Experimental and molecular pathology最新文献_第6页

Small intestinal bacteria accelerate aspirin-induced small intestinal injuries 小肠细菌加速阿司匹林引起的小肠损伤

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-07-14 DOI: 10.1016/j.yexmp.2025.104984

Fumio Kakizaki , Teruo Miyazaki , Hajime Ueda , Junichi Iwamoto , Akira Honda , Tadashi Ikegami

Background

Small intestinal mucosal injuries are observed during treatment with enteric-coated, low-dose aspirin (LDA) through uncertain mechanism(s). Because aspirin (acetylsalicylic acid, ASA) is an acetylated form of the highly cytotoxic salicylic acid (SA), we hypothesized that SA deacetylated by esterases in the small intestine directly causes mucosal injuries. This study explored the mechanism(s) of ASA deacetylation to SA in the small intestinal environment.

Methods

ASA was added to the x, and deacetylation of added ASA and cell damage were evaluated. To explore the ASA deacetylation mechanism(s) in the intestinal environment, ASA was incubated with different pH phosphate buffers (4.01–9.10), pancreatic enzymes, homogenates of pancreas and IEC-6 cell, and caecum bacterial suspension (CBS). ASA and CBS were co-injected into the murine duodenum, and small intestinal damage was evaluated after an hour by histological observation.

Results

Intestinal cell damage was caused dependently on the deacetylation rate of added ASA to SA in the cell and culture media. In vitro, almost ASA was not deacetylated by incubation with different pH buffer, pancreatic enzymes, or IEC-6 cell homogenate, but deacetylation of ASA was significantly promoted with CBS. ASA deacetylation by bacterial esterases(s) was confirmed by adding an esterase-specific inhibitor, potassium fluoride. Furthermore, severe injuries throughout the entire murine small intestine were found after co-injection of ASA and CBS, but not after ASA alone.

Conclusions

Enteric-coated, LDA-induced mucosal injuries in the small intestine are mainly caused by direct cytotoxicity of SA deacetylated by enterobacterial esterase in the small intestine.

背景：在肠包被低剂量阿司匹林（LDA）治疗过程中观察到小肠黏膜损伤，但机制不确定。由于阿司匹林（乙酰水杨酸，ASA）是高细胞毒性水杨酸（SA）的乙酰化形式，我们假设SA在小肠内被酯酶去乙酰化直接导致粘膜损伤。本研究探讨了ASA在小肠环境下脱乙酰化为SA的机制。方法在x细胞中加入ASA，观察其去乙酰化程度及细胞损伤情况。为了探讨ASA在肠道环境中的去乙酰化机制，我们将ASA与不同pH的磷酸盐缓冲液（4.01-9.10）、胰腺酶、胰腺和IEC-6细胞匀浆以及盲肠细菌悬浮液（CBS）孵育。ASA和CBS联合注入小鼠十二指肠，1h后通过组织学观察小肠损伤情况。结果细胞和培养基中添加的ASA对SA的去乙酰化速率对肠细胞的损伤有依赖性。在体外，不同pH缓冲液、胰酶或IEC-6细胞匀浆孵育后，ASA几乎没有去乙酰化，但CBS显著促进了ASA的去乙酰化。通过添加酯酶特异性抑制剂氟化钾证实了细菌酯酶对ASA的去乙酰化作用。此外，ASA和CBS联合注射后，整个小鼠小肠均出现严重损伤，而ASA单独注射后未见损伤。结论senterc包被lda诱导的小肠粘膜损伤主要是由小肠内肠杆菌酯酶脱乙酰化SA直接细胞毒性引起的。

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引用次数: 0

Revisiting TAM polarization: beyond M1- and M2-type TAM toward clinical precision in macrophage-targeted therapy 重新审视TAM极化：超越M1和m2型TAM在巨噬细胞靶向治疗中的临床精确性

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-07-14 DOI: 10.1016/j.yexmp.2025.104982

Qingqing Wang , Wenxue Ma

Tumor-associated macrophages (TAMs) are key regulators of the tumor microenvironment (TME), significantly influencing cancer progression and therapeutic responses. TAMs polarize into M1 or M2 phenotypes, exerting distinct functional roles. M1-type macrophages promote inflammation and tumor cell destruction, whereas M2-type macrophages facilitate immune suppression, angiogenesis, and metastasis. However, inconsistencies and mischaracterizations in the literature regarding TAM classification have led to confusion in the field, potentially impeding the development of effective macrophage-targeted immunotherapies. This commentary highlights the need for clear and standardized nomenclature, clarifies the functional distinctions between M1- and M2- type TAMs, and explores the signaling pathways and environmental factors driving their polarization. We also discuss emerging TAM subtypes and the therapeutic significance of accurate classification, including macrophage reprogramming strategies. Standardizing terminology and addressing misconceptions will be critical to advancing macrophage-based immunotherapies and improving clinical outcomes in cancer treatment.

肿瘤相关巨噬细胞（tam）是肿瘤微环境（TME）的关键调节因子，显著影响癌症进展和治疗反应。tam分化为M1或M2表型，发挥不同的功能作用。m1型巨噬细胞促进炎症和肿瘤细胞破坏，而m2型巨噬细胞促进免疫抑制、血管生成和转移。然而，文献中关于TAM分类的不一致和错误描述导致了该领域的混乱，潜在地阻碍了有效的巨噬细胞靶向免疫疗法的发展。这篇评论强调了明确和标准化命名的必要性，阐明了M1型和M2型tam之间的功能区别，并探讨了驱动其极化的信号通路和环境因素。我们还讨论了新出现的TAM亚型和准确分类的治疗意义，包括巨噬细胞重编程策略。标准化术语和解决误解对于推进巨噬细胞免疫疗法和改善癌症治疗的临床结果至关重要。

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引用次数: 0

Mitochondrial dysfunction in fibrotic diseases: Research progress and MSC-exos therapy 纤维化疾病的线粒体功能障碍：研究进展及MSC-exos治疗

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-07-10 DOI: 10.1016/j.yexmp.2025.104983

Xiaoyun Zhang , Yingyu Wang , Xinyi Guo , Yu Xiao , Weiguo Wan , Hejian Zou , Xue Yang

Fibrosis is a common pathological feature of most chronic diseases progressing to the end stage, with its specific pathogenesis still unclear and lacking effective therapeutic approaches. Mitochondria are essential organelles responsible for energy production and the maintenance of cellular homeostasis. Increasing evidence indicates that mitochondrial dysfunction is closely associated with the onset and progression of fibrotic diseases. In this review, we explore the relationship between mitophagy, oxidative stress, mitochondrial dynamics, mtDNA release, and progression of fibrosis from the perspective of mitochondrial dysfunction. Furthermore, we summarized the latest research advances of mitochondrial dysfunction in lung, liver, kidney and skin fibrosis, and provided an overview of the potential therapeutic use of mesenchymal stem cell-derived exosomes in the treatment of fibrotic diseases by improving mitochondrial function, aiming to deepen the understanding of mitochondrial dysfunction in the pathogenesis of fibrotic diseases and provide new insights into targeting mitochondria in the treatment of fibrotic diseases.

纤维化是大多数慢性疾病进展至终末期的共同病理特征，其具体发病机制尚不清楚，缺乏有效的治疗方法。线粒体是负责能量生产和维持细胞稳态的重要细胞器。越来越多的证据表明，线粒体功能障碍与纤维化疾病的发生和进展密切相关。在本文中，我们从线粒体功能障碍的角度探讨线粒体自噬、氧化应激、线粒体动力学、mtDNA释放和纤维化进展之间的关系。此外，我们总结了线粒体功能障碍在肺、肝、肾和皮肤纤维化中的最新研究进展，并概述了间充质干细胞来源的外泌体通过改善线粒体功能在纤维化疾病治疗中的潜在应用，旨在加深对线粒体功能障碍在纤维化疾病发病机制中的认识，为靶向线粒体治疗纤维化疾病提供新的见解。

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引用次数: 0

Metabolic reprogramming during ineffective erythropoiesis in β-thalassemia/HbE disease β-地中海贫血/HbE病无效红细胞生成过程中的代谢重编程

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-07-01 DOI: 10.1016/j.yexmp.2025.104980

Chanyanat Sukhuma , Donny Nauphar , Khanita Nuamsee , Wasinee Kheansaard , Kittiphong Paiboonsukwong , Alisa Wilantho , Chumpol Ngamphiw , Pornthip Chaichompoo , Sissades Tongsima , Saovaros Svasti , Phatchariya Phannasil

Ineffective erythropoiesis, the main cause of anemia in β-thalassemia disease, is characterized by dramatic expansion of erythroblasts and increased erythroblast cell death. The absence or reduction of β-globin chains causes an accumulation of excess α-globin chains and generates cytotoxic reactive oxidant species, resulting in erythroblast cell death. Metabolism provides energy, building blocks for macromolecule synthesis, and cofactors for antioxidative defense systems. We hypothesized that β-thalassemia erythroblasts might alter their metabolism to cope with increased proliferation and cellular stress. Herein, transcriptomic analysis of basophilic and polychromatic erythroblasts isolated from bone marrow obtained from β-thalassemia/HbE patients showed the global up-regulation of metabolic genes in glycolysis, TCA cycle, pentose phosphate pathway, ATP, and fatty acid synthesis pathway. The expression of metabolic genes during terminal erythropoiesis was further determined by PCR array and RT-qPCR in erythroblast culture obtained from β-thalassemia/HbE patients with mild and severe symptoms. The increased expression of enolase1, isocitrate dehydrogenase 1, and bisphosphoglycerate mutase was observed in mild cases compared to severe patients, suggesting that mild patients might modulate metabolic flux for cellular stress defense mechanisms, reducing disease severity. Moreover, the role of BPGM in regulating erythroid differentiation was demonstrated in K562 cells. Inhibition of BPGM promotes cell differentiation in K562 cells. Understanding metabolic reprogramming in thalassemia erythropoiesis opens new therapeutic approaches for β-thalassemia/HbE treatment. Further research is needed to explore how metabolism affects ineffective erythropoiesis and supports thalassemic erythroblasts' high proliferation and oxidative stress defense.

无效的红细胞生成是β-地中海贫血病中贫血的主要原因，其特征是红母细胞急剧扩增和红母细胞死亡增加。β-珠蛋白链的缺失或减少导致过量α-珠蛋白链的积累，产生细胞毒性反应性氧化物质，导致红母细胞死亡。新陈代谢提供能量，为大分子合成提供基石，并为抗氧化防御系统提供辅助因子。我们假设β-地中海贫血红细胞可能改变其代谢以应对增加的增殖和细胞应激。本研究通过对β-地中海贫血/HbE患者骨髓分离的嗜碱性和多色红细胞的转录组学分析发现，糖酵解、TCA循环、戊糖磷酸途径、ATP和脂肪酸合成途径中代谢基因的整体上调。对轻、重度β-地中海贫血/HbE患者的红母细胞培养物进行PCR阵列和RT-qPCR检测，观察代谢基因在终末红细胞生成过程中的表达。与重症患者相比，轻症患者烯醇化酶1、异柠檬酸脱氢酶1和双磷酸甘油突变酶的表达增加，提示轻症患者可能调节细胞应激防御机制的代谢通量，降低疾病严重程度。此外，BPGM在K562细胞中调节红细胞分化的作用也得到了证实。抑制BPGM可促进K562细胞的分化。了解地中海贫血红细胞生成中的代谢重编程为β-地中海贫血/HbE治疗开辟了新的治疗途径。代谢如何影响无效的红细胞生成并支持地中海贫血红细胞的高增殖和氧化应激防御还有待进一步研究。

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引用次数: 0

Polymerase Ѳ inhibitors combinations with approved and investigational agents in patient-derived tumor multi-cell type (mct) spheroids 聚合酶Ѳ抑制剂与已批准和正在研究的药物联合用于患者源性肿瘤多细胞型（mct）球体

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-06-27 DOI: 10.1016/j.yexmp.2025.104978

Beverly A. Teicher , Thomas S. Dexheimer , Li Chen , Thomas Silvers , Eric M. Jones , Nathan P. Coussens , J. Paul Eder , James H. Doroshow

The potential of novobiocin, recently identified to be a DNA POLѲ inhibitor, to augment cancer chemotherapy was explored in the late 1980s and early 1990s in tumor cells, tumor-bearing mice and in Phase 1 clinical trial in combination with cyclophosphamide or cisplatin. Genetic alterations which may increase or decrease POLѲ inhibitor effects have been elucidated. Thirty patient-derived tumor cell lines with known BRCA, ATM, ATR, POLѲ, XRCC1, PALB2, PARP1, LIG3 alterations as well as know gLOH% and MSI status were screened in a mct-spheroid assay (tumor cells, endothelial cells, mesenchymal stem cells) with a POLѲ inhibitor, novobiocin, ART-558, and RP6685, alone or in simultaneous combination with a FDA-approved or investigational anticancer small molecule with a 7-day exposure and a CellTiter-Glo 3D luminescence endpoint. As single agents, the POLѲ inhibitors had little or no cytotoxicity. In simultaneous combination with ART-558, talazoparib produced greater-than-additive cytotoxicity at the highest concentrations of the POLѲ inhibitors in the 922,993–354-T-J3-PDC endometrial serous carcinoma mct-spheroids. Activity of the Chk1/2 inhibitor prexasertib was potentiated by either ART-558 or RP6685 in the 922,993–354-T-J3 mct-spheroids. The combination of POLѲ inhibitors ART-558 and RP6685, and the Chk1/2 inhibitor prexasertib produced up to 1 log increase in cytotoxicity in the 922,993–354-T-J3 mct-spheroids. Regions of potentiation were evident in the 922,993–354-T-J3-PDC endometrial carcinoma survival surface plots at the highest concentration of paclitaxel tested, while regions of potentiation were evident in the paclitaxel mid-concentrations of the 299,254–011-R-J1-PDC melanoma mct-spheroids survival surface plots as determined by the Bliss independence calculation. DNA POLѲ is recruited to DNA double-strand breaks as a component of repair. POLѲ allosteric inhibitors, novobiocin, ART558 and RP-6685, have entered clinical trial. The current study explores the cytotoxicity of POLѲ inhibitors in combination with anticancer drugs and investigational agents in patient-derived cell lines grown as mct-spheroids.

20世纪80年代末和90年代初，在肿瘤细胞、荷瘤小鼠和与环磷酰胺或顺铂联合进行的一期临床试验中，研究人员探索了新生物素作为DNA POLѲ抑制剂的潜力，以增强癌症化疗。可能增加或减少POLѲ抑制剂作用的遗传改变已被阐明。30例已知BRCA、ATM、ATR、POLѲ、XRCC1、PALB2、PARP1、LIG3改变以及已知gLOH%和MSI状态的患者源性肿瘤细胞系，在mct-spheroid试验（肿瘤细胞、内皮细胞、间质干细胞）中使用POLѲ抑制剂、novobiocin、ART-558和RP6685，单独或同时与fda批准的或正在研究的抗癌小分子联合使用，暴露时间为7天，celltir - glo 3D发光终点。作为单一药物，POLѲ抑制剂几乎没有或没有细胞毒性。在与ART-558联合使用时，在最高浓度的POLѲ抑制剂下，talazoparib在922,993-354-T-J3-PDC子宫内膜浆液性癌mct-spheroid中产生了大于添加性的细胞毒性。ART-558或RP6685在922,993-354-T-J3 mct-spheroid中增强了Chk1/2抑制剂prexasertib的活性。POLѲ抑制剂ART-558和RP6685与Chk1/2抑制剂prexasertib联合使用，在922,993-354-T-J3 mct-spheroid中产生高达1 log的细胞毒性增加。在紫杉醇浓度最高的922,993-354-T-J3-PDC子宫内膜癌生存面图中有明显的增强区域，而在紫杉醇浓度中等的299,254-011-R-J1-PDC黑色素瘤mct-spheroids生存面图中有明显的增强区域，这是由Bliss独立计算确定的。DNA POLѲ被招募到DNA双链断裂作为修复的一个组成部分。POLѲ变构抑制剂novobiocin、ART558和RP-6685已进入临床试验。目前的研究探索POLѲ抑制剂与抗癌药物和研究药物联合在mct-球体生长的患者来源细胞系中的细胞毒性。

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引用次数: 0

Effect of Clostridium butyricum and antibiotics using simultaneous simple suspension in mice with Clostridioides difficile infection 丁酸梭菌与抗生素同时使用单一混悬液对艰难梭菌感染小鼠的影响

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-06-27 DOI: 10.1016/j.yexmp.2025.104979

Hideo Kato , Mao Hagihara , Chihiro Shiraishi , Yuki Asai , Hiroshige Mikamo , Takuya Iwamoto

Background

A simple suspension method, wherein tablets and capsules are disintegrated in warm water (55 °C), is increasingly used in clinical settings. Previously, we demonstrated that probiotic strains were reduced or below limit of detection in a simultaneous simple suspension of probiotic preparations and metronidazole or fidaxomicin. This study investigated its effectiveness in mice with C. difficile infection (CDI).

Methods

Clostridium butyricum products and antibiotics used in this study were the Miya-BM tablet (CBM), metronidazole (Flagyl 250-mg oral tablet), and fidaxomicin (Dafclir 200-mg tablet). Non-infected mice received a simple suspension of CBM and antibiotics simultaneously to assess probiotic viability in the feces. Additionally, C. difficile counts and cytokine production were investigated in CDI-infected mice treated with these suspensions.

Results

C. butyricum was detectable in the feces of non-infected mice receiving simultaneous suspensions of CBM and antibiotics. In CDI-infected mice, simultaneous suspensions significantly reduced C. difficile colony counts in feces compared to CBM or antibiotics alone. Furthermore, suspensions downregulated tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-10 levels, while upregulating interferon-γ (IFN-γ) levels in colon tissues, indicating reduced inflammation and an enhanced immune response.

Conclusions

This study using mice demonstrates the effectiveness of simultaneous simple suspensions of CBM and antibiotics in treating CDI. This approach significantly reduces C. difficile counts, modulates cytokine levels, and maintains probiotic viability, potentially making it a viable option for administration via gastric tubes in clinical settings.

一种简单的悬浮法，其中片剂和胶囊在温水（55°C）中崩解，越来越多地用于临床环境。先前，我们证明了益生菌制剂与甲硝唑或非达霉素同时简单混悬时益生菌菌株的检出限降低或低于检出限。本研究探讨其对艰难梭菌感染（CDI）小鼠的治疗效果。方法本研究使用的丁酸clostridium产品及抗生素为Miya-BM片（CBM）、甲硝唑片（Flagyl 250 mg口服片）、非达霉素片（dafclr 200 mg片）。未感染的小鼠同时接受CBM和抗生素的简单悬浮液，以评估粪便中益生菌的活力。此外，用这些悬浮液处理cdi感染小鼠，观察了艰难梭菌计数和细胞因子的产生。在同时注射CBM和抗生素悬浮液的未感染小鼠的粪便中检测到丁酸。在cdi感染小鼠中，与CBM或单独使用抗生素相比，同时悬液可显著降低粪便中艰难梭菌菌落计数。此外，悬浮液下调肿瘤坏死因子-α (TNF-α)、白细胞介素-6 （IL-6）和IL-10水平，同时上调结肠组织中的干扰素-γ (IFN-γ)水平，表明炎症减少和免疫反应增强。结论本研究证实了中药与抗生素同时单混悬液治疗CDI的有效性。这种方法可以显著减少艰难梭菌计数，调节细胞因子水平，并保持益生菌活力，可能使其成为临床环境中通过胃管给药的可行选择。

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引用次数: 0

Retraction notice to “Matrine protects neuro-axon from CNS inflammation-induced injury” [Experimental and Molecular Pathology 98 (2015) 124–130] “苦参碱保护神经轴突免受中枢神经系统炎症性损伤”的撤稿通知[实验与分子病理学98(2015)124-130]。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-06-01 DOI: 10.1016/j.yexmp.2025.104968

Quan-Cheng Kan , Peng Lv , Xiao-Jian Zhang , Yu-Ming Xu , Guang-Xian Zhang , Lin Zhu

引用次数: 0

Expression of concern: "Matrine ameliorates experimental autoimmune encephalomyelitis by modulating chemokines and their receptors" [Experimental and Molecular Pathology 99 (2015) 212-219]. 关注表达：“苦参碱通过调节趋化因子及其受体改善实验性自身免疫性脑脊髓炎”[experimental and Molecular Pathology 99(2015) 212-219]。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-06-01 Epub Date: 2025-04-03 DOI: 10.1016/j.yexmp.2025.104962

引用次数: 0

Expression of concern: "Upregulation of immunomodulatory molecules by matrine treatment in experimental autoimmune encephalomyelitis" [Experimental and Molecular Pathology 97 (2014) 470-476]. 关注表达：“实验性自身免疫性脑脊髓炎中苦参碱治疗免疫调节分子的上调”[实验与分子病理学97(2014)470-476]。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-06-01 Epub Date: 2025-04-04 DOI: 10.1016/j.yexmp.2025.104961

引用次数: 0

Evaluation of direct-to-PCR (D2P) method for molecular diagnosis of infectious diseases 直接- pcr （D2P）方法在传染病分子诊断中的应用评价

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2025-05-26 DOI: 10.1016/j.yexmp.2025.104972

Rahul Sharma , Vaibhav K. Tamrakar , Rob E. Carpenter , Aditya Sharma , Kamalpreet Suri , Salima Karki , Katelyn Kyser , Randy Sronce , Sadia Almas

This study evaluates the performance of the Direct-to-PCR (D2P) method as a streamlined, extraction-independent alternative to conventional nucleic acid extraction techniques for diagnosing urinary tract infections, sexually transmitted infections, and respiratory tract infections. The D2P approach employs proprietary antimicrobial peptide-based lysis buffers tailored for bacterial, fungal, and viral targets, enabling direct amplification from clinical and contrived specimens without column- or bead-based purification. Comparative analyses were conducted against silica column-based (QIAGEN) and magnetic bead-based (KingFisher) extraction methods using both microbial reference isolates and 116 residual clinical samples. Results demonstrate that the D2P method yields comparable sensitivity and specificity to conventional extraction workflows across a diverse panel of pathogens—including Gram-negative and Gram-positive bacteria, Candida species, ssRNA viruses (e.g., CoV-229E, Parainfluenza Virus 1 and 2), and dsDNA viruses (e.g., HSV, HAdV). Notably, D2P outperformed both QIAGEN and KingFisher in extracting nucleic acids from Candida auris, a multidrug-resistant fungal pathogen. Limit of detection and amplification efficiency remained within acceptable ranges across all platforms, with R² values between 0.92 and 0.99, and slopes consistent with MIQE standards. The D2P protocol reduced total sample processing time from ∼120 min to ∼45 min, minimized hands-on steps, and demonstrated effective performance in turbid or hemolyzed samples—making it suitable for high-throughput and resource-limited settings. However, limitations were observed in samples with high PCR-inhibitor content or low target yield, and broader validation across additional matrices is recommended. These findings support D2P as a reliable, efficient, and scalable molecular diagnostic alternative with broad clinical utility. Integration of D2P into diagnostic workflows could enhance access to rapid, cost-effective pathogen detection in both centralized laboratories and decentralized or point-of-care environments.

本研究评估了直接到pcr （D2P）方法作为传统核酸提取技术诊断尿路感染、性传播感染和呼吸道感染的一种简化的、不依赖提取的替代方法的性能。D2P方法采用专为细菌、真菌和病毒靶点定制的抗菌肽裂解缓冲液，无需柱或珠基纯化，即可从临床和人造标本中直接扩增。对比分析了基于二氧化硅柱（QIAGEN）和基于磁珠（KingFisher）的微生物参考分离物和116份剩余临床样品的提取方法。结果表明，D2P方法在多种病原体(包括革兰氏阴性和革兰氏阳性细菌、念珠菌、ssRNA病毒（如CoV-229E、副流感病毒1和2）和dsDNA病毒（如HSV、hav）中具有与传统提取流程相当的敏感性和特异性。值得注意的是，D2P在提取多重耐药真菌假丝酵母（Candida auris）核酸方面优于QIAGEN和KingFisher。所有平台的检测限和扩增效率均在可接受范围内，R2值在0.92 ~ 0.99之间，斜率与MIQE标准一致。D2P方案将总样品处理时间从~ 120分钟减少到~ 45分钟，最大限度地减少了动手步骤，并且在混浊或溶血样品中表现出有效的性能，使其适用于高通量和资源有限的环境。然而，在高pcr抑制剂含量或低目标产率的样品中观察到局限性，建议在其他基质上进行更广泛的验证。这些发现支持D2P作为一种可靠、有效和可扩展的分子诊断替代方法，具有广泛的临床应用。将D2P整合到诊断工作流程中，可在集中式实验室和分散式或医疗点环境中促进获得快速、具有成本效益的病原体检测。

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引用次数: 0