Attribute Prototype-guided Iterative Scene Graph for Explainable Radiology Report Generation.

The potential of automated radiology report generation in alleviating the time-consuming tasks of radiologists is increasingly being recognized in medical practice. Existing report generation methods have evolved from using image-level features to the latest approach of utilizing anatomical regions, significantly enhancing interpretability. However, directly and simplistically using region features for report generation compromises the capability of relation reasoning and overlooks the common attributes potentially shared across regions. To address these limitations, we propose a novel region-based Attribute Prototype-guided Iterative Scene Graph generation framework (AP-ISG) for report generation, utilizing scene graph generation as an auxiliary task to further enhance interpretability and relational reasoning capability. The core components of AP-ISG are the Iterative Scene Graph Generation (ISGG) module and the Attribute Prototype-guided Learning (APL) module. Specifically, ISSG employs an autoregressive scheme for structural edge reasoning and a contextualization mechanism for relational reasoning. APL enhances intra-prototype matching and reduces inter-prototype semantic overlap in the visual space to fully model the potential attribute commonalities among regions. Extensive experiments on the MIMIC-CXR with Chest ImaGenome datasets demonstrate the superiority of AP-ISG across multiple metrics.

Token-Mixer: Bind Image and Text in One Embedding Space for Medical Image Reporting.

Medical image reporting focused on automatically generating the diagnostic reports from medical images has garnered growing research attention. In this task, learning cross-modal alignment between images and reports is crucial. However, the exposure bias problem in autoregressive text generation poses a notable challenge, as the model is optimized by a word-level loss function using the teacher-forcing strategy. To this end, we propose a novel Token-Mixer framework that learns to bind image and text in one embedding space for medical image reporting. Concretely, Token-Mixer enhances the cross-modal alignment by matching image-to-text generation with text-to-text generation that suffers less from exposure bias. The framework contains an image encoder, a text encoder and a text decoder. In training, images and paired reports are first encoded into image tokens and text tokens, and these tokens are randomly mixed to form the mixed tokens. Then, the text decoder accepts image tokens, text tokens or mixed tokens as prompt tokens and conducts text generation for network optimization. Furthermore, we introduce a tailored text decoder and an alternative training strategy that well integrate with our Token-Mixer framework. Extensive experiments across three publicly available datasets demonstrate Token-Mixer successfully enhances the image-text alignment and thereby attains a state-of-the-art performance. Related codes are available at https://github.com/yangyan22/Token-Mixer.

Development and validation of a risk-prediction model for immune-related adverse events in patients with non-small-cell lung cancer receiving PD-1/PD-L1 inhibitors.

Lung cancer remains the leading cause of cancer deaths worldwide and is the most common cancer in males. Immune-checkpoint inhibitors (ICIs) that target programmed cell death protein-1 (PD-1) or programmed cell death-ligand 1 (PD-L1) have achieved impressive efficacy in the treatment of non-small-cell lung cancer (NSCLC) (Pardoll, 2012; Champiat et al., 2016; Gao et al., 2022). Although ICIs are usually well tolerated, they are often accompanied by immune-related adverse events (irAEs) (Doroshow et al., 2019). Non-specific activation of the immune system produces off-target immune and inflammatory responses that can affect virtually any organ or system (O'Kane et al., 2017; Puzanov et al., 2017). Compared with adverse events caused by chemotherapy, irAEs are often characterized by delayed onset and prolonged duration and can occur in any organ at any stage of treatment, including after cessation of treatment (Puzanov et al., 2017; von Itzstein et al., 2020). They range from rash, pneumonitis, hypothyroidism, enterocolitis, and autoimmune hepatitis to cardiovascular, hematological, renal, neurological, and ophthalmic irAEs (Nishino et al., 2016; Kumar et al., 2017; Song et al., 2020). Hence, we conducted a retrospective study to identify validated factors that could predict the magnitude of the risk of irAEs in patients receiving PD-1/PD-L1 inhibitors; our approach was to analyze the correlation between the clinical characteristics of patients at the start of treatment and relevant indicators such as hematological indices and the risk of developing irAEs. Then, we developed an economical, practical, rapid, and simple model to assess the risk of irAEs in patients receiving ICI treatment, as early as possible.

MiR-101-3p targets KPNA2 to inhibit the progression of lung squamous cell carcinoma cell lines.

We herein discuss the impacts of miR-101-3p on the tumorigenesis-related cell behaviors in lung squamous cell carcinoma (LUSC) by repressing KPNA2. TCGA database was utilized to measure miR-101-3p and KPNA2 levels in LUSC tissues and cells. The interaction of miR-101-3p and KPNA2-3'UTR was determined by dual luciferase assay. Western blot evaluated the protein level of KPNA2. MiR-101-3p was under-expressed in LUSC cells while KPNA2 was overexpressed. Western blot confirmed the impact of KPNA2 expression on cancer cell progression. The negative regulatory impact of miR-101-3p on KPNA2 was also verified. In vitro cell function assays revealed the suppressing effect of high miR-101-3p expression on cell invasion, migration and viability, as well as its promoting effect on apoptosis. Up-regulated miR-101-3p weakened the promoting effect of overexpressed KPNA2 on LUSC malignant progression. To conclude, miR-101-3p repressed viability, invasion, and migration, and facilitated cell apoptosis in LUSC by suppressing KPNA2.

A case of pulmonary inflammatory myofibroblastic tumor treated with bronchoscopic therapy plus lobectomy.

BACKGROUND: Inflammatory myofibroblastic tumor (IMT) is a rare tumor with malignant potential. We presented a case of a young adult who was diagnosed with IMT and treated with loop electrocautery therapy to relieve airway obstruction, followed by lobectomy to complete resection. Recent studies have supported the use of such interventional resection methods. CASE PRESENTATION: A non-smoking 30-year-old woman presented with a 1-month history of progressive dyspnea and productive cough. The Chest X-ray showed a homogenous opacity invading the entire left hemithorax, and the mediastinum content was attracted to the left side. In an effort to avoid pneumonectomy and afford rapid palliation of dyspnea, loop electrocautery was selected as the most appropriate therapy. The left upper lobectomy by thoracoscopy was performed instead of left upper lobe sleeve resection in order to better prevent the recurrence of lung atelectasis. After 6 years of follow-up, no evidence of recurrence has been found till now. CONCLUSION: Interventional bronchoscopy coupled with surgical resection serves not only as a palliative management to bronchial obstruction but also a way to avoid pneumonectomy.

Nanoparticle-enhanced chemo-immunotherapy to trigger robust antitumor immunity.

Mounting evidence suggests that immunotherapies are a promising new class of anticancer therapies. However, the immunosuppressive tumor microenvironment (TME), poor immunogenicity, and off-target toxicity hinder the broader implementation of immunotherapies. Here, we describe a novel strategy combining chemotherapy and immunotherapy to modulate the TME by systemically and concurrently delivering the chemotherapeutic agent SN38 (7-ethyl-10-hydroxycamptothecin) and the STING agonist DMXAA (5,6-dimethylxanthenone-4-acetic acid) into tumors using triblock copolymer nanoparticles, named PS3D1@DMXAA, which enhances antigen cross-presentation and induces the conversion of the immunosuppressive TME to immunogenic TME through the newly found synergistic function between SN38 and STING activation. PS3D1@DMXAA thus shows potent therapeutic efficacy in three mice tumor models and elicits remarkable therapeutic benefit when combined with anti-PD-1 therapy. Our engineered nanosystem offers a rational design of an effective immunotherapy combination regimen to convert uninflamed "cold" tumors into "hot" tumors, addressing the major challenges immunotherapies faced.

A ten-gene signature-based risk assessment model predicts the prognosis of lung adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) is a major cause of cancer death. Therefore, identifying potential prognostic risk factors is critical to improve the survival of patients with LUAD. METHODS: Here, relevant datasets were downloaded from TCGA and GEO databases to screen the differentially expressed genes (DEGs). Univariate Cox analysis, LASSO regression analysis and multivariate Cox analysis were conducted on the DEGs combined with TCGA clinical data, and finally a risk assessment model based on 10 feature genes was constructed. RESULTS: The prognosis of patients was evaluated after the patients were grouped based on the median risk score and the results showed that the survival time of patients in the high-risk group was significantly shorter than that in the low-risk group. ROC analysis showed that the AUC values of the 1, 3, 5-year survival were 0.753, 0.724, and 0.73, respectively, indicating that the model was precise in predicting the prognosis, which was also verified in the external dataset GSE72094. In addition, a significant correlation was found between the risk score and the clinical stages of LUAD, that is, a later stage always corresponded to a higher risk score. Then, we performed survival analysis on the 10 feature genes independently in the TCGA-LUAD dataset through the GEPIA database, finding that the high expression of 6 genes (COL5A2, PLEK2, BAIAP2L2, S100P, ZIC2, SFXN1) was associated with the poor prognosis of LUAD patients. CONCLUSION: To sum, this study established a 10-gene risk assessment model and further evaluated its value in predicting LUAD prognosis, which provided a new method for the prognosis prediction of LUAD.

miR-30a-5p Inhibits Proliferation and Migration of Lung Squamous Cell Carcinoma Cells by Targeting FOXD1.

OBJECTIVE: To investigate the mechanism of miR-30a-5p inhibiting proliferation and migration of lung squamous cell carcinoma (LSCC) cells by targeting FOXD1. METHODS: Bioinformatics was used to analyze differentially expressed genes in the TCGA_LUSC database. qRT-PCR was used to detect the expression levels of miR-30a-5p and FOXD1 in human normal lung epithelial cell line and human LSCC cell lines. The protein expression of FOXD1 was detected by western blot. The cell viability and colony formation abilities were examined by CCK-8 and colony formation assays, respectively. Wound healing and Transwell assays were performed to examine the migration and invasion abilities of cells. The targeted binding sites of miR-30a-5p and FOXD1 were predicted by bioinformatics, and dual luciferase assay was used to verify the targeted binding relationship between miR-30a-5p and FOXD1. RESULT: miR-30a-5p was downregulated in LSCC tissues and cells, while FOXD1 was highly expressed. Overexpression of miR-30a-5p or silencing FOXD1 inhibited cell viability, colony formation ability, migration, and invasion of LSCC cells. miR-30a-5p inhibited the proliferation and migration of LSCC cells by downregulating the expression of FOXD1. CONCLUSION: miR-30a-5p can downregulate the expression of FOXD1 and inhibit the proliferation and migration of LSCC.

Exosome-Derived miR-486-5p Regulates Cell Cycle, Proliferation and Metastasis in Lung Adenocarcinoma via Targeting NEK2.

OBJECTIVE: This study aimed to describe the mechanism of exosome-derived miR-486-5p underlying the cell cycle and progression in lung adenocarcinoma (LUAD). METHODS: Bioinformatics methods were applied for identifying the differentially expressed genes (DEGs) in the GEO-LUAD dataset, predicting where the potential target miRNA was expressed and exploring the corresponding downstream target mRNA. qRT-PCR was conducted to detect the levels of the target genes in cancer cells. Thereafter, a series of in vitro experiments were performed for cell activities evaluation, including CCK-8, EdU, colony formation assay and transwell. Besides, Western blot was applied to determine the protein levels of the migration and invasion-related factors (NEK2, E-cadherin, N-cadherin, Vimentin, MMP-2, and MMP-9). Dual-luciferase reporter gene assay was employed for validating the targeted relationship between the target genes. Furthermore, nude mouse transplantation tumor experiment was conducted to further validate the role of the target miRNA in tumor development, and immunohistochemistry was used for Ki67 detection and TUNEL was applied for cell apoptosis assay. RESULTS: miR-486-5p was observed to be enriched in serum exosomes, and seen to be significantly down-regulated in cancer tissues as well as in cancer serum exosomes. It was proven that exosomes could release miR-486-5p, thus regulating LUAD progression and affecting cell cycle. Moreover, NEK2 was identified as a target of miR-486-5p both in vivo and in vitro. Enrichment analysis revealed that NEK2 was mainly activated in cell cycle and mitosis-related pathways. Meanwhile, NEK2 was found to present significant difference in different TNM stages. Furthermore, rescue experiments indicated that the inhibitory effect of miR-486-5p overexpression on LUAD progression could be abrogated when miR-486-5p and NEK2 were simultaneously up-regulated. CONCLUSION: Exosome-derived miR-486-5p is responsible for cell cycle arrest as well as the inhibition of cell proliferation and metastasis in LUAD via targeting NEK2.

The Functional Effects of Key Driver KRAS Mutations on Gene Expression in Lung Cancer.

Lung cancer is a common malignant cancer. Kirsten rat sarcoma oncogene (KRAS) mutations have been considered as a key driver for lung cancers. KRAS p.G12C mutations were most predominant in NSCLC which was comprised about 11-16% of lung adenocarcinomas (p.G12C accounts for 45-50% of mutant KRAS). But it is still not clear how the KRAS mutation triggers lung cancers. To study the molecular mechanisms of KRAS mutation in lung cancer. We analyzed the gene expression profiles of 156 KRAS mutation samples and other negative samples with two stage feature selection approach: (1) minimal Redundancy Maximal Relevance (mRMR) and (2) Incremental Feature Selection (IFS). At last, 41 predictive genes for KRAS mutation were identified and a KRAS mutation predictor was constructed. Its leave one out cross validation MCC was 0.879. Our results were helpful for understanding the roles of KRAS mutation in lung cancer.

Exploring the Effect of Differentially Expressed Long Non-coding RNAs Driven by Copy Number Variation on Competing Endogenous RNA Network by Mining Lung Adenocarcinoma Data.

Lung cancer is the first cause of cancer death, and gene copy number variation (CNV) is a vital cause of lung cancer progression. Prognosis prediction of patients followed by medication guidance by detecting CNV of lung cancer is emerging as a promising precise treatment in the future. In this paper, the differences in CNV and gene expression between cancer tissue and normal tissue of lung adenocarcinoma (LUAD) from The Cancer Genome Atlas Lung Adenocarcinoma data set were firstly analyzed, and greater differences were observed. Furthermore, CNV-driven differentially expressed long non-coding RNAs (lncRNAs) were screened out, and then, a competing endogenous RNA (ceRNA) regulatory network related to the gene CNV was established, which involved 9 lncRNAs, seven microRNAs, and 178 downstream messenger RNAs (mRNAs). Pathway enrichment analyses sequentially performed revealed that the downstream mRNAs were mainly enriched in biological pathways related to cell division, DNA repair, and so on, indicating that these mRNAs mainly affected the replication and growth of tumor cells. Besides, the relationship between lncRNAs and drug effects was explored based on previous studies, and it was found that LINC00511 and LINC00942 in the CNV-associated ceRNA network could be used to determine tumor response to drug treatment. As examined, the drugs affected by these two lncRNAs mainly targeted metabolism, target of rapamycin signaling pathway, phosphatidylinositol-3-kinase signaling pathway, epidermal growth factor receptor signaling pathway, and cell cycle. In summary, the present research was devoted to analyzing CNV, lncRNA, mRNA, and microRNA of lung cancer, and nine lncRNAs that could affect the CNV-associated ceRNA network we constructed were identified, two of which are promising in determining tumor response to drug treatment.

Exploring the role of Mir204/211 in HNSCC by the combination of bioinformatic analysis of ceRNA and transcription factor regulation.

OBJECTIVES: This study aimed to reveal the regulatory roles of microRNAs in head and neck squamous cell carcinoma (HNSCC) through comprehensive ceRNA, miRNA-transcription factor (TF)-hub gene network and survival analysis. MATERIALS AND METHODS: Expression analysis was performed using the 'edgeR' package based on The Cancer Genome Atlas database. The ceRNA network was screened by intersecting prediction results from miRcode, miRTarBase, miRDB and TargetScan. GSE30784, GSE59102 and GSE107591 from the Gene Expression Omnibus repository were chosen for cross-validation. Hub genes were identified using a protein-protein interaction network constructed by Search Tool for the Retrieval of Interacting Genes. The Transcriptional Regulatory Relationships Unraveled by Sentence-based Text mining (TTRUST) was utilized to map the miRNA-TF-Hub gene network. Patient overall survival was analyzed using the 'survival' package in R. Structural and functional analysis of miR-204/211 was based on miRbase and RNAstructure. RESULTS: A ceRNA network of 178 lncRNAs, 19 miRNAs and 55 mRNAs was generated, and a TF regulatory network with 11 miRNAs, 11 TFs and 18 hub genes was constructed from the 52 hub genes identified through the protein-protein interaction (PPI) network. Survival analysis demonstrated that the dysregulated expression of 11 lncRNAs and 14 mRNAs was highly related to overall survival. Furthermore, miR-204 and miR-211 were significantly involved in the network with identical mature structures, indicating them as key miRNAs in HNSCC. CONCLUSION: This study reveals the comprehensive molecular regulatory networks centralized by miRNAs in HNSCC and uncovers the crucial role of miR-204 and miR-211, which may become potential diagnostic and therapeutic targets.

Cyclosporine A sensitizes lung cancer cells to crizotinib through inhibition of the Ca2+/calcineurin/Erk pathway.

BACKGROUND: Crizotinib has potent anti-tumor activity in patients with advanced MET-amplified non-small cell lung cancer (NSCLC). However, the therapeutic effect is still not satisfying. Thus, developing approaches that improve the efficacy of crizotinib remains a significant challenge. METHODS: MET-amplified NSCLC cell lines were treated with crizotinib and cyclosporine A (CsA). Cell viability was determined by MTS assay. The changes of apoptosis, cell cycle and calcineurin-Erk pathways were assessed by western blot. Xenograft mouse model, primary human NSCLC cells and hollow fiber assays were utilized to confirm the effects of CsA. FINDINGS: We demonstrated that CsA significantly increased the anti-tumor effect of crizotinib on multiple MET-amplified NSCLC cells in vitro and in vivo. Mechanistically, crizotinib treatment led to the activation of Ca2+-calcineurin (CaN)-Kinase suppressor of Ras 2 (KSR2) signaling, resulting in Erk1/2 activation and enhanced survival of cancer cells. CsA effectively blocked CaN-KSR2-Erk1/2 signaling, promoting crizotinib-induced apoptosis and G2/M arrest. Similarly, pharmacologic or genetic inhibition of Erk1/2 also enhanced crizotinib-induced growth inhibition in vitro. Xenograft studies further confirmed that CsA or Erk1/2 inhibitor PD98059 enhanced the anti-cancer activity of crizotinib through inhibition of CaN-Erk1/2 axis. The results were also validated by primary human NSCLC cells in vitro and hollow fiber assays in vivo. INTERPRETATION: This study provides preclinical evidences that combination therapy of CsA and crizotinib is a promising approach for targeted treatment of MET-amplified lung cancer patients. FUND: This work was supported by the National Natural Science Foundation of China, the Key Projects of Natural Foundation of Zhejiang Province, the Ten thousand plan youth talent support program of Zhejiang Province, the Zhejiang Natural Sciences Foundation Grant, and the Zhejiang medical innovative discipline construction project-2016.

Clinical characteristics and programmed cell death ligand-1 expression in adenocarcinoma in situ and minimally invasive adenocarcinoma of lung.

OBJECTIVES: According to the IASLC/ATS/ERS 2011 classification, there are two new conceptions of lung adenocarcinoma, adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA), which are very early stages of lung adenocarcinoma. This study aimed to analyze clinical features of AIS and MIA and determine the expression profile of PD-L1 in AIS and MIA. RESULTS: In all 274 patients, 77 were diagnosed as AIS and 197 as MIA. We accidentally found 4 patients with recurrence, which were all MIA. The median age of the patients at diagnosis was both 52 years. 71.4% were female in AIS as while as 71.1% in MIA. 36.4% patients were observed with ever symptoms in AIS and 28.9% in MIA. 12.9% and 8.6% had smoking history respectively in AIS an MIA. All AIS and MIA cases were PD-L1 negative. There was significant association between symptoms and more mild progression of nodules in chest CT before surgery. MATERIALS AND METHODS: We analyzed some clinical features of 274 patients including age, sex, smoking history, family history, surgery, EGFR mutation, ALK, ROS-1, serum CEA level et al. The expression of PD-L1 was evaluated by immunohistochemical analysis in 37 specimens of MIA and 17 specimens of AIS. CONCLUSIONS: There are no significant differences between AIS and MIA in clinical features. AIS and MIA almost do not express PD-L1 protein and without any lymph node metastasis. The surgery intervention is supposed to be as small as possible.

Apatinib for the treatment of pulmonary epithelioid hemangioendothelioma: A case report and literature review.

RATIONALE: Pulmonary epithelioid hemangioendothelioma (P-EHE) is a rare tumor, with no established standard treatment. Overexpression of vascular endothelial growth factor receptor 2 (VEGFR-2) has been reported in some P-EHE patients. Apatinib, a new small molecule tyrosine kinase inhibitor that specifically targets VEGFR-2, has therapeutic benefits in some advanced tumors. However, its efficacy in P-EHE cases has not been reported. PATIENT CONCERNS: Herein, we presented a 44-year-old man with recurrent hemoptysis for approximately 9 years. DIAGNOSES: After hospitalization, relevant examinations were conducted. The disease was subsequently diagnosed as P-EHE. INTERVENTIONS: The patient underwent pulmonary lobectomy, but subsequently developed multiple metastases. Within the tumor, CD31, CK, and Vimentin were found to be positive, while CD34 was negative. Apatinib was initially administered 250 mg daily doses and after 1 month was increased to 500 mg daily. OUTCOMES: He showed noticeable symptomatic improvements and positive imaging changes in the first month of treatment. However, the disease progressed in the following month, despite the increased apatinib dose. LESSONS: Apatinib is possibly a new treatment for P-EHE. However, further clinical trials are necessary to confirm an effective dose and the efficacy and safety of apatinib in P-EHE treatment.

Cold snare resection for the treatment of benign airway lesions.

The objective was to assess the safety and outcome of cold snare technique used by flexible bronchoscopy in the treatment of airway benign neoplasms. The clinical data of 21 patients, who had airway benign neoplasm and were treated through the cold snare method in Sir Run Run Shaw Hospital, affiliated with the Zhejiang University, were retrospectively analyzed. The relief of the symptoms and occurrence of complications were observed and evaluated. All the tumors were benign and removed by cold snare. Postoperatively, we found that the treatment was completely effective in 12 patients, and there was a significant improvement in 7 patients and a moderate improvement in 2 patients, and no recurrence in follow-up visit. In conclusion, the cold snare technique is an economically feasible, safe, and effective method in the treatment of airway neoplasms.

Wnt/ß-catenin signaling pathway in lung cancer stem cells is a potential target for the development of novel anticancer drugs.

PURPOSE: In the present study, we have analyzed the regulation of Wnt/ß-catenin signaling in lung adenocarcinoma stem cells (CSCs), that are responsible for tumor recurrence. METHODS: Lung cancer samples were studied for the presence of cancer stem like cells and analyzed by flow cytometry. Then, the sorted cells were analyzed for the stem cell surface markers and Wnt/ß-catenin signaling pathways. Moreover, the sorted side population (SP) and non-SP cells were also subjected to drug resistance assay. RESULTS: Western blot analysis showed that the protein level of ß-catenin was highly upregulated in fluorescence activated cells (FACs) sorted SP cells which led to elevated expression of stem cell protein Oct-4 that is responsible for SP cells' self-renewal. RT-PCR revealed that the relative mRNA expression level of Wnt target gene cyclin D was significantly higher (p<0.01) in SP cells, enhancing thus the cell proliferation rate and clone formation efficiency. In addition, the matrigel invasion assay revealed that SP cells were highly invasive than non-SP cells. CONCLUSION: In the present study we demonstrated that lung adenocarcinoma samples contain a small population of tumor-initiating SP cells which possess the characteristic features of CSCs. Wnt/ß-catenin mediated increased expression of ß-catenin, Oct-4 and cyclin D in SP cells but not in non-SP cells was also observed. FACs-purified SP cells are resistant to a number of chemotherapeutic drugs. Our data suggest that the use of novel anticancer drugs, targeting Wnt/ß-catenin signaling pathways, may help eradicate the lung cancers stem cells.

Using oligonucleotide suspension arrays for laboratory identification of bacteria responsible for bacteremia.

The aim of this study was to develop and validate an oligonucleotide suspension array for rapid identification of 15 bacterial species responsible for bacteremia, particularly prevalent in Chinese hospitals. The multiplexed array, based on the QIAGEN LiquiChip Workstation, included 15 oligonucleotide probes which were covalently bound to different bead sets. PCR amplicons of a variable region of the bacterial 23S rRNA genes were hybridized to the bead-bound probes. Thirty-eight strains belonging to 15 species were correctly identified on the basis of their corresponding species-specific hybridization profiles. The results show that the suspension array, in a single assay, can differentiate isolates over a wide range of strains and species, and suggest the potential utility of suspension array system to clinical laboratory diagnosis.

[A high-throughput diagnostic method for detecting pathogenic microbes].

OBJECTIVE: To develop a high-throughput diagnostic method with suspension array technique for detecting pathogenic microbes. METHODS: The probes and positive controls of 56 kinds of pathogenic microbes were designed, synthesized, and used to detect pathogenic microbes with suspension array technique. RESULTS: Fluorescence signals of 56 positive controls were higher than those of the negative controls, and there was no cross-reaction between the probes and positive controls of different microbes. CONCLUSION: Based on suspension array technique, the high-throughput diagnostic method may be useful in clinical detection of pathogenic microbes.

[Human papillomavirus infection in women with cervical lesion of Huzhou area of Zhejiang province].

OBJECTIVE: To observe human papillomavirus (HPV) infection in women with cervical lesions in Huzhou area of Zhejiang province. METHODS: 720 samples of cervical secretion or exfoliated cells were collected from women with cervical lesion in Huzhou area. Human papillomavirus was detected by suspension array technique. RESULTS: Positive HPV infection was detected in 25.42% cases (183/720), with 135 cases of single HPV type, 33 of dual HPV types and 15 of multiple HPV types. HPV16 and HPV58 were the most prevalent types in 183 HPV positive cases. CONCLUSION: The most prevalent high-risk types of HPV are HPV16 and HPV58 in Huzhou area of Zhejiang province.