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Standard therapies for heart failure with preserved ejection fraction (HFpEF) remain controversial. Vagus nerve stimulation (VNS) can downregulate extracellular matrix (ECM) expression and improve the prognosis of patients with heart failure. In order to verify whether the positive effect of VNS on HFpEF is feasible, HFpEF model constructed by Dahl salt-sensitive rats were subjected to VNS. Thirty male Dahl salt-sensitive rats were fed a high-salt diet (inducing HFpEF) and ten were fed a low-salt diet (controls) from the age of 7 weeks old. Roughly 12 weeks later, rats with HFpEF were randomly assigned to VNS (HF-VNS group, n = 13) and sham stimulation (HF-SS group, n = 13). Age-matched controls also underwent sham stimulation (control-SS group, n = 10). Cardiac function, myocardial hypertrophy, and fibrosis were evaluated after 72 h of treatment. Heart rate and systolic blood pressure decreased in rats receiving VNS compared with untreated counterparts. In addition, both systolic and diastolic cardiac function improved concurrently. The concentration of serum brain natriuretic peptide (BNP) concentration and the mRNA and protein expression of ECM proteins in serum and tissues, including collagen type I and III, connective tissue growth factor (CTGF), and transforming growth factor-β1 (TGF-β1) in serum and in tissue (mRNA and protein expression), were remarkably downregulated by VNS. VNS improved cardiac function and mitigated myocardial remodeling in Dahl salt-sensitive rats with HFpEF, which exhibited a good clinical application prospect.

Studies have shown thatWe divided the subjects into the asthma, Mp infection, asthma combined with Mp infection and healthy groups. Patients' peripheral blood was collected for metabolic and interaction analysis. Cytokine levels were measured via serum and exhaled breath condensate (EBC).A total of 150 participating subjects were divided into four groups after exclusion. We found out that there were different metabolic pathways between the healthy and disease groups. The major pathways of both asthma and asthma combined with Mp infection were valine, leucine and isoleucine biosynthesis; malate-aspartate shuttle was the main differential pathway for Mp infection. Moreover, even though three disease groups involved 81 metabolites at the same time, compared with asthma combined with Mp infection, 2 single disease groups still involved different amino acid pathways (phenylalanine, tyrosine and tryptophan biosynthesis; valine, leucine and isoleucine biosynthesis). Interaction analysis showed that Mp infection in asthmatic patients not only activated cytokines, but also activated Toll-like receptors (TLRs) 2 and 6. Finally, the levels of interleukin (IL)-4, IL-8, IL-13 and tumor necrosis factor-α in EBC with asthma combined with Mp infection were significantly higher than the 2 single disease groups.Mp infection in asthmatic children can cause changes in the levels of various amino acids in the body, which were enriched in the pathways such as valine, leucine and isoleucine biosynthesis. Palmitic acid can activate TLR2, and iloprost reduces IL-10 levels, ultimately leading to the increased airway inflammation.

The mechanism behind the aberrant expression of S100A6 in osteosarcoma is seldom reported so far. This study sought to explore the regulatory axis targeting S100A6 involved in osteosarcoma progression. Clinical samples collected from osteosarcoma patients were used to detect the expressions of SNHG1, miR-493-5p, and S100A6 by western bolt analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The effects of S100A6 on proliferation and osteogenic differentiation were investigated by the CCK-8 assay, colony formation assay, Ethynyl deoxyuridine staining, matrix mineralization assay, and alkaline phosphatase assay. The potential of lncRNAs/miRNAs targeting S100A6 was identified by the bioinformatics approach, and the results were verified by the dual luciferase assay and RNA immunoprecipitation assay. Both and rescue experiments were performed to investigate the regulatory relationship between the identified lncRNAs and S100A6. The results showed that S100A6 is highly expressed in osteosarcoma. S100A6 overexpression not only increases the proliferation but also reduces the osteogenic differentiation of osteosarcoma cells, while S1006A silence exerts the opposite effects. Then, SNHG1 is identified to directly interact with miR-493-5p to attenuate miR-493-5p binding to the 3'-untranslated region of S100A6. Notably, S100A6 silence partially rescues the effect of SNHG1 overexpression on proliferation and osteogenic differentiation of osteosarcoma cells. Furthermore, the suppressive role of SNHG1 silence in the growth of osteosarcoma xenograft tumors is countered by S100A6 overexpression. Collectively, this study reveals that S100A6 plays an important role in osteosarcoma progression, and SNHG1 promotes S100A6 expression by competitively sponging miR-493-5p.

Objective. To explore the clinical effect of Sanfeng Tongqiao Diwan in the treatment of allergic rhinitis. Methods. Allergic rhinitis patients included in this study were randomly divided into control group and study group for 7 days of treatment. The control group was treated with Tongqiao Biyan Pian, while the study group was treated with Sanfeng Tongqiao Diwan. Results. After 7 days of treatment, the total effective rate of Sanfeng Tongqiao Diwan was 75.76%, which was higher than that of Tongqiao Biyan Pian (65.62%). The scores of visual analogue scale (VAS), symptom relief, Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ), and Epworth sleepiness scale (ESS) in both groups were significantly improved before and after treatment ( P < 0.05 ), and the improvement was most significant 24 hours after treatment. The adverse reactions in both groups were low. Conclusion. Sanfeng Tongqiao Diwan can significantly alleviate the symptoms and improve the quality of life of patients with allergic rhinitis, with less adverse reactions.

Human coronavirus NL63 (HCoV-NL63) is primarily associated with common cold in children, elderly and immunocompromised individuals. Outbreaks caused by HCoV-NL63 are rare. Here we report a cluster of HCoV-NL63 cases with severe lower respiratory tract infection that arose in Guangzhou, China, in 2018. Twenty-three hospitalized children were confirmed to be HCoV-NL63 positive, and most of whom were hospitalized with severe pneumonia or acute bronchitis. Whole genomes of HCoV-NL63 were obtained using next-generation sequencing. Phylogenetic and single amino acid polymorphism analyses showed that this outbreak was associated with two subgenotypes (C3 and B) of HCoV-NL63. Half of patients were identified to be related to a new subgenotype C3. One unique amino acid mutation at I507 L in spike protein receptor binding domain (RBD) was detected, which segregated this subgenotype C3 from other known subgenotypes. Pseudotyped virus bearing the I507 L mutation in RBD showed enhanced entry into host cells as compared to the prototype virus. This study proved that HCoV-NL63 was undergoing continuous mutation and has the potential to cause severe lower respiratory disease in humans.

Since the development of the first docking program in 1982, the use of docking-based in silico screening for potentially bioactive molecule discovery has become a common strategy in academia and pharmaceutical industry. Up until recently, application of docking programs has largely focused on drugs binding to proteins. However, with the discovery of promising drug targets in nucleic acids, including RNA riboswitches, DNA G-quadruplexes, and extended repeats in RNA, there has been greater interests in developing drugs for nucleic acids. However, due to major biochemical and physical differences in charges, binding pockets, and solvation, existing docking programs, developed for proteins, face difficulties when adopted directly for nucleic acids. In this review, we cover the current field of in silico docking to nucleic acids, available programs, as well as challenges faced in the field.

Neuromyelitis optica spectrum disorder (NMOSD), a relapsing autoimmune disease of the central nervous system, mainly targets the optic nerve and spinal cord. To date, all attempts at the establishment of NMOSD animal models have been based on neuromyelitis optica immunoglobulin G antibody (NMO-IgG) and mimic the disease in part. To solve this problem, we developed a rodent model by opening the blood-brain barrier (BBB) with low frequency ultrasound, followed by injection of NMO-IgG from NMOSD patients and complement to mice suffering pre-existing neuroinflammation produced by experimental autoimmune encephalomyelitis (EAE). In this study, we showed that ultrasound with NMO-IgG and complement caused marked inflammation and demyelination of both spinal cords and optic nerves compared to blank control group, as well as glial fibrillary acidic protein (GFAP) and aquaporin-4 (AQP4) loss of spinal cords and optic nerves compared to EAE mice and EAE mice with only BBB opening. In addition, magnetic resonance imaging (MRI) revealed optic neuritis with spinal cord lesions. We further demonstrated eye segregation defects in the dorsal lateral geniculate nucleus (dLGN) of these NMOSD mice.

BACKGROUND: Traditional Chinese medicine (TCM) has a long history and its own characteristics in the treatment of allergic rhinitis. In this study, the efficacy and safety of patients with allergic rhinitis treated with Sanfeng Tongqiao Diwan were observed to support the clinical medication of patients with allergic rhinitis. METHODS: A total of 61 patients with allergic rhinitis aged 12–70 years from the First Affiliated Hospital of Guangzhou Medical University were included in this study. All the patients were treated with Sanfeng Tongqiao Diwan for a period of 7 days. Return visits were carried out 24 hours after the first medication, the 4th day of medication, and the 7th day of medication, during which the efficacy and safety were assessed. RESULTS: The effective rates of Sanfeng Tongqiao Diwan at 24 hours, 4 days, and 7 days were 49.2%, 60.7%, and 65.6%, respectively. Comparing the severity of various symptoms after treatment to baseline, significant differences were found in nasal secretion (2.95±0.67 vs. 2.26±1.30, P

Intrauterine hyperglycemia can harm a fetus's growth and development, and this can be seen in the umbilical cord blood metabolism disorder. However, the metabolites and metabolic mechanisms involved in the condition remain unknown.Targeted metabolomics using liquid chromatography and MetaboAnalyst were conducted in this study to explore differences in metabolites and metabolic pathways between individuals with hyperglycemia or well-controlled gestational diabetes mellitus (GDM) and healthy controls.Univariate analysis found that the hyperglycemic and healthy control groups differed in 30 metabolites, while the well-controlled GDM and the healthy control groups differed only in three metabolites-ursodeoxycholic acid, docosahexaenoic acid, and 8,11,14-eicosatrienoic acid. Most of these metabolic variations were negatively associated with neonatal weights. Further research showed that the variations in the metabolites were primarily associated with the metabolic pathways of linoleic acid (LA) and alpha-linolenic acid (ALA).Gestational hyperglycemia and well-controlled GDM, which may play a major role by inhibiting the LA and ALA metabolic pathways, have detrimental effects on cord blood metabolism.The main point of this paper is that intrauterine hyperglycemia has a negative effect on cord blood metabolism mainly through the linoleic acid and alpha-linolenic acid metabolic pathways. This is a study to report a new association between well-controlled GDM and cord blood metabolism. This study provides a possible explanation for the association between intrauterine hyperglycemia and neonatal adverse birth outcomes.

Background: Myocardial infarction (MI) refers to a fatal disease, and the border zone (BZ) of myocardial infarction is of high importance to the prognosis of myocardial infarction patients. Autophagy and apoptosis can significantly impact cardiovascular diseases. In the previous studies conducted by the authors, plenty of differential expressions of long non-coding RNA (lncRNA) were reported in the border zone of myocardial infarction. As revealed from the results of bioinformatics analysis, LncRNA may take up a vital part in the pathological process of cardiovascular disease by regulating apoptosis and autophagy. This study aimed to firstly conduct bioinformatics analyses to predict that NR_027324, as a competitive endogenous RNA (ceRNA), binds to miR-103-3p and subsequently regulates the expression of downstream target gene ATG5, to secondly verify the mentioned regulatory relationship by molecular biological experiments, and thirdly to investigate that the above pathways transmit apoptosis and autophagy signals in cardiomyocytes during hypoglycemic and anoxic injuries. Methods: The binding of NR_027324 to miR-103-3p was predicted by the bioinformatics analysis, and then the expression of downstream ATG5 was regulated. By the dual luciferase assay, the binding of NR_027324 to miR-103-3p was confirmed. H9c2 cells underwent the culture under low glucose and hypoxia to simulate cardiomyocytes under ischemia. NR_027324 siRNA and overexpression plasmid vector and miR-103-3p (mimics and inhibitors) were adopted to transfect cells to examine its function in cardiomyocytes. By the reverse transcription-quantitative polymerase chain reaction (RT-PCR), the expression levels of NR_027324, miR-103a-3p and ATG5 were assessed. Cell viability was measured by the MTT assay, and cell injury was analyzed by the lactate dehydrogenase assay (LDH). The western blotting assay was performed to detect the expressions of Bcl2, Bax, Atg5, cleaved-caspase3 and cleaved-caspase9. Moreover, the immunofluorescence assay was used to detect the expression of LC3-I/II as a marker of autophagy.Results: In hypoglycemic and anoxic H9C2 cells, the expressions of NR_027324 and ATG5 were up-regulated, while miR-103-3p showed a down-regulated expression. By the dual luciferase assay, the binding of NR_027324 to miR-103-3p was confirmed. The overexpressed NR_027324 could enhance the reduced cell viability of hypoglycemic and anoxic H9C2 cells and reduce cell damage. Interfering with the expression of NR_027324 could further reduce the viability of hypoglycemic anoxic H9C2 cells, increase injury, inhibit protective autophagy and accelerate apoptosis of hypoglycemic anoxic H9C2 cells. The mentioned pathophysiological processes were achieved by NR_027324 binding to miR-103-3p and then regulating the expression of target gene ATG5.Conclusion: In hypoglycemic and anoxic H9C2 cells, the expressions of NR_027324 and ATG5 are up-regulated, while the expression of miR-103-3p decreases. NR_027324 acts as ceRNA combined with miR-103-3p to regulate ATG5 and control autophagy and apoptosis in cardiomyocytes during hypoglycemic and anoxic injuries.

Haisheng Hu,1,* Chuanxu Cai,2,* Mingshan Xue,1 Jiaying Luo,1 Chenxi Liao,1 Huimin Huang,1,* Baoqing Sun1 1Department of Allergy and Clinical Immunology, State Key Laboratory of Respiratory Disease, National Clinical Research Center of Respiratory Disease, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510120, Guangdong, People’s Republic of China; 2Department of Laboratory Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen People’s Hospital, First Affiliated Hospital of Southern University of Science and Technology, Second Clinical Medical College of Jinan University, Shenzhen, Guangdong 518020, People’s Republic of China*These authors contributed equally to this workCorrespondence: Baoqing Sun First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Road, Guangzhou 510120, Guangdong, People’s Republic of ChinaTel +86 20 8306 2865Fax +86 20 8306 2729Email sunbaoqing@vip.163.comObjective: The aim of this study was to analyse the level of serum matrix metalloproteinases (MMPs) in atopic and non-atopic COPD patients, providing guidance for clinical practice and theory for atopic COPD.Methods: Blood samples from 50 adult male patients with COPD, including 17 atopic and 33 non-atopic patients, were submitted for detection of MMP8, MMP9, surfactant associated protein D (SPD), noradrenaline (NE), leukotriene (LT) B4, recombinant proteoglycan (PRG4), Phadiatop sIgE, and tIgE levels. Patients’ Modified Medical Research Council Dyspnea Scale (mMRC), COPD Assessment Test (CAT), pulmonary function test results, FeNO, blood cell ratio and induced sputum were collected.Results: The level of serum tIgE in patients with atopic COPD [1876.00 kU/l (760.50, 5347.00)] was significantly higher than in patients with non-atopic COPD [377.00 kU/l (93.50, 581.50), P < 0.001]. The MMP8 levels in atopic COPD (1600 ± 1181 ng/mL) were significantly higher than in non-atopic COPD (973.3 ± 921.5 ng/mL, P = 0.0494), but there was no significant difference in MMP9, SPD, NE, LTB4, and PRG4 levels between the two groups. In atopic COPD patients, the rate of leukocyte (rs = 0.63, P < 0.001) and neutrophil (rs = 0.54, P < 0.05) were positively correlated with MMP8 levels, while lymphocyte rate was negatively correlated with MMP8 (rs = − 0.70, P < 0.001) and MMP9 levels (rs = − 0.54, P < 0.05). Optimal scale analysis showed that NE was most closely related to the basophil rate from induced sputum and FeNO levels (Cronbach’s alpha = 85.1%). Interestingly, all atopic COPD patients with mMRC ≥ 2, CAT ≥ 10, and CCQ ≥ 16 exhibited MMP8 levels > 1000 ng/mL.Conclusion: In general, tIgE and MMP8 levels were higher in atopic COPD patients than in non-atopic patients. NE levels were closely correlated with the basophil rate of induced sputum and FeNO levels, which may play an important role in the pathogenesis and development of atopic COPD.Keywords: chronic obstructive pulmonary disease, atopy, matrix metalloproteinases, immunoglobulin E, allergy

Fresh fruit of Rosa roxburghii Tratt has attracted great interest and is used in many functional products in China. However, fresh fruits are perishable products with quite short shelf lives and few studies have focused on dried fruits. Therefore, this study aimed to explore whether the drying process can be used to preserve bioactive components of R roxburghii fruits by comparing phytochemical profiles and antioxidant activities between fresh and dried fruit. As result, a total of 95 compounds, mainly including organic acids, phenols, and flavonoids, were identified in fresh and dried fruits by using ultrahigh-performance liquid chromatography-quadrupole-time of flight mass spectrometry. The relative quantitative result showed that contents of phenols and acylamide were significantly higher ( p

Previous studies have reported that short-term vagus nerve stimulation (VNS) improves cardiac function in rats with chronic heart failure (CHF). The molecular mechanisms are unclear. The potential effect of microRNA (miR)-205 in apoptosis of short-term VNS was examined. A total of 3 weeks after inducing CHF, the rats were divided into three groups: Sham stimulation in sham operated rats, sham stimulation in CHF rats (CHF-SS), and treated with VNS in CHF rats (CHF-VNS). The right vagus nerve of the neck was stimulated for 72 h in CHF rats with rectangular pulses of 40 msec duration at 1 Hz and 5 V. miR-205 was focused on, which exhibited differential expression in the miRNA microarray analysis of CHF rats, and the effects of VNS on apoptosis were examined. It was verified that the expression level of miR-205 in the CHF-SS group was increased, and the expression was reduced in the CHF-VNS group. Furthermore, mimics or inhibitor of miR-205 was transfected into H9c2 to investigate its function on apoptosis. Baculoviral IAP repeat-containing protein 2 (Birc2) was confirmed a target of miR-205 through a dual luciferase reporter assay and western blotting. It was demonstrated that downregulated miR-205 decreased apoptosis in H9c2 cells. The apoptosis-associated proteins were further detected in H9c2 cells and rat tissue. The mRNA and protein expression levels of caspase-3 and Bcl-2-associated X protein were decreased in the CHF-VNS group, the expression of Birc2 and B-cell lymphoma 2 were increased. The results were consistent with the in vitro study in the miR-205 inhibitor group. The present study demonstrated that short-term VNS decreased apoptosis by downregulating miR-205 in rats with CHF. Therefore, the results of the present study provide basic evidence for short-term VNS in the clinical treatment of CHF.

Background The participation of long noncoding RNAs (lncRNAs) in myocardial infarction has recently been noted. However, their underlying roles in the border zone of myocardial infarction remain unclear. This study uses microarrays to determine the profiles of lncRNAs and mRNAs in the border zone. Methods Bioinformatics methods were employed to uncover their underlying roles. Highly dysregulated lncRNAs was further validated via PCR. Results Four hundred seven lncRNAs and 752 mRNAs were upregulated, while 132 lncRNAs and 547 mRNAs were downregulated in the border zone of myocardial infarction. A circos graph was constructed to visualize the chromosomal distribution and classification of the dysregulated lncRNAs and mRNAs. The upregulated mRNAs in the border zone were most highly enriched in cytokine activity, binding, cytokine receptor binding and related processes, as ascertained through Go analysis. Pathway analysis of the upregulated mRNAs showed the most significant changes were in the TNF signaling pathway, cytokine–cytokine receptor interaction and chemokine signaling pathway and similar pathways and interactions. An lncRNA–mRNA co-expression network was established to probe into the underlying functions of the 10 most highly dysregulated lncRNAs based on their co-expressed mRNAs. In the co-expression network, we found 16 genes directly involved in myocardial infarction, including Alox5ap, Itgb2 and B4galt1. The lncRNAs AY212271, EF424788 and MRAK088538, among others, might be associated with myocardial infarction. BC166504 is probably a key lncRNA in the border zone of myocardial infarction. Conclusions The results may have revealed some aberrantly expressed lncRNAs and mRNAs that contribute to the underlying pathophysiological mechanisms of myocardial infarction.

Over the past two decades, interests in DNA and RNA as drug targets have been growing rapidly. Following the trends observed with protein drug targets, computational approaches for drug design have been developed for this new class of molecules. Our efforts toward the development of a universal docking program, Fitted, led us to focus on nucleic acids. Throughout the development of this docking program, efforts were directed toward displaceable water molecules which must be accurately located for optimal docking-based drug discovery. However, although there is a plethora of methods to place water molecules in and around protein structures, there is, to the best of our knowledge, no such fully automated method for nucleic acids, which are significantly more polar and solvated than proteins. We report herein a new method, Splash'Em (Solvation Potential Laid around Statistical Hydration on Entire Macromolecules) developed to place water molecules within the binding cavity of nucleic acids. This fast method was shown to have high agreement with water positions in crystal structures and will therefore provide essential information to medicinal chemists.

Although optic neuritis and myelitis are the core clinical characteristics of neuromyelitis optica spectrum disorders (NMOSD), appropriate animal models of NMOSD with myelitis and optic neuritis are lacking. we developed a mouse model of NMOSD by intravenously injecting 100 µg neuromyelitis optica immunoglobulin G antibody (NMO-IgG) and complement into experimental allergic encephalomyelitis (EAE) mice after reversible blood-brain barrier (BBB) opening by microbubble-enhanced low-frequency ultrasound (MELFUS). Animals were assessed by histopathology. We found noticeable inflammation and demyelination concomitant with the loss of aquaporin-4 (AQP4) and glial fibrillary acidic protein (GFAP) expression in the spinal cord, brain and optic nerve, as well as human IgG and C9neo deposition. Thus, with the help of MELFUS, we established an NMOSD mouse model with the core lesions of NMOSD by applying a considerably lower dose of human NMO-IgG, which may help identify the pathogenesis and facilitate the development of other neuroimmune disease models in the future.

A series of continuous (Na0.5La0.5TiO3)1−x(LaCrO3)x solid solutions with orthorhombic-phase perovskite structure and with LaCrO3 contents (x) in the range from 0 to 1.0 were synthesized by a facile polymerized complex method, and were employed as photocatalysts for H2 evolution under visible-light irradiation. It was found that photocatalytic activities of the solid solutions significantly increased with the increase of x to 0.3, and reached the highest H2-evolution rate of 238.2 μmol h−1 gcat−1 on (Na0.5La0.5TiO3)0.7(LaCrO3)0.3, because the narrowed bandgaps of samples enhanced the generation of charge carriers and the increased lattice distortion of samples could promote the separation and migration of charge carriers. Nevertheless, photocatalytic activities of the solid solutions gradually decreased with the further increase of x from 0.3, since both the bandgaps and lattice distortion rarely changed but Cr6+ and defects gradually increased and thus accelerated the recombination of charge carriers.

Background and Purpose— Intracerebral hemorrhage (ICH) is a neurologically destructive stroke, for which no valid treatment is available. This preclinical study examined the therapeutic effect of PD-L1 (programmed death ligand 1), a B7 family member and a ligand for both PD-1 (programmed death 1) and B7-1 (CD80), in a murine ICH model. Methods— ICH was induced by injecting autologous blood into 252 male C57BL/6 and Rag1 −/− mice. One hour later, ICH mice were randomly assigned to receive an intraperitoneal injection of vehicle, PD-L1, or anti–PD-L1 antibody. Neurological function was assessed along with brain edema, brain infiltration of immune cells, blood–brain barrier integrity, neuron death, and mTOR (mammalian target of rapamycin) pathway products. Results— PD-L1 significantly attenuated neurological deficits, reduced brain edema, and decreased hemorrhage volume in ICH mice. PD-L1 specifically downsized the number of brain-infiltrating CD4 + T cells and the percentages of Th1 and Th17 cells but increased the percentages of Th2 and regulatory T cells. In the PD-L1–treated group, we observed an amelioration of the inflammatory milieu, decreased cell death, and enhanced blood–brain barrier integrity. PD-L1 also inhibited the mTOR pathway. The administration of anti–PD-L1 antibody produced the opposite effects to those of PD-L1 in ICH mice. Conclusions— PD-L1 provided protection from the damaging consequences of ICH.

Few studies addressed trans-regional differences in allergen sensitization between areas within a similar latitudinal range but with distinct geomorphological features. We investigated specific IgE (sIgE) positivity to common allergens in populations from two southern China provinces. Using a uniformed protocol, serum samples were collected from 2778 subjects with suspected atopy in coastal Guangdong and inland Yunnan. The overall prevalence of sIgE positivity were 57.8% (95% CI: 56.0%, 59.6%) from Guangdong vs 60.9% (95% CI: 59.1%, 62.7%) from Yunnan. House dust mite (d1) was the most common allergen in both regions. Among d1-sensitized subjects, only 35.7% (208/583) in Guangdong and 22.9% (147/642) in Yunnan tested positive for d1 alone. Among those poly-sensitized d1-positive subjects, cockroach was the most common co-sensitizing aeroallergen. 41.9% of the d1-sensitized Guangdong subjects showed high-class sIgE reactivity (≥class 4), in contrast to a very low percentage of such reactivity in Yunnan. However, 36.3% of d1-sensitized subjects in Yunnan were concomitantly positive for tree pollen mix. Surprisingly, Yunnan subjects showed high prevalence of sIgE positivity for crabs and shrimps, either by overall or by age-group analysis, compared with their Guangdong counterparts (both P

Capacitive deionization (CDI) is an emerging water desalination technique that holds great potential in solving the global water shortage issue. It is known that, H2O2 formation at the cathode interface causing the performance degradation of activated carbons (ACs) electrode has limited the large-scale implementation of CDI, but up to date there has seldom any effective solution being reported. In this work, we proposed the use of nitrogen-doped carbon spheres (NCSs)-based CDI cathode instead of that made up of activated carbons (ACs). Benefited from the enhanced oxygen reduction ability offering by the abundant active nitrogen dopants, the asymmetrical apparatus assembled by NCSs cathode and ACs anode exhibits an enhanced cycling stability with a retention ratio of 79.6% even after 50 cycles, which surpasses that of symmetrical apparatus (only 18%). This work provides a simple and effective approach to improve the cycling stability of CDI, highlighting the significance of surface nitrogen-doping modification and the importance of interfacial electrochemistry at the nanoscale.

Traditionally, the coagulation and fragmentation process in colloid or nanofluid has been estimated by diffusion-limited cluster aggregation (DLCA) or the population balance model. However, both models fail to give a clear physical meaning when considering the cluster fragmentation. In our present work, we developed a modified DLCA model by adding a new breaking mechanism with a clear physical meaning, which is elucidated by the stress concentration concept in materials science. When an impact (such as a collision) acts on the aggregate, one can compare whether the energy of the impact is larger than its binding energy. If the former is larger, the breaking of aggregates will happen. Otherwise, aggregates cannot be broken. A 2D experiment has been conducted to validate our model. The modeling results showed that Df (the fractal dimension of the clusters) is around 1.34 for the DLCA model, while it is estimated to be 1.43 by our modified model, which is in good agreement with the experimental value of Df = 1.44 ± 0.08. Clearly, our model is more accurate than the DLCA model. The relationship between Df and initial particle size and particle concentration have also been investigated. Our work is expected to add new insight into the evaluation of aggregate morphology and size distribution in various nanoparticle suspension systems.

There is so far a paucity of data about allergen component-resolved diagnosis, and the prevalence of grass pollen allergen components in China, in contrast to those from western countries. Even in this country, allergies to grass pollen allergen components in the vast south are inadequately described. This study aimed to determine the major sensitizing grass pollens in Guangzhou, the largest city in Guangdong province of southern China. Included in this study were 258 patients having allergic rhinitis with or without asthma and 88 healthy controls. ImmunoCap100 was used to examine the serum samples for sIgE to Bermuda, Timothy, and Humulus scandens. Subjects who tested positive were further examined for sIgE to Bermuda antigen Cyn d 1, Timothy antigens Phl p 1/4/5/6/7/11/12, and CCD. The relationship of grass pollen allergy to specific antigen sensitization was assessed. As a result, 22.5% of patients with allergic rhinitis and/or asthma were positive for Bermuda-sIgE, 13.6% for Timothy-sIgE, and 7.0% for Humulus scandens-sIgE. These patients were more likely to be sensitized compared with controls (P

A palladium-catalyzed desulfitative conjugate addition of sodium sulfinates with α,β-unsaturated carbonyl compounds is described. The reaction showed very good selectivity and tolerated a wide range of functionalities under an atmosphere of argon.

A convenient and efficient method for the synthesis of various symmetrical and non-symmetrical trans-stilbene derivatives from benzylic halides in the absence of any transition metals is described. Sodium sulfinates played an important role in this transformation. Various functional groups were well tolerated under the optimized reaction conditions.