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This paper, in allusion to the limitations of traditional transfer alignment methods based on the external measurement equipment or the empirical model of angular deformation, proposes a rapid and accurate transfer alignment method without relying on the empirical angular deformation model. Firstly, the relationship between the actual angular deformation and the angular velocities measured by the gyroscopes in the master and slave inertial navigation systems (INSs) is derived to roughly estimate the angular deformation. Secondly, according to the error characteristics of gyroscopes, the error model of angular deformation is established. Thirdly, expanding the angular deformation error instead of the installation error angle, flexure angle and flexure angle rate into the state vector, a low-order transfer alignment filtering model independent of the empirical angular deformation model is established. The proposed method not only gets rid of the dependence on an empirical angular deformation model, but also realises the rapid and accurate initial alignment of the slave INS without adding any external measurement equipment. The simulations and experiments evidence the validity of the proposed transfer alignment method.

In recent decades, there has been growing concern regarding the effects of human activities on the coastal nutrient cycle. However, interannual variations in the coastal nutrient cycle in response to anthropogenic nutrient input have rarely been quantified. In this study, a hydrodynamic-ecological model capable of describing the nitrogen and phosphorus cycles was used to analyze interannual variations in the nutrient cycle in the central Bohai Sea, a typical semi-enclosed sea in the Northwest Pacific. The results showed an increasing trend of dissolved inorganic nitrogen and particulate nitrogen from 1998 to 2017, whereas different forms of phosphorus showed no obvious interannual variations. The annual nutrient budgets were also quantitatively estimated from 1998 to 2017. This indicates that atmospheric nitrogen deposition plays an important role in interannual variations in the nitrogen cycle. A large amount of nitrogen from anthropogenic inputs was mainly removed by sedimentation processes instead of increasing the standing stock of nitrogen in the sea. With the reduction of anthropogenic inputs, the model showed that a variety of forms of nitrogen concentration decreased linearly, whereas phosphorus concentration increased slightly. Therefore, although environmental governance can effectively alleviate water eutrophication, it is necessary to avoid the situation where the dissolved inorganic nitrogen concentration in the sea becomes too low for phytoplankton to grow, which may determine the primary productivity and eventually affect fishery resources.

High-performance anodes of sodium ion batteries (SIBs) largely depends on rational architecture design and binder-free smart hybridization. Herein, we report TiC/C core/shell nanowires arrays prepared by a one-step chemical vapor deposition (CVD) method and apply it as the anode of SIBs for the first time. The conductive TiC core is intimately decorated with carbon shell. The as-obtained TiC/C nanowires are homogeneously grown on the substrate and show core/shell heterostructure and porous architecture with high electronic conductivity and reinforced stability. Owing to these merits, the TiC/C electrode displays good rate performance and outstanding cycling performance with a capacity of 135.3 mAh/g at 0.1 A/g and superior capacity retention of 90.14% after 1000 cycles at 2 A/g. The reported strategy would provide a promising way to construct binder-free arrays electrodes for sodium ion storage.

Dust deposition can supply nutrients that affect marine phytoplankton, but changing trophic statuses of the surface ocean increase the complexity of interpreting the process. In this study, four onboard incubation experiments amended with various nutrients and dust were performed in the Kuroshio Extension (KE) and Kuroshio–Oyashio transition (TR) of the northwest Pacific (NWP), which are characterised by lower and higher trophic statuses, respectively. According to the nutrient-addition experiments, phytoplankton were limited by nitrogen (N) in the KE, and limited by iron (Fe) or co-limited by Fe and phosphorus (P) in the TR. Dust additions supplied a considerable amount of N and Fe but negligible amount of P to stimulate phytoplankton growth, as indicated by chlorophyll a (Chl a) concentration. In the KE incubations, dust additions enhanced the shift of phytoplankton size structure towards larger cells from dominantly pico-sized (0.2–2 μm) Chl a to comparable contributions from each size class (i.e. pico-, nano-: 2–20 μm, micro-: >20 μm). On the basis of the large shift of size structure towards nano- or micro-phytoplankton in the unamended control treatments in the TR, dust additions furtherly promoted the shift towards micro-phytoplankton becoming the dominant contributor to the total Chl a. The collective analysis of the data from experiments in both regions revealed that, the extent of phytoplankton growth stimulation and the shift towards larger cells were enhanced gradually with increasing amounts of nutrient uptake (including N, P, and silicon). The nutrient uptake ratios of phytoplankton converged towards the Redfield ratio in comparison to the wider range of nutrient ratios in the dust-amended seawater. This study suggested consistencies in the dynamic of phytoplankton growth, shift of size structure, and nutrient uptake following dust additions in the KE and TR, although the trophic status and limiting nutrient varied between these two regions.

Biological aerosols play an important role in atmospheric chemistry, clouds, climate, and public health. Here, we studied the morphology and composition of primary biological aerosol particles (PBAPs) collected in the Lesser Khingan Mountain boreal forest of China in summertime using transmission electron microscopy (TEM) and scanning electron microscopy (SEM). C, N, O, P, K, and Si were detected in most of the PBAPs, and P represented a major marker to discriminate the PBAPs. Of all detected particles >100 nm in diameter, 13% by number were identified as PBAPs. We found that one type of PBAPs mostly appeared as similar rod-like shapes with an aspect ratio > 1.5. Size distribution of the rod-like PBAPs displays two typical peaks at 1.4 μm and 3.5 μm, which likely are bacteria and fungal particles. The second most PBAPs were identified as fungal spores with ovoid, sub-globular or elongated shapes with a smooth surface and small protuberances with their dominant size range of 2–5 μm. Moreover, we found some large brochosomal clusters containing hundreds of brochosomes with a size range of 200–700 nm and a shape like a truncated icosahedron. We estimated that mass concentration of PBAPs approximately 1.9 μg m−3 and contributed 47% of the in situ PM2.5–10 mass. The detection frequency and concentration of PBAPs were higher at night than in the daytime, suggesting that the relative humidity dramatically enhanced the PBAPs emissions in the boreal forest. Our study also showed that the fresh PBAPs displayed weak hygroscopicity with a growth factor of ~1.09 at RH = 94%. TEM analysis revealed that about 20% of the rod-like PBAPs were internally mixed with metal, mineral dust, and inorganic salts in the boreal forest air. This work for the first time provides the overview of individual PBAPs from nanoscale to microscale in Chinese boreal forest air.

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The Bohai Sea is a typical semi-enclosed sea in the northwest Pacific, which is subject to serious eutrophication due to human activities. Similar to hydrographic variables such as water temperature and salinity, the nutrient concentrations and ratios in the Bohai Sea also exhibit seasonal variations. However, the effects of external inputs, biological processes, and benthic processes on these seasonal variations have not been quantified to date. To address this issue, a physical-biological coupled model was developed to capture the seasonal nutrient cycling in the central Bohai Sea. The simulation results revealed apparent seasonal variations in the concentrations of dissolved inorganic nitrogen (DIN), dissolved inorganic phosphorus (DIP), and dissolved silicate (DSi). The N/P ratio (as the molar ratio of DIN/DIP) also exhibited an apparent seasonal variation, with the maximum and minimum values in surface water occurring in summer (100) and winter (30), respectively. The Si/N ratio (as the molar ratio of DSi/DIN) was slightly higher in summer than in other seasons. The budget for three types of nutrient indicated that the biological processes determined the seasonal variations in nutrient concentrations and the N/P ratio. The external inputs of nutrients via river input, atmospheric deposition, and sediment release were probably important in summer when they could alleviate the reduced nutrient concentrations due to biological processes. To maintain a reasonable nitrogen budget, it was necessary to include benthic nitrogen loss, which removed a large amount of inorganic nitrogen in summer and autumn. In addition, the variation of N/P ratio of phytoplankton uptake can reduce the ratio of DIN to DIP in surface water by ~20 in summer as compared to the calculation with a fixed N/P ratio (16:1) in phytoplankton uptake.

Magnetoplasmonics, combining magnetic and plasmonic functions, has attracted increasing attention owing to its unique magnetic and optical properties in various nano-architectures. In this work, Ag, CoFeB and ITO layers are fabricated on anodic aluminum oxide (AAO) porous films to form hybrid multi-layered nanoporous thin films by magnetron sputtering deposition process. The designed nanostructure supports localized surface plasmon resonance (LSPR) and tunable magneto-optical (MO) activity, namely, the sign inversion, which can be controlled by AAO porous film geometry (pore diameter and inter-pore spacing) flexibly. The physical mechanism of this special MO phenomena is further analyzed and discussed by the correlation of Kerr rotation and electronic oscillations controlled by the surface plasmon resonance that is related to the nanoporous structure.

Biological aerosols play an important role in atmospheric chemistry, clouds, climate, and public health. Here, we studied the morphology and composition of primary biological aerosol particles (PBAPs) collected in the Lesser Khingan Mountain boreal forest of China in summertime using transmission electron microscopy and scanning electron microscopy. Of all detected particles > 100 nm in diameter, 13 % by number were identified as PBAPs. In addition, 57 % of the PBAPs were identified as bacteria, followed by brochosomes (24 %) and fungi (19 %). The dominant size of bacteria was 1–4 μm, fungi was 2–4 μm, and brochosomes was 300–500 nm. The number size distribution of PBAPs coupled with the mass concentrations of PM2.5 and PM10 were used to estimate the total mass concentration of PBAPs, which is approximately 1.9 μg m−3 and accounts for 47 % of the in situ PM2.5–10 mass. C, N, O, P, K, and Si are detected in all PBAP particles, and P represented a major marker to identify PBAPs. Moreover, there is a higher frequency and concentration of PBAPs at night compared with day. Bacterial and fungal particles displayed weak hygroscopicity with a growth factor of ~ 1.09 at RH = 94 %. Electron microscopy shows that approximately 20 % of the bacterial particles were internally mixed with metal, mineral dust, and inorganic salts in the boreal forest air. This work provides a database for both further understanding physicochemical state of individual PBAP particles from natural sources and expanding the scope of atmospheric implications.

For decades, E2F1 has been recognized as a retinoblastoma protein (RB) binding transcription factor that regulates the cell cycle. E2F1 binds preferentially to RB and accelerates the cell cycle in most cancer cells. However, it is thought that E2F1 modulates cell proliferation in other ways as well. Herein, it has been discovered that in pathological tissues derived from hepatocellular carcinoma (HCC) patients, E2F1 correlates positively with IQGAP3 and that both of these factors are highly expressed (N = 164, R = 0.6716). In addition, a high level of E2F1 or IQGAP3 predicted poor survival in HCC patients. Further study determined that E2F1 transactivates IQGAP3, the GTPase binding protein in MHCC-97H cells. Co-immunoprecipitation analysis indicated that IQGAP3 interacts with PKCδ and competitively inhibits the interaction between PKCδ and PKCα, resulting in phosphorylation of PKCα activation and promotion of cell proliferation. This study reveals that highly expressed E2F1 not only transactivates cell-cycle-related factors but also promotes HCC proliferation by activating the phosphorylation of PKCα.

Rural residential emissions contribute significantly to regional air pollution in China, but our understanding on how residential solid fuel burning influences the village outdoor air quality is limited. In this study, we compared the fine particulate matter (PM2.5) composition and individual particle characteristics from 11 to 18 January 2017 at a village and an urban site in northern China. At the village site, each day was divided into four periods: cooking (07:30–10:00; 16:00–17:00), daytime (10:00–16:00), heating (17:00–24:00), and midnight (00:00–07:30) periods. The highest PM2.5 concentration occurred during the cooking period (236 ± 88 μg m−3), which was characterized by high concentrations of K+ and abundant primary OM-K particles (i.e., organic matter mixed with K-salts) emitted from residential biomass burning. The second highest PM2.5 concentration was found during the heating period (161 ± 97 μg m−3), and the PM2.5 contained abundant spherical primary OM particles (i.e., tarballs) emitted from residential coal burning. The primary emissions from residential solid fuel burning resulted in 75% of the village OM by mass consisting of primary OM and 67% of the village aerosol particles by number internally mixing with primary OM particles. The village PM2.5 composition was different from that of the urban PM2.5, with the former containing more OM (47% vs 32%) and less secondary inorganic ions (30% vs 46%). Individual primary OM-K and tarballs were abundant in the village air. These results suggest a large contribution of village residential emissions in the winter to village air pollution. Our study highlights that the residential health in villages of northern China should be paid more attention because of high PM2.5 concentrations and abundant toxic particles during the cooking and heating periods per day in winter.

Metal–organic frameworks (MOFs) have been generating a great deal of interest due to their high specific surface area, regular pore structure, and adjustable aperture. However, only a few studies explored their application in the field of photovoltaic devices. In the present work, MIL-125(Ti), one kind of MOFs, was investigated as the precursor for TiO2 photoanode of dye-sensitized solar cells for the first time. Herein, pure anatase TiO2 with a hierarchical structure was synthesized through the decomposition of MIL-125(Ti), which avoids the use of templates and fussy operation of sol–gel methods. The obtained TiO2 has a specific surface area of 147 m2 g–1 and a mean pore size value of 10 nm. When used as a photoanode material in dye-sensitized solar cells, the device gave rise to an overall energy conversion efficiency of 7.20%, which is better than the performance of the P25 based photoanode.

The Water Sediment Regulation Scheme (WSRS) is a unique engineering measure that has been regularly performed to reduce reservoir sedimentation and increase the flood capacity of the Yellow River in China since 2002. As a side effect, the WSRS greatly increases the monthly input flux of nutrients to the Bohai Sea (BHS) in summer, potentially exacerbating eutrophication levels therein and subsequently affecting the growth of phytoplankton. However, its influence on the Chlorophyll-a (Chl-a) dynamics over the BHS is still poorly understood. In this study, two approaches were adopted to investigate it: 1) long-term in-situ observations and satellite-derived data of surface Chl-a were used to study its seasonal variations before and since 2002, and 2) one 1D physical-biological coupled model was developed to evaluate the impact of WSRS on seasonal Chl-a. The results showed that the surface Chl-a exhibited two peaks in spring and autumn until 2002, but has exhibited only one peak in spring-summer since 2002. Satellite-derived Chl-a concentrations in spring-summer since 2002 have increased by 56% compared to those until 2002. The simulated results showed that the change in Yellow River discharge induced by the WSRS has resulted in the appearance of high concentrations of Chl-a in summer over the Central Bohai Sea since 2002. The WSRS increased the ratio of added Chl-a owing to the riverine nutrients to total Chl-a by 19% compared to that until 2002. Overall, WSRS greatly affects the seasonal cycling of Chl-a in the Bohai Sea, and the side effect needs to be considered.

Aberrant expression of histone deacetylases (HDACs) has been detected in a variety of cancers, which disrupts the balance between cell proliferation and apoptosis in favor of continuous growth. A previous study demonstrated that HDAC5 contributes to the proliferation of hepatocellular carcinoma (HCC) cells, but a clear understanding of the mechanism has not yet been provided. In the present work, we found that the levels of HDAC5 were significantly higher in HCC tissues and cells than in adjacent tissues and normal hepatic cells. In addition, knockdown of HDAC5 attenuated the proliferation of Hep3B and HepG2 cells. Through profiling the expressions of proliferation and apoptosis-related genes in Hep3B cells following HDAC5 knockdown, p63 and maspin were found obviously up-regulated in HDAC5-deprived cells compared with the control. Further investigations confirmed that HDAC5 knockdown induced TAp63 expression in HCC cells, accompanied with increased H3K9 acetylation at the TAp63 promoter. Overexpression of TAp63 led to proliferation inhibition by inducing cell cycle arrest. Additionally, TAp63 that was required for the maspin upregulation resulted from HDAC5 knockdown. Phenotype experiments showed that interrupting either TAp63 or maspin recovered the proliferative and tumorigenic capabilities of HCC cells with HDAC5 knockdown. Clinical analysis showed that HDAC5 was negatively correlated with TAp63 and maspin in HCC tissues. In addition, a high level of HDAC5 as well as a low level of TAp63 or maspin predicted poor survival in HCC patients. Taken together, this study proposes the existence of an aberrant HDAC5-TAp63-maspin pathway conferring HCC progression through proliferation induction, which suggests novel intervention targets for the disease.

A GeO2/RGO composite was successfully fabricated via alternating deposition of graphene oxide (GO) and GeO2 on the surface of a Ni foam substrate using a facile dip-coating method cooperated with in situ hydrolysis of GeCl4. This material was directly used as a binder-free anode for LIBs and exhibited high reversible capacity (1716 mA h g−1 at 0.2 A g−1, 702 mA h g−1 at 16 A g−1), good cycling performance (1159 mA h g−1 at 1 A g−1 after 500 cycles) and excellent rate capability. In addition, a reversible capacity as high as 621 mA h g−1 can be retained when cycled to 500 cycles at a rate as high as 8 A g−1.

Hypoxia plays a critical role in the progression and metastasis of hepatocellular carcinoma by activating the key transcription factor, hypoxia-inducible factor-1. This study aims to identify the novel mechanisms underlying the dysregulation of hypoxia-inducible factor-1α in hepatocellular carcinoma. We found that histone deacetylase 5, a highly expressed histone deacetylase in hepatocellular carcinoma, strengthened the migration and invasion of hepatocellular carcinoma cells under hypoxia but not normoxia condition. Furthermore, histone deacetylase 5 induced the transcription of hypoxia-inducible factor-1α by silencing homeodomain-interacting protein kinase-2 expression, which was also dependent on hypoxia. And then knockdown of hypoxia-inducible factor-1α decreased the expressions of mesenchymal markers, N-cadherin, and Vimentin, as well as matrix metalloproteinases, MMP7 and MMP9; however, the epithelial marker, E-cadherin, increased. Phenotype experiments showed that the migration and invasion of hepatocellular carcinoma cells were impaired by knockdown of histone deacetylase 5 or hypoxia-inducible factor-1α but rescued when eliminating homeodomain-interacting protein kinase-2 in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2-hypoxia-inducible factor-1α pathway in hypoxia-induced metastasis. Finally, clinical analysis confirmed the positive correlation between histone deacetylase 5 and hypoxia-inducible factor-1α in hepatocellular carcinoma specimens and a relatively poor prognosis for the patients with high levels of histone deacetylase 5 and hypoxia-inducible factor-1α. Taken together, our findings demonstrated a novel mechanism underlying the crosstalk between histone deacetylase 5 and hypoxia-inducible factor-1 in hepatocellular carcinoma.

The ATBF1/ZFHX3 gene at 16q22 is the second most frequently mutated gene in human prostate cancer and has reduced expression or mislocalization in several types of human tumors. Nonetheless, the hypothesis that ATBF1 has a tumor suppressor function in prostate cancer has not been tested. In this study, we examined the role of ATBF1 in prostatic carcinogenesis by specifically deleting Atbf1 in mouse prostatic epithelial cells. We also examined the effect of Atbf1 deletion on gene expression and signaling pathways in mouse prostates. Histopathologic analyses showed that Atbf1 deficiency caused hyperplasia and mouse prostatic intraepithelial neoplasia (mPIN) primarily in the dorsal prostate but also in other lobes. Hemizygous deletion of Atbf1 also increased the development of hyperplasia and mPIN, indicating a haploinsufficiency of Atbf1. The mPIN lesions expressed luminal cell markers and harbored molecular changes similar to those in human PIN and prostate cancer, including weaker expression of basal cell marker cytokeratin 5 (Ck5), cell adhesion protein E-cadherin, and the smooth muscle layer marker Sma; elevated expression of the oncoproteins phospho-Erk1/2, phospho-Akt and Muc1; and aberrant protein glycosylation. Gene expression profiling revealed a large number of genes that were dysregulated by Atbf1 deletion, particularly those that encode for secretory and cell membrane proteins. The four signaling networks that were most affected by Atbf1 deletion included those centered on Erk1/2 and IGF1, Akt and FSH, NF-κB and progesterone and β-estradiol. These findings provide in vivo evidence that ATBF1 is a tumor suppressor in the prostate, suggest that loss of Atbf1 contributes to tumorigenesis by dysregulating membrane and secretory proteins and multiple signaling pathways, and provide a new animal model for prostate cancer.

In the present work, a one-step synthetic route is developed for fabricating hierarchical anatase TiO2 microspheres for the first time. These microspheres are composed of ultrathin rod-like structures in the radial direction, in which ultrathin rods consisted of tiny octahedra via a growth model of oriented attachment. Based on XRD and electron microscopic analyses, a mechanism for the growth of the microspheres is proposed. This material displays a large capacity of 157.3 mA h g−1 at 1 C after 200 cycles and also exhibits high rate performance and excellent cycling stability. These high performance characteristics may be due to the intrinsic characteristics of the hierarchical porous anatase TiO2 microspheres, in which the porous structure can permit facile diffusion of the electrolyte. They can also enhance the contact between the electrode surface and the electrolyte, while the ultrathin rods can shorten the transport distance of Li-ions and electrons during electrochemical cycling. At the same, the porous microsphere can also accommodate volume changes in the charge–discharge process.

In this study, a simple hydrothermal route was developed for the synthesis of the square-like anatase TiO 2 nanocrystals starting from TiOA and NH 4 F raw materials. The synthesized nanocrystals exhibited a high percentage 64% of exposed {0 0 1} facets and highly crystalline. The size of square-like nanocrystals was found to be ca. 50–80 nm and their thickness was 10–20 nm. It was found that the intermediate TiOF 2 QDs formed before the hydrothermal reaction played a key role for the formation of square-like anatase TiO 2 nanocrystals. Based on a series of experimental results, a possible mechanism for the formation of square-like anatase TiO 2 nanocrystals with a highly exposed {0 0 1} facet was proposed.

Platelets express a variety of membrane and secreted glycoproteins, but the importance of glycosylation to platelet functions is poorly understood. To explore the importance of O-glycosylation, we generated mice with a targeted deletion of Cosmc in murine endothelial/hematopoietic cells (EHC) (EHC Cosmc −/ y ). X-linked Cosmc encodes an essential chaperone that regulates protein O-glycosylation. This targeted mutation resulted in lethal perinatal hemorrhage in the majority of mice, and the surviving mice displayed severely prolonged tail-bleeding times and macrothrombocytopenia. EHC Cosmc − /y platelets exhibited a marked decrease in GPIb-IX-V function and agonist-mediated integrin αIIbβ3 activation, associated with loss of interactions with von Willebrand factor and fibrinogen, respectively. Significantly, three O-glycosylated glycoproteins, GPIbα, αIIb, and GPVI normally on platelet surfaces that play essential roles in platelet functions, were partially proteolyzed in EHC Cosmc − /y platelets. These results demonstrate that extended O-glycans are required for normal biogenesis of the platelets as well as the expression and functions of their essential glycoproteins, and that variations in O-glycosylation may contribute to altered hemostasis.

Hydrothermal carbonization of sucrose was used to controllably synthesize Montroseite VOOH and Paramontroseite VO2 nanoparticles carbonaceous core-shell microspheres. After calcinations, V2O3-VO2-C core-shell microspheres were obtained. When they were used as cathode materials in lithium-ion battery (LIB), it was found that Montroseite VOOH carbonaceous core-shell microspheres exhibited higher discharge capacity than Paramontroseite VO2 counterpart, while the content of V2O3 had some large effects on the electrochemical properties of V2O3-VO2C core-shell microspheres.

Loss of T-synthase (uridine diphosphate galactose:N-acetylgalactosaminyl-α1-Ser/Thr β3galactosyltransferase), a key enzyme required for the formation of mucin-type core 1 O-glycans, is observed in several human diseases, including cancer, Tn syndrome and IgA nephropathy, but current methods to assay the enzyme use radioactive substrates and complicated isolation of the product. Here we report the development of a novel fluorescent assay to measure its activity in a variety of tumor cell lines. Deficiencies in T-synthase activity correlate with mutations in the gene encoding the molecular chaperone Cosmc that is required for folding the T-synthase. This new high-throughput assay allows for facile screening of tumor specimens and other biological material for T-synthase activity and could be used diagnostically.

Spinel Li2ZnTi3O8 nanorods were first synthesized using titanate nanowires as a precursor. The synthesized nanorods are highly crystalline and used as an anode material in a rechargeable Li-ion battery. A large capacity of 220 mA h g−1 was kept after 30 cycles at a current density of 0.1 A g−1, which is close to the theoretic capacity. The electrochemical measurements indicate that the anode material made of spinel Li2ZnTi3O8 nanorods displayed a highly reversible capacity and excellent cycling stability. Keywords: Li2ZnTi3O8, Nanorods, Anode, Spinel, Lithium-ion battery

MnV2O6 nanobelts have successfully been synthesized via a hydrothermal route. The obtained nanobelts are highly crystalline and their thickness is found to be ca. 20–30 nm. These nanobelts were first used as the anode materials in a rechargeable lithium-ion battery, which exhibits a very reversible discharge/charge capacity and excellent cycling stability even at a current density as high as 1 A g−1. This might be attributed to the intrinsic characteristics of MnV2O6 nanobelts.

In this study, orthorhombic LiMnO 2 nanoplates have successfully been synthesized via a simple hydrothermal route. The synthesized nanoplates are highly crystalline and their thickness is found to be ca. 10–50 nm. A lithium battery using LiMnO 2 nanoplates as the active materials of the electrode exhibits a second discharge capacity of 235 mAh g −1 at a current density of 0.01 Ag −1 . Cycling test indicates that the electrode composed of LiMnO 2 nanoplates shows a high reversible charge/discharge capacity and relative stable cycling performance.

In this study, large single-crystal anatase TiO 2 bipyramids were first successfully synthesized using a simple hydrothermal route. The synthesized bipyramids were characterized by XRD, SEM and TEM measurements, and found that these bipyramids are highly crystalline anatase TiO 2 with a size up to 3.6 μm between the two ends. On the other hand, it was also found that the size and shape of bipyramids were significantly influenced by the pH value. Based on a series of experimental results, a possible model for the process of dissolving-coalescing-growing, has been proposed for the formation of large anatase TiO 2 bipyramids.

Background & Aims: The isolation and culture of primary enteric neurons is a difficult process and yields a small number of neurons. We developed fetal and postnatal enteric neuronal cell lines using H-2K b -tsA58 transgenic mice (immortomice) that have a temperature-sensitive mutation of the SV40 large tumor antigen gene under the control of an interferon γ–inducible H-2K b promoter element. Methods: Enteric neuronal precursors were isolated from the intestines of E13-mouse fetuses and second day postnatal mice using magnetic immunoselection with a p75NTR antibody. The cells were maintained at the permissive temperature, 33°C, and interferon-γ for 24 or 48 hours, and then transferred to 39°C in the presence of glial cell line–derived neurotrophic factor for 7 days for further differentiation. Neuronal markers were assessed by reverse-transcription polymerase chain reaction, Western blot, and immunocytochemistry. Neuronal function was assessed by transplanting these cells into the colons of Piebald or nNOS −/− mice. Results: Expression analysis of cells showed the presence of neuronal markers peripherin, PGP9.5, HuD, tau, synaptic marker synaptophysin, characteristic receptors of enteric neurons, Ret, and 5-hydroxytryptamine–receptor subtypes at 33°C and 39°C. Nestin, S-100β, and α-smooth muscle actin were expressed minimally at 39°C. Glial cell line–derived neurotrophic factor resulted in increased phosphorylation of Akt in these cells, similar to primary enteric neurons. Transplantation of cells into the piebald or nNOS −/− mice colon improved colonic motility. Conclusions: We have developed novel enteric neuronal cell lines that have neuronal characteristics similar to primary enteric neurons. These cells can help us in understanding newer therapeutic options for Hirschsprung's disease.

Pancreatic beta-cell mass increases in response to increased demand for insulin, but the factors involved are largely unknown. Glial cell line-derived neurotrophic factor (GDNF) is a growth factor that plays a role in the development and survival of the enteric nervous system. We investigated the role of GDNF in regulating beta-cell survival.Studies were performed using the beta-TC-6 pancreatic beta-cell line, isolated mouse pancreatic beta cells, and in vivo in transgenic mice that overexpress GDNF in pancreatic glia. GDNF receptor family alpha1 and c-Ret receptor expression were assessed by reverse-transcription polymerase chain reaction and immunofluorescence microscopy. Apoptosis was evaluated by assessing caspase-3 cleavage. Phosphoinositol-3-kinase signaling pathway was analyzed by Akt phosphorylation. Glucose homeostasis was assessed by performing intraperitoneal glucose tolerance tests. Insulin sensitivity was assessed using intraperitoneal injection of insulin.We demonstrate the presence of receptors for GDNF, GFRalpha1, and c-Ret on beta cells. GDNF promoted beta-cell survival and proliferation and protected them from thapsigargin-induced apoptosis (P.0001) in vitro. Exposure of beta-cells to GDNF also resulted in phosphorylation of Akt and GSK3beta. Transgenic mice that overexpress GDNF in glia exhibit increased beta-cell mass, proliferation, and insulin content. No differences in insulin sensitivity and c-peptide levels were noted. Compared with wild-type mice, GDNF-transgenic mice have significantly lower blood glucose levels and improved glucose tolerance (P.01). GDNF-transgenic mice are resistant to streptozotocin-induced beta-cell loss (P.001) and subsequent hyperglycemia.We demonstrate that over expression of GDNF in pancreatic glia improves glucose tolerance and that GDNF may be a therapeutic target for improving beta-cell mass.

Although leptin is a key adipokine promoting liver fibrosis, adiponectin may prevent liver injury. To determine the role of these adipokines in liver fibrosis and to understand their expression in vivo, fa/fa rats and their lean littermates were subjected to bile duct ligation (BDL). Histomorphometry for collagen and α-smooth muscle actin (α-SMA) revealed that lean rats, but not fa/fa littermates, had significant fibrosis with abundant hepatic stellate cell (HSC) activation. The lean-BDL rats had significantly higher leptin concentrations in the hepatic vein than lean sham-operated, fa/fa BDL, or fa/fa sham-operated rats. Co-localization of leptin and α-SMA in activated HSCs was observed by immunohistochemistry. Real-time reverse transcriptase-polymerase chain reaction and Western blot analysis confirmed the presence of leptin and α-SMA in activated, but not quiescent, HSCs, whereas only quiescent HSCs synthesized adiponectin mRNA and protein. Adiponectin overexpression in activated HSCs reduced proliferation, augmented apoptosis, and reduced expression of α-SMA and proliferating cell nuclear antigen. Adiponectin receptors (AdipoR1 and AdipoR2) were detected in both activated and quiescent HSCs, but only activated HSCs produced significant apoptosis after treatment with either globular or full-length adiponectin. Adiponectin may act to reverse HSC activation, maintain HSC quiescence, or significantly, may have important therapeutic implications in liver fibrosis.

Ternary oxide Zn(2)Ti(3)O(8) nanowires were first synthesized and used as the anode material in a rechargeable lithium-ion battery, which displayed a very reversible charge-discharge capacity and excellent cycling stability.

In many different human disorders, the cellular glycome is altered. An interesting but poorly understood alteration occurs in the mucin-type O-glycome, in which there is aberrant expression of the truncated O-glycans Tn (GalNAcα1-Ser/Thr) and its sialylated version sialyl-Tn (STn) (Neu5Acα2,6GalNAcα1-Ser/Thr). Both Tn and STn are tumor-associated carbohydrate antigens and tumor biomarkers, since they are not expressed normally and appear early in tumorigenesis. Moreover, their expression is strongly associated with poor prognosis and tumor metastasis. The Tn and STn antigens are also expressed in other human diseases and disorders, such as Tn syndrome and IgA nephropathy. The major pathological mechanism for expression of the Tn and STn antigens is compromised T-synthase activity, resulting from alteration of the X-linked gene that encodes for Cosmc, a molecular chaperone specifically required for the correct folding of T-synthase to form active enzyme. This review will summarize our current understanding of the Tn and STn antigens in terms of their biochemistry and role in pathology.

In the present work, the nanocomposite of MoO2-ordered mesoporous carbon (MoO2-OMC) was synthesized for the first time using a carbon thermal reduction route and the mesoporous carbon as the nanoreactor. The synthesized nanocomposite was characterized by X-ray diffraction (XRD), thermogravimetric analysis (TGA), N2 adsorption-desorption, scanning electron microscopy (SEM), and transmission electron microscopy (TEM) measurements. Furthermore, this nanocomposite was used as an anode material for Li-ion intercalation and exhibited large reversible capacity, high rate performance, and good cycling stability. For instance, a high reversible capacity of 689 mAh g(-1) can remain after 50 cycles at a current density of 50 mA g(-1). It is worth mentioning that the MoO2-OMC nanocomposite electrode can attain a high reversible capacity of 401 mAh g(-1) at a current density as high as 2 A g(-1). These results might be due to the intrinsic characteristics of nanocomposite, which offered a better accommodation of the strain and volume changes and a shorter path for Li-ion and electron transport, leading to the improved capacity and enhanced rate capability.

A key feature in the molecular pathogenesis of liver fibrosis requires maintenance of the activated hepatic stellate cell (HSC) phenotype by both proliferation and inhibition of apoptosis. We provide evidence that leptin is a potent HSC mitogen and dramatically inhibits stellate cell apoptosis. Leptin proved to be as potent an HSC mitogen as platelet-derived growth factor (PDGF) as assessed by bromodeoxyuridine (BrdU) incorporation in isolated primary HSCs; data using fluorescent propidium iodide (PI) uptake revealed that leptin, like PDGF, increased HSC populations in the S- and G2/M-phases of the cell cycle. Leptin resulted in a robust increase in cyclin D1 expression. Using the chemical inhibitor of Janus kinase 2 (Jak2) activity, AG 490, and overexpression of the suppressor of cytokine signaling 3 (SOCS-3), we show that blockade of leptin receptor (Ob-Rb) phosphorylation blocks leptin-induced HSC proliferation. Leptin-associated phosphorylation of both extracellular regulated kinase (p44/p42, Erk) and Akt is also prohibited. Further, the PI-3 kinase inhibitor LY294002 and MAPK inhibitor PD98059 were found to significantly reduce leptin-induced HSC proliferation, thereby indicating that leptin induced HSC proliferation is Akt- and Erk-dependent. Akt was also protective against HSC apoptosis. Leptin abolished both cycloheximide-induced and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, demonstrated by reduced caspase-3 activity, HSC-TUNEL staining, and DNA fragmentation. We conclude that leptin acts as a direct hepatic stellate cell survival agonist. Importantly, we have demonstrated that leptin-induced HSC proliferation and survival by Ob-Rb phosphorylation are both Erk- and Akt-dependent.