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<title>MS 2018 Focus Issue1</title>
<link>http://hdl.handle.net/10608/9705</link>
<description/>
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<rdf:li rdf:resource="http://hdl.handle.net/10608/9998"/>
<rdf:li rdf:resource="http://hdl.handle.net/10608/9997"/>
<rdf:li rdf:resource="http://hdl.handle.net/10608/9996"/>
<rdf:li rdf:resource="http://hdl.handle.net/10608/9995"/>
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<dc:date>2026-04-05T19:56:16Z</dc:date>
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<item rdf:about="http://hdl.handle.net/10608/9998">
<title>Exploring the dynamic changes between pulmonary and cutaneous sarcoidosis based on gene expression</title>
<link>http://hdl.handle.net/10608/9998</link>
<description>Exploring the dynamic changes between pulmonary and cutaneous sarcoidosis based on gene expression
Sheng, Youyu; Yang, Yuxin; Wu, Yun; Yang, Qinping
Sarcoidosis is a disease involving the growth of abnormal inflammatory granulomas and affecting multisystems. It has an unknown etiology. The lung and the skin are the most commonly involved organs. Although large amounts of research have focused on the pathogenesis of sarcoidosis, little is known about the link between cutaneous sarcoidosis and pulmonary sarcoidosis. Moreover, the gene expression profiles provide a novel way to find diagnostic or prognostic biomarkers. Therefore, the aim of this study was to analyze the differentially expressed genes (DEGs) in pulmonary sarcoidosis and cutaneous sarcoidosis patients and to compare them to healthy individuals. DEGs and their biological functions are dynamically dysregulated, and several common disease-related genes and mutual disease progression-related genes were identified which linked pulmonary sarcoidosis and cutaneous sarcoidosis together. The biological functional pathways regulated by these DEGs may allow to define the common mechanism shared by different type of sarcoidosis, providing novel insight into the common pathogenesis of sarcoidosis and opening the way to the development of new therapeutic strategies.
</description>
<dc:date>2018-01-01T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/10608/9997">
<title>Complement protein C5a enhances the β-amyloid-induced neuro-inflammatory response in microglia in Alzheimer’s disease</title>
<link>http://hdl.handle.net/10608/9997</link>
<description>Complement protein C5a enhances the β-amyloid-induced neuro-inflammatory response in microglia in Alzheimer’s disease
An, Xiao-qun; Xi, Wei; Gu, Chen-yun; Huang, Xiao
Objective: The dysregulation of neuro-inflammation is one of the attributes of the pathogenesis of Alzheimer’s disease (AD). Over-expression of complement proteins co-localizes with neurofibrillary tangles, thereby indicating that a complement system may be involved in neuro-inflammation. Here, we report the influence of complement activation on the neuro-inflammation using a microglial cell line. Methods: first, we performed a cytotoxic assay using the microglial cells BV-2. Second, after treatment of BV-2 cells with Aβ42 and/ or C5a, the anaphylatoxin derived from C5, we determined the expression levels of the pro-inflammatory factors TNF-α, IL-1β, and IL-6. Finally, we explored whether this neuroinflammatory response was mediated by JAK/ STAT3 signaling. Results: C5a had an enhanced effect on the neural cell viability of BV-2 cells treated with Aβ42. In addition, C5a also increased the Aβ-induced neuro-inflammatory response, and these effects were blocked by the C5aR antagonist, PMX205. Finally, we demonstrated that the neuro-inflammatory responses induced by Aβ and C5a were mediated through JAK/STAT3 signaling. By blocking this pathway with an antagonist, AG490, the expression of TNF-α, IL-1β, and IL-6 was alleviated. Conclusion: The complement protein C5a could exaggerate the Aβ-induced neuroinflammatory response in microglia, and C5aR may be a potential therapeutic tool for AD treatment.
</description>
<dc:date>2018-01-01T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/10608/9996">
<title>Relationship between depression and blood cytokine levels in lung cancer patients</title>
<link>http://hdl.handle.net/10608/9996</link>
<description>Relationship between depression and blood cytokine levels in lung cancer patients
Liu, Wen-Juan; Wang, Xiao-Dan; Wu, Wei; Huang, Xiao
Objective: To study the correlation between depression and blood cytokine levels in lung cancer patients. Methods: 92 patients with advanced lung cancer were evaluated for depression using the scoring index of depression self-rating scale. Lack of depression (n=24), mild depression (n=45), and moderate depression (n=23) were found in the cohort. Meanwhile, 40 healthy subjects were selected as the control group. The levels of IL-10, IL-6, IL-8, and TNF-α in each group were detected by sandwich enzyme-linked immunosorbent assays, and their correlation with the degree of depression was analyzed. Results: The levels of IL-10, IL-6, IL-8, and TNF-α were all higher than those in the control group (P&lt;0.05). Moreover, the depression statuses of patients with lung cancer were positively correlated with IL-10, IL-6, and TNF-α levels (r = 0.705, 0.301, and 0.446, P&lt;0.01); however, the level of IL-8 was not relevant (r=0.136, p&gt;0.05). Conclusion: Serum levels of IL-10, IL-6, and TNF-α are associated with depression scoring in patients with lung cancer.
</description>
<dc:date>2018-01-01T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/10608/9995">
<title>Analysis of the association between CDH2 gene polymorphism and osteoarthritis risk</title>
<link>http://hdl.handle.net/10608/9995</link>
<description>Analysis of the association between CDH2 gene polymorphism and osteoarthritis risk
Zhao, Guanglei; Shi, Jingsheng; Xia, Jun
Objective: to define the cadherin 2 (CDH2) gene polymorphism in Chinese osteoarthritis and control populations and to explore the correlation between CDH2 gene polymorphism and the risk of osteoarthritis. Method: a total of 476 patients with osteoarthritis were collected and 380 control subjects were included in the study. Clinical data such as gender, age and functional score were collected. The blood and tissue samples were collected and genotyped by PCR. Data analysis was performed using SPSS 19.0, Hapioview 4.2 and SNPstats softwares. Results: the association of rs11083271 and osteoarthritis was initially validated in this study population (P = 0.016, OR = 1.43 (1.07- 1.93)]. The risk of OA was significantly higher in heterozygous T/C than in homozygous T/T and C/C in rs11083271. By adjusting the age, according to gender stratification analysis, the heterozygous T/C genotype in rs11083271 significantly increased the risk of OA incidence in males [p = 0.011, 3.40 (1.55-7.43)]. The remaining rs sites were not significantly associated with OA. Notably, the association of rs11564299 with OA, regardless of genotyping, gene frequency and RNA expression levels in the study population, was not confirmed. Conclusion: in this study, we have analyzed the association between CDH2 gene polymorphism and OA in Chinese population. We found that rs11083271 heterozygous T/C genotype significantly increases the risk of OA and the severity of the disease. By contrast, the rs11564299 locus and OA have no significant correlation in the Chinese population. The role of rs11083271 in the regulation of CDH2 expression levels and the mechanisms by which it impacts OA remain to be further studied.
</description>
<dc:date>2018-01-01T00:00:00Z</dc:date>
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