Journal of Clinical Laboratory Analysis最新文献

Background: The carbapenemase-producing Klebsiella pneumoniae (CRKP) is a global health problem associated with nosocomial and opportunistic infection and gastrointestinal colonization. A rapid detection method for carbapenemase genes is necessary for effective treatment and to prevent dissemination of carbapenemase genes.

Methods: In this study, a hexaplex recombinase polymerase amplification assay was established for detection of five common carbapenemase genes (bla_KPC, bla_NDM, bla_OXA-48-like, bla_IMP, and bla_VIM) and waaQ as a K. pneumoniae-specific target. The carbapenemase genes from 129 CRKP strains isolated from pediatric inpatients and 50 carbapenemase-susceptible strains were identified by hexaplex RPA and validated with the Modified Carbapenem Inactivation Method (mCIM) and PCR sequencing results.

Results: The duplex to hexaplex primer concentrations were successfully optimized. Single-tube RPA reaction could be completed at 37°C in 25-30 min. The limit of detection of each target varied from 0.1 to 10 ng. No cross-reactivity of hexaplex primers was observed against five Gram-positive and four Gram-negative pathogenic bacteria in pediatric infections. The sensitivity and specificity were 100% with perfect concordance with both reference methods.

Conclusion: Therefore, the hexaplex RPA has potential for rapid carbapenemase genes detection in limited resource settings.

Wang R, Zhao J, Wei Q, et al. Potential of circulating lncRNA CASC2 as a biomarker in reflecting the inflammatory cytokines, multi-organ dysfunction, disease severity, and mortality in sepsis patients. J Clin Lab Anal. 2022;36:e24569. https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcla.24569.

Due to differing institutional requirements regarding the designation of corresponding authors, the affiliation of Qingchun Dai¹ designates the corresponding author position at the end of the list, whereas the affiliation of Cuicui Liu² requires it to be placed at the beginning. After comprehensive discussion and mutual agreement among all co-authors, it has been collectively decided to revise the author order by changing the positions of these two corresponding authors.

The updated authorship sequence is shown below:

Rui Wang¹ | Jinglin Zhao¹ | Qi Wei¹ | Hao Wang¹ | Chao Zhao² | Caihong Hu² | Yu Han¹ | Zhi Hui¹ | Long Yang¹ | Cuicui Liu² | Qingchun Dai¹.

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RETRACTION: C. Deng, B. Zhang, Y. Zhang, X. Xu, D. Xiong, X. Chen, and J. Wu, “ A Long Non-Coding RNA OLBC15 Promotes Triple-Negative Breast Cancer Progression Via Enhancing ZNF326 Degradation,” Journal of Clinical Laboratory Analysis 34, no. 8 (2020): e23304, https://doi.org/10.1002/jcla.23304.

The above article, published online on 24 April 2020, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the authors; the journal Editor-in-Chief, Rong Fu; and Wiley Periodicals, LLC. The corresponding author Jiaojiao Wu contacted the journal to request that the article be retracted for the following reasons: 1. An inability to reproduce key experimental results; 2. Technical errors in the experimental protocols that may have compromised the reliability and reproducibility of the data (inconsistencies in RNA pulldown assay conditions, potential cross-contamination in cell line experiments, and insufficient validation of antibody specificity for ZNF326 detection); and 3. Discrepancies in the original data, calling into question the western blot images in Figures 4B, 5A, and 5B; the quantification data for migration assays; and IHC scoring consistency in clinical samples. Following an investigation, images in Figures 4 and 5 were found to be duplicated from earlier publications: Figure 4D being from Figure 3A in Koo et al. 2017 (https://doi.org/10.1158/1535-7163.MCT-17-0077), Figure 5B being from Figure 5B in Shen et al. 2019 (https://doi.org/10.1002/jcla.23122), and Figure 5E being from Figure 2G in Li et al. 2018 (https://doi.org/10.2147/CMAR.S183355). Due to the scope of these errors, the editor has lost confidence in the results reported, and therefore the article must be retracted.

Objective: Diabetic Foot Ulcers (DFUs) represent a prevalent and serious complication of diabetes, frequently resulting in persistent wounds and delayed healing. This research explores the healing effects of mesenchymal stem cells (MSCs) on DFUs and examines the involvement of Notch signaling in this therapeutic process.

Methods: BALB/c mice were induced with diabetes using streptozotocin (STZ) and divided into five groups: Control, Model, MSCs Treatment, MSCs + Notch Inhibition, and MSCs + Notch Activation. Wound healing was monitored, and tissue samples were analyzed using histological and molecular techniques.

Results: Our results demonstrated that MSCs treatment significantly accelerated wound healing, as evidenced by improved histopathology and enhanced expression of CD31, VEGF, FGF, and PECAM-1 in MSCs-treated groups. Notch activation further enhanced MSCs-mediated healing, as shown by increased Notch1 and Jagged-1 protein levels. Conversely, the MSCs + Notch Inhibition Group showed reduced healing and similar results to the Model Group, with lower expression of Notch1 and Jagged-1.

Conclusion: These findings suggest that MSCs promote DFU healing, and Notch signaling plays a crucial role in enhancing MSC-mediated repair. Our results highlight the potential of MSC-based therapies combined with Notch pathway modulation as a promising strategy for improving DFU treatment and wound healing in diabetic patients.

Background: Immune-mediated bone marrow failure (AA) is characterized by T cell-mediated destruction of hematopoietic stem and progenitor cells (HSPCs). The JAK-STAT signaling pathway plays a crucial role in regulating immune responses, and JAK inhibitors have shown potential in treating immune-mediated disorders. This study investigates the effects of MMB, a JAK inhibitor, in a mouse model of immune-mediated bone marrow failure to evaluate its impact on hematopoiesis and immune cell function.

Methods: In this study, immune-mediated AA was induced in B6D2F1 female mice through irradiation and lymphocyte infusion. The mice were treated with MMB monotherapy at doses of 6.25 and 12.5 mg/kg for 14 days. Peripheral blood cell counts, bone marrow cell counts, plasma cytokine levels, T lymphocyte subsets, Fas/FasL expression, and hematopoietic stem and progenitor cell (HSPC) levels were analyzed to assess the effects of MMB treatment on immune function and hematopoiesis.

Results: MMB treatment exacerbated the reduction in peripheral blood cell counts in marrow failure mice and decreased bone marrow hematopoietic cell numbers. Concurrently, MMB also reduced cytokine levels. The treatment also led to a significant reduction in CD4⁺ T cells and Tregs in both the spleen and bone marrow, while the low-dose MMB group exhibited a decrease in CD8+ T cell count. Additionally, MMB did not significantly improve HSPC levels, and a decrease in the more primitive LSK and LT-HSC populations was observed. However, later-stage stem and progenitor cells, such as ST-HSCs, MPPs, and CMPs, showed an increase in numbers. The treatment also resulted in downregulation of Fas expression on non-T cells, while FasL expression on lymphocytes increased.

Conclusion: MMB treatment exacerbated peripheral blood cell reduction and impaired bone marrow hematopoiesis in the immune-mediated AA mouse model. Although MMB modulated T lymphocyte subsets, it did not significantly improve hematopoietic stem and progenitor cell function. These findings highlight the need for further research to explore the potential and limitations of JAK inhibitors like MMB in the treatment of immune-mediated bone marrow failure.

Objective: To develop and validate a clinical prediction model for differentiating non-small cell lung cancer (NSCLC) from benign pulmonary diseases (BPD).

Methods: The retrospective study included 226 participants in the training set (134 with NSCLC and 92 with BPD) and 98 participants in the validation set (62 with NSCLC and 36 with BPD). A logistic regression model was constructed using variables such as sex, hemoptysis, serum biomarkers (carcinoembryonic antigen [CEA] and total protein [TP]), and CT features (volume ratio of solid density region [VR_2A], volume of calcified density area [VR_3], total volume [TV], CT variance [CTV], and maximum surface area [MSA]). The model was validated on an independent cohort, and its performance was evaluated using area under the curve (AUC), accuracy, calibration curves, and decision curves. Additionally, a nomogram was developed for clinical application, and its acceptance and convenience among clinicians were assessed.

Results: The prediction model achieved an AUC-ROC of 0.95 in the training set and 0.82 in the validation set. Calibration and decision curves demonstrated that the model had reliable diagnostic performance and good clinical application value.

Conclusion: The integrated prediction model combining clinical features, laboratory biomarkers, and CT features shows promise for improving the accuracy of differentiating NSCLC from BPD. Further studies are warranted to explore its potential in clinical practice.

Caner V. Tanir F. “Investigation of Occupational Health and Safety Levels in Genetic Disease Centers in Istanbul,” Journal of Clinical Laboratory Analysis (2025) 39: e70015.

The Acknowledgement section was inadvertently omitted from the published article. To comply with academic regulations and ensure transparency, the Acknowledgement section below has been added to the proof.

Acknowledgements

“This study was produced from the PhD thesis of Vedat Caner, titled ‘Investigation of Occupational Health and Safety Levels in Genetic Disease Centers in Istanbul’ (Turkish: İstanbul'daki Genetik Hastalık Tanı Merkezlerinin İş Sağlığı ve Güvenliği Düzeylerinin Araştırılması), completed at Cukurova University in 2024, under the supervision of Prof. Dr. Ferdi Tanır.”

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Background: RNA-based fusion panels using targeted next-generation sequencing of formalin-fixed paraffin-embedded tumour tissue specimens are used for various tumour types to detect rearrangements/fusions. Using bioinformatic approaches, the data obtained from RNA sequencing (RNA-Seq) can also be used for small nucleotide variants analysis (single nucleotide variants and indels).

Methods: The performance characteristics of applying Small nucleotide variant analysis Using RNA Fusion panel (SMURF) analysis to RNA-Seq (RNA sequencing) data obtained from an RNA-based fusion panel was evaluated and compared to results obtained from a dedicated DNA-based panel.

Results: This demonstrated that an RNA fusion panel can be enhanced to identify small nucleotide variants to maximise the utility of this panel. Although coverage depth across various genes, based on gene expression, was found to be quite variable, which is expected, there were certain genes found to consistently display coverage depth suitable for variant identification, such as GNAS, GNAQ, NRAS, and CTNNB1.

Conclusion: This analysis suggests that the variants in these genes can be confidently reported from RNA-Seq data obtained from an RNA-based fusion panel.