Kawasaki disease coronary artery lesions prediction with monocyte-to-high-density lipoprotein ratio.

OBJECTIVE: The aim of this study was to evaluate the predictive value of the monocyte-to-high-density lipoprotein ratio (MHR) in Kawasaki disease (KD) complicated with coronary artery lesions (CALs) and to construct a nomogram prediction model. METHODS: The medical records of KD inpatients diagnosed in the Department of Pediatrics of Lanzhou University Second Hospital from May 2015 to September 2021 were retrospectively analyzed. ROC curves were applied to evaluate the predictive value of MHR in KD complicated with CALs, and logistic regression analysis was used to screen independent risk factors. We constructed a nomogram model and performed internal validation. RESULTS: A total of 568 KD patients were enrolled in the study. MHR was significantly higher in KD patients complicated with CALs and was identified as an independent risk factor for CALs (OR: 1.604, 95% CI: 1.292-1.990). The area under the ROC curve for MHR in predicting CALs was 0.661. The C-index of the nomogram model constructed by incorporating MHR was 0.725 (95% CI: 0.682-0.768), and the calibration curve revealed good agreement between the predicted and actual probabilities. CONCLUSIONS: MHR may not be suitable as a single biomarker to predict the occurrence of CALs, but the nomogram model constructed in combination with other independent risk factors had acceptable predictive performance. IMPACT: The inflammatory response plays an important role in the pathogenesis of Kawasaki disease. The monocyte-to-high-density lipoprotein ratio is a novel systemic inflammation marker. The monocyte-to-high-density lipoprotein ratio is an independent risk factor for Kawasaki disease complicated with coronary artery lesions. The nomogram established by incorporating the monocyte-to-high-density lipoprotein ratio has satisfactory predictive performance for coronary artery lesion formation.

Opsoclonus-myoclonus syndrome associated with neuroblastoma: Insights into antitumor immunity.

Opsoclonus-myoclonus syndrome (OMS) is a rare neurological disorder. Half of these cases occur in children with neuroblastoma. Neuroblastoma patients with OMS usually have better oncological outcomes than those without OMS even after stratification by tumor stage and age, indicating that factors mediating OMS may also inhibit tumor cell proliferation. Although the mechanisms underlying OMS remain undefined, the cytokines and lymphocytes alterations in the cerebrospinal fluid support the concept that it is a pattern of neuroinflammation due to an autoimmune effect. The presence of lymphoid follicles consisting of follicular dendritic cells, CD20+ B lymphocytes, CD3+ T lymphocytes, and CD68+ macrophages in the tumor microenvironment in OMS-associated neuroblastoma support the autoimmune nature of this disorder. This review focuses on the clinical and genetic features of OMS-associated neuroblastoma, and we update readers on immune features of neuroblastoma with or without OMS to gain insights into antitumor immunity as it relates to tumor biology and prognosis.

miRNA-146a-5p mitigates stress-induced premature senescence of D-galactose-induced primary thymic stromal cells.

Senescent thymic stromal cells (TSCs) producing senescence-associated secretory phenotype (SASP) may play a role at later phases of thymic involution. However, the etiology and mechanisms responsible for TSC senescence remain to be elucidated. In the present study, the effects of oxidative stress on TSCs and role of miRNA-146a-5p in stress-induced premature senescence (SIPS) were identified. D-galactose (D-gal) induced oxidative stress in primary TSCs and a limited cumulative oxidative stress induced premature senescence but not apoptosis of TSCs. miRNA-146a-5p overexpression can mitigate the SIPS by targeting tumor necrosis factor receptor-associated factor 6 (TRAF6) instead of increasing autophagy clearance. Furthermore, exogenous miRNA-146a-5p reversed the upregulation of chemokines including Cxcl5, pro-inflammatory cytokines, and antimicrobial peptides in TSCs with SIPS. In conclusion, the accumulated oxidative stress may be partially responsible for senescence in TSCs and modulation of miRNA-146a-5p may attenuate this process.

Roles of metabolic regulation in developing Quercus variabilis acorns at contrasting geologically-derived phosphorus sites in subtropical China.

BACKGROUND: Phosphorus (P) -rich soils develop in phosphorite residing areas while P-deficient soils are ubiquitous in subtropical regions. Little has been reported that how metabolites participate in the seed development and the processes involved in their coping with contrasting-nutrient environments. RESULTS: Here we quantified the metabolites of Quercus variabilis acorns in the early (July), middle (August), late (September) development stages, and determined element (C, H, O, N, P, K, Ca, Mg, S, Fe, Al, Mn, Na, Zn, and Cu) concentrations of acorns in the late stage, at geologically-derived contrasting-P sites in subtropical China. The primary metabolic pathways included sugar metabolism, the TCA cycle, and amino acid metabolism. Most metabolites (especially C- and N-containing metabolites) increased and then decreased from July to September. Acorns between the two sites were significantly discriminated at the three stages, respectively, by metabolites (predominantly sugars and organic acids). Concentrations of P, orthophosphoric acid and most sugars were higher; erythrose was lower in late-stage acorns at P-rich sites than those at P-deficient sites. No significant differences existed in the size and dry mass of individual acorns between oak populations at the two sites. CONCLUSIONS: Oak acorns at the two sites formed distinct metabolic phenotypes related to their distinct geologically-derived soil conditions, and the late-stage acorns tended to increase P-use-efficiency in the material synthesis process at P-deficient sites, relative to those at P-rich sites.

Multiscale Time-Sharing Elastography Algorithms and Transfer Learning of Clinicopathological Features of Uterine Cervical Cancer for Medical Intelligent Computing System.

Intelligent medical diagnosis and computing system faces many challenges in complex object recognition, large-scale data imaging and real-time diagnosis, such as poor real-time computing, low efficiency of data storage and low recognition rate of lesions. In order to solve the above problems, this paper proposes a medical intelligent computing system and a series of algorithms for the clinical pathology of cervical cancer based on the multi-scale imaging and transfer learning framework. Firstly, based on data dimensions, imaging errors and other factors, this paper designs a multi-scale time-sharing elastic imaging algorithm based on image reconstruction time and data sample characteristics. Then, taking the burst imaging cohort and the calculation data set of new cervical cancer cases as the objects, based on the difficulties of cervical cancer feature modeling, this paper proposes the transfer learning algorithm of clinical and pathological features of cervical cancer. Finally, a medical intelligent computing system for cervical cancer pathology analysis and calculation with high efficiency and reliability is established. A series of proposed algorithms are compared with single-scale Retinex (SSR), which is based on single-scale Retinex migration learning (SSR-TL). The experimental results show that the proposed algorithm in cervical cancer pathological imaging and scoring, as well as the feature extraction and recognition of lesions, especially the efficiency of system execution, is obviously due to the comparison algorithm.

Screening the expression characteristics of several miRNAs in G93A-SOD1 transgenic mouse: altered expression of miRNA-124 is associated with astrocyte differentiation by targeting Sox2 and Sox9.

MicroRNAs (miRNAs) are suspected to be a contributing factor in amyotrophic lateral sclerosis (ALS). Here, we assess the altered expression of miRNAs and the effects of miR-124 in astrocytic differentiation in neural stem cells of ALS transgenic mice. Differentially expressed miRNA-positive cells (including miR-124, miR-181a, miR-22, miR-26b, miR-34a, miR-146a, miR-219, miR-21, miR-200a, and miR-320) were detected by in situ hybridization and qRT-PCR in the spinal cord and the brainstem. Our results demonstrated that miR-124 was down-regulated in the spinal cord and brainstem. In vitro, miR-124 was down-regulated in neural stem cells and up-regulated in differentiated neural stem cells in G93A-superoxide dismutase 1 (SOD1) mice compared with WT mice by qRT-PCR. Meanwhile, Sox2 and Sox9 protein levels showed converse change with miR-124 in vivo and vitro. After over-expression or knockdown of miR-124 in motor neuron-like hybrid (NSC34) cells of mouse, Sox2 and Sox9 proteins were noticeably down-regulated or up-regulated, whereas Sox2 and Sox9 mRNAs remained virtually unchanged. Moreover, immunofluorescence results indicated that the number of double-positive cells of Sox2/glial fibrillary acidic protein (GFAP) and Sox9/glial fibrillary acidic protein (GFAP) was higher in G93A-SOD1 mice compared with WT mice. We also found that many Sox2- and Sox9-positive cells were nestin positive in G93A-SOD1 mice, but not in WT mice. Furthermore, differentiated neural stem cells from G93A-SOD1 mice generated a greater proportion of astrocytes and lower proportion of neurons than those from WT mice. MiR-124 may play an important role in astrocytic differentiation by targeting Sox2 and Sox9 in ALS transgenic mice. Cover Image for this issue: doi: 10.1111/jnc.14171.

Narrative review: precision medicine applications in neuroblastoma-current status and future prospects.

Background and Objective: Neuroblastoma (NB) is a common malignant tumor in children, and its treatment remains challenging. Precision medicine, as an individualized treatment strategy, aims to improve efficacy and reduce toxicity by combining unique patient- and tumor-related factors, bringing new hope for NB treatment. In this article, we review the evidence related to precision medicine in NB, with a focus on potential clinically actionable targets and a series of targeted drugs associated with NB. Methods: We conducted an extensive search in PubMed, EMBASE, and Web of Science using key terms and database-specific strategies, filtered for time and language, to ensure a comprehensive collection of literature related to precision medicine in NB. The main search terms consisted of "neuroblastoma", "precision medicine", "pediatrics", and "targeting". The articles included in this study encompass those published from 1985 to the present, without restrictions on the type of articles. Key Content and Findings: ALK inhibitors and MYCN inhibitors have been developed to interfere with tumor cell growth and dissemination, thereby improving treatment outcomes. Additionally, systematic testing to identify relevant driver mutations is crucial and can be used for diagnosis and prognostic assessment through the detection of many associated molecular markers. Furthermore, liquid biopsy, a non-invasive tumor detection method, can complement tissue biopsy and play a role in NB by analyzing circulating tumor DNA and circulating tumor cells to provide genetic information and molecular characteristics of the tumor. Recently, trials conducted by many pediatric oncology groups have shown the urgent need for new approaches to cure relapsed and refractory patients. Conclusions: The purpose of this review is to summarize the latest advances in clinical treatment of NB, to better understand and focus on the development of promising treatment approaches, and to expedite the transition to the precision medicine clinical relevance in NB patients.

Digital economy development boosts urban resilience-evidence from China.

Focusing on the impact of the digital economy on urban resilience is beneficial to the sustainable development of cities. This paper empirically examines the impact of digital economic development on urban resilience and its mechanisms by measuring urban resilience and the level of urban digital economy with the entropy-weighted TOPSIS method using the data of 252 Chinese cities from 2011 to 2020. The findings show that digital economic development effectively promotes urban resilience at the 1% significance level, and this conclusion remains valid after a series of endogeneity and robustness tests. The channel mechanism suggests that the development of the digital economy can improve urban resilience by optimizing urban distributional effects and promoting the upgrading of urban industrial structures. This paper discusses the nonlinear relationship between the two using the MMQR model and the threshold model. The results show that urban resilience development level is in a higher quartile of cities, and digital economy development has a greater impact on urban resilience improvement. Meanwhile, there are two threshold values for the nonlinear impact of the digital economy on urban resilience, which are 0.026 and 0.082, respectively. Further, the spatial effect between the two is also verified. From the perspective of heterogeneity analysis, the digital economy development of high-class cities, key city clusters, and cities in eastern and western regions has a greater effect on urban resilience. This study can provide ideas and inspiration for countries to enhance urban resilience and promote sustainable urban development through the development of the digital economy.

Wnt Signaling is altered by spinal cord neuronal dysfunction in amyotrophic lateral sclerosis transgenic mice.

Amyotrophic lateral sclerosis (ALS) is a chronic neurodegenerative disease characterized by progressive degeneration of the motor neurons in the cortex, brainstem, and spinal cord. The etiology and mechanisms of selective motor neuron loss in ALS remain unknown. Wnt signaling is involved in neurodegenerative processes but little is known about the kinetic changes in Wnt signaling during ALS progression. In this study we used transcriptional microarray analysis to examine the expression of Wnt signaling components in the spinal cords of ALS transgenic SOD1(G93A) mice at different stages. We found that ALS onset led to the upregulation of Wnt signaling components and target genes involved in growth regulation and proliferation. We also determined the expression of Wnt inhibitory factor-1 (Wif1) and Wnt4 in the spinal cord of ALS transgenic mice at different stages by Western blot and immunofluorescence analysis. The protein levels of Wif1 and Wnt4 in the spinal cords of ALS transgenic mice were upregulated compared to those in wild-type mice. Moreover, the expression of Wif1 and Wnt4 in mature GFAP+ astrocytes was increased at the end stage of ALS. Our findings demonstrate that Wnt signaling is altered by spinal cord neuronal dysfunction in adult ALS transgenic mice, which provides new insight into ALS pathogenesis.

Micro-perspective of listed companies in China: Digital development promotes the green transformation of the manufacturing industry.

In the context of the rapid development of the global digital economy, it is of great significance to explore the greening transformation of the manufacturing industry from the micro-perspective of enterprise digital development. This paper empirically examines the impact and mechanism of enterprise digital development on the greening transformation of the manufacturing industry using the 2010-2020 data of Chinese A-share listed companies in the manufacturing industry as a sample. The study shows that enterprise digital development can significantly promote the greening transformation of China's manufacturing industry, and this conclusion still holds after a series of robustness tests. Technological innovation and financing constraints are important mediating mechanisms. Further research found that the impact of enterprise digital development on the greening transformation of China's manufacturing industry has a positive nonlinear effect, and its marginal effect shows a weakening trend. Heterogeneity analysis shows that, from the perspective of micro characteristics, digital development is more able to promote the green transformation of state-owned and large enterprises. From a macro-regional perspective, digital development can better promote the green transformation of the manufacturing industry in eastern cities, key city clusters, and high-level cities. The findings of this paper can provide corresponding insights for "revitalizing the manufacturing industry", and also provide decision-making references for countries aiming to make the manufacturing industry bigger and stronger.

A study on the changing trend and influencing factors of hospitalization costs of schizophrenia in economically underdeveloped areas of China.

The public health problems caused by schizophrenia are becoming increasingly prominent and can place a huge economic burden on society. This study takes Gansu Province as an example to analyze the level and changing trend of the economic burden of schizophrenia inpatients in economically underdeveloped areas of China. Using a multi-stage stratified cluster sampling method, 39,054 schizophrenics from 197 medical and health institutions in Gansu Province were selected as the research objects, and their medical expenses and related medical records were obtained from the medical information system. The rank sum test and Spearman rank correlation were used for univariate analysis. Quantile regression and random forest were used to analyze the influencing factors. The results show that the average length of stay of schizophrenics in Gansu Province of China was 52.01 days, and the average hospitalization cost was USD1653.96 from 2014 to 2019. During the six years, the average hospitalization costs per time decreased from USD2136.85 to USD1401.33. The average out-of-pocket costs per time decreased from USD1238.78 to USD267.68. And the average daily hospitalization costs increased from USD38.18 to USD41.25. The main factors influencing hospitalization costs are length of stay, proportion of medications, and schizophrenic subtype. The hospitalization costs per time of schizophrenics in Gansu Province have decreased but remain at a high level compared to some other chronic non-communicable diseases. In the future, attention should be paid to improving the efficiency of medical institutions, enhancing community management, and promoting the transformation of the management model of schizophrenia.

The Bidirectional Relationship between Chronic Kidney Disease and Hyperuricemia: Evidence from a Population-Based Prospective Cohort Study.

BACKGROUND: Although several studies have examined the association between chronic kidney disease (CKD) and hyperuricemia (HUA), the direction of the association remains unclear. We aimed to investigate whether there was a bidirectional association between them. METHODS: The present study was conducted in three analyses. Analysis I included 25,433 participants free of HUA at baseline to evaluate the associations between CKD and estimated glomerular filtration rate (eGFR) with incident HUA. Analysis II had 28,422 participants free of CKD at baseline to analyze the relationships between HUA and serum uric acid (sUA) with new-onset CKD. Cox proportional hazards regression models were applied to evaluate the association involved in Analysis I and II. Analysis III included 31,028 participants with complete data and further dissected the bidirectional association between sUA and eGFR using cross-lag models. RESULTS: New-onset HUA and CKD were observed in the first round of the follow-up study among 1597 and 1212 participants, respectively. A significantly higher risk of HUA was observed in individuals with CKD compared to individuals without CKD (HR = 1.58, 95% CI: 1.28-1.95). The adjusted HRs (95% CIs) of HUA were 3.56 (2.50-5.05) for the participants in the group of eGFR less than 60 mL·min-1·1.73 m-2, 1.61 (1.42-1.83) for those in the group of eGFR between 60 and 90 mL·min-1·1.73 m-2, and 1.74 (1.42-2.14) for those in the group of eGFR more than 120 mL·min-1·1.73 m-2, compared with the group of eGFR between 90 and 120 mL·min-1·1.73 m-2. A higher risk of CKD was also observed in individuals with HUA compared to individuals without HUA (HR = 1.28, 95% CI: 1.12-1.47). Compared with the first quintile of sUA, the adjusted HR (95% CI) of CKD was 1.24 (1.01-1.51) for the participants in the fourth quantile. There was a bidirectional relationship between sUA and eGFR, with the path coefficients (ρ1 = -0.024, p < 0.001) from baseline eGFR to follow-up sUA and the path coefficients (ρ2 = -0.015, p = 0.002) from baseline sUA to follow-up eGFR. CONCLUSIONS: The present study indicated that CKD and HUA were closely associated, and there was a bidirectional relationship between sUA and eGFR.

Induced Pluripotent Stem Cells and Their Applications in Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that results in the loss of motor function in the central nervous system (CNS) and ultimately death. The mechanisms underlying ALS pathogenesis have not yet been fully elucidated, and ALS cannot be treated effectively. Most studies have applied animal or single-gene intervention cell lines as ALS disease models, but they cannot accurately reflect the pathological characteristics of ALS. Induced pluripotent stem cells (iPSCs) can be reprogrammed from somatic cells, possessing the ability to self-renew and differentiate into a variety of cells. iPSCs can be obtained from ALS patients with different genotypes and phenotypes, and the genetic background of the donor cells remains unchanged during reprogramming. iPSCs can differentiate into neurons and glial cells related to ALS. Therefore, iPSCs provide an excellent method to evaluate the impact of diseases on ALS patients. Moreover, patient-derived iPSCs are obtained from their own somatic cells, avoiding ethical concerns and posing only a low risk of immune rejection. The iPSC technology creates new hope for ALS treatment. Here, we review recent studies on iPSCs and their applications in disease modeling, drug screening and cell therapy in ALS, with a particular focus on the potential for ALS treatment.

Activation of the Wnt/ß-catenin signaling pathway is associated with glial proliferation in the adult spinal cord of ALS transgenic mice.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the progressive and fatal loss of motor neurons. In ALS, there is a significant cell proliferation in response to neurodegeneration; however, the exact molecular mechanisms of cell proliferation and differentiation are unclear. The Wnt signaling pathway has been shown to be involved in neurodegenerative processes. Wnt3a, ß-catenin, and Cyclin D1 are three key signaling molecules of the Wnt/ß-catenin signaling pathway. We determined the expression of Wnt3a, ß-catenin, and Cyclin D1 in the adult spinal cord of SOD1(G93A) ALS transgenic mice at different stages by RT-PCR, Western blot, and immunofluorescence labeling techniques. We found that the mRNA and protein of Wnt3a and Cyclin D1 in the spinal cord of the ALS mice were upregulated compared to those in wild-type mice. In addition, ß-catenin translocated from the cell membrane to the nucleus and subsequently activated transcription of the target gene, Cyclin D1. BrdU and Cyclin D1 double-positive cells were increased in the spinal cord of these mice. Moreover, Wnt3a, ß-catenin, and Cyclin D1 were also expressed in both neurons and astrocytes. The expression of Wnt3a, ß-catenin or Cyclin D1 in mature GFAP(+) astrocytes increased. Moreover, BrdU/Cyclin D1/GFAP triple-positive cells were detected in the ALS mice. Our findings suggest that neurodegeneration activates the Wnt/ß-catenin signaling pathway, which is associated with glial proliferation in the adult spinal cord of ALS transgenic mice. This mechanism may be significant in clinical gene therapy.

Elevated cytokinin content in ipt transgenic creeping bentgrass promotes drought tolerance through regulating metabolite accumulation.

Increased endogenous plant cytokinin (CK) content through transformation with an adenine isopentyl transferase (ipt) gene has been associated with improved plant drought tolerance. The objective of this study is to determine metabolic changes associated with elevated CK production in ipt transgenic creeping bentgrass (Agrostis stolonifera L.) with improved drought tolerance. Null transformants (NTs) and plants transformed with ipt controlled by a stress- or senescence-activated promoter (SAG12-ipt) were exposed to well-watered conditions or drought stress by withholding irrigation in an environmental growth chamber. Physiological analysis confirmed that the SAG12-ipt line (S41) had improved drought tolerance compared with the NT plants. Specific metabolite changes over the course of drought stress and differential accumulation of metabolites in SAG12-ipt plants compared with NT plants at the same level of leaf relative water content (47% RWC) were identified using gas chromatography-mass spectroscopy. The metabolite profiling analysis detected 45 metabolites differentially accumulated in response to ipt expression or drought stress, which included amino acids, carbohydrates, organic acids, and organic alcohols. The enhanced drought tolerance of SAG12-ipt plants was associated with the maintenance of accumulation of several metabolites, particularly amino acids (proline, γ-aminobutyric acid, alanine, and glycine) carbohydrates (sucrose, fructose, maltose, and ribose), and organic acids that are mainly involved in the citric acid cycle. The accumulation of these metabolites could contribute to improved drought tolerance due to their roles in the stress response pathways such as stress signalling, osmotic adjustment, and respiration for energy production.

Anchoring NiO Nanosheet on the Surface of CNT to Enhance the Performance of a Li-O2 Battery.

Li2O2, as the cathodic discharge product of aprotic Li-O2 batteries, is difficult to electrochemically decompose. Transition-metal oxides (TMOs) have been proven to play a critical role in promoting the formation and decomposition of Li2O2. Herein, a NiO/CNT catalyst was prepared by anchoring a NiO nanosheet on the surface of CNT. When using the NiO/CNT as a cathode catalyst, the Li-O2 battery had a lower overpotential of 1.2 V and could operate 81 cycles with a limited specific capacity of 1000 mA h g-1 at a current density of 100 mA g-1. In comparison, with CNT as a cathodic catalyst, the battery could achieve an overpotential of 1.64 V and a cycling stability of 66 cycles. The introduction of NiO effectively accelerated the generation and decomposition rate of Li2O2, further improving the battery performance. SEM and XRD characterizations confirmed that a Li2O2 film formed during the discharge process and could be fully electrochemical decomposed in the charge process. The internal network and nanoporous structure of the NiO/CNT catalyst could provide more oxygen diffusion channels and accelerate the decomposition rate of Li2O2. These merits led to the Li-O2 battery's better performance.

High fat diet-induced obesity leads to depressive and anxiety-like behaviors in mice via AMPK/mTOR-mediated autophagy.

Depression is one of the most common mental illnesses in modern society. In recent years, several studies show that there are disturbances in lipid metabolism in depressed patients. High-fat diet may lead to anxiety and depression, but the mechanisms involved remain unclear. In our study, we found that 8 weeks of high-fat feeding effectively induced metabolic disorders, including obesity and hyperlipidemia in mice. Interestingly, the mice also showed depressive and anxiety-like behaviors. We further found activated microglia and astrocyte, increased neuroinflammation, decreased autophagy and BDNF levels in mice after high-fat feeding. Besides, high-fat feeding can also inhibit AMPK phosphorylation and induce mTOR phosphorylation. After treating with the mTOR inhibitor rapamycin, autophagy and BDNF levels were elevated. The number of activated microglia and astrocyte, and pro-inflammation levels were reduced. Besides, rapamycin can also reduce the body weight and serum lipid level in high fat feeding mice. Depressive and anxiety-like behaviors were also ameliorated to some extent after rapamycin treatment. In summary, these results suggest that high-fat diet-induced obesity may lead to depressive and anxiety-like behaviors in mice by inhibiting AMPK phosphorylation and promoting mTOR shift to phosphorylation to inhibit autophagy. Therefore, improving lipid metabolism or enhancing autophagy through the AMPK/mTOR pathway could be potential targets for the treatment of obesity depression.

Shufeng Jiedu capsule ameliorates olfactory dysfunction via the AMPK/mTOR autophagy pathway in a mouse model of allergic rhinitis.

BACKGROUND: Shufeng Jiedu capsule (SFJDC) has been widely used as a conventional Chinese pharmaceutical agent for various upper respiratory infections, including acute lung injury, acute respiratory distress syndrome and allergic rhinitis (AR). However, its mechanism in AR remains unclear. PURPOSE: The present study aimed to decipher the antiallergic inflammatory effect of SFJDC in an AR model with olfactory dysfunction. Specifically, we wanted to explore whether SFJDC can improve the olfactory abnormality in AR mice and reduce the levels of inflammatory factors in the olfactory epithelium (OE) and olfactory bulb (OB). METHODS: To address the above issues, we constructed an AR model using C57BL/6 mice, which were sensitised and challenged with ovalbumin (OVA) by intraperitoneal injection. SFJDC (0.045 or 0.18 g/kg) was delivered by gavage administration 1 h prior to the intraperitoneal injection of OVA. The control mice received saline alone. Then, the animals were assessed according to the presence of nasal symptoms and nasal inflammation, and a buried food test was used to evaluate olfactory function. The levels of proteins involved in the AMPK/mTOR autophagy pathway in the OE and OB were investigated by western blotting and fluorescence staining. RESULTS: After OVA induction of AR and drug administration, we found that SFJDC significantly ameliorated the nasal symptoms and allergic inflammatory reaction of the nasal mucosa superior to cetirizine. A behavioural test indicated that the mice with AR had olfactory dysfunction, and SFJDC can ameliorate this behavior deficiency. Meanwhile, SFJDC clearly reduced the neuroinflammation level in OE tissue. In addition, SFJDC increased p-mTOR and decreased p-AMPK, beclin1, LC3 and cleaved caspase-3 levels in the OE. CONCLUSIONS: In addition to antibacterial and antiviral activities, SFJDC has marked anti-inflammatory effects in AR mice. Its mechanism of action in the nasal cavity involves inhibition of upregulated anti-inflammatory cytokines, modulation of autophagy and apoptosis levels and regulation of autophagy through the AMPK/mTOR pathway in the OE tissue of AR mice. Hence, SFJDC is a promising drug for AR, and clinical trials should further validate the therapeutic impact of SFJDC on AR with olfactory dysfunction.

UV radiation-responsive proteins in rice leaves: a proteomic analysis.

Depletion of stratospheric ozone has led to increased UV radiation reaching the surface of the Earth. This may damage plants. Using physiological, proteomic and quantitative real-time PCR (qPCR) methods, we systematically studied the response of 16-day-old rice seedlings to UV [0.67 W m(-2) biologically effective UVB (UVB(BE)) and 0.28 W m(-2) UVA] exposure for 6, 12 and 24 h. UV exposure resulted in the appearance of light brown patches on leaves, a decrease in the net photosynthetic rate (Pn), lipid peroxidation, accumulation of UV-absorbing compounds (including flavonoids and other phenolic pigments) and differential expression of 22 proteins. Both physiological and molecular responses became stronger with increasing UV exposure time, indicating the effects of UV accumulation on plants. UV-induced responses included (i) phytohormone-regulative responses (up-regulation of proteins related to phytohormone synthesis such as IAA and ethylene); (ii) injurious responses (photosynthesis suppression, lipid peroxidation and visible injury); and (iii) protective responses (accumulation of UV-absorbing compounds and differential expression of proteins involved in detoxification/antioxidation, defense, protein processing, RNA processing, carbohydrate metabolism and secondary metabolism). The identification of UV-responsive proteins provided a better understanding of the molecular mechanism of plant responses to UV stress. Proteomic and qPCR analysis identified one up-regulated and two induced proteins with important functions: tryptophan synthase α chain (production of radical oxygen species), glyoxalase I (detoxification/antioxidation) and a Bet v I family protein (defense). These results will contribute to future research into their roles in UV stress responses in plants.

Identification of proteins associated with water-deficit tolerance in C4 perennial grass species, Cynodon dactylon×Cynodon transvaalensis and Cynodon dactylon.

The study was conducted to examine differential proteomic responses to water-deficit stress in hybrid bermudagrass [Cynodon dactylon (L.) Pers. ×Cynodon transvaalensis Burtt Davy, cv. Tifway] and common bermudagrass (C. dactylon, cv. C299). Plants were exposed to water-deficit stress for 15 days by withholding irrigation in a growth chamber. Leaf electrolyte leakage increased and photochemical efficiency and relative water content declined under water-deficit stress, but the extent of changes in each of the physiological parameters for 'Tifway' was less pronounced than those for 'C299'. Total proteins of leaves were extracted from well-watered and water-deficit plants and separated by two-dimensional gel electrophoresis. Of the 750 protein spots reproducibly detected, 32 proteins had increases in the abundance and 22 proteins exhibited decreases in the abundance in at least one genotype under water-deficit stress. A significantly higher number of proteins were found to accumulate in 'Tifway' than in 'C299' and 16 proteins with increasing abundance were detected only in 'Tifway' under water-deficit stress. All stress-responsive proteins were subjected to mass spectrometry analysis, which were mainly involved in metabolism, energy, cell growth/division, protein synthesis and stress defense. Functional analysis of differential drought-responsive proteins between the two genotypes suggests that the superior water-deficit tolerance in 'Tifway' bermudagrass could be mainly associated with less severe decline in the abundance level of proteins involved in photosynthesis (chlorophyll a-b, ATP synthase subunit alpha, phosphoribulokinase and ribulose-1,5-bisphosphate carboxylase/oxygenase) and greater increase in the abundance level of antioxidant defense proteins (superoxide dismutase, ascorbate peroxidase, dehydroascorbate reductase and peroxiredoxin), demonstrating that maintaining photosynthesis and active antioxidant defense mechanisms may play a critical role in C(4) grass adaptation to water-deficit stress.