Allograft inflammatory factor-1 (AIF-1) plays an important role in various inflammatory conditions. Our previous study demonstrated that AIF-1 was over-expressed in the liver of BALB/c mice infected with Schistosoma japonicum and played significant role in the pathogenesis of schistosomiasis. The aim of this study was to focus on the effect of AIF-1 treatment on liver fibrosis and necrosis of BALB/c mice infected with S. japonicum. Seventy-two BALB/c mice were infected with cercariae of S. japonicum and then divided into three groups: AIF-1-treated group, saline-treated group, and control group. The vital signs, liver function, egg load, and hepatic pathological changes of the mice were assessed, and the levels of AIF-1 and TNF-α in the liver and spleen were measured at 5, 8, and 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum suppressed the expression of TNF-α and increased the effectiveness of AIF-1 in the liver and spleen at 14 weeks postinfection. Histopathological analysis and Masson trichrome staining for the liver tissues showed that the liver fibrosis and necrosis were alleviated previously compared with other infected mice at 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum can alleviate hepatic fibrosis and necrosis which indicate that AIF-1 use may prevent and cure the liver fibrosis.
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http://dx.doi.org/10.1007/s00436-014-3915-8 | DOI Listing |
Sci Rep
December 2024
State Key Laboratory for Diagnosis, Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, China.
Influenza virus infections are a serious danger to people's health worldwide as they are responsible for seasonal flu outbreaks. There is an urgent need to improve the effectiveness and durability longevity of the immune response to influenza vaccines. We synthesized the CpG HP021 and examined the impact of it on the immune response to an influenza vaccine.
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December 2024
Fujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, Institute for Basic Medical Sciences, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
High-fat diet (HFD) induces low-grade chronic inflammation, contributing to obesity and insulin resistance. However, the precise mechanisms triggering obesity-associated metabolic inflammation remain elusive. In this study, we identified epigenetic factor Brd4 as a key player in this process by regulating the expression of Ccr2/Ccr5 in colonic macrophage.
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December 2024
Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Sepsis is defined as a dysfunctional, life-threatening response to infection leading to multiorgan dysfunction and failure. During the past decade, studies have highlighted the relationship between sepsis and aging. However, the role of aging-related mechanisms in the progression and prognosis of sepsis remains unclear.
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December 2024
Division of Zoonosis Research, National Institute of Animal Health, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Salmonella enterica serovar 4,[5],12:i:- sequence type 34 (ST34) has recently become a global concern for public and animal health. The acquisition of mobile genetic element ICEmST, which contains two copper tolerance gene clusters, cus and pco, influences the epidemic success of this clone. Copper is used as a feed additive in swine at levels that potentially lead to selection pressure for Enterobacteriaceae; however, it remains unclear whether the copper tolerance system of ICEmST functions in vivo.
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December 2024
Department of Gynaecology, The Affiliated Wuxi People's Hospital of Nanjing Medical University/Wuxi Medical Center, Nanjing Medical University/Wuxi People's Hospital, 299 Qingyang Road, Wuxi, 214023, Jiangsu, China.
Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in cancer progression. We found lncRNA DNM1P35 is elevated in ovarian tumors compared to normal tissues, and demonstrated that lncRNA DNM1P35 promoted cancer cell proliferation, migration and invasion in SK-OV-3 and OVCAR-3 cell lines. Furthermore, lncRNA DNM1P35 also facilitated the epithelial-mesenchymal transition (EMT) of ovarian cancer cells.
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