Search

Byline: Tian-tian. Zhu, Chao-Nan. Zhu, Ning. Huang, Xin. Yu, Guang-rui. Wan, Shuang-xi. Wang, Ping. Song, Jian. Xu, Peng. Li, Ya-ling. Yin OBJECTIVES: This work aimed to determine tert-Butylhydroquinone (TBHQ)'s effects [...]

The evaluation of the scientific and technological (S&T) innovation efficiency of universities is important for the 'double first-class' construction in China. However, related research often only considers desirable outputs while ignoring undesirable ones, which tends to produce biased evaluation results. For this reason, this study takes the ratio of unemployed graduates as undesirable output, and uses the global Malmquist – Luenberger index method to evaluate the S&T innovation efficiency of 31 relevant universities in China during 2013–2017, then develops a panel Tobit model to analyse its influencing factors. The results reveal that: first, during the sample period, the S&T innovation efficiency of those universities improved overall, and technical progress was the main driver. Second, excluding undesirable output will result in an overestimate of the S&T innovation efficiency of universities. Third, the S&T innovation efficiency of universities features regional distribution, with high efficiency in the west and low efficiency in the east. Moreover, different regions have different drivers for the improvement of S&T innovation efficiency of universities, with technical progress for the east and technical efficiency changes for the central and west. Finally, the 'double first-class' construction proposal in China has significantly promoted the improvement of S&T innovation efficiency in universities. [ABSTRACT FROM AUTHOR]

Based on the data of 31 provinces in China during 2004–2015 and the models of panel threshold regression and panel quantile regression, this paper investigates the impact of China's higher education on regional carbon emissions. The results indicate that there exists threshold effect of both China's higher education scale and quality on regional carbon emissions per capita. Specifically, in terms of higher education scale, its further progress may facilitate the positive effect on carbon emissions per capita when technology is above threshold. As for higher education quality, its further growth may moderate the positive effect on carbon emissions per capita when income exceeds threshold; it also can promote its constrained effect on carbon emissions per capita when exceeding the technology threshold; and the continuous improvement of higher education quality may help to reduce carbon emissions per capita. Besides, the positive impact of higher education scale on carbon emissions per capita appears smaller in regions with more carbon emissions per capita; meanwhile, only in the regions with larger carbon emissions per capita, may higher education quality promote carbon emissions per capita, while the curbing impact of technology level is relatively constant among different regions with various carbon emissions. [ABSTRACT FROM AUTHOR]

The proliferation of pulmonary artery smooth muscle cells (PASMCs) is an important cause of pulmonary vascular remodeling in pulmonary hypertension (PH). It has been reported that miR-137 inhibits the proliferation of tumor cells. However, whether miR-137 is involved in PH remains unclear. In this study, male Sprague-Dawley rats were subjected to 10% O2 for 3 weeks to establish PH, and rat primary PASMCs were treated with hypoxia (3% O2) for 48 h to induce cell proliferation. The effect of miR-137 on PASMC proliferation and calpain-2 expression was assessed by transfecting miR-137 mimic and inhibitor. The effect of calpain-2 on PASMC proliferation was assessed by transfecting calpain-2 siRNA. The present study found for the first time that miR-137 was downregulated in pulmonary arteries of hypoxic PH rats and in hypoxia-treated PASMCs. miR-137 mimic inhibited hypoxia-induced PASMC proliferation and upregulation of calpain-2 expression in PASMCs. Furthermore, miR-137 inhibitor induced the proliferation of PASMCs under normoxia, and knockdown of calpain-2 mRNA by siRNA significantly inhibited hypoxia-induced proliferation of PASMCs. Our study demonstrated that hypoxia-induced downregulation of miR-137 expression promoted the proliferation of PASMCs by targeting calpain-2, thereby potentially resulting in pulmonary vascular remodeling in hypoxic PH. [ABSTRACT FROM AUTHOR]

A new Sr(II)-based metal organic framework (MOF) formulated as [Sr(HTATB)(H2O)2(DMF)4 (1) has been prepared by reaction of Sr(NO3)2 with the rigid tricarboxylic acid linker 4,4′,4″-s-triazine-2, 4, 6-triyltribenzoic acid (H3TATB) in a mixed solvent of N,N-dimethylformamide (DMF) and water. Complex 1 has been characterized by powder X-ray diffraction (PXRD), elemental analysis (EA) and single crystal X-ray diffraction (SCXRD). In light of its large inner spaces as well as widely distributed open metal sites, the guest-free 1 (1a) has been used as a crystalline vessel for delivering small-molecule chemotherapeutics such as 5-fluorouracil (5-Fu), which exhibits an outstanding loading capacity around 36.48 wt%. Furthermore, the cumulative release value of 5-Fu at 48 h was about 96.5% in phosphate buffer saline (PBS). In addition, the 3-(4,5-dimethyl-2-thiazolyl)−2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was employed to evaluate the in vitro cytotoxicity of the carrier 5-Fu loaded 1a against the human melanoma cell lines. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Acupuncture & Tuina Science is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Pulmonary arterial hypertension (PAH) is characterized by the apoptosis resistance and hyperproliferation of pulmonary artery smooth muscle cells (PASMCs). Its pathogenesis has not been revealed. Here, we carried out experiments to investigate the functions of miR‐140‐5p and tumor necrosis factor‐α (TNF‐α). Methods: We selected GSE703 from Gene Expression Omnibus (GEO) Database to conduct microarray analysis using R software and Gene Set Enrichment Analysis (GSEA). Combing bioinformatics results, the upregulation of miR‐140‐5p inhibited PAH progression through targeting TNF‐α. RNA expression was measured by quantitative real‐time polymerase chain reaction (RT‐qPCR) and protein level was measured by western blot analysis and enzyme‐linked immunosorbent assays (ELISA). We conducted monocrotaline (MCT) injection to rats to form PAH animal models. The lung tissues were observed by hematoxylin–eosin (HE) staining and Sirius red‐picric acid staining. Right ventricular systolic pressure (RVSP) and the ratio of right ventricle (RV)‐to‐left ventricle (LV) plus septum (S) weight (RV/[LV + S]) were measured in MCT‐induced animal models. Overexpression of miR‐140‐5p and TNF‐α were utilized to research the proliferation, migration, and phenotypic variation of hypoxia‐mediated PASMCs. The binding between miR‐140‐5p and TNF‐α 3′‐untranslated region (3′‐UTR) was confirmed via luciferase reporter assay. Results: Downregulation of miR‐140‐5p and upregulation of TNF‐α were observed in PAH rat model and hypoxia‐mediated PASMCs. And we proved that overexpression of miR‐140‐5p could suppress the proliferation, migration, and phenotypic variation of PASMCs, therefore inhibiting PAH pathogenesis. Luciferase assay verified that miR‐140‐5p targeted TNF‐α directly. A converse correlation was also shown between miR‐140‐5p and TNF‐α in PASMCs. Conclusions: miR‐140‐5p and TNF‐α are important regulators in PAH pathology and may serve as a therapeutic target for PAH. miR‐140‐5p might inhibit the occurrence and development of pulmonary arterial hypertension (PAH) by repressing tumor necrosis factor‐α (TNF‐α) expression via the TNF signaling pathway. These findings may help in the search of promising strategies for achieving better treatment outcome in patients diagnosed with PAH. [ABSTRACT FROM AUTHOR]

PhD enrolment quota allocation proves the key concern for China’s universities to promote institutional reform and improve research level, and it is often characterized by the zero sum game among schools within a university. Therefore, this article develops a new indicator system for PhD enrolment quota allocation and efficiency evaluation in China, and then it reallocates the quotas considering the preferences of decision-makers and the efficiency based on the historical data during 2011-2015 in a research-oriented university in China. The results indicate that, first, the preferences of decision-makers in the university for article publications and research funds may significantly affect the allocation of PhD enrolment quotas among schools. Second, when the linear combination weighting method is used, the overall efficiency for PhD enrolment allocation proves the highest, among various weighting methods concerned. Finally, to improve the overall efficiency of the 19 schools, five social science schools and four engineering schools have to cut their PhD enrolment quotas; among them, three engineering schools should reduce the largest redundant quotas sharply. The methods and results in this article are conducive to the allocation of education resources which have the zero sum feature and are often accompanied with undesirable outputs. [ABSTRACT FROM AUTHOR]

The new compound based on Wells-Dawson-type arsenomolybdate: [{Cu 10 (pz) 11 Cl 4 }{As 2 III As 2 V Mo 6 V Mo 12 VI O 62 }]·H 2 O ( 1 ) has been hydrothermally synthesized and characterized by single-crystal X-ray diffraction analysis, X-ray powder diffraction (XRPD), XPS spectroscopy and thermogravimetric analysis (TG). Compound 1 is consisted of two As caps Wells-dawson-type arsenomolybdate and {Cu 10 (py) 11 } complexes by chloride bridge. In addition, the antitumor effects of the title compound 1 were studied on three human lung cancer cells (A549, SK-LU-1 and SW1573). The results showed that compared with the positive reference drug carboplatin, compound 1 displayed efficient antitumor activity. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PH) mainly results from excessive proliferation of pulmonary artery smooth muscle cells (PASMCs) and displays mitochondrial abnormalities such as mitochondrial fragmentation. Epigallocatechin-3-gallate (EGCG), an efficient antiproliferative compound in green tea, has recently been demonstrated to inhibit PASMCs proliferation. However, the pre-clinical issues as to whether EGCG attenuates PH and the underlying mechanisms have yet to be addressed. The present study was undertaken to investigate the therapeutic effects of EGCG on PH and its effects on mitochondrial fragmentation in PASMCs. Rats exposed to hypoxia (10% O 2 , 3 weeks) developed PH. EGCG (50, 100 or 200 mg/kg/d, i.g.) dose-dependently attenuated right ventricular systolic pressure, pulmonary vascular remodeling and right ventricular hypertrophy, increased expression of mitochondrial fusion protein - mitofusin-2 (MFN-2), and promoted mitochondrial fusion as evidenced by decreased number and volume of mitochondria in PASMCs of pulmonary arteries. Notably, EGCG (50 μM) downregulated hypoxia-induced (3% O 2 , 48 h) PASMCs mitochondrial fragmentation and inhibited PASMCs proliferation via KLF-4/MFN-2/p-Erk signaling pathway. Collectively, our data demonstrated that EGCG exerts antiproliferative effects via regulating mitochondrial fragmentation of PASMCs and EGCG holds the promise as a drug against PH. [ABSTRACT FROM AUTHOR]

Background Pulmonary hypertension (PH) is a proliferative disorder associated with enhanced proliferation and suppressed apoptosis of pulmonary artery smooth muscle cells (PASMCs). Our lately study demonstrated that let-7g inhibited hypoxia-induced proliferation of PASMCs via repressing c-myc-Bmi-1-p16 signaling pathway. However, the upstream of let-7g has not yet been fully defined. Previous studies have shown that LOX-1, a target of let-7g, could also regulate the expression of let-7g in human aortic endothelial cells. In this present study, we aimed to investigate whether there is a negative feedback regulation between microRNA let-7g and LOX-1 in hypoxia-induced proliferation of PASMCs. Methods SD Rats were exposed to hypoxia (10% O 2 , 3 weeks) to induce PH. HE staining was used to evaluate pulmonary artery remodeling. in situ hybridization and immunohistochemistry were performed to assess the expression and distribution of let-7g and LOX-1, respectively. MTS, EDU and flow cytometry were performed to evaluate PASMCs proliferation. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were conducted to assess the expression of let-7g, LOX-1, calpain-1,-2,-4, and OCT-1. Results The expression of let-7g was significantly down-regulated in pulmonary arteries of hypoxia-induced PH rats accompanied by pulmonary vascular remodeling, whereas let-7g mimic inhibited hypoxia-induced proliferation of PASMCs and up-regulation of LOX-1 expression. LOX-1 blocking reversed hypoxia-induced down-regulation of let-7g expression. Calpains, protein kinase C and OCT-1 were involved in negative feedback regulation between let-7g and LOX-1. Conclusion Negative feedback regulation between let-7g and LOX-1 mediated hypoxia-induced proliferation of in PASMCs. [ABSTRACT FROM AUTHOR]

The authors have retrieved the experimental literature on moxibustion in treatment of heat syndrome in recent years, and summarized the mechanism of moxibustion in treatment of heat syndrome from such aspects as antipyretic and anti-infective effect of moxibustion, the effect on peripheral metabolism of humoral factors and the level of central neurotransmitter, and the regulation of immune function through sorting and analysis, thus providing experimental evidences for the feasibility and effectiveness of “moxibustion can be used for heat syndrome”, and providing ideas and direction for future researches. [ABSTRACT FROM AUTHOR]

Pulmonary vascular remodeling (PVR) is the pathological basis of pulmonary hypertension (PH). Incomplete understanding of PVR etiology has hindered drug development for this devastating disease, which exhibits poor prognosis despite the currently available therapies. Endothelial-to-mesenchymal transition (EndMT), a process of cell transdifferentiation, has been recently implicated in cardiovascular diseases, including PH. But the questions of how EndMT occurs and how to pharmacologically target EndMT in vivo have yet to be further answered. Herein, by performing hematoxylin–eosin and immunofluorescence staining, transmission electron microscopy and Western blotting, we found that EndMT plays a key role in the pathogenesis of PH, and importantly that aspirin, a FDA-approved widely used drug, was capable of ameliorating PVR in a preclinical rat model of hypoxia-induced PH. Moreover, aspirin exerted its inhibitory effects on EndMT in vitro and in vivo by suppressing HIF-1α/TGF-β1/Smads/Snail signaling pathway. Our data suggest that EndMT represents an intriguing drug target for the prevention and treatment of hypoxic PH and that aspirin may be repurposed to meet the urgent therapeutic needs of hypoxic PH patients. [ABSTRACT FROM AUTHOR]

Environmental pollution and its health risks to human beings have been becoming increasingly serious in China, and the health status of the individuals is not only affected by their environment but also by their own characteristics and socio-economic status. Based on the survey data of China Family Panel Studies (2014), three hierarchical linear models at three levels of individual, family, and community were developed to investigate the influencing factors of individual health status. The results indicate that: (1) there exists significant difference among individual health status, of which 16% and 9.11% are caused by the family and community levels, respectively; (2) the average health status of men is better than that of women by 6.95%. As for the difference in health effects produced by gender, total household income can reduce this difference; (3) age has significant negative health effects, while the level of education has positive effect on individual health status; and (4) the health effects of pollution is mainly reflected by its interaction with gender; in particular, when men and women face the same level of pollution exposure, men are more susceptible. [ABSTRACT FROM AUTHOR]

[Display omitted] The pulmonary vascular remodeling (PVR), the pathological basis of pulmonary hypertension (PH), entails pulmonary artery smooth muscle cells (PASMCs) phenotypic switching, but appreciation of the underlying mechanisms is incomplete. Exosomes, a novel transfer machinery enabling delivery of its cargos to recipient cells, have been recently implicated in cardiovascular diseases including PH. The two critical questions of whether plasma-derived exosomes drive PASMCs phenotypic switching and what cargo the exosomes transport, however, remain unclear. Herein, by means of transmission electron microscopy and protein detection, we for the first time, characterized lectin like oxidized low-density lipoprotein receptor-1 (LOX-1) as a novel cargo of plasma-derived exosomes in PH. With LOX-1 knockout (Olr1-/-) rats-derived exosomes, we demonstrated that exosomal LOX-1 could be transferred into PASMCs and thus elicited cell phenotypic switching. Of importance, Olr1-/- rats exhibited no cell phenotypic switching and developed less severe PH, but administration of wild type rather than Olr1-/- exosomes to Olr1-/- rats recapitulated the phenotype of PH with robust PASMCs phenotypic switching. We also revealed that exosomal LOX-1 triggered PASMCs phenotypic switching, PVR and ultimately PH via ERK1/2-KLF4 signaling axis. This study has generated proof that plasma-derived exosomes confer PH by delivering LOX-1 into PASMCs. Hence, exosomal LOX-1 represents a novel exploitable target for PH prevention and treatment. [ABSTRACT FROM AUTHOR]

Abstract Objective: This study aimed to investigate the functions of lncRNA H19 on glomerular endothelial structural damage of diabetic nephropathy (DN). Materials and Methods: Rats were fed a high sugar and fat high feed die, and intraperitoneally administrated with streptozotocin (30 mg/kg) to induce DN model. Meanwile, rat glomerular endothelial cells (rGEnCs) were treated with high a level of glucose （HG, 30 mM glucose）to induce structural damage. Results: Our results showed that H19 level was drastically increased in diabetic glomeruli and high-glucose (HG)-stimulated rat glomerular endothelial cells (rGEnCs). Deficiency of H19 ameliorated microalbumin, creatinine, BUN, and histopathological alterations in diabetic rats. In addition, H19 deficiency significantly attenuated the damage of endothelial structure by upregulating the expression of junction proteins ZO-1 and Occludin, glycolcalyx protein Syndecan-1, and endothelial activation marker sVCAM-1 and sICAM-1 in diabetic rats. The in vitro results also showed that H19-siRNA alleviated glycocalyx shedding, tight junctions damage, and endothelial activation in HG-stimulated rGEnCs. Moreover, H19 deficiency significantly enhanced the expression of p-Akt and p-eNOS and NO concentration in vitro and in vivo. Pre-treatment with Akt inhibitor LY294002 abrogated these favourable effects mediated by H19 deficiency. Discussion and Conclusion: These results indicate that H19 deficiency could mitigate the structural damage of glomerular endothelium in DN via activating Akt/eNOS pathway. [ABSTRACT FROM AUTHOR]

Background Endothelial cell apoptosis contributes to cardiovascular diseases such as hypertension, atherosclerosis. MicroRNA regulates endothelial cell function but its role in endothelial cell apoptosis remains to be fully elucidated. This study aims to investigate the role of miR-590-5p in endothelial cell apoptosis and dissect the underlying mechanisms. Methods Flow cytometric analysis, Hoechst 33258 staining and Western blotting were performed to evaluate human umbilical vein endothelial cell (HUVEC) apoptosis induced by Angiotensin (Ang) II. Western blotting and real-time quantitative PCR were conducted to assess the expression of LOX-1. DCFH-DA staining was carried out to measure the generation of reactive oxygen species (ROS). Results Ang II-induced HUVEC apoptosis was accompanied by downregulation of miR-590-5p; administration of miR-590-5p mimics attenuated HUVEC apoptosis and decreased ROS generation, as indicated by reduced fraction of apoptotic HUVECs and decreased caspase-3 activity. LOX-1 expression was increased by Ang II, and miR-590-5p mimics reduced LOX-1 expression in HUVECs in the absence or presence of Ang II. Pharmacologic or genetic block of LOX-1 with small interference RNA or TS92 (LOX-1 neutralizing antibody) significantly ameliorated HUVEC apoptosis, as evidenced by reduced number of apoptotic HUVECs, inhibited caspase-3 activation and suppressed mitochondrial cytochrome C release. Moreover, LOX-1 siRNA or TS92 treatment dramatically reduced ROS production in HUVECs treated with Ang II. Conclusion Our data demonstrated that miR-590-5p downregulation promoted Ang II-induced endothelial cell apoptosis by elevating LOX-1 expression and consequently increasing ROS generation. Thus, restoration of miR-590-5p or block of LOX-1 could be therapeutically exploited to alleviate endothelial cell apoptosis. [ABSTRACT FROM AUTHOR]

Objectives: To analyze the effect of acupuncture at the acupoints for Yizhi Tiaoshen (benefiting the intelligence and regulating the spirit) on the functional connectivity between the hippocampus and the whole brain in the patients with Alzheimer's disease (AD), and reveal the brain function mechanism of acupuncture in treatment of AD using resting state functional magnetic resonance imaging (rs-fMRI)., Methods: Sixty patients with mild to moderate AD were randomly divided into an acupuncture + medication group (30 cases, 3 cases dropped out) and a western medication group (30 cases, 2 cases dropped out). In the western medication group, the donepezil hydrochloride tablets were administered orally, 2.5 mg to 5 mg each time, once daily; and adjusted to be 10 mg each time after 4 weeks of medication. Besides the therapy as the western medication group, in the acupuncture + medication group, acupuncture was supplemented at the acupoints for Yizhi Tiaoshen , i.e. Baihui (GV 20), Sishencong (EX-HN 1), and bilateral Shenmen (HT 7), Neiguan (PC 6), Zusanli (ST 36), Sanyinjiao (SP 6) and Xuanzhong (GB 39). The needles were retained for 30 min in one treatment, once daily; and 6 treatments were required weekly. The duration of treatment was 6 weeks in each group. The general cognitive function was assessed by the mini-mental state examination (MMSE) and Alzheimer's disease assessment scale-cognitive part (ADAS-Cog) before and after treatment in the two groups. Using the rs-fMRI, the changes in the functional connectivity (FC) of the left hippocampus and the whole brain before and after treatment were analyzed in the patients of the two groups (11 cases in the acupuncture + medication group and 12 cases in the western medication group)., Results: After treatment, compared with those before treatment, MMSE scores increased and ADAS-Cog scores decreased in the two groups ( P< 0.05); MMSE score was higher, while the ADAS-Cog score was lower in the acupuncture + medication group when compared with those in the western medication group ( P ≤0.05). After treatment, in the western medication group, FC of the left hippocampus was enhanced with the left fusiform gyrus, the inferior frontal gyrus of the left triangular region, the bilateral superior temporal gyrus and the right superior parietal gyrus ( P <0.05), while FC was weakened with the left inferior temporal gyrus, the left middle frontal gyrus and the right dorsolateral superior frontal gyrus when compared with that before treatment ( P< 0.05). After treatment, in the acupuncture + medication group, FC of the left hippocampus was increased with the right gyrus rectus, the left inferior occipital gyrus, the right superior temporal gyrus and the left middle occipital gyrus ( P< 0.05), and it was declined with the left thalamus ( P< 0.05) when compared with those before treatment. After treatment, in the acupuncture + medication group, FC of the left hippocampus was strengthened with the bilateral inferior temporal gyrus, the bilateral middle temporal gyrus, the right gyrus rectus, the bilateral superior occipital gyrus, the left lenticular nucleus putamen, the left calcarine fissure and surrounding cortex, the inferior frontal gyrus of the left insulae operculum, the left medial superior frontal gyrus and the right posterior central gyrus ( P <0.05) compared with that of the western medication group., Conclusions: Acupuncture at the acupoints for Yizhi Tiaoshen improves the cognitive function of AD patients, and its main brain functional mechanism is related to intensifying the functional connectivity of the left hippocampus with the default network (inferior temporal gyrus, middle temporal gyrus and superior frontal gyrus, gyrus rectus), as well as with the sensory (posterior central gyrus) and visual (calcarine fissure and surrounding cortex and superior occipital gyrus) brain regions.

Objectives: This study aimed to evaluate the effects and the underlying mechanisms of tertiary butylhydroquinone (TBHQ) on diabetic liver steatosis and cell survival., Materials and Methods: We performed streptozocin injection and used a high-sugar-high-fat diet for mice to develop an animal model of type 2 diabetes mellitus (T2DM). Bodyweight, blood glucose levels, and content of insulin were measured on all of the mice. The liver tissues were observed by hematoxylin-eosin staining. Protein levels of the liver were measured by Western blot analysis in mice. Primary hepatocytes were induced by hypochlorous acid (HClO) and insulin to form insulin resistance (IR). Primary hepatocyte apoptosis was observed by Hoechst staining. The PI3K/AKT signaling pathway and β-arrestin-2 factor were evaluated by Western blot assay., Results: TBHQ reduced the blood glucose level and content of insulin in serum, increased body weight, and effectively alleviated liver steatosis in diabetic mice. TBHQ significantly up-regulated the expression of p-PI3K, p-AKT, GLUT4, GSK3β, and β-arrestin-2 in the liver of diabetic mice. Cell experiments confirmed that TBHQ increased the survival ability of primary hepatocytes, and TBHQ improved the expression of p-PI3K, p-AKT, GLUT4, and GSK3β by activating β-arrestin-2 in primary hepatocytes., Conclusion: TBHQ could alleviate liver steatosis and increase cell survival, and the mechanism is due in part to β-arrestin-2 activation., Competing Interests: The authors have no conflicts of interest to declare.

Aims: We have previously reported that nano-selenium quantum dots (SeQDs) prevented endothelial dysfunction in atherosclerosis. This study is to investigate whether amorphous SeQDs (A-SeQDs) increase endogenous tetrahydrobiopterin biosynthesis to alleviate pulmonary arterial hypertension., Results: Both A-SeQDs and C-SeQDs were stable under physiological conditions, while the size of A-SeQDs was smaller than C-SeQDs by high resolution-transmission electron microscopy scanning. In monocrotaline-injected mice, oral administration of A-SeQDs was more effective to decrease pulmonary arterial pressure, compared to C-SeQDs and organic selenium. Further, A-SeQDs increased both nitric oxide productions and intracellular BH4 levels, upregulated dihydrofolate reductase activity in lungs, and improved pulmonary arterial remodeling. Gene deletion of dihydrofolate reductase abolished these effects produced by A-SeQDs in mice. Finally, the blood levels of tetrahydrobiopterin and selenium were decreased in patients with pulmonary arterial hypertension., Conclusion: A-SeQDs increase intracellular tetrahydrobiopterin to prevent pulmonary arterial hypertension through recoupling endothelial nitric oxide synthase., Methods: Two polymorphs of SeQDs and A-SeQDs, and a crystalline form of SeQDs (C-SeQDs) were prepared through self-redox decomposition of selenosulfate precursor. Mice were injected with monocrotaline to induce pulmonary arterial hypertension in vivo . Pulmonary arterial pressure was measured.

Fatty acids (FAs) are transported by serum albumin in plasma. Studies have been undertaken to address the binding of MCFAs or LCFAs to human plasma albumin (HPA) and bovine serum albumin (BSA) by characterizing the binding affinities. Previous research on FA binding to serum albumin was usually performed in dilute solutions that are not sufficiently concentrated for the interpretation of the significance of the results under normal physiological conditions. How macromolecular crowded media affect fatty acids and bovine serum albumin (BSA) binding remains unknown. In this article, we investigated the mechanism of FA-BSA binding in a polyethylene glycol crowding environment by using thermodynamic and spectroscopic methods. Molecular crowding increased the binding constant for saturated medium-chain fatty acids (MCFAs) but significantly decreased the binding constant for unsaturated long-chain FAs. The binding sites tended to increase in all the cases. Further investigation revealed that crowding media might loosen the structure of BSA, facilitating MCFA-BSA binding. This research is useful for understanding the transportation of FAs by BSA under physiological conditions and may also help to control digestion by the eventual incorporation of macromolecular crowding agents into food formulations.

Purpose: The goal of this study was to clarify the reporting patterns of self-reported adverse drug reactions (ADRs) in China., Methods: A variety of sources were searched, including the official website of China FDA, the national center for ADR monitoring center, publications from PubMed, and so on. We retrieved the relevant information and made descriptive and comparative analysis from the year 2009 to 2013., Results: The ADR reporting numbers were 638,996, 692,904, 852,799, 1,200,000 and 1,317,000 from 2009 to 2013, respectively. Healthcare professionals contributed significantly, and their proportion always exceeded 80% before 2012. The average report per million inhabitants has increased from 479 to 983 from 2009 to 2013. However, the proportion of new or serious report was always below 25%. The reports mainly concern anti-infective agents and traditional Chinese medicine (TCM), especially TCM injection. The proportion of ADR reports in geriatric patients has increased for 4 consecutive years., Conclusions: ADR report numbers and reporting rates in China are on the rise. However, the proportion of new or serious reports as well as the proportion of reports contributed by consumers and pharmaceutical companies are still quite low. More attention should be paid to the elderly, anti-infective agents and TCM, especially TCM injections.