RVdb: a comprehensive resource and analysis platform for rhinovirus research.

Rhinovirus (RV), a prominent causative agent of both upper and lower respiratory diseases, ranks among the most prevalent human respiratory viruses. RV infections are associated with various illnesses, including colds, asthma exacerbations, croup and pneumonia, imposing significant and extended societal burdens. Characterized by a high mutation rate and genomic diversity, RV displays a diverse serological landscape, encompassing a total of 174 serotypes identified to date. Understanding RV genetic diversity is crucial for epidemiological surveillance and investigation of respiratory diseases. This study introduces a comprehensive and high-quality RV data resource, designated RVdb (http://rvdb.mgc.ac.cn), covering 26 909 currently identified RV strains, along with RV-related sequences, 3D protein structures and publications. Furthermore, this resource features a suite of web-based utilities optimized for easy browsing and searching, as well as automatic sequence annotation, multiple sequence alignment (MSA), phylogenetic tree construction, RVdb BLAST and a serotyping pipeline. Equipped with a user-friendly interface and integrated online bioinformatics tools, RVdb provides a convenient and powerful platform on which to analyse the genetic characteristics of RVs. Additionally, RVdb also supports the efforts of virologists and epidemiologists to monitor and trace both existing and emerging RV-related infectious conditions in a public health context.

Layered Double Hydroxide Derivatives for Polyolefin Upcycling.

While Ru-catalyzed hydrogenolysis holds significant promise in converting waste polyolefins into value-added alkane fuels, a major constraint is the high cost of noble metal catalysts. In this work, we propose, for the first time, that Co-based catalysts derived from CoAl-layered double hydroxide (LDH) are alternatives for efficient polyolefin hydrogenolysis. Leveraging the chemical flexibility of the LDH platform, we reveal that metallic Co species serve as highly efficient active sites for polyolefin hydrogenolysis. Furthermore, we introduced Ni into the Co framework to tackle the issue of restricted hydrogenation ability associated with contiguous Co-Co sites. In-situ analysis indicates that the integration of Ni induces electron transfer and facilitates hydrogen spillover. This dual effect synergistically enhances the hydrogenation/desorption of olefin intermediates, resulting in a significant reduction in the yield of low-value CH4 from 27.1 to 12.6%. Through leveraging the unique properties of LDH, we have developed efficient and cost-effective catalysts for the sustainable recycling and valorization of waste polyolefin materials.

Stable Interfacial Ruthenium Species for Highly Efficient Polyolefin Upcycling.

The present polyolefin hydrogenolysis recycling cases acknowledge that zerovalent Ru exhibits high catalytic activity. A pivotal rationale behind this assertion lies in the propensity of the majority of Ru species to undergo reduction to zerovalent Ru within the hydrogenolysis milieu. Nonetheless, the suitability of zerovalent Ru as an optimal structural configuration for accommodating multiple elementary reactions remains ambiguous. Here, we have constructed stable Ru0-Ruδ+ complex species, even under reaction conditions, through surface ligand engineering of commercially available Ru/C catalysts. Our findings unequivocally demonstrate that surface-ligated Ru species can be stabilized in the form of a Ruδ+ state, which, in turn, engenders a perturbation of the σ bond electron distribution within the polyolefin carbon chain, ultimately boosting the rate-determining step of C-C scission. The optimized catalysts reach a solid conversion rate of 609 g·gRu-1·h-1 for polyethylene. This achievement represents a 4.18-fold enhancement relative to the pristine Ru/C catalyst while concurrently preserving a remarkable 94% selectivity toward valued liquid alkanes. Of utmost significance, this surface ligand engineering can be extended to the gentle mixing of catalysts in ligand solution at room temperature, thus rendering it amenable for swift integration into industrial processes involving polyolefin degradation.

Correlation between the triglyceride-glucose index and left ventricular global longitudinal strain in patients with chronic heart failure: a cross-sectional study.

BACKGROUND: Left ventricular global longitudinal strain (GLS) holds greater diagnostic and prognostic value than left ventricular ejection fraction (LVEF) in the heart failure (HF) patients. The triglyceride-glucose (TyG) index serves as a reliable surrogate for insulin resistance (IR) and is strongly associated with several adverse cardiovascular events. However, there remains a research gap concerning the correlation between the TyG index and GLS among patients with chronic heart failure (CHF). METHOD: 427 CHF patients were included in the final analysis. Patient demographic information, along with laboratory tests such as blood glucose, lipids profiles, and echocardiographic data were collected. The TyG index was calculated as Ln [fasting triglyceride (TG) (mg/dL) × fasting plasma glucose (FPG) (mg/dL)/2]. RESULTS: Among CHF patients, GLS was notably lower in the higher TyG index group compared to the lower TyG index group. Following adjustment for confounding factors, GLS demonstrated gradual decrease with increasing TyG index, regardless of the LVEF level and CHF classification. CONCLUSION: Elevated TyG index may be independently associated with more severe clinical left ventricular dysfunction in patients with CHF.

Rutin mitigates fluoride-induced nephrotoxicity by inhibiting ROS-mediated lysosomal membrane permeabilization and the GSDME-HMGB1 axis involved in pyroptosis and inflammation.

Fluoride is known to induce nephrotoxicity; however, the underlying mechanisms remain incompletely understood. Therefore, this study aims to explore the roles and mechanisms of lysosomal membrane permeabilization (LMP) and the GSDME/HMGB1 axis in fluoride-induced nephrotoxicity and the protective effects of rutin. Rutin, a naturally occurring flavonoid compound known for its antioxidative and anti-inflammatory properties, is primarily mediated by inhibiting oxidative stress and reducing proinflammatory markers. To that end, we established in vivo and in vitro models. In the in vivo study, rats were exposed to sodium fluoride (NaF) throughout pregnancy and up until 2 months after birth. In parallel, we employed in vitro models using HK-2 cells treated with NaF, n-acetyl-L-cysteine (NAC), or rutin. We assessed lysosomal permeability through immunofluorescence and analyzed relevant protein expression via western blotting. Our findings showed that NaF exposure increased ROS levels, resulting in enhanced LMP and increased cathepsin B (CTSB) and D (CTSD) expression. Furthermore, the exposure to NaF resulted in the upregulation of cleaved PARP1, cleaved caspase-3, GSDME-N, and HMGB1 expressions, indicating cell death and inflammation-induced renal damage. Rutin mitigates fluoride-induced nephrotoxicity by suppressing ROS-mediated LMP and the GSDME/HMGB1 axis, ultimately preventing fluoride-induced renal toxicity occurrence and development. In conclusion, our findings suggest that NaF induces renal damage through ROS-mediated activation of LMP and the GSDME/HMGB1 axis, leading to pyroptosis and inflammation. Rutin, a natural antioxidative and anti-inflammatory dietary supplement, offers a novel approach to prevent and treat fluoride-induced nephrotoxicity.

TFEB ameliorates DEHP-induced neurotoxicity by activating GAL3/TRIM16 axis dependent lysophagy and alleviating lysosomal dysfunction.

Di-(2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer with known neurotoxic effects. However, the specific mechanism underlying this neurotoxicity remains unclear. This study aimed to investigate the role of lysosomal function and lysophagy in DEHP-induced neurotoxicity, with a particular focus on the regulatory role of Transcription factor EB (TFEB). To achieve this, we utilized in vitro models of DEHP-exposed SH-SY5Y cells and HT22 cells. Our findings revealed that DEHP exposure led to lysosomal damage and dysfunction. Moreover, we observed impaired autophagic degradation, characterized by elevated levels of LC3II and p62. DEHP treatment downregulated the expression of TFEB, GAL3, and TRIM16, while upregulating the expression of PARP. This led to the inhibition of GAL3/TRIM16 axis dependent lysophagy and ultimately excessive apoptosis in neuronal cells. Importantly, TFEB overexpression alleviated lysosomal dysfunction, activated lysophagy, and mitigated DEHP-induced apoptosis. Overall, our results suggest that DEHP induces not only lysosomal dysfunction, but also inhibits lysophagy through the suppression of GAL3/TRIM16 axis. Consequently, impaired clearance of damaged lysosomes occurs, culminating in neuronal apoptosis. Taken together, our findings highlight the critical role of TFEB in regulating lysophagy and lysosomal function. Furthermore, TFEB may serve as a potential therapeutic target for mitigating DEHP-induced neuronal toxicity.

TFE3-mediated impairment of lysosomal biogenesis and defective autophagy contribute to fluoride-induced hepatotoxicity.

Excessive fluoride exposure can cause liver injury, but the specific mechanisms need further investigation. We aimed to explore the role of impaired lysosomal biogenesis and defective autophagy in fluoride-induced hepatotoxicity and its potential mechanisms, focusing on the role of transcription factor E3 (TFE3) in regulating hepatocyte lysosomal biogenesis. To this end, we established a Sprague-Dawley (SD) rat model exposed to sodium fluoride (NaF) and a rat liver cell line (BRL3A) model exposed to NaF. The results showed that NaF exposure diminished liver function and led to apoptosis as well as autophagosome accumulation and impaired autophagic degradation. In addition, NaF exposure caused compromised lysosome biogenesis and decreased lysosomal degradation, and inhibited TFE3 nuclear translocation. Notably, the mTOR inhibitors rapamycin (RAPA) and Ad-TFE3 promoted lysosomal biogenesis and enhanced lysosomal degradation function. Furthermore, RAPA and Ad-TFE3 reduced NaF-induced apoptosis by alleviating impaired autophagic degradation. In conclusion, NaF impairs lysosomal biogenesis by inhibiting TFE3 nuclear translocation, decreasing lysosomal degradation function, resulting in impaired autophagic degradation, and ultimately inducing apoptosis. Therefore, TFE3 may be a promising therapeutic target for fluoride-induced hepatotoxicity.

Cross-talk between autophagy and ferroptosis contributes to the liver injury induced by fluoride via the mtROS-dependent pathway.

Fluoride can induce hepatotoxicity, but the mechanisms responsible are yet to be investigated. This study sought to investigate the role and mechanism of mitochondrial reactive oxygen species (mtROS), autophagy, and ferroptosis in fluoride-induced hepatic injury with a focus on the role of mtROS-mediated cross-talk between autophagy and ferroptosis. To this end, an in vivo Sprague-Dawley rat model and in vitro BRL3A cells were exposed to sodium fluoride (NaF). The results revealed that NaF exposure diminished the mitochondrial membrane potential, increased mtROS production and TOMM20 expression, and induced autophagic flux blockage and ferroptosis in vivo and in vitro. Furthermore, the autophagy activator (RAPA) enhanced GPX4 expression while inhibiting ACSL4 expression, reduced the accumulation of ferrous ions in BRL3A cells, and restored lipid peroxidation levels, thus inhibiting ferroptosis. Fer-1, a ferritinase inhibitor, downregulated the expression of LC3-II and p62, increased the number of autolysosomes while decreasing the number of autophagosomes, and alleviated the blockage of autophagic flux by improving autophagic degradation. These results suggest the occurrence of a cross-talk between autophagy and ferroptosis. The mtROS inhibitor (Mito-TEMPO) could alleviate autophagic flux blockage and inhibit ferroptosis in NaF-induced liver injury. In addition, the cross-talk between NaF-induced autophagy and ferroptosis was dependent on the mtROS pathway.

The inhibition of TRPML1/TFEB leads to lysosomal biogenesis disorder, contributes to developmental fluoride neurotoxicity.

Fluoride is capable of inducing developmental neurotoxicity; regrettably, the mechanism is obscure. We aimed to probe the role of lysosomal biogenesis disorder in developmental fluoride neurotoxicity-specifically, the regulating effect of the transient receptor potential mucolipin 1 (TRPML1)/transcription factor EB (TFEB) signaling pathway on lysosomal biogenesis. Sprague-Dawley rats were given fluoridated water freely, during pregnancy to the parental rats to 2 months after delivery to the offspring. In addition, neuroblastoma SH-SY5Y cells were treated with sodium fluoride (NaF), with or without mucolipin synthetic agonist 1 (ML-SA1) or adenovirus TFEB (Ad-TFEB) intervention. Our findings revealed that NaF impaired learning and memory as well as memory retention capacities in rat offspring, induced lysosomal biogenesis disorder, and decreased lysosomal degradation capacity, autophagosome accumulation, autophagic flux blockade, apoptosis, and pyroptosis. These changes were evidenced by the decreased expression of TRPML1, nuclear TFEB, LAMP2, CTSB, and CTSD, as well as increased expression of LC3-II, p62, cleaved PARP, NLRP3, Caspase1, and IL-1ß. Furthermore, TRPML1 activation and TFEB overexpression both restored TFEB nuclear protein expression and promoted lysosomal biogenesis while enhancing lysosomal degradation capacity, recovering autophagic flux, and attenuating NaF-induced apoptosis and pyroptosis. Taken together, these results show that NaF promotes the progression of developmental fluoride neurotoxicity by inhibiting TRPML1/TFEB expression and impeding lysosomal biogenesis. Notably, the activation of TRPML1/TFEB alleviated NaF-induced developmental neurotoxicity. Therefore, TRPML1/TFEB may be promising markers of developmental fluoride neurotoxicity.

PRKAA1 induces aberrant mitophagy in a PINK1/Parkin-dependent manner, contributing to fluoride-induced developmental neurotoxicity.

Chronic fluoride exposure can cause developmental neurotoxicity, however the precise mechanisms remain unclear. To explore the mechanism of mitophagy in fluoride-induced developmental neurotoxicity, specifically focusing on PRKAA1 in regulating the PINK1/Parkin pathway, we established a Sprage Dawley rat model with continuous sodium fluoride (NaF) exposure and an NaF-treated SH-SY5Y cell model. We found that NaF exposure increased the levels of LC3-Ⅱ and p62, impaired autophagic degradation, and subsequently blocked autophagic flux. Additionally, NaF exposure increased the expression of PINK1, Parkin, TOMM-20, and Cyt C and cleaved PARP in vivo and in vitro, indicating NaF promotes mitophagy and neuronal apoptosis. Meanwhile, phosphoproteomics and western blot analysis showed that NaF treatment enhanced PRKAA1 phosphorylation. Remarkably, the application of both 3-methyladenosine (3-MA; autophagy inhibitor) and dorsomorphin (DM; AMPK inhibitor) suppressed NaF-induced neuronal apoptosis by restoring aberrant mitophagy. In addition, 3-MA attenuated an increase in p62 protein levels and NaF-induced autophagic degradation. Collectively, our findings indicated that NaF causes aberrant mitophagy via PRKAA1 in a PINK1/Parkin-dependent manner, which triggers neuronal apoptosis. Thus, regulating PRKAA1-activated PINK1/Parkin-dependent mitophagy may be a potential treatment for NaF-induced developmental neurotoxicity.

Applications of Prolamin-Based Edible Coatings in Food Preservation: A Review.

Foods are susceptible to deterioration and sour due to external environmental influences during production and storage. Coating can form a layer of physical barrier on the surface of foods to achieve the purpose of food preservation. Because of its good barrier properties and biocompatibility, prolamin-based film has been valued as a new green and environment-friendly material in the application of food preservation. Single prolamin-based film has weaknesses of poor toughness and stability, and it is necessary to select appropriate modification methods to improve the performance of film according to the application requirements. The practical application effect of film is not only affected by the raw materials and the properties of the film itself, but also affected by the selection of preparation methods and processing techniques of film-forming liquid. In this review, the properties and selection of prolamins, the forming mechanisms and processes of prolamin-based coatings, the coating techniques, and the modifications of prolamin-based coatings were systematically introduced from the perspective of food coating applications. Moreover, the defects and deficiencies in the research and development of prolamin-based coatings were also reviewed in order to provide a reference for the follow-up research on the application of prolamin-based coatings in food preservation.

Entropy Confinement Promotes Hydrogenolysis Activity for Polyethylene Upcycling.

Chemical upcycling that catalyzes waste plastics back to high-purity chemicals holds great promise in end-of-life plastics valorization. One of the main challenges in this process is the thermodynamic limitations imposed by the high intrinsic entropy of polymer chains, which makes their adsorption on catalysts unfavorable and the transition state unstable. Here, we overcome this challenge by inducing the catalytic reaction inside mesoporous channels, which possess a strong confined ability to polymer chains, allowing for stabilization of the transition state. This approach involves the synthesis of p-Ru/SBA catalysts, in which Ru nanoparticles are uniformly distributed within the channels of an SBA-15 support, using a precise impregnation method. The unique design of the p-Ru/SBA catalyst has demonstrated significant improvements in catalytic performance for the conversion of polyethylene into high-value liquid fuels, particularly diesel. The catalyst achieved a high solid conversion rate of 1106 g ⋅ gRu -1 ⋅ h-1 at 230 °C. Comparatively, this catalytic activity is 4.9 times higher than that of a control catalyst, Ru/SiO2 , and 14.0 times higher than that of a commercial catalyst, Ru/C, at 240 °C. This remarkable catalytic activity opens up immense opportunities for the chemical upcycling of waste plastics.

A deep learning radiomics model may help to improve the prediction performance of preoperative grading in meningioma.

PURPOSE: This study aimed to investigate the clinical usefulness of the enhanced-T1WI-based deep learning radiomics model (DLRM) in differentiating low- and high-grade meningiomas. METHODS: A total of 132 patients with pathologically confirmed meningiomas were consecutively enrolled (105 in the training cohort and 27 in the test cohort). Radiomics features and deep learning features were extracted from T1 weighted images (T1WI) (both axial and sagittal) and the maximum slice of the axial tumor lesion, respectively. Then, the synthetic minority oversampling technique (SMOTE) was utilized to balance the sample numbers. The optimal discriminative features were selected for model building. LightGBM algorithm was used to develop DLRM by a combination of radiomics features and deep learning features. For comparison, a radiomics model (RM) and a deep learning model (DLM) were constructed using a similar method as well. Differentiating efficacy was determined by using the receiver operating characteristic (ROC) analysis. RESULTS: A total of 15 features were selected to construct the DLRM with SMOTE, which showed good discrimination performance in both the training and test cohorts. The DLRM outperformed RM and DLM for differentiating low- and high-grade meningiomas (training AUC: 0.988 vs. 0.980 vs. 0.892; test AUC: 0.935 vs. 0.918 vs. 0.718). The accuracy, sensitivity, and specificity of the DLRM with SMOTE were 0.926, 0.900, and 0.924 in the test cohort, respectively. CONCLUSION: The DLRM with SMOTE based on enhanced T1WI images has favorable performance for noninvasively individualized prediction of meningioma grades, which exhibited favorable clinical usefulness superior over the radiomics features.

Comparison of the Endophytic Bacterial Microbiota of Asymptomatic and Symptomatic Ginger Rhizomes During the Activation of Adventitious Bud Development.

Bacterial infections are the cause of rhizome rot in ginger (Zingiber officinale). Key members of the endophytic microbial community in ginger rhizomes have not been identified, and their impact on the decay of rhizomes during the activation of adventitious bud development has not been investigated. High-throughput, 16S rRNA amplicon sequencing and inoculation experiments were used to analyze the microbial diversity, community structure and composition, and pathogenicity of isolated bacteria. Our results indicated that the composition of the endophytic microbiota underwent a shift during the progression of rhizome rot disease. Enterobacteriaceae, Lachnospiraceae, and the bacterial genera Clostridium, Bacteroides, Acrobacter, Dysgonomonas, Anaerosinus, Pectobacterium, and Lactococcus were relatively abundant in the bacterial community of rhizomes exhibiting bacterial decay symptoms but were also present in asymptomatic rhizomes. The presence of Enterobacteriaceae and Pseudomonadaceae were positively correlated (ρ = 0.83) at the beginning of the sampling period in the symptomatic group, while a positive correlation (ρ = 0.89) was only observed after 20 days in the asymptomatic group. These data indicate that the co-occurrence of Enterobacteriaceae and Pseudomonadaceae may be associated with the development of ginger rot. Bacterial taxa isolated from ginger rhizomes, such as Enterobacter cloacae, E. hormaechei, and Pseudomonas putida, induced obvious rot symptoms when they were inoculated on ginger rhizomes. Notably, antibiotic-producing bacterial taxa in the Streptococcaceae and Flavobacteriaceae were also relatively abundant in rhizomes with rot and appeared to be linked to the onset of rhizome rot disease. Our results provide important information on the establishment and management of disease in ginger rhizomes.

CircFOXK2 Promotes the Progression of Osteoarthritis by Regulating the miR-4640-5p/NOTCH2 Axis.

OBJECTIVE: Osteoarthritis (OA) is the most common age-related chronic and disabling joint disease, frequently causing pain and disability in the adult population. Given that there are no proven disease-modifying drugs for OA, it is urgent to gain a deeper understanding of OA pathogenesis. This study intended to uncover the circFOXK2 regulation in OA. METHODS: Firstly, in vitro OA cell model was constructed by treating murine chondrocytes with interleukin (IL)-1ß. Then, a series of functional assays were conducted to evaluate the effect of circFOXK2 on OA progression in murine chondrocytes. Bioinformatics analysis and mechanism investigations were performed to investigate the competitive endogenous RNA (ceRNA) network of circFOXK2 in OA. RESULTS: CircFOXK2 is overexpressed in IL-1ß-treated chondrocyte. We confirmed the cyclic structure and cytoplasmic distribution of circFOXK2. Functionally, circFOXK2 promotes chondrocyte apoptosis and extracellular matrix (ECM) degradation but inhibiting chondrocyte proliferation. Mechanically, circFOXK2 competitively binds to microRNA-4640-5p (miR-4640-5p) to enhance NOTCH2 expression in OA, affecting OA progression. Besides, circFOXK2 could motivate the Notch pathway to accelerate OA progression. CONCLUSION: CircFOXK2/miR-4640-5p/NOTCH2 axis stimulates the Notch pathway to promote the transcription of inflammatory cytokines (IL33, IL17F and IL6), consequently facilitating OA progression in murine chondrocytes.

Stiffness of photocrosslinkable gelatin hydrogel influences nucleus pulposus cell propertiesin vitro.

A key early sign of degenerative disc disease (DDD) is the loss of nucleus pulposus (NP) cells (NPCs). Accordingly, NPC transplantation is a treatment strategy for intervertebral disc (IVD) degeneration. However, in advanced DDD, due to structural damage of the IVD and scaffold mechanical properties, the transplanted cells are less viable and secrete less extracellular matrix, and thus, are unable to efficiently promote NP regeneration. In this study, we evaluated the encapsulation of NPCs in a photosensitive hydrogel made of collagen hydrolysate gelatin and methacrylate (GelMA) to improve NP regeneration. By adjusting the concentration of GelMA, we prepared hydrogels with different mechanical properties. After examining the mechanical properties, cell compatibility and tissue engineering indices of the GelMA-based hydrogels, we determined the optimal hydrogel concentration of the NPC-encapsulating GelMA hydrogel for NP regeneration as 5%. NPCs effectively combined with GelMA and proliferated. As the concentration of the GelMA hydrogel increased, the survival, proliferation and matrix deposition of the encapsulated NPCs gradually decreased, which is the opposite of NPCs grown on the surface of the hydrogel. The controllability of the GelMA hydrogels suggests that these NPC-encapsulating hydrogels are promising candidates to aid in NP tissue engineering and repairing endogenous NPCs.

Groundwater quality assessment using a new integrated-weight water quality index (IWQI) and driver analysis in the Jiaokou Irrigation District, China.

Groundwater is an important water resource in arid and semi-arid regions. The impact of human activities on groundwater is increasing. After 60 years running, the groundwater quality and its formation mechanism are imperative questions needed to be answered in Jiaokou Irrigation District, Guanzhong Basin, China. In this study, the quality of groundwater in Jiaokou Irrigation District was assessed by a new integrated-weight water quality index (IWQI), and the groundwater chemistry is studied through integrated statistical, geostatistical and hydrogeochemical approaches. The patterns for the average anion and cation concentrations were HCO3- > SO42- > Cl- > NO3- > CO32- > NO2-, and Na+ > Mg2+ > Ca2+ > K+ > NH4+, respectively. Statistics showed that the major water chemistry types were HCO3-Na, SO4·Cl-Na, and Cl·SO4-Na. A new integrated-weight water quality index (IWQI) was proposed based on the entropy-weighted method and CRITIC method and showed excellent performance for explaining and evaluating the groundwater quality. The IWQI results show 65.33% of groundwater, mainly distributed in the central and western parts of this study area, was unsuitable for drinking. Furthermore, SO42－, HCO3－, Cl－, NO3－, and Na+ had more important effects on groundwater quality. The weathering process affecting groundwater quality in the study area is carbonate dissolution, followed by silicate weathering and evaporite dissolution, whereas the major geochemical processes include the dissolution and precipitation of calcite, as well as the dissolution of dolomite and gypsum (anhydrite). Cation exchange also plays an important role in the hydrogeochemical evolution of groundwater with a long residence time. Anthropogenic activities affecting groundwater quality included long-term irrigation infiltration and excessive use of fertilizers. The findings and the results of the study can improve understanding of the processes driving groundwater chemistry in Jiaokou Irrigation District, and can be used for reference to other similar regions in the world.

Anisotropic Seeded Growth of Ag Nanoplates Confined in Shape-Deformable Spaces.

Conventional templating synthesis confines the growth of seeds in rigid spaces to achieve faithful morphological replication. Herein, we explore the use of spherical shape-deformable polymeric nanoshells to regulate the anisotropic growth of Ag nanoplates. The flexible shells deform adaptively to accommodate the initial overgrowth of the seeds but restrict the growth in the directions where the shells are fully stretched, eventually producing nanoplates with an unconventional circular profile. The diameter of the final Ag nanoplates can be precisely predicted by stretching and flattering the nanoshells into a plate-like capsule while retaining their original internal surface area. Furthermore, unlike conventional templates, the polymer shells eventually turn themselves into a conformal coating that binds to the surface of the full-grown Ag nanoplates and significantly enhances their stability against oxidative etching.

Integrated transcriptomic and metabolomic analyses to characterize the anti-cancer effects of (-)-epigallocatechin-3-gallate in human colon cancer cells.

(-)-Epigallocatechin-3-gallate (EGCG) is the main bioactive component in tea (Camellia sinensis) catechins, and exhibits potential antitumor activity against colorectal cancer (CRC). However, the underlying mechanisms are largely unclear. We investigated the effects of EGCG on activities of CRC cells and the exact molecular mechanism. We used human colon cancer cells (HT-29) and exposed them to EGCG at various concentrations. The MTT assay, flow cytometry, and TUNEL staining were used to study the underlying mechanisms of EGCG (proliferation, apoptosis, autophagy). Western blotting was used to measure expression of marker proteins of the cell cycle, apoptosis, and autophagy. Using a combined microarray-based transcriptomic and ultra-high-performance liquid chromatography coupled with quadrupole-time-of-flight tandem mass spectrometry (UHPLC-QTOF/MS)-based metabolomic approach, we investigated the perturbed pathways induced by EGCG treatment at transcript and metabolite levels. Transcriptomic analyses showed that 486 genes were differentially expressed between untreated and EGCG-treated cells. Also, 88 differentially expressed metabolites were identified between untreated and EGCG-treated cells. The altered metabolites were involved in the metabolism of glutathione, glycerophospholipids, starch, sucrose, amino sugars, and nucleotide sugars. There was substantial agreement between the results of transcriptomics and metabolomics analyses. Our data indicate that the anticancer activity of EGCG against HT-29 cells is mediated by induction of cell-cycle arrest, apoptosis, and autophagy. EGCG modulates cancer-cell metabolic pathways. These results provide a platform for future molecular mechanistic studies of EGCG.

Bushen-Tiansui Formula Improves Cognitive Functions in an Aß 1-42 Fibril-Infused Rat Model of Alzheimer's Disease.

Bushen-Tiansui Formula (BTF) was empirically updated from a classical prescription named Kong-Sheng-Zhen-Zhong pill. It is based on the traditional Chinese medicine theory of the mutual relationship between the brain and the kidney and is intended to treat neurodegenerative diseases. This formulation has been used for several years to treat patients with Alzheimer's disease- (AD-) like symptoms in our clinical department. However, the medicinal ingredients and the mechanisms by which BTF improves cognition and memory functions have not been characterized. In this study, we used UPLC-MS to generate a chromatographic fingerprinting of BTF and identified five possible active ingredients, including stilbene glycoside; epimedin A1, B, and C; and icariin. We also showed that oral administration of BTF reversed the cognitive defects in an Aß 1-42 fibril-infused rat model of AD, protected synaptic ultrastructure in the CA1 region, and restored the expression of BDNF, synaptotagmin (Syt), and PSD95. These effects likely occurred through the BDNF-activated receptor tyrosine kinase B (TrkB)/Akt/CREB signaling pathway. Furthermore, BTF exhibited no short-term or chronic toxicity in rats. Together, these results provided a scientific support for the clinical use of BTF to improve learning and memory in patients with AD.