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"Li, Jie-Liang"
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هذه هي الصين : قوة تسير نحو العالم
يركز كتاب \"هذه هي الصين\" على سرد قصص تنمية الصين في العصر الجديد. وقد غير الدكتور تشانغ وي وي طريقته المعروفة بالتوجيه والإرشاد في البرامج الأيديولوجية والنظرية في الماضي، وعبر عنها بلغة شعبية سائغة، وحجج منطقية صارمة، وبيانات حقيقية، وتصادمات صريحة للأفكار، وتقنيات عرض مبتكرة لمساعدة الجمهور على فهم النموذج الصيني والطريق الصيني، وتعزيز ثقتهم بمستقبل الصين.
Book
Human Intestinal Epithelial Cells Release Antiviral Factors That Inhibit HIV Infection of Macrophages
As a rich source of CD4
T cells and macrophages, the gastrointestinal (GI) tract is a major target site for HIV infection. The interplay between GI-resident macrophages and intestinal epithelial cells (IECs) constitutes an important element of GI innate immunity against pathogens. In this study, we investigated whether human IECs have the ability to produce antiviral factors that can inhibit HIV infection of macrophages. We demonstrated that IECs possess functional toll-like receptor 3 (TLR3), the activation of which resulted in induction of key interferon (IFN) regulatory factors (IRF3 and IRF7), IFN-β, IFN-λ, and CC chemokines (MIP-1α, MIP-1β, RANTES), the ligands of HIV entry co-receptor CCR5. In addition, TLR3-activated IECs release exosomes that contained the anti-HIV factors, including IFN-stimulated genes (ISGs: ISG15, ISG56, MxB, OAS-1, GBP5, and Viperin) and HIV restriction miRNAs (miRNA-17, miRNA-20, miRNA-28, miRNA-29 family members, and miRNA-125b). Importantly, treatment of macrophages with supernatant (SN) from the activated IEC cultures inhibited HIV replication. Further studies showed that IEC SN could also induce the expression of antiviral ISGs and cellular HIV restriction factors (Tetherin and APOBEC3G/3F) in HIV-infected macrophages. These findings indicated that IECs might act as an important element in GI innate immunity against HIV infection/replication.
Journal Article
IFN-λ3 Inhibits HIV Infection of Macrophages through the JAK-STAT Pathway
Interferon lambda 3 (IFN-λ3) is a newly identified cytokine with antiviral activity, and its single nucleotide polymorphisms are strongly associated with the treatment effectiveness and development of chronic hepatitis C virus infection. We thus examined the potential of IFN-λ3 to inhibit HIV replication and the possible mechanisms of the anti-HIV action by IFN-λ3 in human macrophages.
Under different conditions (before, during, and after HIV infection), IFN-λ3 significantly inhibited viral replication in macrophages, which was associated with the induction of multiple antiviral cellular factors (ISG56, MxA, OAS-1, A3G/F and tetherin) and IFN regulatory factors (IRF-1, 3, 5, 7 and 9). This anti-HIV action of IFN-λ3 could be compromised by the JAK-STAT inhibitor. In addition, IFN-λ3 treatment of macrophages induced the expression of toll-like receptor 3 (TLR3) and two key adaptors (MyD88 and TRIF) in type I IFN pathway activation. However, HIV infection compromised IFN-λ3-mediated induction of the key elements in JAK-STAT signaling pathway.
These data indicate that IFN-λ3 exerts its anti-HIV function by activating JAK-STAT pathway-mediated innate immunity in macrophages. Future in vivo studies are necessary in order to explore the potential for developing IFN-λ3-based therapy for HIV disease.
Journal Article
Impact of type 2 and steroid-Induced diabetes mellitus on prognosis in patients with multiple myeloma
Objective
This study aimed to investigate the association between type 2 diabetes mellitus (T2DM) and steroid-induced diabetes mellitus (SIDM) with prognosis in patients with multiple myeloma (MM).
Methods
A retrospective analysis was conducted on patients initially diagnosed with MM at Henan Provincial Cancer Hospital between January 2005 and December 2016. Patients were categorized into three groups: MM without diabetes mellitus, MM with T2DM, and MM with SIDM.
Results
A cohort of 1,463 patients were included in this study, comprising 818 patients with MM without diabetes mellitus, 217 with MM and T2DM, and 428 with MM and SIDM. Independent predictors of overall survival (OS) in the entire cohort included age (hazard ratio [HR] = 1.011, 95% confidence interval [CI]: 1.007–1.016,
p <
0.001), International Staging System (ISS) stage III (HR = 1.463, 95% CI: 1.273–1.681,
p
< 0.001), hematopoietic stem cell transplantation (HSCT) (HR = 0.334, 95% CI: 0.286–0.390,
p
< 0.001), chromosomal abnormalities (HR = 11.999, 95% CI: 9.688–14.860,
p
< 0.001), T2DM (HR = 1.606, 95% CI: 1.409–1.829,
p
< 0.001), and SIDM (HR = 1.224, 95% CI: 1.038–1.444,
p
= 0.016). Among patients with MM and SIDM, age (HR = 1.047, 95% CI: 1.037–1.057,
p
< 0.001), ISS stage III (HR = 1.796, 95% CI: 1.389–2.322,
p
< 0.001), lactate dehydrogenase (HR = 1.004, 95% CI: 1.002–1.006,
p
< 0.001), HSCT (HR = 0.284, 95% CI: 0.213–0.382,
p
< 0.001), and chromosomal abnormalities (HR = 14.59, 95% CI: 9.822–21.674,
p
< 0.001) were independently associated with OS. In patients with MM and T2DM, ISS stage II (HR = 2.008, 95% CI: 1.418–2.844,
p
< 0.001), ISS stage III (HR = 3.126, 95% CI: 2.110–4.631,
p
< 0.001), HSCT (HR = 0.264, 95% CI: 0.173–0.403,
p
< 0.001), and chromosomal abnormalities (HR = 32.677, 95% CI: 17.632–60.560,
p
< 0.001) were independently associated with OS.
Conclusion
Both T2DM and SIDM were independently associated with poorer prognosis in patients with MM.
Journal Article
Heroin Abuse and/or HIV Infection Dysregulate Plasma Exosomal miRNAs
Exosomes play an important role in cell-to-cell communication as they can transfer functional molecules such as microRNAs (miRNAs) from one cell to another, exerting biological and immunological functions. Here, we investigated the impact of HIV infection and/or heroin use on the expression of the miRNAs in plasma exosomes. We found that HIV infection or heroin use upregulated the majority (98%) of a panel of plasma exosomal miRNAs associated with immune regulation and inflammation. We also observed the enhanced effect of HIV infection and heroin use on some of these upregulated miRNAs. Our further investigation showed that the levels of four of neuro-inflammation-related miRNAs (146a, 126, 21, and let-7a) were higher in HIV-infected heroin users as compared with the control subjects. These findings indicate that the dysregulations of the plasma exosomal miRNAs support further studies to determine the role of the miRNAs in HIV and/or heroin use-mediated immune modulation and neuro-inflammation.
Graphical abstract
Journal Article
Neuroprotective Activity of ( - )-Epigallocatechin Gallate against Lipopolysaccharide-Mediated Cytotoxicity
Lipopolysaccharide- (LPS-) mediated systemic inflammation plays a critical role in neurodegenerative diseases. The present study was conducted to evaluate the protective effects of epigallocatechin gallate (EGCG), the major component in green tea, on LPS-mediated inflammation and neurotoxicity. LPS treatment of macrophages induced expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6). However, EGCG pretreatment of macrophages significantly inhibited LPS-mediated induction of these cytokines. In addition, EGCG significantly diminished LPS-induced inflammatory cytokines in the peripheral mononuclear blood cells (PBMCs). Supernatant from EGCG-pretreated and LPS-activated macrophage cultures was found to be less cytotoxic to neurons than that from non-EGCG-pretreated and LPS-activated macrophage cultures. Furthermore, EGCG treatment of neurons could inhibit LPS-induced production of reactive oxygen species (ROS). Thus EGCG represents a potent and useful neuroprotective agent for inflammation-mediated neurological disorders.
Journal Article
IFN-λ Inhibits Drug-Resistant HIV Infection of Macrophages
Type III interferons (IFN-λs) have been demonstrated to inhibit a number of viruses, including HIV. Here, we further examined the anti-HIV effect of IFN-λs in macrophages. We found that IFN-λs synergistically enhanced anti-HIV activity of antiretrovirals [azidothymidine (AZT), efavirenz, indinavir, and enfuvirtide] in infected macrophages. Importantly, IFN-λs could suppress HIV infection of macrophages with the drug-resistant strains, including AZT-resistant virus (A012) and reverse transcriptase inhibitor-resistant virus (TC49). Mechanistically, IFN-λs were able to induce the expression of several important anti-HIV cellular factors, including myxovirus resistance 2 (Mx2), a newly identified HIV post-entry inhibitor and tetherin, a restriction factor that blocks HIV release from infected cells. These observations provide additional evidence to support the potential use of IFN-λs as therapeutics agents for the treatment of HIV infection.
Journal Article
Regulatory Effect and Mechanism of Erythroblastic Island Macrophages on Anemia in Patients with Newly Diagnosed Multiple Myeloma
To examine the clinical characteristics and anemia-related factors in patients with newly diagnosed multiple myeloma (NDMM), as well as the effect and mechanism of erythroblastic islands (EBIs) and EBI macrophages in NDMM patients with anemia.
We collected and analyzed clinical data to find anemia-related factors. Using flow cytometry, the numbers and ratios of erythroblasts and EBI macrophages were determined. RNA sequencing (RNA-seq) was used to determine the differences of EBI macrophages in NDMM patients with or without anemia.
Based on the clinical characteristics of NDMM patients with anemia, MCV, abnormal levels of albumin, osteolytic lesions, and Durie-Salmon (DS) stage are risk factors for anemia. Patients with anemia have fewer erythroblasts, erythroblastic islands (EBIs), and EBI macrophages in their bone marrow than patients without anemia. RNA-seq analysis of EBI macrophages from the bone marrow of patients with and without anemia revealed that macrophages from patients with anemia are impaired and tend to promote the production of interleukin-6, which has been demonstrated to be an essential survival factor of myeloma cells and protects them from apoptosis.
In NDMM patients with anemia, EBI macrophages are impaired, which causes anemia in those patients. Our finding highlights the significance of EBI macrophages in anemia in NDMM patients and provides a new strategy for recovery from anemia in these patients.
Journal Article
Development of chromosome-specific potential intron polymorphism markers in watermelon
Intron length polymorphism (ILP) marker is one of the popular molecular markers. Despite the effectiveness of ILP markers in some plants has been reported, while none in watermelon compared to others marker systems. In this study, a genome-wide survey of intron length markers for watermelon genome-annotated genes was performed. According to the genomic information of watermelon, the intron position was extracted by comparison with
Arabidopsis thaliana
, and the primers were designed by ePrimer3. A total of 51,585 potential intron polymorphism (PIP) markers spanning 11 watermelon chromosomes were identified and designed. All these PIP markers on the watermelon genome were verified by ePCR, and 50,093 (98.51%) markers revealed single-locus amplification. The marker genes on chromosome 10 have the strongest collinearity with genes on other chromosomes. Further, two primers were randomly selected from the designed primers, and electrophoresis on 8% polyacrylamide gel was carried out in 48 watermelon cultivars demonstrated the potential utility of the developed markers. This study reported the development of PIP markers in watermelon for the first time, and provided abundant marker resources for genetic variation research, functional gene discovery and genome-assisted breeding of watermelon.
Journal Article
Soybean-derived Bowman-Birk Inhibitor (BBI) Inhibits HIV Replication in Macrophages
The Bowman-Birk inhibitor (BBI), a soybean-derived protease inhibitor, is known to have anti-inflammatory effect in both
in vitro
and
in vivo
systems. Macrophages play a key role in inflammation and immune activation, which is implicated in HIV disease progression. Here, we investigated the effect of BBI on HIV infection of peripheral blood monocyte-derived macrophages. We demonstrated that BBI could potently inhibit HIV replication in macrophages without cytotoxicity. Investigation of the mechanism(s) of BBI action on HIV showed that BBI induced the expression of IFN-β and multiple IFN stimulated genes (ISGs), including Myxovirus resistance protein 2 (Mx2), 2′,5′-oligoadenylate synthetase (OAS-1), Virus inhibitory protein (viperin), ISG15 and ISG56. BBI treatment of macrophages also increased the expression of several known HIV restriction factors, including APOBEC3F, APOBEC3G and tetherin. Furthermore, BBI enhanced the phosphorylation of IRF3, a key regulator of IFN-β. The inhibition of IFN-β pathway by the neutralization antibody to type I IFN receptor (Anti-IFNAR) abolished BBI-mediated induction of the anti-HIV factors and inhibition of HIV in macrophages. These findings that BBI could activate IFN-β-mediated signaling pathway, initialize the intracellular innate immunity in macrophages and potently inhibit HIV at multiple steps of viral replication cycle indicate the necessity to further investigate BBI as an alternative and cost-effective anti-HIV natural product.
Journal Article