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Dissolved organic carbon (DOC) in lakes serves as a substrate for heterotrophic bacterial growth, a regulator of the global carbon cycle, and a light absorption agent. DOC in eutrophic lakes is greatly influenced by phytoplankton phenology and terrigenous input by rivers. Therefore, it is necessary and significant to dynamically monitor the concentration, storage, and riverine exchange flux of DOC. By using in-situ DOC measurements from 2004 until 2018 (N = 2019), a machine learning algorithm, namely, a multilayer back-propagation neural network (MBPNN) model, was developed in this work to improve the remote sensing estimation of DOC concentrations in eutrophic Lake Taihu. The model yielded a mean estimation error of 15.14% for the testing dataset. The monthly mean DOC concentration significantly increased from 2003 to 2018 (N = 192, p

Low-frequency high-magnitude storms can flush disproportionate amounts of terrigenous dissolved organic carbon (DOC) and particulate organic carbon (POC) into rivers during a short period. However, previous studies focused on the impacts of storms on organic carbon transport in headwater streams that are minimally influenced by human activities and are far from lakes. To better estimate the lake carbon budget and manage lake water environments, we need to understand the transport of storm-induced organic carbon into lakes by eutrophic rivers. Based on daily and hourly time-series monitoring data, this paper systematically studied the influences of storm precipitation on DOC and POC transport in the eutrophic Tiaoxi River entering Lake Taihu, the 3rd largest freshwater lake in China. The results showed that seven storms transported 59% of the annual total organic carbon into Lake Taihu in 2019, and all storms resulted in transport peaks. During the storm period on August 9-16, 2019, DOC was negatively related to the water level (r = -0.44, p0.05), but POC responded positively (r = 0.52, p0.05); allochthonous organic carbon contents were elevated, but the autochthonous components were diluted. Moreover, the storm-induced input of riverine organic carbon influenced the lake water environment across a large region, and the impacts lasted more than 10 days. These findings have important implications for accurately estimating riverine organic carbon fluxes into lakes and making better-informed decisions about when to pump drinking water from lakes.

Free fatty acids (FFAs) increase in visceral fat and are inferred to be one of the underlying inducers of adipose tissue inflammation. In our previous study, it was demonstrated that ginsenoside Rb1 stimulates endothelial nitric oxide synthase (eNOS) and Sirtuin 1 to protect against endothelial cell senescence. In the present study, 3T3‑L1 adipocytes were exposed to 0.5 mM FFAs with or without Rb1 (10‑40 µM). Monocyte chemotactic protein‑1 (MCP‑1) and interleukin‑6 (IL‑6) secretion was measured using ELISA. Tumor necrosis factor‑α (TNF‑α) expression and nuclear factor‑κB (NF‑κB) p65 phosphorylation were detected using western blot analysis. Oxidative stress was determined via measuring intracellular reactive oxygen species (ROS) and nitric oxide (NO) production. The results demonstrated that MCP‑1 and IL‑6 secretion, as well as TNF‑α expression, were significantly increased following FFA treatment, which was attenuated by Rb1 in a dose‑dependent manner. Furthermore, Rb1 attenuated FFA‑induced NF‑κB phosphorylation, suggesting that the inhibitory effect of Rb1 on inflammatory cytokines was partially mediated through blockade of NF‑κB phosphorylation. Further experiments demonstrated that Rb1 ameliorated FFA‑induced ROS generation and NO reduction through upregulation of superoxide dismutase 2 and eNOS expression. Taken together, these results demonstrate proinflammatory and pro‑oxidant effects of FFA on 3T3‑L1 adipocytes, which are effectively ameliorated by Rb1. Suppression of inflammatory responses and oxidative stress may be a novel mechanism for attenuating the effect of Rb1 on adipocyte dysfunction.

CSNK2B, which encodes the beta subunit of casein kinase II (CK2), plays an important role in neuron morphology and synaptic transmission. Variants in CSNK2B associated with epilepsy and/or intellectual disability (ID)/developmental delay (DD) have been reported in five cases only. Among the 816 probands suspected hereditary epilepsy whose initial report of trio-based whole exome sequencing (WES) were negative, 10 de novo pathogenic or likely pathogenic variants of CSNK2B in nine probands were identified after reanalysis of their raw Trio-WES data. Six of the nine epileptic patients had ID/DD. The age of seizure onset of these nine patients with CSNK2B variants ranged from 2–12 months. Eight patients had age of seizure onset of less than 6 months. The epilepsy of most probands (8/9) was generalized tonic-clonic seizure and clustered (6/9). Most patients had normal electroencephalogram (5/9) and brain magnetic resonance image (7/9) results. Most patients (7/9) had easy-to-control seizures. Levetiracetam was the most commonly used drug in seizure-free patients (5/7). The variants detected in five patients (5/9, 55.6%) were located in the zinc-binding domain. In summary, our research provided evidence that variants in CSNK2B are associated with epilepsy with or without ID/DD. CSNK2B-related epilepsy is relatively easy to be controlled. The zinc-binding domain appears to be the hotspot region for mutation.

Oxidative low-density lipoprotein (ox-LDL) induces endothelium senescence and promotes atherosclerosis. Ginsenoside Rb1 (gRb1) has been proved to protect human umbilical vein cells (HUVECs), but its effect on ox-LDL-induced endothelium senescence and the underlying mechanism remains unknown. This study is to explore the involvement of the SIRT1/Beclin-1/autophagy axis in the effect of gRb1 on protecting endothelium against ox-LDL-induced senescence. Hyperlipidemia of Sprague Dawley rats was induced by high-fat diet, and gRb1 was intraperitoneal injected. A senescence model of HUVECs induced by ox-LDL was also established. The results showed that gRb1 alleviated hyperlipidemia-induced endothelium senescence and ox-LDL-induced HUVECs senescence. GRb1 also restored the reductions in SIRT1 and autophagy, which were involved in the anti-senescence effects. Beclin-1 acetylation was reduced, and the correlation between SIRT1 and Beclin-1 was increased by gRb1. Results of our study demonstrated the anti-senescence function of gRb1 against hyperlipidemia in the endothelium, and the underlying mechanism involves the SIRT1/Beclin-1/autophagy axis.

The salinity of the Arctic Ocean is influenced by the fresh water input from sea ice melting, river discharge and precipitation, and its variation could provide a useful reference for the study of changes in Arctic environment. Since the SMOS satellite launched in 2009, there have been three microwave salinity satellites (Aquarius, SMOS and SMAP satellites) that could provide us sea surface salinity (SSS) data from space. In this study, we compared the SSS products derived from these three salinity satellites: the Aquarius satellite data have a limited spatial resolution and a short time series of less than 5 years, the SMOS SSS product for the Arctic from Barcelona Expert Center provide a 7-year record of the Arctic SSS in 2011-2017, the SMAPSSS data is more sensitive in low salinity regions. With the data from the SMAP and SMOS satellites, we presented a general view on summertime SSS variation during 2011-2017 in the Arctic area. The SSS maps showed that the SSS mainly varied in the plume area and were stable in the Arctic open sea. Satellite-derived salinity could detect the extremely low SSS area caused by sea ice melting and continental runoff. We extracted the ice-melt water area by combing the microwave salinity satellite data and the ocean color satellite data, which could exclude the continental fresh water input. The result showed consistence with sea ice concentration and former literature. The distribution of the ice-melt water could be of great significance for the study of Arctic sea ice anomaly and relative biogeochemical changes.

To delineate the clinical and genetic characteristics of patients with Allan-Herndon-Dudley syndrome (AHDS).Genetic testing was carried out by next generation sequencing on 117 patients featuring intellectual disability and developmental delay. Clinical information including clinical manifestation, brain magnetic resonance imaging(MRI）, thyroid hormone levels, and electrocardiogram was collected for those with SLC16A2 mutations.Five male patients with SLC16A2 gene mutations were identified, including 2 affected brothers and 3 sporadic cases. The ages of the patients ranged from 8 months to 8 years. All patients presented with severe intellectual disability and developmental delay including poor head control, inability to sit independently, no speech, and poor response to external stimuli. All patients presented with hypotonia, dystonia, and positive pyramidal signs. Three patients had sinus tachycardia. All patients had abnormal thyroid hormone levels with elevated free triiodothyronine (FTAHDS is characterized by severe psychomotor developmental delay as well as congenital hypotonia, dystonia and positive pyramidal signs. Affected males may present with distinctive thyroid hormone abnormalities including increased FT

Purpose This study aimed to investigate the genetic etiology of epilepsy in a cohort of Chinese children. Methods Targeted next-generation sequencing (NGS) was performed for 120 patients with unexplained epilepsy, including 71 patients with early-onset epileptic encephalopathies, and 16 patients with Dravet syndrome (including three patients with a Dravet-like phenotype) but without SCN1A pathogenic variants. Results Pathogenic variants of 14 genes were discovered in 22 patients (18%). A de novo KCND3 pathogenic variant (c.1174G > A, p.Val392Ile) was identified in a boy with refractory epilepsy, psychomotor regression, attention deficit, and visual decline. Pathogenic variants in other coding genes were excluded via whole exome sequencing. This KCND3 variant was previously confirmed to be pathogenic by Giudicessi, et al. However, the clinical profile was different: sudden death at 20 years old without any medical history of neurological disorders, nor with any diseases typically caused by KCND3 pathogenic variants such as Brugada syndrome, spinocerebellar ataxia type 19/22 or ataxia accompanied by epilepsy. This indicates that we have identified a new KCND3 phenotype. In addition, we also uncovered a GRIN1 pathogenic variant and a novel HCN1 pathogenic variant in the Dravet cohort. Conclusion Our study highlights the significant utility of NGS panels in the genetic diagnosis of pediatric epilepsy. Our findings indicate that KCND3 pathogenic variants may be responsible for a wider phenotypic spectrum than previously thought, by including childhood epileptic encephalopathy. Furthermore, this study provides evidence that GRIN1 and HCN1 are candidate genes for Dravet and Dravet-like phenotypes.

Based on time-series satellite-retrieved records of the marine ecological environment from Aqua/MODIS, we investigated changes in the sea surface temperature (SST), photosynthetically active radiation (PAR), Secchi Disc depth (SDD), and chlorophyll-a concentration (Chla) in 12 Eurasian marginal seas from 2003 to 2014. Results showed that the SST increased in all 12 marginal seas, with the enclosed marginal seas (i.e., Black Sea, Baltic Sea, Japan Sea, Mediterranean Sea, and Persian Gulf) exhibiting relatively higher rates of increase. The PAR generally decreased, except in the European marginal seas, though not significantly. Similar to the changes in the SST, the SDD increased in all 12 marginal seas, with a maximum rate of 3.02%/year (or 0.25 m/year, p = 0.0003) found in the Persian Gulf. As expected, Chla generally decreased in the tropical marginal seas, but increased in the high-latitude marginal seas. The different relationships between SST and Chla changes indicate the complexity of global warming effects on marine phytoplankton in different marginal seas.

Table S1. List of 512 candidate genes. (DOCX 20 kb)

The Bay of Bengal (BOB) is a semi-enclosed marginal sea in the northeastern part of the Indian Ocean. The South China Sea (SCS) is almost an enclosed marginal sea and is part of the northwestern Pacific Ocean. Both of them are tropical marginal seas, and have similar hydrological properties, such as high surface temperature, stable thermocline, deep euphotic zone, etc. Moreover, they are all greatly affected by East Asian monsoon and typhoons. However, there are also several significant differences between them. The current circulation structures in the South China Sea are more complex with significant season variations. A large amount of fresh water through river inputs is one of the remarkable hydrological characteristics in the Bay of Bengal. In addition, the Bay of Bengal has a large volume of precipitation. Therefore, it is naturally interesting to investigate the different response of the marine ecological properties represented by chlorophyll concentration to climate change. The Sea-Viewing Wide Field-of-View Sensor (SeaWiFS) and Moderate Resolution Imaging Spectroradiometer (MODIS) mission have provided a successive, long-term observations of global ocean color from space. In this study, we investigate the Chl-a trends in the BOB and SCS during the SeaWiFS and MODIS observation periods (1998-2010 and 2003-2016), respectively. In 1998-2010, Chl-a increased in the western central basin of BOB, while it decreased in almost all other parts. During 2003-2016, Chl-a significantly increased in the western part of BOB, and reduced in the southern part. In the SCS, Chl-a in almost the whole region increased during the SeaWiFS observation period. In 2003-2016, the major rising trends appeared in China and Vietnam coast, the Beibu Gulf, and the Gulf of Thailand. The Chl-a of the Straits of Malacca and the Karimata Straits showed downward trends. The rise in temperature might be the main cause of the Chl-a decrease in the BOB. The deepened MLD and/or decreasing SST may contribute to the increasing Chl-a of the BOB and SCS. Remarkably, coastal Chl-a has continued to rise over the past 19 years. The freshwater input might have significant effect on it.

Two unusual phytoplankton bloom events were identified in the southwestern Bay of Bengal from MODIS-derived chlorophyll-a concentration data collected between 2003 and 2015. The occurrence of the unusual phytoplankton bloom in December 2005 (called Bloom 1 in this study) has been reported in the literature to be triggered by multiple forcings, including strong cyclonic eddy, frequent typhoons, and strong wind-induced mixing. Interestingly, the other unusual phytoplankton bloom (called Bloom 2 in this study) was identified in almost the same location in December 2013. Further, it is the strongest bloom during our study period with large area of high Chl-a > 1.0 mg/m3 and shared some similar features with Bloom 1, such as wide coverage and long duration. At the same time, there were also frequent typhoons and a cyclonic eddy. The possible causes of Bloom 2 were examined using time series of multi-satellite datasets, including sea surface height anomalies (SSHA), sea surface temperature (SST), together with Argo profile data. We found that the cyclonic eddy might be not yet the dominant factor for Bloom 2 as the eddy was much weaker than that of Bloom 1. Specially, SST in December 2013 was lowest among all the December from 2003 to 2015. That is, the stratification is weakest. Therefore, the weak stratification can be broken easily by mixing induced by typhoons and cyclonic eddies and finally result in the strong bloom. This comparative studies could provide us some insight in understanding the role of eddies and tropical cyclones in phytoplankton dynamics in the Bay of Bengal.

23 candidate genes identified in the Chinese family with epilepsy, by whole-exome sequencing. (DOCX 16Â kb)

The record of seizures attack of patients with SCN8A mutations. This file included the seizure frequency of patients with SCN8A mutations, at different periods. (DOCX 16Â kb)

485 genes in the targeted-next generation sequencing panel. (PDF 45Â kb)

Aims Hypoxia induces vascular inflammation by a mechanism not fully understood. Emerging evidence implicates O -GlcNAc transferase (OGT) in inflammation. This study explored the role of OGT in hypoxia-induced vascular endothelial inflammatory response. Methods and results Hypoxia was either induced (1% O2 chamber) or mimicked by exposure to hypoxia-mimetic agents in cultured endothelial cells. Hypoxia increased hypoxia-inducible factor (HIF-1α) and inflammatory response (gene and protein expression of interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and E-selectin) but, surprisingly, reduced OGT protein (not mRNA) levels. Hypoxia-mimetic CoCl2 failed to reduce OGT when proteasome inhibitors were present, suggesting proteasome involvement. Indeed, CoCl2 enhanced 26S proteasome functionality evidenced by diminished reporter (UbG76V-GFP) proteins in proteasome reporter cells, likely due to increased chymotrypsin-like activities. Mechanistically, β-TrCP1 mediated OGT degradation, since siRNA ablation of this E3 ubiquitin ligase stabilized OGT. Administration of the oxidative stress inhibitors reversed both proteasome activation and OGT degradation. Furthermore, up-regulation of OGT by stabilization, overexpression, or activation mitigated CoCl2-elicited inflammatory response. These observations were recapitulated in a mouse (C57BL/6J) model mimicking hypoxia, in which lung tissues presented higher levels of HIF-1α, proteasome activity, and inflammatory response, but lower levels of OGT ( n = 5/group, hypoxia vs. normoxia, P < 0.05). However, administration of an activator of OGT (glucosamine: 1 mg/g/day, vehicle: saline, ip, 5 days) abolished the up-regulation of proteasome activity and inflammatory response ( n = 5/group, the treated vs. untreated hypoxia groups, P < 0.05). Conclusions 26S proteasome-mediated OGT reduction contributed to hypoxia-induced vascular endothelial inflammatory response. Modulation of OGT may represent a new approach to treat diseases characterized by hypoxic inflammation.

Our previous studies have shown that ginsenoside Rb1 prevents endothelial cells from senescence through modulating redox status. Oxidative stress and inflammation are involved in aging and age-related phenomenon. This study was performed to investigate the role of ginsenoside Rb1 in aged mice.

The second author Jiarui Li is now listed as a co–first author according to her contribution to this paper. The list of authors who contributed equally now reads: Qingping Zhang, Xiaoxu Yang, Jiaping Wang, and Jiarui Li. This has now been corrected in both the PDF and HTML versions of the Article.

The Persian Gulf and the Gulf of Oman locate at the northwest of the Arabian Sea, with the total area more than 50,0000 km2. The Persian Gulf is a semi-enclosed subtropical sea with high water temperature, extremely high salinity, and an average depth of 50 meters. By the Strait of Hormuz, the Persian Gulf is connected to the Gulf of Oman which is significantly affected by the monsoonal winds and by water exchange between the Arabian Sea and the Persian Gulf. Algal blooms occurred frequently in the Persian Gulf and the Gulf of Oman, and some of them are harmful algal blooms which may lead to massive fish death and thereby serious economic loss. Due to the widely spatial coverage and temporal variation, it is difficult to monitoring the dynamic of the algal bloom based on in situ measurement. In this study, we used the remote sensing data from the Moderate Resolution Imaging Spectroradiometer (MODIS) onboard the Aqua satellite to investigate a massive algal bloom event in the Persian Gulf and the Gulf of Oman during 2008-2009. The time series of MODIS-derived chlorophyll concentration (Chl-a) indicated that the bloom event with high Chl-a concentration (~60 percent higher than corresponding climatological data) appeared to lasting more than 8 months from autumn of 2008 to spring of 2009. In addition, the bloom was widespread from the Persian Gulf to the Gulf of Oman and neighboring open ocean. The MODIS-derived net primary production (NPP) collected from MODIS showed the same trend with Chl-a. Multiple forces including upwelling, dust deposition was taken into account to elucidate the mechanisms for the long-lasting algal bloom. The time series chlorophyll concentration of the Persian Gulf emerges a significant seasonal pattern with maximum concentrations seen during the winter time and lowest during the summer. It also indicated slight disturbances occurred in June (May/July) and December (November/ January) in some years. The sea surface temperature and water transparency in the Persian Gulf increased with the rates of 0.3% (

Tsutsugamushi disease is a zoonotic disease caused by Orientia tsutsugamushi in which humans are accidental hosts. Infective endocarditis associated with Tsutsugamushi disease has not been previously reported. We are describing a case of Tsutsugamushi disease presenting with aortic valve endocarditis. The clinical data of a 67-year-old female with O. tsutsugamushi-induced aortic valve endocarditis was summarized retrospectively and analyzed with a literature review. Treatment of O. tsutsugamushi-induced aortic valve endocarditis with chloramphenicol is recommended.

Objective— Although the connection of oxidative stress and inflammation has been long recognized in diabetes mellitus, the underlying mechanisms are not fully elucidated. This study defined the role of 26S proteasomes in promoting vascular inflammatory response in early diabetes mellitus. Methods and Results— The 26S proteasome functionality, markers of autophagy, and unfolded protein response were assessed in (1) cultured 26S proteasome reporter cells and endothelial cells challenged with high glucose, (2) transgenic reporter (Ub G76V –green fluorescence protein) and wild-type (C57BL/6J) mice rendered diabetic, and (3) genetically diabetic (Akita and OVE26) mice. In glucose-challenged cells, and also in aortic, renal, and retinal tissues from diabetic mice, enhanced 26S proteasome functionality was observed, evidenced by augmentation of proteasome (chymotrypsin-like) activities and reduction in 26S proteasome reporter proteins, accompanied by increased nitrotyrosine-containing proteins. Also, whereas inhibitor of the nuclear factor κ-light-chain-enhancer of activated B cells α proteins were decreased, an increase was found in nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) nucleus translocation, which enhanced the NF-κB–mediated proinflammatory response, without affecting markers of autophagy or unfolded protein response. Importantly, the alterations were abolished by MG132 administration, small interfering RNA knockdown of PA700 (proteasome activator protein complex), or superoxide scavenging in vivo. Conclusion— Early hyperglycemia enhances 26S proteasome functionality, not autophagy or unfolded protein response, through peroxynitrite/superoxide-mediated PA700-dependent proteasomal activation, which elevates NF- ĸB-mediated endothelial inflammatory response in early diabetes mellitus.

To study the mechanism of the transforming growth factor-β(TGF-β) in Ginsenoside Rb1 against the replicative senescence of human umbilical vein endothelial cells (HUVECs). Replicative Senescence model was established by serial subcultivation of primary HUVECs in vitro. Then, Cells were divided

Tubular ZnO clusters and rods have been fabricated using a simple template-free hydrothermal method by controlling the reaction temperature, pH value and reaction time. The obtained ZnO products were characterized using scanning electron microscopy, high-resolution transmission electron microscopy, X-ray diffraction, photoluminescence spectra and UV-vis diffuse reflectance spectroscopy. The results show that the formation of the tubular ZnO clusters and rods involves both a growth process and a dissolution process. The reaction temperature and reaction time play important roles in the formation of the ZnO clusters and rods with tubular morphologies. The possible formation mechanism of tubular ZnO is discussed.

Pyrochlore-type K{sub 2}Ta{sub 2}O{sub 6} compound cannot be obtained by a conventional solid-state reaction. Here, we report the synthesis of K{sub 2}Ta{sub 2}O{sub 6} and tetragonal tungsten bronze (TTB)-type K{sub 6}Ta{sub 10.8}O{sub 30} nanopowders using a facile and low-cost sol-gel method at low temperature. The as-prepared samples were characterized by XRD, TG-DSC, FESEM, UV-vis diffuse reflectance spectrum and XPS. The compound K{sub 2}Ta{sub 2}O{sub 6} was formed at 700 {sup o}C and reached complete crystallization at 750 {sup o}C, and decomposed into pure K{sub 6}Ta{sub 10.8}O{sub 30} with the volatilization of K{sub 2}O at 900 {sup o}C. The transformation of K{sub 2}Ta{sub 2}O{sub 6} to K{sub 6}Ta{sub 10.8}O{sub 30} is reported for the first time. The band gap of the pure K{sub 2}Ta{sub 2}O{sub 6} and K{sub 6}Ta{sub 10.8}O{sub 30} samples was found to be about 4.16 and 3.63 eV, respectively. The as-prepared K{sub 2}Ta{sub 2}O{sub 6} sample exhibited an efficient photocatalytic activity for the decomposition of azo dye acid red G (ARG) and 4-nitrophenol (4-NP, a typical persistent organic pollutant) solution under UV irradiation. According to the experimental results, the mechanism of the photocatalytic reaction over K{sub 2}Ta{sub 2}O{sub 6} was discussed.

Nuclear factor-κB plays a critical role in endothelial senescence. However, the mechanisms remain unclear. We hypothesized that the alteration of S-Nitrosylation of NF-κB p65 may contribute to hydrogen peroxide-induced endothelial cell senescence. The human umbilical vein endothelial cells (

Sr 6 Bi 2 O 9 powders were synthesized by a sol–gel method using Bi(NO 3 ) 3 ·5H 2 O and Sr(NO 3 ) 2 as the starting materials and were characterized by X-ray diffraction (XRD), UV–vis diffuse reflectance spectrum (UV–vis DRS), Fourier transform infrared (FT-IR) spectrum and Raman spectrum. The as-prepared Sr 6 Bi 2 O 9 powders showed an efficient photocatalytic activity in the decomposition of 4BS dye (a widely used azo dye) and 4-nitrophenol (4-NP, a priority pollutant) under visible light irradiation ( λ > 400 nm). TA-PL analysis reveals that HO was not the dominant photooxidant. The radical scavengers experiments indicated that the main active species was O 2 − in the photocatalytic degradation of dye under visible irradiation. A possible photodegradation mechanism of organic pollutants by the visible light driven Sr 6 Bi 2 O 9 was discussed.

ZnMoO 4 with a rhombus sheet or flower-like structure, α-ZnMoO 4 and needle-like ZnMoO 4 ·0.8 H 2 O were successfully synthesized by simple hydrothermal crystallization processes with citric acid. ZnMoO 4 ·0.8 H 2 O was easily synthesized in a shorter reaction time (2 h) at a higher reactant concentration. It gradually transformed into ZnMoO 4 with a monoclinic wolframite tungstate structure with an increased reaction time, and pure ZnMoO 4 was obtained with a longer reaction time (8 h). Citric acid (CA) played an important role in controlling the morphology of the as-obtained molybdates. The α-ZnMoO 4 and ZnMoO 4 were synthesized by heating ZnMoO 4 ·0.8 H 2 O at 130 °C for 4 h and 8 h, respectively, under hydrothermal conditions. With transforming of ZnMoO 4 ·0.8 H 2 O to α-ZnMoO 4 and further to ZnMoO 4 , the needle-like crystals gradually disappeared and were transformed into crystals with rhombus sheet morphology and then further to pentacle or flower-like crystals that can be ascribed to continuous splitting and growing of the rhombus sheets.

Nanosized Bi3NbxTa1−xO7 photocatalysts were prepared by a facile and low-cost sol−gel method using stable, less toxic Ta2O5, Nb2O5, and Bi(NO3)3·5H2O as the raw materials. The as-prepared samples were characterized by X-ray diffraction, transmission electron microscopy, Fourier transformation infrared spectroscopy, X-ray photoelectron spectroscopy, and UV−vis diffuse reflectance spectroscopy. The Bi3NbxTa1−xO7 nanoparticles exhibited an efficient photocatalytic activity in the decomposition of acid red G (ARG) dye solution under visible light irradiation. Besides decoloring, the typical sample Bi3Nb0.6Ta0.4O7 also showed an excellent photocatalytic property for the removal of the cyanotoxin, microcystin-LR (MC-LR, an emerging contaminant from the Contaminant Candidate Lists (CCLs 1-3) of the USEPA). The excellent visible light photocatalytic activity of the samples was mainly attributed to their narrow band gaps, small particle size, and the oxygen vacancies on the surface of the catalysts. According to e...

To investigate the effects of Ginsenoside Rb1 on Homocysteine(HCY)-induced endothelial dysfunction and inflammatory response. With the informed consents of puerperants, the normal fetal umbilical cords were obtained through uterine-incision delivery in Third Affiliated Hospital, Sun Yat-sun

We analyzed left ventricular diastolic function in patients with pregnancy-induced hypertension using tissue Doppler imaging to assess any velocity differences at different points around the annulus. Sixty-three patients (aged 21–38 years old, mean 28 ± 7 years) with pregnancy-induced

To study the mechanism of the oxidative damage in Ginsenoside Rb1 against the intrinsic aging of mouse brain. Female C57BL/6 mice were divided into three groups randomly: control group(4 months, n=12); model group(24 months, n=12) and drug group(24 months, n=12). In drug group, ginsenoside Rb1(20mg

To investigate the relationship between apolipoprotein (apo) A and the extent of coronary artery lesions in Chinese type 2 diabetics with coronary heart disease. Totally 184 type 2 diabetic patients diagnosed with coronary heart disease by coronary angiography were enrolled. The level of apoA was