Implementation of the Fuzzy C-Means Clustering Algorithm in Meteorological Data

Yinghua Lu,Tinghuai Ma,Changhong Yin,Xiaoyu Xie,Wei Tian,ShuiMing Zhong 보안공학연구지원센터 2013 International Journal of Database Theory and Appli Vol.6 No.6

Microbial short-chain fatty acids: a bridge between dietary fibers and poultry gut health — A review

Ali Qasim,Ma Sen,La Shaokai,Guo Zhiguo,Liu Boshuai,Gao Zimin,Farooq Umar,Wang Zhichang,Zhu Xiaoyan,Cui Yalei,Li Defeng,Shi Yinghua 아세아·태평양축산학회 2022 Animal Bioscience Vol.35 No.10

The maintenance of poultry gut health is complex depending on the intricate balance among diet, the commensal microbiota, and the mucosa, including the gut epithelium and the superimposing mucus layer. Changes in microflora composition and abundance can confer beneficial or detrimental effects on fowl. Antibiotics have devastating impacts on altering the landscape of gut microbiota, which further leads to antibiotic resistance or spread the pathogenic populations. By eliciting the landscape of gut microbiota, strategies should be made to break down the regulatory signals of pathogenic bacteria. The optional strategy of conferring dietary fibers (DFs) can be used to counterbalance the gut microbiota. DFs are the non-starch carbohydrates indigestible by host endogenous enzymes but can be fermented by symbiotic microbiota to produce shortchain fatty acids (SCFAs). This is one of the primary modes through which the gut microbiota interacts and communicate with the host. The majority of SCFAs are produced in the large intestine (particularly in the caecum), where they are taken up by the enterocytes or transported through portal vein circulation into the bloodstream. Recent shreds of evidence have elucidated that SCFAs affect the gut and modulate the tissues and organs either by activating G-protein-coupled receptors or affecting epigenetic modifications in the genome through inducing histone acetylase activities and inhibiting histone deacetylases. Thus, in this way, SCFAs vastly influence poultry health by promoting energy regulation, mucosal integrity, immune homeostasis, and immune maturation. In this review article, we will focus on DFs, which directly interact with gut microbes and lead to the production of SCFAs. Further, we will discuss the current molecular mechanisms of how SCFAs are generated, transported, and modulated the pro-and anti-inflammatory immune responses against pathogens and host physiology and gut health. The maintenance of poultry gut health is complex depending on the intricate balance among diet, the commensal microbiota, and the mucosa, including the gut epithelium and the superimposing mucus layer. Changes in microflora composition and abundance can confer beneficial or detrimental effects on fowl. Antibiotics have devastating impacts on altering the landscape of gut microbiota, which further leads to antibiotic resistance or spread the pathogenic populations. By eliciting the landscape of gut microbiota, strategies should be made to break down the regulatory signals of pathogenic bacteria. The optional strategy of conferring dietary fibers (DFs) can be used to counterbalance the gut microbiota. DFs are the non-starch carbohydrates indigestible by host endogenous enzymes but can be fermented by symbiotic microbiota to produce shortchain fatty acids (SCFAs). This is one of the primary modes through which the gut microbiota interacts and communicate with the host. The majority of SCFAs are produced in the large intestine (particularly in the caecum), where they are taken up by the enterocytes or transported through portal vein circulation into the bloodstream. Recent shreds of evidence have elucidated that SCFAs affect the gut and modulate the tissues and organs either by activating G-protein-coupled receptors or affecting epigenetic modifications in the genome through inducing histone acetylase activities and inhibiting histone deacetylases. Thus, in this way, SCFAs vastly influence poultry health by promoting energy regulation, mucosal integrity, immune homeostasis, and immune maturation. In this review article, we will focus on DFs, which directly interact with gut microbes and lead to the production of SCFAs. Further, we will discuss the current molecular mechanisms of how SCFAs are generated, transported, and modulated the pro-and anti-inflammatory immune responses against pathogens and host physiology and gut health.

Novel Push-Front Fibonacci Windows Model for Finding Emerging Patterns with Better Completeness and Accuracy

Tubagus Mohammad Akhriza,Yinghua Ma,Jian Hua Li 한국전자통신연구원 2018 ETRI Journal Vol.40 No.1

To find the emerging patterns (EPs) in streaming transaction data, the streaming is first divided into some time windows containing a number of transactions. Itemsets are generated from transactions in each window, and then the emergence of itemsets is evaluated between two windows. In the tilted-time windows model (TTWM), it is assumed that people need support data with finer accuracy from the most recent windows, while accepting coarser accuracy from older windows. Therefore, a limited array's elements are used to maintain all support data in a way that condenses old windows by merging them inside one element. The capacity of elements that accommodates the windows inside is modeled using a particular number sequence. However, in a stream, as new data arrives, the current array updating mechanisms lead to many null elements in the array and cause data incompleteness and inaccuracy problems. Two models derived from TTWM, logarithmic TTWM and Fibonacci windows model, also inherit the same problems. This article proposes a novel push-front Fibonacci windows model as a solution, and experiments are conducted to demonstrate its superiority in finding more EPs compared to other models.

MicroRNA 34c Gene Down-regulation via DNA Methylation Promotes Self-renewal and Epithelial-Mesenchymal Transition in Breast Tumor-initiating Cells

Yu, Fengyan,Jiao, Yu,Zhu, Yinghua,Wang, Ying,Zhu, Jingde,Cui, Xiuying,Liu, Yujie,He, Yinghua,Park, Eun-Young,Zhang, Hongyu,Lv, Xiaobin,Ma, Kelong,Su, Fengxi,Park, Jong Hoon,Song, Erwei American Society for Biochemistry and Molecular Bi 2012 The Journal of biological chemistry Vol.287 No.1

5-Formylhonokiol exerts anti-angiogenesis activity $via$ inactivating the ERK signaling pathway

Zhu, Wei,Fu, Afu,Hu, Jia,Wang, Tianen,Luo, Youfu,Peng, Ming,Ma, Yinghua,Wei, Yuquan,Chen, Lijuan Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.3

Our previous report has demonstrated that 5-formylhonokiol (FH), a derivative of honokiol (HK), exerts more potent anti-proliferative activities than honokiol in several tumor cell lines. In present study, we first explored the antiangiogenic activities of 5-formylhonokiol on proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVECs) for the first time $in$ $vitro$. Then we investigated the $in$ $vivo$ antiangiogenic effect of 5-formylhonokiol on zebrafish angiogenesis model. In order to clarify the underlying molecular mechanism of 5-formylhonokiol, we investigated the signaling pathway involved in controlling the angiogenesis process by western blotting assay. Wound-healing results showed that 5-formylhonokiol significantly and dose-dependently inhibited migration of cultured human umbilical vein enthothelial cells. The invasiveness of HUVEC cells was also effectively suppressed at a low concentration of 5-formylhonokiol in the transwell assay. Further F-actin imaging revealed that inhibitory effect of 5-formylhonokiol on invasion may partly contribute to the disruption of assembling stress fiber. Tube formation assay, which is associated with endothelial cells migration, further confirmed the anti-angiogenesis effect of 5-formylhonokiol. In $in$ $vivo$ zebrafish angiogenesis model, we found that 5-formylhonokiol dose-dependently inhibited angiogenesis. Furthermore, western blotting showed that 5-formylhonokiol significantly down-regulated extracellular signal-regulated kinase (ERK) expression and inhibited the phosphorylation of ERK but not affecting the total protein kinase B (Akt) expression and related phosphorylation, suggesting that 5-formylhonokiol might exert anti-angiogenesis capacity $via$ down-regulation of the ERK signal pathway. Taken together, these data suggested that 5-formylhonokiol might be a viable drug candidate in antiangiogenesis and anticancer therapies.

5-Formylhonokiol exerts anti-angiogenesis activity via inactivating the ERK signaling pathway

Wei Zhu,Lijuan Chen,Afu Fu,Jia Hu,Tianen Wang,Youfu Luo,Ming Peng,Yinghua Ma,Yuquan Wei 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.3

Our previous report has demonstrated that 5-formylhonokiol (FH), a derivative of honokiol (HK), exerts more potent anti-proliferative activities than honokiol in several tumor cell lines. In present study, we first explored the antiangiogenic activities of 5-formylhonokiol on proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVECs) for the first time in vitro. Then we investigated the in vivo antiangiogenic effect of 5-formylhonokiol on zebrafish angiogenesis model. In order to clarify the underlying molecular mechanism of 5-formylhonokiol, we investigated the signaling pathway involved in controlling the angiogenesis process by western blotting assay. Wound-healing results showed that 5-formylhonokiol significantly and dose-dependently inhibited migration of cultured human umbilical vein enthothelial cells. The invasiveness of HUVEC cells was also effectively suppressed at a low concentration of 5-formylhonokiol in the transwell assay. Further F-actin imaging revealed that inhibitory effect of 5-formylhonokiol on invasion may partly contribute to the disruption of assembling stress fiber. Tube formation assay, which is associated with endothelial cells migration,further confirmed the anti-angiogenesis effect of 5-formylhonokiol. In in vivo zebrafish angiogenesis model, we found that 5-formylhonokiol dose-dependently inhibited angiogenesis. Furthermore, western blotting showed that 5-formylhonokiol significantly down-regulated extracellular signal-regulated kinase (ERK) expression and inhibited the phosphorylation of ERK but not affecting the total protein kinase B (Akt)expression and related phosphorylation, suggesting that 5-formylhonokiol might exert anti-angiogenesis capacity via down-regulation of the ERK signal pathway. Taken together, these data suggested that 5-formylhonokiol might be a viable drug candidate in antiangiogenesis and anticancer therapies.