NG2 cells are a population of CNS cells that are distinct from neurons, mature oligodendrocytes, astrocytes, and microglia. These cells can be identified by their NG2 proteoglycan expression. NG2 cells have a highly branched morphology, with abundant processes radiating from the cell body, and express a complex set of voltage-gated channels, AMPA/kainate, and GABA receptors. Neurons notably form classical and nonclassical synapses with NG2 cells, which have varied characteristics and functions. Neuron-NG2 cell synapses could fine-tune NG2 cell activities, including the NG2 cell cycle, differentiation, migration, and myelination, and may be a novel potential therapeutic target for NG2 cell-related diseases, such as hypoxia-ischemia injury and periventricular leukomalacia. Furthermore, neuron-NG2 cell synapses may be correlated with the plasticity of CNS in adulthood with the synaptic contacts passing onto their progenies during proliferation, and synaptic contacts decrease rapidly upon NG2 cell differentiation. In this review, we highlight the characteristics of classical and nonclassical neuron-NG2 cell synapses, the potential functions, and the fate of synaptic contacts during proliferation and differentiation, with the emphasis on the regulation of the NG2 cell cycle by neuron-NG2 cell synapses and their potential underlying mechanisms.
The surgical treatment of pulmonary aspergilloma is challenging and controversial. This study was designed to evaluate the clinical profile, indications and surgical outcomes of pulmonary aspergilloma operated on in our institute. A total of 256 patients with pulmonary aspergilloma underwent surgical treatment from 1975 to 2010. The patients were divided into two groups: Group A (simple aspergilloma, n = 96) and Group B (complex aspergilloma, n = 160). The principal underlying lung disease was tuberculosis (71.1%). The surgical procedures consisted of 212 lobectomies in both groups; eight cavernoplasties, 10 bilobectomies, 16 pneumonectomies and six thoracoplasties in Group B; four segmentectomies and six wedge resections in Group A. Postoperative complications occurred in 40 patients (15.6%). The major complications were residual pleural space (3.9%), prolonged air leak (3.1%), bronchopleural fistula (1.6%), excessive bleeding (1.6%), respiratory insufficiency (1.9%) and empyema (1.2%). No intraoperative deaths occurred. The overall mortality within 30 days post-operation was 1.2%, occurring only in Group B. There was no statistically significant difference in the postoperative morbidity between Groups A and B (P = 0.27). With the good selection of patients, meticulous surgical techniques and good postoperative management, aggressive surgical treatment with anti-fungal therapy for pulmonary aspergilloma is safe and effective, and can achieve favourable outcomes.
Fungal infection; Haemoptysis; Pulmonary aspergilloma; Surgery
A facile approach was developed to prepare multi-walled carbon nanotubes/graphene nanoplatelets hybrid materials through covalent bond formation. First, poly(acryloyl chloride) was grafted onto oxidized multi-walled carbon nanotubes through the reaction between the acyl chloride groups of poly and the hydroxyl groups of oxidized multi-walled carbon nanotubes. Second, the remaining acyl chloride groups of poly were allowed to react with the hydroxyl groups of hydroxylated graphene nanoplatelets. Scanning electron microscopy and transmission electron microscopy data showed that the multi-walled carbon nanotubes and graphene nanoplatelets were effectively connected with each other. And Fourier transform infrared spectroscopy data indicated the formation of covalent bonds between carbon nanotubes and graphene nanoplatelets. Conformational changes were monitored by Raman spectroscopy. This novel kind of carbon hybrid materials may have the potential application in a wide field, especially in increasing the toughness and strength of the matrix resin.
Multi-walled carbon nanotubes; Graphene; Hybrid materials; Poly(acryloyl chloride); Microstructure
Pollen tube growth and endosperm development are important for fertilization and seed formation. The genetic mechanism of the processes remains poorly understood. This study reports the functional characterization of AtTFIIB1 in pollen tube growth and endosperm development. AtTFIIB1 shares 86% and 44% similarity with AtTFIIB2 and AtTFIIB3/AtpBRP2, respectively. It is expressed in many tissues including vegetative nuclei and generative cells of pollen grains and pollen tubes, endosperm, and embryos. It is thus different from AtTFIIB2, whose expression is not found in the endosperm and vegetative nucleus of mature pollen, and AtTFIIB3/AtpBRP2, which is expressed mostly in male gametophytes and weakly in seeds. Mutations in AtTFIIB1 caused a drastic retardation of pollen tube growth and endosperm development, as well as impaired pollen tube guidance and reception, leading to disruption of fertilization and seed development. Expression of AtTFIIB2 driven by the AtTFIIB1 promoter could restore the defective pollen tube growth, guidance, and reception completely, but only partially recovered the seed development in attfiib1, whilst expression of AtTFIIB3/AtpBRP2 driven by the AtTFIIB1 promoter could rescue only the defective attfiib1 seeds. All these results suggest that AtTFIIB1 plays important roles in pollen tube growth, guidance, and reception as well as endosperm development and is partially functionally different from AtTFIIB2 and AtTFIIB3/AtpBRP2.
Arabidopsis; AtTFIIB1; endosperm; fertilization; pollen; transcription factor.
A pulsed laser engineering approach is developed to prepare novel functional graphene paper with graphitic nanospheres homogeneously decorated on the surface and the superior performance of engineered paper is revealed in matrix-free mass spectrometry (MS) detection and imaging. We demonstrate that the stability of graphene paper under intense irradiation can be dramatically increased through a designed laser engineering process by forming densely packed graphitic nanospheres on the paper surface. Moreover, the surface hydrophobicity is enhanced and electric conductivity is improved. The engineered graphene paper can image the invisible micro-patterns of trace amount molecules and increases the detection limit towards diverse molecules by over two orders of magnitude compared to the pristine graphene paper and commercial products in MS analysis.
EPAC proteins are the guanine nucleotide exchange factors that act as the intracellular receptors for cyclic AMP. Two variants of EPAC genes including EPAC1 and EPAC2 are cloned and are widely expressed throughout the brain. But, their functions in the brain remain unknown. Here, we genetically delete EPAC1 (EPAC1-/-), or EPAC2 (EPAC2-/-) or both EPAC1 and EPAC2 genes (EPAC-/-) in the forebrain of mice. We show that EPAC null mutation impairs long-term potentiation (LTP) and that this impairment is paralleled with the severe deficits in spatial learning and social interactions and is mediated in a direct manner by miR-124 transcription and Zif268 translation. Knockdown of miR-124 restores Zif268 and hence reverses all aspects of the EPAC-/- phenotypes, whereas expression of miR-124 or knockdown of Zif268 reproduces the effects of EPAC null mutation. Thus, EPAC proteins control miR-124 transcription in the brain for processing spatial learning and social interactions.
FAS/FASL system plays a central role in maintaining peripheral immune tolerance. Human SLE is a prototypic systemic autoimmune disease characterized by expansion of autoreactive lymphocytes. It remains unclear whether a defective FAS/FASL system is involved in the pathogenesis of SLE. In this study, we have discovered a novel nucleotide insertion in FAS mRNA. We demonstrate that this novel FAS mutation occurs at mRNA levels, likely through a site-specific mRNA editing process. The mRNA editing mutation is unique for human FAS because the similar mRNA editing event is absent in other human TNFR family genes with death domains (DR5, DR6, and TNFR1) and in murine FAS. The adenine insertion mutation in the coding region message causes the alteration of human FAS mRNA reading frame. Functionally, cells expressing the edited FAS (edFAS) were refractory to FAS-mediated apoptosis. Surprisingly, cells from SLE patients produced significantly more edFAS products compared to cells from normal healthy controls. Additionally, we demonstrated that persistent engagement of T cell receptor increases human FAS mRNA editing in human T cells. Our data suggest that the site-specific FAS mRNA editing mutation may play a critical role in human immune responses and in the pathogenesis of human chronic inflammatory diseases.
FAS; mRNA editing; apoptosis; Systemic Lupus Erythematosus
Marek’s disease virus (MDV) is a highly cell-associated oncogenic α-herpesvirus that causes a disease characterised by T-cell lymphomas. The pathogenesis, or the nature of the interaction of the virus and the host, in the thymus are still unclear.
In this study, we identified 119 differentially expressed proteins using two-dimensional electrophoresis and mass spectrometry from the thymuses of chickens infected with the RB1B strain of MDV. These differentially expressed proteins were found mainly at 21, 28 and 35 days post-infection. More than 20 of the differentially expressed proteins were directly associated with immunity, apoptosis, tumour development and viral infection and replication. Five of these proteins, ANXA1, MIF, NPM1, OP18 and VIM, were further confirmed using real-time PCR. The functional associations and roles in oncogenesis of these proteins are discussed.
This work provides a proteomic profiling of host responses to MDV in the thymus of chickens and further characterises proteins related to the mechanisms of MDV oncogenesis and pathogenesis.
Vascular gene transfer is a powerful tool for investigating and treating vascular diseases; however, its utility is limited by brevity of transgene expression and vector-associated inflammation. Helper-dependent adenovirus (HDAd), an advanced-generation Ad that lacks all viral genes, is superior to first-generation Ad (FGAd) in normal rabbit arteries. We compared HDAd to FGAd in arteries of cholesterol-fed rabbits, a model of early atherogenesis in which transgene expression might be decreased, and inflammation increased.
Methods and Results-
Carotid arteries of chow- and cholesterol-fed rabbits were infused with FGAd, HDAd, or medium. HDAd expressed a transgene at least as well in arteries of cholesterol-fed rabbits as in arteries of chow-fed rabbits and expressed more durably than FGAd. In arteries of cholesterol-fed rabbits, HDAd stimulated less intimal growth, lipid deposition, and inflammation than FGAd. Neither vector affected phenylephrine-induced contraction or nitroprusside-mediated relaxation; however, both vectors decreased maximal acetylcholine-stimulated vasorelaxation. Relative absence of intimal growth in HDAd arteries could interfere with the utility of this model for testing atheroprotective genes; however, both co-infusion of FGAd and extension of cholesterol feeding yielded larger intimal lesions, on which atheroprotective genes could be tested.
HDAd is superior to FGAd for expression of transgenes in atherosclerosis-prone arteries.
atherosclerosis; vascular gene therapy; helper-dependent adenovirus; intima; rabbit
In the title compound, [Fe(C5H5)(C17H16NO4)], the O=C—C=C—N mean plane is twisted with respect to the mean planes of the benzene and substituted cyclopentadienyl rings by 44.2 (2) and 13.8 (3)°, respectively. Furthermore, the O=C—C=C—N mean plane and the O=C—O(ester) plane make a dihedral angle of 55.5 (6)°. Consistent with this large dihedral angle, the linking C—C bond [1.507 (6) Å] does not show any (delocalized) double-bond character.
Chicken anemia virus (CAV) is the causative agent of chicken infectious anemia. CAV putative intergenotypic recombinants have been reported previously. This fact is based on the previous classification of CAV sequences into three genotypes. However, it is unknown whether intersubtype recombination occurs between the recently reported four CAV genotypes and five subtypes of genome sequences.
Phylogenetic analysis, together with a variety of computational recombination detection algorithms, was used to investigate CAV approximately full genomes. Statistically significant evidence of intersubtype recombination was detected in the parent-like and two putative CAV recombinant sequences. This event was shown to occur between CAV subgroup A1 and A2 sequences in the phylogenetic trees.
We revealed that intersubtype recombination in CAV genome sequences played a role in generating genetic diversity within the natural population of CAV.
The title compound, [Fe(C11H11N2O)2], crystallizes with two independent molecules in the asymmetric unit which have have different conformations. In one molecule, the two ferrocene cyclopentadienyl rings are fully eclipsed and the two pyrazole rings are syn to each other; in the other, the two cyclopentadienyl rings are synclinal and the pyrazole rings are anti. In both molecules, the acetyl group attached to the pyrazole ring is oriented away from the iron–cyclopentadienyl group of ferrocene.
The fused bis-butterfly-shaped title compound, [Fe4(CS4)(CO)12], possesses an orthothiocarbonate (CS4
4−) ligand that acts as a bridge between two Fe2(CO)6 units. A short intramolecular S⋯S contact [2.6984 (8) and 2.6977 (8) Å] occurs in each S2Fe2(CO)6 fragment.
Chicken anemia virus (CAV) is the causative agent of chicken infectious anemia (CIA). A high prevalence of CAV has been reported in China. However, VP1 sequences of Chinese isolates show no clear genotype clustering or correlation with geographic origin. Therefore, the present study aimed to detect and characterize CAV isolates from China based on sequence and phylogenetic analysis of the VP1, VP2 and VP3 genes.
Of 460 spleen samples tested by PCR, 47 (10.22%) were found to be positive for CAV. A total of 25 CAV, approximately full genomes, from different commercial farms were characterized. Phylogenetic analysis of the Chinese CAV sequences together with strains from different countries resulted in four distinct groups (A-D) with significant high bootstrap values. The Chinese viral sequences were located as four different clusters within groups A and D. All the Chinese CAV genomes characterized in this study had glutamine (Q) at amino acid position 394, which indicated that all are highly pathogenic. Mutations associated with attenuation and weaker reactivity with monoclonal antibody 2A9 were absent in the Chinese sequences.
We revealed that CAV prevalence was lower than that reported previously in commercial farms in China. We also showed four distinct sequence groups (A-D), and genetic variability in local CAV sequences that could be divided into four groups based on phylogenetic analysis.
Urokinase-type plasminogen activator (uPA) is expressed at increased levels in stenotic, atherosclerotic human arteries. However, the biological roles of uPA in the artery wall are poorly understood. Previous studies associate uPA with both acute vasoconstriction and chronic vascular remodeling and attribute uPA-mediated vasoconstriction to the kringle—not the catalytic—domain of uPA. We used an in vivo uPA overexpression model to test the hypothesis that uPA-induced vasoconstriction is a reversible vasomotor process that can be prevented—and uPA fibrinolytic activity preserved—by: 1) removing the growth factor and kringle domains; or 2) anchoring uPA to the endothelial surface. To test this hypothesis we constructed adenoviral vectors that express: wild-type rabbit uPA (AduPA); a uPA mutant lacking the NH2-terminal growth-factor and kringle domains (AduPAdel); a mutant lacking catalytic activity (AduPAS→A), and a cell-surface anchored mutant (AdTMuPA). uPA mutants were expressed and characterized in vitro and in carotid arteries in vivo. uPAS→A had no plasminogen activator activity. Activity was similar for uPA and uPAdel, whereas AdTMuPA had only cell-associated activity. AduPAS→A arteries were not constricted. AduPA, AduPAdel, and AdTM-uPA arteries were constricted (approximately 30% smaller lumens; P ≤ 0.008 vs AdNull arteries). Papaverine reversed constriction of AduPA arteries. uPA-mediated arterial constriction is a vasomotor process that is mediated by uPA catalytic activity, not by the NH2-terminal domains. Anchoring uPA to the endothelial surface does not prevent vasoconstriction. uPA catalytic activity, generated by artery wall cells, may contribute to lumen loss in human arteries. Elimination of uPA vasoconstrictor activity requires concomitant loss of fibrinolytic activity.
The elevation of serum alanine aminotransferase (ALT) is regarded as an indicator of liver damage based on the presumption that ALT protein is specifically and abundantly expressed in the liver. However, ALT elevation is also observed in non-liver injury conditions (e.g., muscle injury) and in apparently healthy people. Conversely, serum ALT activity is normal in many patients with confirmed liver diseases (e.g., cirrhosis and hepatitis C infection). To improve the diagnostic value of the ALT assay and to understand the molecular basis for serum ALT changes in various pathophysiological conditions, we have cloned rat ALT isoenzyme ALT1 and ALT2 cDNAs, examined their tissue expressions at the mRNA and protein levels, and determined ALT1 and ALT 2 serum levels in response to liver damage in rodents. Quantitative real-time PCR (qRT-PCR) analysis shows that ALT1 mRNA is widely distributed and mainly expressed in intestine, liver, fat tissues, colon, muscle and heart, in the order of high to low expression level, whereas ALT2 gene expression is more restricted, mainly in liver, muscle, brain, and white adipose tissue. The tissue distribution pattern of ALT1 and ALT2 proteins largely agrees with their mRNA expression. Interestingly, hepatic ALT2 protein is about four times higher in male rats than female rats. In addition, ALT isoenzymes distribute differentially at the subcellular level in that ALT1 is a cytoplasmic protein and ALT2 a mitochondrial protein, supporting bioinformatic prediction of mitochondrial localization of ALT2. Finally, using animal models of hepatoxicity induced by carbon tetrachloride and acetaminophen, we found that both serum ALT1 and ALT2 protein levels were significantly elevated and correlated with ALT activity, providing, for the first time, the molecular basis for the elevated total serum ALT activity.
Five isolates (JS09GY2, JS09GY3, JS09GY4, JS09GY5, and JS09GY6) of avian leukosis virus subgroup J (ALV-J) were isolated from six infected commercial layer flocks displaying both hemangioma and myeloid leukosis (ML), which shared the same parental line, in China in 2009.
All six of the commercial layer chickens examined showed hemangiomas on their body surface or feet. Some developed hemangiomas in their internal organs, causing hepatorrhexis and blood loss. Histopathologically different stages of hemangiomas with ML in the liver, heart, and spleen, were observed. Five viral isolates were obtained from infected DF1 cells incubated with the spleen tissue or serum of the birds from the six flocks. By full genome sequences analysis, a 19-nucleotide repeat sequence was identified in the primer binding site (PBS)-leader region of isolates JS09GY3 and JS09GY6, located between sites 249 and 250 according to the sequence of reference strain HPRS103, and also present in Rous sarcoma virus strain Schmidt–Ruppin B (RSV-SRB), Rous associated virus type 1 (RAV-1), and Rous associated virus type 2 (RAV-2). The predicted Gp85 proteins of isolates JS09GY2, JS09GY3, JS09GY5, and JS09GY6 were highly variable. Interestingly, the E elements of these four examined isolates showed a key deletion at site 30, which produced a new c-Ets-1 binding site. An 11-bp insertion was also found in the E element of isolate JS09GY3 located between bp 66 and 67 according to the sequence of reference strain HPRS103, while almost all previously reported Chinese strains showed an almost identical deletion of 127 bp in the same region.
Five ALV-J isolates were obtained from six field infected commercial layer chickens. Coexistence of hemangioma and ML were observed in these infected cases both macro- and microscopically. Complete proviral genome sequences of two isolates (JS09GY3 and JS09GY6) and the partial sequences of the other two isolates (JS09GY2 and JS09GY5) were determined. The isolates were found to be recombinants of ALV-J with a PBS-leader sequence originating from other retroviruses. The Gp85 protein with an amino acid deletion, a contiguous 11-bp insertion mutation in the E element, and a novel binding site, were noted in the proviral genomes.
Recombinant avian leukosis virus; Subgroup J; Layer chickens; Hemangioma; Myeloid leukosis
The molecule of the title compound, C18H19N3O, displays a trans configuration with respect to the C=N double bond. The dihedral angle between the planes of the two benzene rings is 2.62 (11)°. A strong intramolecular O—H⋯N hydrogen bond stabilizes the molecular conformation.
The title complex, [Co(C22H14N4)2]Cl2, has been synthesized by a solvothermal reaction of the 4′-(4-cyanophenyl)-2,2′:6′,2′′-terpyridine ligand with CoCl2·6H2O. The cobalt(II) ion is six-coordinated by two tridentate ligands in a distorted octahedral geometry. The benzene rings form dihedral angles of 30.02 (7) and 30.26 (7)° with the mean planes of the terpyridine ring systems. The chloride anions are statistically disordered over two positions with refined site occupancies of 0.601 (2) and 0.399 (2).
In the molecule of the zwitterionic title compound, C17H11N3O, the naphthalene ring system is planar [maximum deviation = 0.029 (3) Å] and is oriented at a dihedral angle of 3.55 (3)° with respect to the benzene ring. An intramolecular N—H⋯O hydrogen bond results in the formation of a planar six-membered ring. In the crystal structure, intermolecular C—H⋯O interactions link the molecules into centrosymmetric dimers.
The title compound, C4H12NO3
−, was obtained from dichloroacetic acid and 2-amino-2-(hydroxymethyl)propane-1,3-diol. In the crystal structure, the cations and anions are connected by intermolecular N—H⋯O and O—H⋯O hydrogen bonding, forming a two-dimensional array parallel to (001). The crystal used for analysis was a merohedral twin, as indicated by the Flack parameter of 0.67 (6).
The molecule of the title compound, C17H21N3O, displays a trans configuration with respect to the C=N double bond. The dihedral angle between the planes of the two benzene rings is 50.96 (11)° and a strong intramolecular O—H⋯N hydrogen bond is present. An intermolecular N—H⋯O hydrogen-bonding interaction stabilizes the crystal structure.
The molecule of the title Schiff base, C16H15N3, is non-planar and displays a trans configuration with respect to the C=N double bond. The two benzene rings make a dihedral angle of 49.24 (3)°.
The HOXA10 homeobox gene controls embryonic uterine development and adult endometrial receptivity. The three-amino-acid loop extension (TALE) family homeobox genes like myeloid ecotropic viral integration site 1 (MEIS) provide enhanced target gene activation and specificity in HOX-regulated cellular processes by acting as HOX cofactors.
METHODS AND RESULTS
Analysis of an Affymetrix data set in the public domain showed high expression of MEIS1 in human endometrium. MEIS1 expression was confirmed during the human menstrual cycle by RT–PCR and in situ hybridization and was increased during the secretory compared with proliferative phase of the cycle (P = 0.0001), the time of implantation. To assess the importance of maternal Meis1 expression in a mouse model, the uteri of Day 2 pregnant mice were injected with Meis1 over-expression or small interfering RNA (siRNA) constructs. Blocking Meis1 expression by siRNA before implantation significantly reduced average implantation rates (P = 0.00001). Increased or decreased Meis1 expression significantly increased or decreased the expression of integrin β3, a transcriptional target of HOXA10 and an important factor in early embryo-endometrium interactions (P = 0.006). Manipulating Meis1 expression before implantation also dramatically affected the number of pinopodes, uterine endometrial epithelial projections that develop at the time of endometrial receptivity.
The results suggest that in mouse, meis1 contributes to regulating endometrial development during the menstrual cycle and establishing the conditions necessary for implantation.
embryonic implantation; endometrium; HOXA10; integrin β3; MEIS1
Despite the progresses in developing pulsatile impeller pump and impeller total heart, as well as in applying streamlined impeller vanes, the best results in application of artificial heart pumps have been achieved by nonpulsatile univentricular assist pump with straight impeller vanes until now. It seems all efforts and successes have been done in vain because artificial heart rejects Hi-Tech! This paper recalls some important achievements in R&D of artificial heart in past 25 years and shares author’s experiences with the readers.