The role of electrochemical biosensors in SARS-CoV-2 detection: a bibliometrics-based analysis and review

The global pandemic of COVID-19, which began in late 2019, has resulted in extremely high morbidity and severe mortality worldwide, with important implications for human health, international trade, and national politics. Severe acute respiratory syndrome coronavirus (SARS-CoV-2) is the primary pathogen causing COVID-19. Analytical chemistry played an important role in this global epidemic event, and detection of SARS-CoV-2 even became a part of daily life. Analytical chemists have devoted much effort and enthusiasm to this event, and different analytical techniques have shown very rapid development. Electrochemical biosensors are highly efficient, sensitive, and cost-effective and have been used to detect many highly pathogenic viruses long before this event. However, another fact is that electrochemical biosensors are not the technology of choice for most detection applications. This review describes for the first time the role played by electrochemical biosensors in SARS-CoV-2 detection from a bibliometric perspective. This paper analyzed 254 relevant research papers up to June 2022. The contributions of different countries and institutions to this topic were analyzed. Keyword analysis was used to explore different methodological attempts of electrochemical detection techniques. More importantly, we are trying to find an answer to the question: do electrochemical biosensors have the potential to become a genuinely employable detection technology in an outbreak of infectious disease?

This review describes for the first time the role played by electrochemical biosensors in SARS-CoV-2 detection from a bibliometric perspective.     

微切口超声乳化术对糖尿病合并白内障患者眼表的影响

目的：探讨白内障超声乳化手术中2.2及3.0mm透明角膜切口对2型糖尿病患者术后泪膜功能及眼表的影响。
　　方法：收集2015-01/10在我院接受超声乳化术的2型糖尿病患者150例150眼。按照随机数字表,将其分为两组,A组微切口组(75例75眼)行2.2mm透明角膜微切口白内障超声乳化术, B 组小切口组(75例75眼)行常规3.0 mm透明角膜切口白内障超声乳化术,两组资料的人口统计学特征差异无统计学意义。观察并比较两组患者术前及术后1wk,1、3、6mo的眼表疾病指数( ocular surface disease index,OSDI)、角膜知觉、泪膜破裂时间( break-up time,BUT)和基础泪液分泌试验( Schirmer’s Ⅰtest,SⅠt)指标的变化。
　　结果：术后1wk,1、3mo,两组患者的 OSDI 评分均高于术前,且B组的OSDI评分明显高于A组,差异有统计学意义(均P<0.05);两组患者的角膜知觉均较术前降低,且B组的角膜知觉明显低于A组,差异具有统计学意义(均P<0.05);两组患者的SⅠt均低于术前,且B组的SⅠt明显低于A组,差异具有统计学意义(均 P<0.05)。术后1wk,1mo,两组患者的BUT均低于术前,且B组的BUT明显低于A组,差异具有统计学意义(均 P<0.05)。术后6mo,A组患者的OSDI、角膜知觉、BUT和SⅠt与术前相比差异不明显,无统计学意义(均P>0.05);B组患者的OSDI评分和角膜知觉与术前相比差异明显,具有统计学意义(均P<0.05);BUT和SⅠt与术前相比差异不明显,无统计学意义(均P>0.05)。
　　结论：2.2mm透明角膜微切口对眼表及泪膜的影响较小,对并发白内障的2型糖尿病患者尤为适用。     

IL‐27 improves adoptive CD8+ T cells’ antitumor activity via enhancing cell survival and memory T cell differentiation

IL‐27 is an anti‐inflammatory cytokine that triggers enhanced antitumor immunity, particularly cytotoxic T lymphocyte responses. In the present study, we sought to develop IL‐27 into a therapeutic adjutant for adoptive T cell therapy using our well‐established models. We have found that IL‐27 directly improved the survival status and cytotoxicity of adoptive OT‐1 CD8⁺ T cells in vitro and in vivo. Meanwhile, IL‐27 treatment programs memory T cell differentiation in CD8⁺ T cells, characterized by upregulation of genes associated with T cell memory differentiation (T‐bet, Eomes, Blimp1, and Ly6C). Additionally, we engineered the adoptive OT‐1 CD8⁺ T cells to deliver IL‐27. In mice, the established tumors treated with OT‐1 CD8⁺ T‐IL‐27 were completely rejected, which demonstrated that IL‐27 delivered via tumor antigen–specific T cells enhances adoptive T cells’ cancer immunity. To our knowledge, this is the first application of CD8⁺ T cells as a vehicle to deliver IL‐27 to treat tumors. Thus, this study demonstrates IL‐27 is a feasible approach for enhancing CD8⁺ T cells’ antitumor immunity and can be used as a therapeutic adjutant for T cell adoptive transfer to treat cancer.     

KIF23 is a potential biomarker of diffuse large B cell lymphoma: Analysis based on bioinformatics and immunohistochemistry

Diffuse Large B Cell Lymphoma (DLBCL), the most common form of blood cancer. The genetic and clinical heterogeneity of DLBCL poses a major barrier to diagnosis and treatment. Hence, we aim to identify potential biomarkers for DLBCL.Differentially expressed genes were screened between DLBCL and the corresponding normal tissues. Kyoto Encyclopedia of Genes and Genomes and Gene oncology analyses were performed to obtain an insight into these differentially expressed genes. PPI network was constructed to identify hub genes. survival analysis was applied to evaluate the prognostic value of those hub genes. DNA methylation analysis was implemented to explore the epigenetic dysregulation of genes in DLBCL.In this study, Kinesin family member 23 (KIF23) showed higher expression in DLBCL and was identified as a risk factor in DLBCL. The immunohistochemistry experiment further confirmed this finding. Subsequently, the univariate and multivariate analysis indicated that KIF23 might be an independent adverse factor in DLBCL. Upregulation of KIF23 might be a risk factor for the overall survival of patients who received an R-CHOP regimen, in late-stage, whatever with or without extranodal sites. Higher expression of KIF23 also significantly reduced 3, 5, 10-year overall survival. Furthermore, functional enrichment analyses (Kyoto Encyclopedia of Genes and Genomes, Gene oncology, and Gene Set Enrichment Analysis) showed that KIF23 was mainly involved in cell cycle, nuclear division, PI3K/AKT/mTOR, TGF-beta, and Wnt/beta-catenin pathway in DLBCL. Finally, results of DNA methylation analysis indicated that hypomethylation in KIF23''s promoter region might be the result of its higher expression in DLBCL.The findings of this study suggested that KIF23 is a potential biomarker for the diagnosis and prognosis of DLBCL. However, further studies were needed to validate these findings.     

口腔溃疡豚鼠血清中谷胱甘肽过氧化物酶活性的研究

目的：研究口腔溃疡豚鼠血清中谷胱甘肽过氧化物酶（GSH-PX）的活性。方法：用90%苯酚溶液灼烧豚鼠左侧面颊,造成口腔溃疡模型,观察豚鼠口腔溃疡模型的溃疡面积、溃疡程度及溃疡组织病理变化,测定血清中GSH-PX活性。结果：用苯酚溶液造豚鼠口腔溃疡模型成功,d1～d5,模型组与空白组相比,口腔溃疡程度显著,血清中GSH-PX活性显著降低（P<0.01）。口腔溃疡豚鼠随着时间的变化溃疡面积逐渐缩小,血清中GSH-PX活性逐渐增强。结论：血清中GSH-PX对口腔溃疡的自愈有促进作用。     

地塞米松对脓毒血症鼠Peyer小结Tfh细胞的影响

目的：测定脓毒血症鼠Peyer小结内滤泡辅助性T细胞（T follicular helper,Tfh）的变化,分析地塞米松（dexamethasone,Dex）对脓毒血症Tfh细胞的可能作用。方法：昆明小鼠诱导脓毒血症模型,模型诱导成功后随机分2组,脓毒血症组（SE组,n=12）、脓毒血症＋Dex处理组（DE组,n=12）。另设对照组（NC组,n=12）。测定血清白介素-6（interleukin-6,IL-6）、降钙素原（procalcitonin,PCT）、中性粒细胞明胶酶相关载脂蛋白（neutrophil gelatinase-associated lipocalin,NGAL）水平。Peyer小结Ⅰ型1-磷酸鞘氨醇（Sphingosine 1-Phosphate 1,S1P1）、CXC趋化因子配体13（CXC chemokine ligand 13,CXCL13）免疫组化染色。Western blot分别检测Peyer小结IL-21、程序性死亡分子-1（programmed death 1,PD-1）、胞嘧啶脱氨酶（enzyme activation-induced cytidine deaminase,AID）蛋白的表达。流式细胞仪测定3组Peyer小结Tfh细胞占T淋巴细胞的百分率。结果：与NC组相比,SE组血清IL-6（19.7±5.20 vs 10.7±3.60 ng·L~（-1））、PCT（1.56±0.92 vs 0.31±0.09μg·L~（-1））、NGAL（0.44±0.11 vs 0.35±0.09 mg·L（-1））升高（P〈0.05或0.01）,Peyer小结S1P1（0.22±0.06 vs 0.14±0.04）、CXCL13（0.25±0.07 vs 0.15±0.04）的表达增加（P〈0.01）,IL-21（0.60±0.08 vs 0.35±0.08）、PD-1（0.30±0.04 vs 0.20±0.05）、AID（0.23±0.05 vs 0.18±0.03）蛋白的表达亦升高（P〈0.05或0.01）,Tfh细胞占T淋巴细胞（8.30±2.00 vs 5.69 vs 1.64%）的百分率升高（P〈0.01）。Dex治疗可降低SE鼠血清IL-6（19.7±5.20 vs 12.8±3.40 ng·L~（-1））、PCT（1.56±0.92 vs 0.71±0.44μg·L~（-1））水平（P〈0.05或0.01）,降低Peyer小结S1P1（0.22±0.06 vs 0.17±0.05）、CXCL13（0.25±0.07 vs 0.19±0.06）的表达（P〈0.05或0.01）,下调Peyer小结IL-21（0.60±0.08 vs 0.48±0.09）、PD-1（0.30±0.04 vs 0.26±0.06）、AID（0.23±0.05 vs0.19±0.04）蛋白的表达（P〈0.05）,降低Tfh细胞占T淋巴细胞（8.30±2.00 vs 6.56±1.59%）的百分率（P〈0.05）。结论：Peyer小结Tfh细胞可能参与脓毒血症的发病机制,Dex抑制Peyer小结Tfh的活化,对Peyer小结微环境起保护作用。     

正常人眼眶脂肪及眼外肌中抵抗素的表达

目的了解抵抗素在人眼眶脂肪组织及眼外肌组织中mRNA及蛋白表达情况。方法RT-PCR法检测人眼眶脂肪组织及眼外肌组织中抵抗素mRNA的表达情况；免疫组织化学法检测抵抗素蛋白在人眼眶脂肪组织及眼外肌组织中的表达。结果PCR产物电泳结果示抵抗素产物片段约500bp，脂肪组织中含量高于眼外肌组织。抵抗素蛋白表达位于胞浆，免疫组织化学显示人眼眶脂肪组织及眼外肌组织中有抵抗素蛋白存在。结论在人眼眶脂肪组织及眼外肌组织中可检测到抵抗素mRNA及蛋白的表达，抵抗素可能与眼眶炎性疾病，如Graves眼病、炎性假瘤等有一定的关系。     

芪竹方中单体及配伍对人胃癌细胞MGC-803抑制作用研究

目的:观察芪竹方单体成分薯蓣皂苷、莪术醇及两者配伍对人胃癌细胞MGC-803的增殖抑制作用,初步探讨芪竹方复方在抗肿瘤治疗中的有效成分及作用机制。方法:选用5个剂量的薯蓣皂苷、莪术醇单药组,及2个剂量的两药配伍组在24h、48h 2个不同时间点作用人胃癌细胞MGC-803,采用MTT法检测药物对MGC-803的增殖抑制率。结果:一定浓度范围内,薯蓣皂苷及莪术醇均对MGC-803细胞的增殖有剂量、时间依赖性抑制作用,且两药配伍使用较单药能产生更好的抑制作用。结论:薯蓣皂苷及莪术醇可能为芪竹方抑制人胃癌细胞MGC-803增殖的有效成分。     

Intravenous injection of oncolytic picornavirus SVV-001 prolongs animal survival in a panel of primary tumor–based orthotopic xenograft mouse models of pediatric glioma

Background

Seneca Valley virus (SVV-001) is a nonpathogenic oncolytic virus that can be systemically administered and can pass through the blood–brain barrier. We examined its therapeutic efficacy and the mechanism of tumor cell infection in pediatric malignant gliomas.

Methods

In vitro antitumor activities were examined in primary cultures, preformed neurospheres, and self-renewing glioma cells derived from 6 patient tumor orthotopic xenograft mouse models (1 anaplastic astrocytoma and 5 GBM). In vivo therapeutic efficacy was examined by systemic treatment of preformed xenografts in 3 permissive and 2 resistant models. The functional role of sialic acid in mediating SVV-001 infection was investigated using neuraminidase and lectins that cleave or competitively bind to linkage-specific sialic acids.

Results

SVV-001 at a multiplicity of infection of 0.5 to 25 replicated in and effectively killed primary cultures, preformed neurospheres, and self-renewing stemlike single glioma cells derived from 4 of the 6 glioma models in vitro. A single i.v. injection of SVV-001 (5 × 10¹² viral particles/kg) led to the infection of orthotopic xenografts without harming normal mouse brain cells, resulting in significantly prolonged survival in all 3 permissive and 1 resistant mouse models (P < .05). Treatment with neuraminidase and competitive binding using lectins specific for α2,3-linked and/or α2,6-linked sialic acid significantly suppressed SVV-001 infectivity (P < .01).

Conclusion

SVV-001 possesses strong antitumor activity against pediatric malignant gliomas and utilizes α2,3-linked and α2,6-linked sialic acids as mediators of tumor cell infection. Our findings support the consideration of SVV-001 for clinical trials in children with malignant glioma.