stimulus grating moving. The OKN was recorded by means of electromagnetic search scleral coil technique. In MG patients, the open-loop gains of OKN increased significantly after the intramuscular injection of an acetylcholinesterase inhibitor, neostigmine, while the closed-loop OKN gains were not significantly changed. Both the closed-loop and open-loop OKN gains of normal subjects and nonmyasthenic patients were not increased for the administration of neostigmine. The experimental results indicated that the open-loop OKN gain could be sensitive to reflect the changes of the function of neuromuscular junction in MG patients.

Send your questions or comments to :Mail to: Nicolas Lenfant, Thierry Hotelier, Yves Bourne, Pascale Marchot and Arnaud Chatonnet.Please cite: Lenfant 2013 Nucleic.Acids.Res. or Marchot Chatonnet 2012 Prot.Pept Lett.

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