Objective To measure the peak skin dose (PSD) in two cardiovascular interventional procedures,including coronary angiography (CA) and percutaneous transluminal coronary angioplasty (PTCA) using radiochromic film.Methods Gafchromic XR-RV3 film was selected to measure PSD in two hospitals.The films were placed on the table underneath the patient during interventional surgery.The kV,mA,fluoroscopy time,dose-area product (DAP),and cumulative dose at reference point and other relevant information were recorded for all cases.Using the Epson V750 flatbed scanner for scanning and analyzing film,FilmQA software was chosen to analyze the pixel value of red,green and blue color channels.The PSD was determined using red channel data.The correlation and linear regression analysis between PSD and device-displayed parameters was carried out.Results PSD were measured using XR-RV3 film for 26 CA and 19 CA + PTCA procedures.For CA procedures,maximum fluoroscopy time,cumulative dose and DAP were 17.62 min,1 498.50 mGy and 109.68 Gy · cm2,respectively.The maximum PSD was 361.20 mGy.However,for CA + PTCA procedures,maximum fluoroscopy time,cumulative dose and DAP were 64.48 min,6 976.20 mGy and 5 336.00 Gy· cm2,respectively.One patient with CA + PTCA procedures was found to have received the PSD value more than 2 Gy,up to 2 195.70 mGy.DAP was found to be a good indicator (R2 =0.815,P ＜0.05) of PSD for CA procedure,and correlated with cumulative dose (R2 =0.916,P ＜ 0.05) for CA + PTCA procedures.Conclusions The PSD value of some patients in cardiac interventional procedures would exceed 2 Gy,the threshold of deterministic effects recommended by ICRP.The dose-related parameters value showed on DSA device can only used to estimate PSD roughly.Using XR-RV3 film accurate measurement of the PSD in interventional projects is a very fast and effective method.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous syestem (CNS) triggered by an autoimmune mechanism, which is the main cause of neurological disability in young people. In MS, a variety of glial cells participate in the pathogenesis and development of the disease, and oligodendrocytes (OL) and myelin cytes are destroyed by autoimmune mediated inflammation. Impaired OL production of oligodendrocyte progenitor cells (OPC) leads to persistent demyelination, myelin fragment accumulation and axonal injury, with clinical manifestation of CNS disability. Microglia (MG), which is involved in the inflammatory response and removal of myelin debris, plays a pivotal role in OPC differentiation and OL maturation, thereby directly or indirectly influencing the process of myelin regeneration. An interactive mechanism exists between these 2 components. The comprehension of the interrelationship between the 2 factors can provide enhanced insights into the pathogenesis of MS and facilitate the development of novel therapeutic strategies, thereby addressing pivotal scientific challenges encountered in clinical management of MS. Therefore, this review summarizes the dynamic changes of microglia in MS and its classic animal models, explores the internal relationship between MG and OL in this process, and focuses on the beneficial effects of targeted regulation of microglia, thereby promoting OPC differentiation and myelin regeneration, in order to provide a new research direction for MS treatment.

The continuous advancement of molecular detection technology has greatly propelled the develop-ment of precision medicine for lung cancer.However,tumor heterogeneity is closely associated with tumor metastasis,recurrence,and drug resistance.Additionally,different lung cancer patients with the same genetic mutation may exhibit varying treatment responses to different therapeutic strategies.Therefore,the development of modern precision medicine urgently requires the precise formulation of personalized treatment strategies through personalized tumor models.Lung cancer organoid(LCO)can highly simulate the biological characteristics of tumor in vivo,facilitating the application of innovative drugs such as antibody-drug conjugate in precision medicine for lung cancer.With the development of co-culture model of LCO with tumor microenvironment and tissue engineering technology such as microfluidic chip,LCO can better preserve the biological characteristics and functions of tumor tissue,further improving high-throughput and automated drug sensitivity experiment.In this review,we combine the latest research progress to summarize the applica-tion progress and challenges of LCO in precision medicine for lung cancer.

Lung cancer is one of the leading causes of cancer-related morbidity and mortality. Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) have become the standard treatment for EGFR-mutated advanced non-small cell lung cancer (NSCLC). Unfortunately, drug resistance is inevitable in most cases. EGFR-TKI combined with angiogenesis inhibitors is a treatment scheme being explored to delay the therapeutic resistance, which is called "A+T treatment". Several clinical trials have demonstrated that the A+T treatment can improve the progression free survival (PFS) of the NSCLC patients. However, compared to EGFR-TKI monotherapy, the benefits of the A+T treatment based on different EGFR-TKIs, as well as its safety and exploration prospects are still unclear. Therefore, we reviewed the literature related to all three generations EGFR-TKIs combined with angiogenesis inhibitors, and summarized the mechanism, benefit, safety, optimal target population of A+T treatment.
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Angiogenesis Inhibitors/therapeutic use* ; Carcinoma, Non-Small-Cell Lung/genetics* ; ErbB Receptors/genetics* ; Humans ; Lung Neoplasms/genetics* ; Mutation ; Protein Kinase Inhibitors/therapeutic use*

Minute pulmonary meningothelial-like nodules (MPMNs) are benign small lesions in the lungs, with similar pathological characteristics to the meningeal epithelium. MPMNs have similar imaging manifestations to malignant tumors, which can lead to misdiagnosis in clinical practice. There is no consensus on the pathogenesis of MPMNs, with some suggest that MPMNs derive from reactive proliferation, while others suggest that MPMNs share a common origin and molecular mechanism with meningiomas in the central nervous system. Understanding the characteristics of MPMNs and studying their pathogenesis will help improve the understanding and diagnosis of MPMNs. In this article, we reviewed the clinical, pathological, imaging characteristics, differential diagnosis and pathogenesis of MPMNs. We also analyze the existing research advances regarding the pathogenesis and propose prospects for further research.
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Due to the advancement of 16S rRNA sequencing technology, the lower respiratory tract microbiota, which was considered non-existent, has been revealed. The correlation between these microorganisms and diseases such as tumor has been a hot topic in recent years. As the bacteria in the surrounding can infiltrate the tumors, researchers have also begun to pay attention to the biological behavior of tumor bacteria and their interaction with tumors. In this review, we present the characteristic of the lower respiratory tract bacteria and summarize recent research findings on the relationship between these microbiota and lung cancer. On top of that, we also summarize the basic feature of bacteria in tumors and focus on the characteristic of the bacteria in lung cancer. The relationship between bacteria in lung cancer and tumor development is also been discussed. Finally, we review the potential clinical applications of bacterial communities in the lower respiratory tract and lung cancer, and summarize key points of sample collection, sequencing, and contamination control, hoping to provide new ideas for the screening and treatment of tumors.
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Humans ; Lung Neoplasms ; RNA, Ribosomal, 16S/genetics* ; Bacteria/genetics* ; Microbiota ; Respiratory System ; Lung/microbiology*