Browsing by Author "Song, Liang"

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    Nitrogen-doped PtNi Catalysts on PBI-functionalized Carbon Support for the Oxygen Reduction Reaction in PEMFC
    (American Chemical Society, 2022) Li, Chenzhao; Song, Liang; Zhao, Xueru; Sasaki, Kotaro; Xie, Jian; Mechanical and Energy Engineering, Purdue School of Engineering and Technology
    PtM (M = 3d transition metals) alloys are known as the promising oxygen reduction reaction catalysts and have been considered as the replacement of pure Pt catalysts for the commercialization of proton exchange membrane fuel cells. Although great progress has been made in the past three decades, the performance and durability of PtM catalysts still face stringent challenges from practical applications. Functionalization of a catalyst carbon support with nitrogen-contained groups can add charges onto its surface, which can be utilized to build a more complete ionomer/catalyst interface, to reduce the catalyst particle size, and to improve particle size distribution. Nitriding of PtNi catalysts can effectively improve the catalyst activity and stability by the modification of lattice strain. Hereby, we propose a synergistic approach of combining polybenzimidazole-grafted Vulcan XC72 carbon as the catalyst carbon support and the nitriding of PtNi to develop PtNiN/XC72-polybenzimidazole catalysts. Such PtNiN/XC72-PBI catalysts exhibit the excellent performance of fuel cell membrane electrode assembly (i.e., mass activity, 440 mA mgPt–1; electrochemical surface area, 51 m2 gPt–1; and rated power density, 836 mW cm–2) as well as promising catalyst stability. The developed PtNiN/XC72-PBI meets the US DOE 2020 targets of mass activity for the fuel cell catalysts. This work provides a novel approach and a promising pathway on the development of the catalyst using such a synergistic approach─modification of the catalyst structure by nitrogen doping and functionalization of carbon support by polybenzimidazole for both high performance and high durability.
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    Prenatal inflammation exposure-programmed cardiovascular diseases and potential prevention
    (Elsevier, 2018) Deng, Youcai; Song, Liang; Nie, Xuqiang; Shou, Weinian; Li, Xiaohui; Pediatrics, School of Medicine
    In recent years, the rapid development of medical and pharmacological interventions has led to a steady decline in certain noncommunicable chronic diseases (NCDs), such as cancer. However, the overall incidence of cardiovascular diseases (CVDs) has not seemed to decline. CVDs have become even more prevalent in many countries and represent a global health threat and financial burden. An increasing number of epidemiological and experimental studies have demonstrated that maternal insults not only can result in birth defects but also can cause developmental functional defects that contribute to adult NCDs. In the current review, we provide an overview of evidence from both epidemiological investigations and experimental animal studies supporting the concept of developmental reprogramming of adult CVDs in offspring that have experienced prenatal inflammation exposure (PIE) during fetal development (PIE-programmed CVDs), a disease-causing event that has not been effectively controlled. This review describes the epidemiological observations, data from animal models, and related mechanisms for the pathogenesis of PIE-programmed CVDs. In addition, the potential therapeutic interventions of PIE-programmed CVDs are discussed. Finally, we also deliberate the need for future mechanistic studies and biomarker screenings in this important field, which creates a great opportunity to combat the global increase in CVDs by managing the adverse effects of inflammation for prepregnant and pregnant individuals who are at risk for PIE-programmed CVDs.
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    Prenatal inflammation exposure-programmed hypertension exhibits multi-generational inheritance via disrupting DNA methylome
    (Nature, 2021-09-30) Guan, Xiao; Dan, Guo-rong; Yang, Yao; Ji, Yan; Lai, Wen-jing; Meng, Meng; Mo, Bang-hui; Huang, Pei; You, Ting-ting; Deng, Ya-fei; Song, Liang; Guo, Wei; Yi, Ping; Yu, Jian-hua; Gao, Yuan; Shou, Wei-nian; Chen, Bing-bo; Deng, You-cai; Li, Xiao-hui; Pediatrics, School of Medicine
    The multi-generation heredity trait of hypertension in human has been reported, but the molecular mechanisms underlying multi-generational inheritance of hypertension remain obscure. Recent evidence shows that prenatal inflammatory exposure (PIE) results in increased incidence of cardiovascular diseases, including hypertension. In this study we investigated whether and how PIE contributed to multi-generational inheritance of hypertension in rats. PIE was induced in pregnant rats by intraperitoneal injection of LPS or Poly (I:C) either once on gestational day 10.5 (transient stimulation, T) or three times on gestational day 8.5, 10.5, and 12.5 (persistent stimulation, P). Male offspring was chosen to study the paternal inheritance. We showed that PIE, irrespectively induced by LPS or Poly (I:C) stimulation during pregnancy, resulted in multi-generational inheritance of significantly increased blood pressure in rat descendants, and that prenatal LPS exposure led to vascular remodeling and vasoconstrictor dysfunction in both thoracic aorta and superior mesenteric artery of adult F2 offspring. Furthermore, we revealed that PIE resulted in global alteration of DNA methylome in thoracic aorta of F2 offspring. Specifically, PIE led to the DNA hypomethylation of G beta gamma (Gβγ) signaling genes in both the F1 sperm and the F2 thoracic aorta, and activation of PI3K/Akt signaling was implicated in the pathologic changes and dysregulated vascular tone of aortic tissue in F2 LPS-P offspring. Our data demonstrate that PIE reprogrammed DNA methylome of cells from the germline/mature gametes contributes to the development of hypertension in F2 PIE offspring. This study broadens the current knowledge regarding the multi-generation effect of the cumulative early life environmental factors on the development of hypertension.