The distribution of sialic acid receptors of avian influenza virus in the reproductive tract of laying hens.

The susceptibility of the host to influenza virus is determined by the distribution of the sialic acid (SA) receptors on host cell membrane. Avian influenza virus (AIV) preferentially binds to SA α-2,3-galactose (SA α2,3-gal) linked receptors, while human strains bind to sialic acid α2,6-galactose (SA α2,6-gal) linked receptors. Here, we describe the SA patterns and distributions in the reproductive tract of hens by employing two specific lectins, Maackia amurensis agglutinin (MAA) for SA α2,3-gal and sambucus nigra agglutinin (SNA) for SA α 2,6-gal receptors. Our results revealed that both SA α2,3-gal and SA α2,6-gal receptors exist in the reproductive tract of hens, including magnum, isthmus, uterus and vagina except for infundibulum. The distribution of SAα-2,3-gal receptor was more abundantly in the columnar epithelium cells of magnum, isthmus and uterus. Only minimal positive results for SA α-2,6-gal receptors were detected in the columnar epithelium cells of magnum, isthmus, uterus and vagina. Furthermore, AIV in tissues of the reproductive tract tissues of laying hens were detected by SYBR green-based reverse transcription and polymerase chain reaction (RT-PCR). Results showed that both viral loads and pathological changes in different parts of the reproductive tract were positively correlated with the expression of both receptors. Our results revealed that the reproductive tract of hens may provide an environment for the replication of both avian and human influenza viruses.

Hydrocarbon Accumulation Periods in the Upper Paleozoic Strata of the Western Ordos Basin, China, Based on Fluid Inclusions and Basin Modeling.

The upper Paleozoic strata in the western part of the Ordos Basin have rich oil and gas resources but low exploration levels. These strata were subjected to multiple tectonic events, such as the Caledonian, Hercynian, Indosinian, and Himalayan movements, which led to a relatively complex process of hydrocarbon accumulation in the study area. These strata also have obvious structural segmentation in the north-south direction. However, the accumulation periods of the upper Paleozoic strata in different structural sections of the western Ordos Basin and their differences are poorly understood. A total of 65 sandstone samples from the upper Paleozoic reservoirs in 16 representative wells were selected for fluid inclusion analyses. The results of fluid inclusion analyses, combined with the burial-thermal histories of representative wells, were used to determine the hydrocarbon accumulation periods of the main layers and summarize their patterns in different structural regions and layers. The results show that the formation of fluid inclusions in the main upper Paleozoic strata can be divided into two stages. The first-stage inclusions mainly occur in secondary quartz edges, and the second-stage inclusions mainly occur in healed microcracks. The inclusion types are dominantly hydrocarbon-bearing, brine, and minor nonhydrocarbon gas inclusions. The hydrocarbon components are mostly CH4 and minor asphaltene, and the nonhydrocarbon gases are dominantly CO2 and minor SO2. The homogenization temperatures of the brine inclusions associated with hydrocarbon inclusions in major layers in the study area have a wide distribution and multiple peaks; the main peaks in the central part of a given tectonic area are slightly lower than those in the eastern part, and the main peaks in a given location tend to increase with decreasing burial depth. Hydrocarbon accumulation in the upper Paleozoic strata in the study area mainly occurred in the Early and Middle Jurassic and Early Cretaceous. The Early and Middle Jurassic were the mature oil and gas accumulation periods, and the Early Cretaceous was the high-maturity natural gas accumulation period and the most critical accumulation period. The accumulation period in the central part of a given structural region occurred earlier than that in the eastern part, and the accumulation period in different layers in a given location gradually shifted at a later time from deep to shallow.

Improving Superconducting Performance of Fe(Se, Te) with In Situ Formed Grain-Boundary Strengthening and Flux Pinning Centers.

It is well known that the existence of interstitial Fe is a great obstacle to enhancing the superconducting properties of the Fe(Se, Te) system. In this work, a silver and oxygen codoping effect toward enhancement of the superconductivity and flux pinning in Fe(Se, Te) bulks is reported. The oxygen ions from SeO2 can induce the precipitation of interstitial Fe as Fe2O3, thus simultaneously optimizing the superconducting properties of Fe(Se, Te) and forming extra flux pinning centers, while the existence of Ag can enhance the intergrain connections of the polycrystalline material by improving the electron transport at grain boundaries. Compared with the undoped sample, the critical current density, the upper critical field, and the thermally activated flux flow activation energy are greatly enhanced by 4.7, 1.7, and 1.5 times, respectively. The novel synthesis technique and optimized properties of this work can pave the way for the development of high-performance Fe(Se, Te) superconducting wires or tapes.

Altered expression of Dscam in temporal lobe tissue from human and experimental animals.

Down syndrome cell adhesion molecule (Dscam) is a neural adhesion molecule that plays an essential role in the establishment of neural circuits. Considerable evidence suggests that Dscam is required for axon guidance and dendritic arborization. Our aim was to investigate the expression of Dscam in the temporal lobes of patients with intractable epilepsy (IE) and of experimental animals. In this study, we used immunohistochemistry, immunofluorescence, and western blotting to examine Dscam expression in thirty-five surgical samples from brains of IE patients and 15 control brain samples. We also measured the levels of Dscam during the entire epileptic process in a rat model of temporal lobe epilepsy. Dscam expression in IE patients was significantly higher compared with that in the controls. In addition, Dscam was also highly expressed in the rat brain during the different phases of the epileptic process. It is the first time to find abnormal expression of Dscam in the brain tissues in patients with IE. And this finding provides an experimental evidence for the study of neuronal circuit remodeling and synaptic plasticity in IE, furthermore, our results also suggest that Dscam may be involved in the generation and the development of IE.

Boosting Superconducting Properties of Fe(Se, Te) via Dual-Oscillation Phenomena Induced by Fluorine Doping.

Fluorine-doped Fe(Se, Te) has been successfully synthesized using the melting method. A dual-oscillation effect was found in the F-doped sample, which combined both microstructural oscillation and chemical compositional oscillation. The microstructural oscillation could be attributed to alternate growth of tetragonal ß-Fe(Se, Te) and hexagonal δ-Fe(Se, Te), which formed a pearlite-like structure and led to the enhancement of δ l flux pinning due to the alternating distributed nonsuperconducting δ-Fe(Se, Te) phase. The chemical compositional oscillations in ß-Fe(Se, Te) phase were because of the inhomogeneously distributed Se and Te, which changes the pinning mechanism from surface pinning in the undoped sample to Δκ pinning in the 5% F-doped one. As a result, the critical current, upper critical field, and thermally activated flux-flow activation energy of FeSe0.45Te0.5F0.05 were enhanced by 7, 2, and 3 times, respectively. Our work revealed the physical insights into F-doping resulting in high-performance Fe(Se, Te) superconductors and inspired a new approach to optimize superconductivities in iron-based superconductors through phase and element manipulations.

High electrochemical performance of nanocrystallized carbon-coated LiFePO4 modified by tris(pentafluorophenyl) borane as a cathode material for lithium-ion batteries.

Tris(pentafluorophenyl) borane (C18BF15) was first adopted as a boron source, which clearly demonstrated its modification effects. XPS and EDX mapping proved that boron can be successfully doped into a carbon layer. The high number of defects in the carbon induced by boron was demonstrated via Raman spectroscopy and thus, the electric conductivity of LiFePO4 was greatly enhanced. The boron-doped composite possessed a higher specific discharge capacity and rate capability than the undoped sample. For instance, the reversible specific capacity for the boron-doped cathode reached 165.8 mA h g-1 at 0.5C, which was almost close to its theoretical capacity (166 mA h g-1). Even at a high rate of 5C, it still possessed a high specific capacity of 124.8 mA h g-1. This provides for the possibility that boron-doped carbon-coated LiFePO4 cathodes may deliver high energy and power density for rechargeable lithium-ion batteries.

Quantification of microRNA-210 in the cerebrospinal fluid and serum: Implications for Alzheimer's disease.

The aim of the present study was to investigate the potential clinical application of the genetic marker microRNA (miRNA)-210 in the cerebrospinal fluid (CSF) and serum of patients with Alzheimer's disease (AD). The enrolled patients were divided into the mild cognitive impairment (MCI) and AD groups. Healthy individuals were used as the controls. The mRNA and protein expression of vascular endothelial growth factor (VEGF) in the CSF and serum samples was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, respectively. The expression of miRNA-210 in the CSF and serum was detected by RT-qPCR. The results revealed that the mRNA and protein expression levels of VEGF in the CSF and serum were decreased in the MCI and AD groups compared with those in the control group. The greater the severity of the dementia, the lower the mRNA and protein expression of VEGF. Similar to the trend observed for VEGF, the miRNA-210 expression in the CSF and serum decreased as the severity of the AD increased. miRNA-210 is thus not only indicative of AD pathogenesis, but may also provide novel insights into the prevention and treatment of the disease.

Change of MicroRNA-134, CREB and p-CREB expression in epileptic rat.

OBJECTIVE: To To investigate the changes of MicroRNA-134, CREB and p-CREB expression in epileptic rat brains in order to elucidate the molecular mechanisms of epilepsy, providing new ideas for clinical treatment. METHODS: Sixty-four Spraque-Dawley (SD) rats were divided into groups randomly, including control group, six hours after seizure group, 24-hour group, three-day group, one-week group, two-week group, four-week group, and eight-week group. All groups were placed under a pilocarpine-induced epilepsy model except the control group, and all rats were decapitated in different points of time. Brain specimens were taken for quantitative PCR experiments, immunohistochemistry and Western blot experiments. The results of the epilepsy model groups and the control group were compared. RESULTS: There were no significant differences between the six hours after seizure group, the 24-hour group and the control group about the MicroRNA-134 levels. MicroRNA-134 in the hippocampus tissue of the three-day group significantly reduced compared with the control group; same result was observed with the one-week, two-week, four-week and eight-week groups. The CREB and p-CREB levels in the three-day group's rat hippocampus significantly increased compared with the control group; and the high levels of CREB and p-CREB were constantly maintained in the one-week, two-week, four-week and eight-week groups. CONCLUSIONS: The MicroRNA-134 level of the epileptic rat hippocampus is significantly lower than normal after three days, and continues to maintain a low level; while CREB and p-CREB levels are rsignificantly increased after three days, and continue to remain at a high level. MicroRNA-134 plays a role in inhibiting synaptic plasticity by inhibiting CREB and p-CREB expressions.

Increased expression of annexin A7 in temporal lobe tissue of patients with refractory epilepsy.

Annexin A7 is a member of the family of annexins, which are thought to function in the regulation of calcium homeostasis and the fusion of vesicles. Refractory epilepsy may be related to the imbalance of calcium homeostasis. Our aims are to investigate the expression of Annexin A7 in epileptic brains in comparison with human controls and to explore Annexin A7's possible role in refractory epilepsy. We examined the expression of Annexin A7 via immunohistochemistry, double-label immunofluorescence and western blot. The expression of Annexin A7 was shown to be significantly increased in patients with refractory epilepsy. Double-label immunofluorescence and confocal microscopy disclosed Annexin A7 immunoreactivity in the neurons, which were recognized by the antibody of neuron specific enolase (NSE). The result showed that Annexin A7 may be involved in the pathophysiology of refractory epilepsy and may play a role in developing and maintaining the epilepsy.

Expression and localization of annexin A7 in the rat lithium-pilocarpine model of acquired epilepsy.

BACKGROUND: Annexin A7 (synexin, ANXA7) is a member of annexins, which plays an essential role in the regulation of calcium homeostasis. Considerable evidence shows that the pathogenetic mechanism of acquired epilepsy (AE) has been related to the imbalance of calcium homeostasis. The aim of this study was to investigate ANXA7 expression and cellular localization in the cortex and hippocampus in the rat lithium-pilocarpine model of AE. METHODS: Totally 81 adult healthy male Wistar rats were randomly divided into control group (n = 9) and experimental group (n = 72), the experimental group contained eight subgroups according to sacrifice time (n = 9) (6-hour, 24-hour, 48-hour, 72-hour, 7-day, 15-day, 1-month, and 2-month). In the experimental group, rats were intraperitoneally injected by lithium-pilocarpine to induce AE model. We examined the expression and localization of ANXA7 via immunohistochemistry, double-label immunofluorescence with the use of neuron specific enolase (NSE) antibody, glial fibrillary acidic protein (GFAP) antibody and propidium iodide (PI), respectively. The data of optical density value were analyzed by analysis of variance. RESULTS: ANXA7 expression increased significantly in the experimental groups especially in the acute period (6 hours, 24 hours, and 48 hours after the onset of seizure) using immunohistochemistry. Double-label immunofluorescence and confocal microscopy disclosed that ANXA7 localized in the neurons but not in astrocytes and did not localize in the nucleus, which were performed with anti-NSE, anti-GFAP and PI respectively. CONCLUSION: ANXA7 may play a potential role in the pathogenetic mechanisms of the rat lithium-pilocarpine model of AE.

Abnormal expression and spatiotemporal change of Slit2 in neurons and astrocytes in temporal lobe epileptic foci: A study of epileptic patients and experimental animals.

Repellent guidance molecules provide targeting information to outgrowing axons along predetermined pathways during development. These molecules may also play a role in synaptic reorganization in the adult brain and thereby promote epileptogenesis. Our aim was to investigate the expression of Slit2, one of repellent guidance molecules, in temporal lobe epileptic foci from epileptic patients and experimental animals. Thirty-five temporal neocortex tissue samples from patients with intractable temporal lobe epilepsy (TLE) and fifteen histological normal temporal lobes from controls were selected. Fifty-four Sprague-Dawley rats were divided randomly into six groups, including five groups with epilepsy induced by lithium-pilocarpine administration and one control group. Temporal lobe tissue samples were taken from rats at 1, 7, 14, 30, and 60 days post-seizure and from controls. Expression of Slit2 was assessed by immunohistochemistry, immunofluorescence, and Western blot analysis. Slit2 was mainly expressed in neurons in human controls and in both neurons and astrocytes in TLE patients. Slit2 expression was significantly higher in TLE patients as compared with the controls. Slit2-positive cells were mainly neurons in the rat temporal lobe tissues of the control group, the acute period group, and the latent period group, while the Slit2-positive cells were mainly astrocytes in chronic phase. Compared with controls, Slit2 expression in animals in the TLE group gradually decreased from days 1 to 14 post-seizure, but then increased over the levels seen in controls, to peak levels at days 30 and 60. These results suggest that Slit2 may play an important role in the pathogenesis of TLE.