Enterotoxin-related genes PPFIA4 and SCN3B promote colorectal cancer development and progression.

To identify the role of enterotoxin-related genes in colorectal cancer (CRC) development and progression. Upregulated differentially expressed genes shared by three out of five Gene Expression Omnibus (GEO) data sets were included to screen the key enterotoxin-induced oncogenes (EIOGs) according to criteria oncogene definition, enrichment, and protein-protein interaction (PPI) network analysis, followed by prognosis survival, immune infiltration, and protential drugs analyses was performed via integration of RNA-sequencing data and The Cancer Genome Atlas-derived clinical profiles. We screened nine common key EIOGs from at least three GEO data sets. A Cox proportional hazards regression models verified that more alive cases, decreased overall survival, and highest 4-year survival prediction in CRC patients with high-risk score. Protein tyrosine phosphatase receptor type F polypeptide-interacting protein alpha-4 (PPFIA4), STY11, SCN3B, and SPTBN5 were shared in the same PPI network. Immune infiltration results showed that SCN3B and synaptotagmin 11 expression were obviously associated with B cell, macrophage, myeloid dendritic cell, neutrophils, and T cell CD4+ and CD8+ in both colon adenocarcinoma and rectal adenocarcinoma. CHIR-99021, MLN4924, and YK4-279 were identified as the potential drugs for treatment. Finally, upregulated EIOGs genes PPFIA4 and SCN3B were found in colon adenocarcinoma and PPFIA4 and SCN3B were proved to promote cell proliferation and migration in vitro. We demonstrated here that EIOGs promoting a malignancy phenotype was related with poor survival and prognosis in CRC, which might be served as novel therapeutic targets in CRC management.

Wafer-Scale Periodic Poling of Thin-Film Lithium Niobate.

Periodically poled lithium niobate on insulator (PPLNOI) offers an admirably promising platform for the advancement of nonlinear photonic integrated circuits (PICs). In this context, domain inversion engineering emerges as a key process to achieve efficient nonlinear conversion. However, periodic poling processing of thin-film lithium niobate has only been realized on the chip level, which significantly limits its applications in large-scale nonlinear photonic systems that necessitate the integration of multiple nonlinear components on a single chip with uniform performances. Here, we demonstrate a wafer-scale periodic poling technique on a 4-inch LNOI wafer with high fidelity. The reversal lengths span from 0.5 to 10.17 mm, encompassing an area of ~1 cm2 with periods ranging from 4.38 to 5.51 µm. Efficient poling was achieved with a single manipulation, benefiting from the targeted grouped electrode pads and adaptable comb line widths in our experiment. As a result, domain inversion is ultimately implemented across the entire wafer with a 100% success rate and 98% high-quality rate on average, showcasing high throughput and stability, which is fundamentally scalable and highly cost-effective in contrast to traditional size-restricted chiplet-level poling. Our study holds significant promise to dramatically promote ultra-high performance to a broad spectrum of applications, including optical communications, photonic neural networks, and quantum photonics.

Evaluation of the Growth, Sporulation, Fungicide Efficacy, and Host Range of Ramularia sphaeroidea.

Ramularia sphaeroidea was primarily identified based on the characteristics of its conidia and several sequences. The fungus causes severe leaf spot disease on hairy vetch (Vicia villosa var. glabrescens) in Yunnan Province in China. The growth, sporulation, fungicide efficacy, and host range of the pathogen were evaluated to aid in disease management. Different types of culture media and carbon and nitrogen sources were used to evaluate the growth of R. sphaeroidea. Oatmeal, maltose, and potassium nitrate agar had a higher amount of sporulation. Difenoconazole (10%) was the most effective fungicide against the leaf disease caused by R. sphaeroidea. In addition, foliar inoculation sprays were used to assess the host range of R. sphaeroidea in six different plant species, including alfalfa (Medicago sativa L.), sainfoin (Onobrychis viciifolia Scop.), erect milkvetch (Astragalus adsurgens Pall.), common vetch (Vicia sativa L.), red clover (Trifolium pratense L.), and white clover (Trifolium repens L.). R. sphaeroidea successfully infected these plants, indicating that it has a wider host range than hairy vetches.

Cellular iron depletion enhances behavioral rhythm by limiting brain Per1 expression in mice.

AIMS: Disturbances in the circadian rhythm are positively correlated with the processes of aging and related neurodegenerative diseases, which are also associated with brain iron accumulation. However, the role of brain iron in regulating the biological rhythm is poorly understood. In this study, we investigated the impact of brain iron levels on the spontaneous locomotor activity of mice with altered brain iron levels and further explored the potential mechanisms governing these effects in vitro. RESULTS: Our results revealed that conditional knockout of ferroportin 1 (Fpn1) in cerebral microvascular endothelial cells led to brain iron deficiency, subsequently resulting in enhanced locomotor activity and increased expression of clock genes, including the circadian locomotor output cycles kaput protein (Clock) and brain and muscle ARNT-like 1 (Bmal1). Concomitantly, the levels of period circadian regulator 1 (PER1), which functions as a transcriptional repressor in regulating biological rhythm, were decreased. Conversely, the elevated brain iron levels in APP/PS1 mice inhibited autonomous rhythmic activity. Additionally, our findings demonstrate a significant decrease in serum melatonin levels in Fpn1cdh5 -CKO mice compared with the Fpn1flox/flox group. In contrast, APP/PS1 mice with brain iron deposition exhibited higher serum melatonin levels than the WT group. Furthermore, in the human glioma cell line, U251, we observed reduced PER1 expression upon iron limitation by deferoxamine (DFO; iron chelator) or endogenous overexpression of FPN1. When U251 cells were made iron-replete by supplementation with ferric ammonium citrate (FAC) or increased iron import through transferrin receptor 1 (TfR1) overexpression, PER1 protein levels were increased. Additionally, we obtained similar results to U251 cells in mouse cerebellar astrocytes (MA-c), where we collected cells at different time points to investigate the rhythmic expression of core clock genes and the impact of DFO or FAC treatment on PER1 protein levels. CONCLUSION: These findings collectively suggest that altered iron levels influence the circadian rhythm by regulating PER1 expression and thereby modulating the molecular circadian clock. In conclusion, our study identifies the regulation of brain iron levels as a potential new target for treating age-related disruptions in the circadian rhythm.

Rational design of a polypropylene composite foam with open-cell structure via graphite conductive network for sound absorption.

An exciting result is reported in this study where a polypropylene (PP) foam with a high open-cell content was achieved by constructing a thermally conductive network for the first time. PP and nano-graphite particles were used as substrate and filler, respectively, to prepare the PP-graphite (PP-G) composite foam by twin-screw blending, hot pressing, and supercritical CO2 foaming. The nano-graphite particles can effectively adjust the microstructure of the PP-G foam and achieve a high porosity. When the amount of nano-graphite is 10.0 wt%, the PP-G foam exhibits optimal sound absorption performance, compression resistance, heat insulation, and hydrophobic properties. In the human-sensitive frequency range of 1000-6000 Hz, the corresponding average SAC is above 0.9, and the internal tortuosity is 5.27. After 50 cycles of compression, the compressive stress is 980 kPa and the SAC loss is only 7.8%. This study also innovatively proposed a new strategy to achieve the simple and rapid preparation of open-cell PP foams by increasing the thermal conductivity of the foaming substrate.

Transmembrane serine protease 6, a novel target for inhibition of neuronal tumor growth.

Transmembrane serine protease 6 (Tmprss6) has been correlated with the occurrence and progression of tumors, but any specific molecular mechanism linking the enzyme to oncogenesis has remained elusive thus far. In the present study, we found that Tmprss6 markedly inhibited mouse neuroblastoma N2a (neuro-2a) cell proliferation and tumor growth in nude mice. Tmprss6 inhibits Smad1/5/8 phosphorylation by cleaving the bone morphogenetic protein (BMP) co-receptor, hemojuvelin (HJV). Ordinarily, phosphorylated Smad1/5/8 binds to Smad4 for nuclear translocation, which stimulates the expression of hepcidin, ultimately decreasing the export of iron through ferroportin 1 (FPN1). The decrease in cellular iron levels in neuro-2a cells with elevated Tmprss6 expression limited the availability of the metal forribo nucleotide reductase activity, thereby arresting the cell cycle prior to S phase. Interestingly, Smad4 promoted nuclear translocation of activating transcription factor 3 (ATF3) to activate the p38 mitogen-activated protein kinases signaling pathway by binding to ATF3, inducing apoptosis of neuro-2a cells and inhibiting tumor growth. Disruption of ATF3 expression significantly decreased apoptosis in Tmprss6 overexpressed neuro-2a cells. Our study describes a mechanism whereby Tmprss6 regulates the cell cycle and apoptosis. Thus, we propose Tmprss6 as a candidate target for inhibiting neuronal tumor growth.

Engineering a Z-Scheme Heterostructure on ZnIn2S4@NH2-MIL-125 Composites for Boosting the Photocatalytic Performance.

Constructing a Z-scheme heterostructure on a metal-organic framework (MOF) composite with an explicit charge transfer mechanism at the interface is considered to be an effective strategy for improving the photocatalytic performance of MOFs. Herein, an internal electric field (IEF)-induced Z-scheme heterostructure on the ZnIn2S4@NH2-MIL-125 composite is designed and fabricated by a facile electrostatic self-assembly process. Systematic investigations reveal that close interfacial contact and difference in work function between NH2-MIL-125 and ZnIn2S4 enable the formation of the IEF, which drives the Z-scheme charge transfer as revealed by the in situ irradiated X-ray photoelectron spectroscopy (ISI-XPS), photoirradiated Kelvin probe force microscope (KPFM) measurement, electron paramagnetic resonance (EPR) radical trapping experiment, as well as density functional theory (DFT) calculation; meanwhile, directions of the interfacial IEFs are determined. Benefiting from the unique merit of IEF-induced Z-scheme charge transfer, the optimized ZnIn2S4@NH2-MIL-125 composite exhibits significantly enhanced photocatalytic activity for the photoreduction of 4-nitroaniline (4-NA) to p-phenylenediamine (PPD) under visible light irradiation. This work not only provides in-depth insights for charge transfer in the IEF-induced Z scheme heterostructure but also affords useful inspirations on designing the Z-scheme MOF composite to boost the photocatalytic performance.

Hepcidin deficiency impairs hippocampal neurogenesis and mediates brain atrophy and memory decline in mice.

BACKGROUND: Hepcidin is the master regulator of iron homeostasis. Hepcidin downregulation has been demonstrated in the brains of Alzheimer's disease (AD) patients. However, the mechanism underlying the role of hepcidin downregulation in cognitive impairment has not been elucidated. METHODS: In the present study, we generated GFAP-Cre-mediated hepcidin conditional knockout mice (HampGFAP cKO) to explore the effect of hepcidin deficiency on hippocampal structure and neurocognition. RESULTS: We found that the HampGFAP cKO mice developed AD-like brain atrophy and memory deficits. In particular, the weight of the hippocampus and the number of granule neurons in the dentate gyrus were significantly reduced. Further investigation demonstrated that the morphological change in the hippocampus of HampGFAP cKO mice was attributed to impaired neurogenesis caused by decreased proliferation of neural stem cells. Regarding the molecular mechanism, increased iron content after depletion of hepcidin followed by an elevated level of the inflammatory factor tumor necrosis factor-α accounted for the impairment of hippocampal neurogenesis in HampGFAP cKO mice. These observations were further verified in GFAP promoter-driven hepcidin knockdown mice and in Nestin-Cre-mediated hepcidin conditional knockout mice. CONCLUSIONS: The present findings demonstrated a critical role for hepcidin in hippocampal neurogenesis and validated the importance of iron and associated inflammatory cytokines as key modulators of neurodevelopment, providing insights into the potential pathogenesis of cognitive dysfunction and related treatments.

A novel detection method for wheat aging based on the delayed luminescence.

Wheat aging plays an important role in assessing storage wheat quality and its subsequent processing purposes. The conventional detection methods for wheat aging are mainly involved in chemical techniques, which are time-consuming as well as waste part of wheat samples for each detection. Although some physical detection methods have obtained gratifying results, it is extremely hard to expand their application fields but to stay in the theory stage. For this reason, a novel nondestructive detection model for wheat aging based on the delayed luminescence (DL) has been proposed in this paper. Specifically, after collecting enough sample data, we first took advantage of certain hyperbolic function to fit DL signal, and then used four parameters of the hyperbolic function to feature the decay trend of the DL signal. Secondly, in order to better feature the DL signal, we extracted other six features together with above four features to form the input feature vector. Finally, as the bidirectional long short-term memory (Bi-LSTM) network lacked error-correcting performance, the Bi-LSTM network based on Walsh coding (Walsh-Bi-LSTM) mechanism was proposed to establish the detection model, which made the detection model have the error-correcting performance by reasonably splitting the multi-classification target task. Shown by experimental results, the newly proposed wheat aging detection model is able to achieve 94.00% accuracy in the testing dataset, which can be used as a green and nondestructive method to timely reflect wheat aging states.

Germination and Invasion of Paraphoma radicina on Roots of a Susceptible and a Resistant Alfalfa Cultivar (Medicago sativa).

Alfalfa Paraphoma root rot (APRR) (Paraphoma radicina) is a recently described alfalfa disease widely distributed in China, first reported in 2020. So far, the resistance levels of 30 alfalfa cultivars to APRR have been characterized; however, the resistance mechanisms among these cultivars remain unknown. In the present study, the alfalfa resistance mechanisms against APRR were investigated by studying the difference of P. radicina infecting susceptible (Gibraltar) and resistant (Magnum II) alfalfa cultivars under the light microscope and scanning electronic microscope. The conidial germination and germ tube growth in the root exudates of different resistant cultivars were also compared. The results revealed that conidial germination, germ tube development, and P. radicina penetration into root tissues of resistant plants were delayed. In susceptible and resistant cultivars, P. radicina infected roots by penetrating epidermal cells and the intercellular space between epidermal cells. During the infection process, germ tubes penetrated the root surface directly or formed appressoria. However, the penetration percentage on the susceptible cultivar was significantly higher than on the resistant cultivar, irrespective of the infection route. Moreover, disintegrated conidia and germ tubes were observed on resistant cultivar roots at 48 h postinoculation. The conidial germination and germ tube growth in root exudates of susceptible cultivars were significantly higher than in resistant cultivars. The current findings implied that the alfalfa resistance mechanism might be related to root exudates. These findings could provide insights into the alfalfa resistance mechanism following P. radicina infection.

Iron overload suppresses hippocampal neurogenesis in adult mice: Implication for iron dysregulation-linked neurological diseases.

AIMS: Adult hippocampal neurogenesis is an important player in brain homeostasis and its impairment participates in neurological diseases. Iron overload has emerged as an irreversible factor of brain aging, and is also closely related to degenerative disorders, including cognitive dysfunction. However, whether brain iron overload alters hippocampal neurogenesis has not been reported. We investigated the effect of elevated iron content on adult hippocampal neurogenesis and explored the underlying mechanism. METHODS: Mouse models with hippocampal iron overload were generated. Neurogenesis in hippocampus and expression levels of related molecules were assessed. RESULTS: Iron accumulation in hippocampus remarkably impaired the differentiation of neural stem cells, resulting in a significant decrease in newborn neurons. The damage was possibly attributed to iron-induced downregulation of proprotein convertase furin and subsequently decreased maturation of brain-derived neurotrophic factor (BDNF), thus contributing to memory decline and anxiety-like behavior of mice. Supportively, knockdown of furin indeed suppressed hippocampal neurogenesis, while furin overexpression restored the impairment. CONCLUSION: These findings demonstrated that iron overload damaged hippocampal neurogenesis likely via iron-furin-BDNF pathway. This study provides new insights into potential mechanisms on iron-induced neurotoxicity and the causes of neurogenesis injury and renders modulating iron homeostasis and furin expression as novel therapeutic strategies for treatment of neurological diseases.

Sculpting Mesoscopic Helical Chirality into Covalent Organic Framework Nanotubes from Entirely Achiral Building Blocks.

The diversification of chirality in covalent organic frameworks (COFs) holds immense promise for expanding their properties and functionality. Herein, we introduce an innovative approach for imparting helical chirality to COFs and fabricating a family of chiral COF nanotubes with mesoscopic helicity from entirely achiral building blocks for the first time. We present an effective 2,3-diaminopyridine-mediated supramolecular templating method, which facilitates the prefabrication of helical imine-linked polymer nanotubes using unprecedented achiral symmetric monomers. Through meticulous optimization of crystallization conditions, these helical polymer nanotubes are adeptly converted into imine-linked COF nanotubes boasting impressive surface areas, while well preserving their helical morphology and chiroptical properties. Furthermore, these helical imine-linked polymers or COFs could be subtly transformed into corresponding more stable and functional helical ß-ketoenamine-linked and hydrazone-linked COF nanotubes with transferred circular dichroism via monomer exchange. Notably, despite the involvement of covalent bonding breakage and reorganization, these exchange processes overcome thermodynamic disadvantages, allowing mesoscopic helical chirality to be perfectly preserved. This research highlights the potential of mesoscopic helicity in conferring COFs with favourable chiral properties, providing novel insights into the development of multifunctional COFs in the field of chiral materials chemistry.

Konjac Mannan Oligosaccharides enhanced intestinal barrier function to improve alcoholic nervous injury / 中国药理学通报

Aim Excessive cerebral inflammation caused by chronic alcohol intake is an important risk factor for central nervous system injury. The purpose of this study was to explore the protective effect of konjac mannan oligosaccharide (KMOS) on central nervous system inflammation in alcohol-fed mice and its mechanism. Methods The chronic alcohol fed model of C57BL/6J mice was established using Gao-binge method. And the different doses of KMOS were gavaged every day for 6 weeks. The neuronal damage and microglia activation were evaluated in cerebral cortex and hippocampus. The damage of colon tissue was assessed and serum LPS concentrations were measured. In vitro, Caco-2 cells were stimulated with LPS to establish intestinal mucosal injury model. Results Chronic alcohol intake can cause brain neuron damage in mice, and different doses of KMOS effectively reduced the activation state of microglia, decreased the expression of inflammatory factors caused by the activation of the NLRP3 inflammasome and alleviated neuronal damage in the brain tissue of alcohol-fed mice. The results of colon tissue analysis showed that the use of KMOS effectively reduced the concentration of endotoxin LPS in serum of alcohol-fed mice, alleviated the pathological injury and inflammatory response of colon tissue, and enhanced the expression of Occludin in intestinal tissue. In vitro experiments also showed that KMOS significantly inhibited the inflammatory reaction of Caco-2 cells exposed to alcohol and increased the expression of Occludin protein. Conclusions KMOS treatment effectively inhibited intestinal inflammation caused by alcohol intake, repaired intestinal barrier to prevent the entry of intestinal LPS into brain tissue, decreased the activation of microglia, and then improved brain neuron damage. KMOS had the potential to prevent alcoholic nerve injury.

Regulating PI3K/Akt Signaling Pathway by Traditional Chinese Medicine to Improve Cognitive Impairment： A Review / 中国实验方剂学杂志

Cognitive impairment refers to the abnormality of the hippocampus， cortex and other parts of the brain， which is manifested by the decline of cognitive abilities such as learning， memory and attention. With the increase in people's work pressure and bad living habits， the incidence of cognitive impairment is getting higher and higher， which seriously affects people's normal life. However， there are adverse reactions such as gastrointestinal reactions and extrapyramidal reactions in Western drug treatment for cognitive impairment. Therefore， the development of a drug with relatively minimal adverse reactions is of great significance. Traditional Chinese medicine （TCM） has the characteristics of "multi-component， multi-pathway and multi-target"， and the incidence of adverse reactions is relatively low. Studies have shown that the pathogenesis of cognitive impairment is closely related to oxidative stress， inflammation， apoptosis， autophagy and other processes of neurons in the cerebral cortex and hippocampus. Phosphatidylinositol 3-kinase （PI3K）-protein kinase B （Akt） signal pathway plays an important role in the transmission of intracellular and intracellular signals， and in the regulation of cellular inflammation， apoptosis， autophagy， etc. TCM monomers， TCM extracts， and TCM compounds exert anti-inflammatory， antioxidant， anti-apoptotic and autophagy regulation effects by regulating the PI3K/Akt signaling pathway to improve cognitive impairment. This review first summarized the composition and regulatory process of the PI3K/Akt signaling pathway， and then discussed the research progress on the improvement of cognitive impairment through the improvement of oxidative stress， inflammation， apoptosis and autophagy of neurons. Finally， the recent research status of the regulation of this signaling pathway by TCM extracts， TCM monomers and TCM compounds to improve cognitive impairment was summarized. This study provides a theoretical basis for the future study of new TCM related to cognitive impairment.

Brain Iron Homeostasis and Mental Disorders.

Iron plays an essential role in various physiological processes. A disruption in iron homeostasis can lead to severe consequences, including impaired neurodevelopment, neurodegenerative disorders, stroke, and cancer. Interestingly, the link between mental health disorders and iron homeostasis has not received significant attention. Therefore, our understanding of iron metabolism in the context of psychological diseases is incomplete. In this review, we aim to discuss the pathologies and potential mechanisms that relate to iron homeostasis in associated mental disorders. We propose the hypothesis that maintaining brain iron homeostasis can support neuronal physiological functions by impacting key enzymatic activities during neurotransmission, redox balance, and myelination. In conclusion, our review highlights the importance of investigating the relationship between trace element nutrition and the pathological process of mental disorders, focusing on iron. This nutritional perspective can offer valuable insights for the clinical treatment of mental disorders.

Iron Metabolism, Redox Balance and Neurological Diseases.

Iron is essential for life, and the dysregulation of iron homeostasis can lead to severe pathological changes in the neurological system [...].

Ferroptosis-related factors in the substantia nigra are associated with Parkinson's disease.

Ferroptosis is an iron-dependent, lipid peroxidation-driven cell death pathway, while Parkinson's disease (PD) patients exhibit iron deposition and lipid peroxidation in the brain. Thus, the features of ferroptosis highly overlap with the pathophysiological features of PD. Despite this superficial connection, the possible role(s) of ferroptosis-related (Fr) proteins in dopaminergic neurons and/or glial cells in the substantia nigra (SN) in PD have not been examined in depth. To explore the correlations between the different SN cell types and ferroptosis at the single-cell level in PD patients, and to explore genes that may affect the sensitivity of dopaminergic neurons to ferroptosis, we performed in silico analysis of a single cell RNA sequence (RNA-seq) set (GSE178265) from the Gene Expression Omnibus (GEO) database. We identified differentially expressed genes (DEGs) in the different cell types in the human SN, and proceeded to perform enrichment analysis, constructing a protein-protein interaction network from the DEGs of dopaminergic neurons with the Metascape database. We examined the intersection of Fr genes present in the FerrDb database with DEGs from the GSE178265 set to identify Fr-DEGs in the different brain cells. Further, we identified Fr-DEGs encoding secreted proteins to implicate cell-cell interactions in the potential stimulation of ferroptosis in PD. The Fr-DEGs we identified were verified using the bulk RNA-seq sets (GSE49036 and GSE20164). The number of dopaminergic neurons decreased in the SN of PD patients. Interestingly, non-dopaminergic neurons possessed the fewest DEGs. Enrichment analysis of dopaminergic neurons' DEGs revealed changes in transmission across chemical synapses and ATP metabolic process in PD. The secreted Fr-DEGs identified were ceruloplasmin (CP), high mobility group box 1 (HMGB1) and transferrin (TF). The bulk RNA-seq set from the GEO database demonstrates that CP expression is increased in the PD brain. In conclusion, our results identify CP as a potential therapeutic target to protect dopaminergic neurons by reducing neurons' sensitivity to ferroptosis.

Investigation and analysis of porcine epidemic diarrhea cases and evaluation of different immunization strategies in the large-scale swine farming system.

BACKGROUND: Porcine epidemic diarrhea (PED) is a contagious intestinal disease caused by porcine epidemic diarrhea virus (PEDV) characterized by vomiting, diarrhea, anorexia, and dehydration, which has caused huge economic losses around the world. However, it is very hard to find completely valid approaches to control the transmission of PEDV. At present, vaccine immunity remains the most effective method. To better control the spread of PED and evaluate the validity of different immunization strategies, 240 PED outbreak cases from 577 swine breeding farms were collected and analyzed. The objective of the present study was to analyze the epidemic regularity of PEDV and evaluate two kinds of different immunization strategies for controlling PED. RESULTS: The results showed that the main reasons which led to the outbreak of PED were the movement of pig herds between different pig farms (41.7%) and delaying piglets from the normal production flow (15.8%). The prevalence of PEDV in the hot season (May to October) was obviously higher than that in the cold season (January to April, November to December). Results of different vaccine immunity cases showed that immunization with the highly virulent live vaccine (NH-TA2020 strain) and the commercial inactivated vaccine could significantly decrease the frequency of swine breeding farms (5.9%), the duration of PED epidemic (1.70 weeks), and the week batches of dead piglets (0.48 weeks weaned piglets), compared with immunization with commercial attenuated vaccines and inactivated vaccine of PED. Meanwhile, immunization with the highly virulent live vaccine and the commercial inactivated vaccine could bring us more cash flows of Y̶275,274 per year than immunization with commercial live attenuated vaccine and inactivated vaccine in one 3000 sow pig farm within one year. CONCLUSION: Therefore, immunization with highly virulent live vaccine and inactivated vaccine of PED is more effective and economical in the prevention and control of PED in the large-scale swine farming system.

Alternaria gansuense, a Plant Systematic Fungal Pathogen Producing Swainsonine in Vivo and in Vitro.

Astragalus adsurgens (A. adsurgens), which is considered a forage in China, grows widely in Eurasia and North America. However, Alternaria gansuense (A. gansuense) (synonym: Embellisia astragali) systematically infects A. adsurgens, producing swainsonine (SW), which poisons domesticated animals. In this study, we hypothesized that the A. gansuense SW-producing fungus is morphologically and molecularly related to the locoweed endophyte, Alternaria oxytropis (A. oxytropis), which systematically grows in host plants. Therefore, pure cultures of the fungi from diseased plants or endophytic interactions were collected from fields and assayed for SW via high-performance liquid chromatography linked to mass spectroscopy (HPLC-MS). The production of SW was also detected in A. adsurgens, A. oxytropis and diseased plants by assaying for the presence of the ß-ketoacyl synthase (KS) gene, which is required for SW synthesis. Diseased A. adsurgens and pure cultures of A. gansuense have SW and the healthy-looking A. adsurgens plants also contained SW, probably because they were infected with A. gansuense. Therefore, A. adsurgens-infected A. gansuense are not safe for livestock consumption.

Brain Iron Metabolism, Redox Balance and Neurological Diseases.

The incidence of neurological diseases, such as Parkinson's disease, Alzheimer's disease and stroke, is increasing. An increasing number of studies have correlated these diseases with brain iron overload and the resulting oxidative damage. Brain iron deficiency has also been closely linked to neurodevelopment. These neurological disorders seriously affect the physical and mental health of patients and bring heavy economic burdens to families and society. Therefore, it is important to maintain brain iron homeostasis and to understand the mechanism of brain iron disorders affecting reactive oxygen species (ROS) balance, resulting in neural damage, cell death and, ultimately, leading to the development of disease. Evidence has shown that many therapies targeting brain iron and ROS imbalances have good preventive and therapeutic effects on neurological diseases. This review highlights the molecular mechanisms, pathogenesis and treatment strategies of brain iron metabolism disorders in neurological diseases.