The paper analyzes the potential drawbacks of the current medical liability insurance from the perspectives of hospitals, insurance companies and patients. It puts forward suggestions for the sustainable development of medical liability insurance, viz. involvement of insurance brokers in coordinately solving the issue of application for medical liability insurance, involvement of loss assessors in solving medical disputes, adoption of compulsory medical liability insurance in due time, and further expansion of the scope and categories of insurance.

OBJECTIVE: To investigate the effect of miR-204 on the invasion and metastasis of breast cancer by targeted regulation of HNRNPA2B1. METHODS: The bioinformatics database was used to obtain data of the expressions of miR-204 in breast cancer patients and the survival rate of the patients. RT-qPCR was used to detect the expression of miR-204 in breast cancer cell lines. The expression vector GV369-miR-204 was used to overexpress miR-204 in MDA-MB-231 cells. Transwell assay was performed to detect the effect of miR-204 on the migration and invasion ability of the breast cancer cells. The key genes (hub genes) of miR-204 were determined by bioinformatics method. A dual luciferase assay was used to analyze the targeting relationship between miR-204 and HNRNPA2B1. The expression of HNRNPA2B1 in MDA-MB-231 cells after miR-204 overexpression was detected by Western blotting, and Transwell assay was used to examine the changes in the cell invasion ability. RESULTS: The expression of miR-204 was decreased in both breast cancer tissues, and was significantly lower in breast cancer MDA-MB-231 cells than in MCF-10A cells ( < 0.05). The decreased expression of miR-204 was associated with poorer prognosis of breast cancer patients ( < 0.05). Upregulation of miR-204 in MDA-MB-231 cells significantly inhibited the invasion and migration of the cells ( < 0.05). Analysis of the data from the Starbase revealed that the expression of miR-204-5p was negatively correlated with the expression of HNRNPA2B1, and the expression of HNRNPA2B1 was increased in breast cancer patients ( < 0.05) in association with a poorer prognosis of the patients ( < 0.05). Dual luciferase assay demonstrated that miR-204 could bind to HNRNPA2B1 in a target-specific manner. Western blotting and Transwell assay showed that miR-204 significant inhibited the migration and invasion ability of breast cancer cells by targeting HNRNPA2B1 ( < 0.05). CONCLUSIONS miR-204 expression is decreased in breast cancer tissues and cells, and its overexpression can inhibit the invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1.
Breast Neoplasms ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; Neoplasm Invasiveness ; Neoplasm Metastasis

Cachexia is a common complication in patients with lung cancer. It aggravates the toxic and side effects of chemotherapy, hinders the treatment plan, weakens the responsiveness of chemotherapy, reduces the quality of life, increases complications and mortality, and seriously endangers the physical and mental health of patients with lung cancer. The causes and pathogenesis of tumor cachexia are extremely complex, which makes its treatment difficult and complex. Controlling cachexia in lung cancer patients requires many means such as anti-tumor therapy, inhibition of inflammatory response, nutritional support, physical exercise, and relief of symptoms to exert the synergistic effect of multimodal therapy against multiple mechanisms of tumor cachexia. To date, there has been a consensus within the discipline that no single therapy can control the development of cachexia. Some therapies have made some progress, but they need to be implemented in combination with multimodal therapy after fully assessing the individual characteristics of lung cancer patients. This article reviews the application of drug therapy and nutritional support in lung cancer patients, and looks forward to the research direction of cachexia control in lung cancer patients.
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Cachexia/therapy* ; Combined Modality Therapy ; Humans ; Lung Neoplasms/drug therapy* ; Neoplasms/complications* ; Nutritional Support/adverse effects* ; Quality of Life

BACKGROUND: Derlin 3 (DERL3) is downregulated in colorectal cancer (CRC) samples. Its level is closely linked to lymphatic metastasis or distant metastasis rate in CRC patients. However, its biological behavior in lung adenocarcinoma were rarely reported. The aim of this study is to investigate the ectopic expression of DERL3 in lung adenocarcinoma tissues and its effect on the invasion and metastasis of lung adenocarcinoma A549 cell line to reveal the possible mechanism of invasion and metastasis of lung adenocarcinoma. METHODS: Lung adenocarcinoma microarray gene chip data included 3 cases of lymph node metastasis and 3 cases of lung adenocarcinoma tissue without lymph node metastasis. The GEDS and Kaplan-Meier plot queries the survival curve and expression level of DERL3. Western blot was used to detect the expression of DERL3 in lung adenocarcinoma cells. The efficiency of knockdown DERL3 gene was detected by Western blot assay. Transwell detected the number of cells passing through the basement membrane of the transwell. EDU assay detected cell proliferation ability. Western blot detected the expression of epithelial-mesenchymal transition related proteins E-cadherin and Vimentin. RESULTS: The microarray gene chip results showed that compared with lung adenocarcinoma tissues without lymph node metastasis, 1,314 mRNAs in lung adenocarcinoma tissues with lymph node metastasis were up-regulated, 400 mRNAs were down (P<0.05). The expression of DERL3 increased in lung adenocarcinoma (P<0.05). The results of survival curve showed that the lung cancer patients with high expression of DERL3 with poor prognosis (P<0.05). Western blot results indicated that plasmid transfection was successful. Knockdown of DERL3 suppressed the ability of proliferation, invasion and migration in A549 cells (P<0.05). After knockdown of DERL3, the expression level of Vimentin was decreased, while E-cadherin expression increased (P<0.05). CONCLUSIONS Knockdown of DERL3 inhibited the proliferation, invasion and metastasis of A549 cells.

BACKGROUND: MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression, influence cellular processes, and promote disease development. Variations in miRNA expression have been observed in many diseases, including hepatitis, cardiovascular disease, and cancer. The aim of this study is to investigate the effect of miR-144-3p on the invasion and metastasis of lung adenocarcinoma by targeting recombinant insulin receptor substrate 1 (IRS1). METHODS: The expression of miR-144-3p in patients with lung adenocarcinoma was queried through bioinformatics database. MirTarPathway was used to analyze the KEGG enrichment pathway of miRNA. The expression and plasmid transfection efficiency of miR-144-3p in lung adenocarcinoma cell lines were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Transwell assay was used to detect the changes of cell invasion and migration ability in different groups. Bioinformatics determined the key genes (Hub genes) of miR-144-3p; Double luciferase target assay was used to detect the mutual binding of miR-144 and IRS1. Western blot assay was used to detect the expression of IRS1 in different cell lines and the expression of after overexpression of miR-144. RESULTS: The expression of miR-144-3p in lung adenocarcinoma tissues was decreased, qRT-PCR results indicated that the expression of miR-144-3p in lung adenocarcinoma cell A549 was significantly decreased (P<0.05), and the overexpressed plasmid was successfully transfected (P<0.05). Overexpression of miR-144 decreased the ability of cell migration and invasion (P<0.05). The expression of IRS1 was up-regulated in lung adenocarcinoma tissues. Survival analysis showed that patients with lung adenocarcinoma with high IRS1 expression had a poor prognosis (P<0.05). Double luciferase assay results showed that miR-144 could specifically identify 3'-UTR of IRS1 and inhibit reporter enzyme expression (P<0.05). Western blot indicated that the expression of IRS1 was increased in A549 cells (P<0.05). After overexpression of miR-144, the expression level of IRS1 protein was decreased (P<0.05). Transwell experiment proved that miR-144-3p could inhibit invasion and metastasis of lung adenocarcinoma cells by targeting IRS1 (P<0.05). CONCLUSIONS MiR-144-3p inhibits the invasion and migration of A549 cells through targeted regulation of IRS1, thus playing an anticancer role in tumors.

BACKGROUND: Lung adenocarcinoma (LUAD) is the most common clinical histological subtype of lung cancer and microRNAs (miRNAs) are a type of small non-coding RNAs which play a central role in cells. miR-30b-3p plays a key effect in many types of carcinoma, but there is still very little research on how it works in lung adenocarcinoma. The role and mechanism of miR-30b-3p in the proliferation and invasion of LUAD were explored in this study, to provide new targets for inhibiting the proliferation and invasion of LUAD. METHODS: NCBI database was used to screen out miRNA with obvious differential expression, and the differential expression and survival curve were searched by StarBase database. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of miR-30b-3p in each lung adenocarcinoma cell line. 5-ethynyl-2'-deoxyuridine (EdU) cell proliferation assay and Transwell invasion assay were used to detect the proliferation and invasion of A549 cells in each group. The target genes of miR-30b-3p were determined by the target gene prediction websites. Western blot assay was used to detect the expression of COX6B1 in each group of A549 cells. Double luciferase assay was used to verify the targeted binding relationship between miR-30b-3p and COX6B1. RESULTS: The expression of miR-30b-3p in lung adenocarcinoma tissues and lung adenocarcinoma cells was downregulated (P<0.05). Low expression levels of miR-30b-3p were associated with poor prognosis in patients with lung adenocarcinoma (P=0.005,8). Overexpression of miR-30b-3p could inhibit the proliferation and the invasion of lung adenocarcinoma cells (P<0.05). Double luciferase assay proved that miR-30b-3p could target and bind to COX6B1 (P<0.05). Western blot analysis showed that the overexpression of miR-30b-3p could downregulate the expression of COX6B1 in A549 cells (P<0.05). EdU cell proliferation assay and Transwell invasion assay showed that the overexpression of miR-30b-3p could reverse the promoting effect of upregulation of COX6B1 on proliferation and invasion in lung adenocarcinoma cells (P<0.05). CONCLUSIONS miR-30b-3p acts as a tumor suppressor gene in lung adenocarcinoma, and it can inhibit the proliferation and invasion of lung adenocarcinoma by targeting the expression of COX6B1.
Adenocarcinoma of Lung/pathology* ; Cell Line, Tumor ; Cell Movement/genetics* ; Cell Proliferation/genetics* ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/pathology* ; MicroRNAs/metabolism*

BACKGROUND: Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer, and any change of miRNAs expression will affect the degree of target regulation, thus affecting intracellular homeostasis. This study verified that miR-186-5p could inhibit the proliferation, migration and invasion of LUAD cells by regulating PRKAA2. METHODS: Previous investigations found that the expression of miR-186-5p was markedly suppressed in LUAD. Bioinformatics method is used to predict the target protein related to ferroptosis downstream and inquire about its expression level in LUAD and its influence on the survival of patients. Double luciferase verified the binding site of PRKAA2 and miR-186-5p. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression of PRKAA2. The effects of miR-186-5p of LUAD cells as well as the mechanism by which miR-186-5p inhibits Fer-1's sensitivity to ferroptosis were confirmed by EdU, Transwell, and scratch assays. The effect of miR-186-5p on the amount of reactive oxygen species (ROS) in LUAD cells was discovered using ROS experiment. Malondialdehyde (MDA) and glutathione (GSH) experiments were used to detect the effects of miR-186-5p and PRKAA2 on ferroptosis index of LUAD cells. The concentration of lipid ROS (L-ROS) in LUAD cells were measured using the L-ROS tests to determine the effects of miR-186-5p and PRKAA2. RESULTS: The expression of PRKAA2 is up-regulated, and a high level of PRKAA2 expression was associated with a poor prognosis for patients with LUAD. Overexpression of miR-186-5p decreased the gene and protein expression of PRKAA2. By promoting ferroptosis, miR-186-5p overexpression prevented lung cancer cells from proliferating, invading, and migrating. ROS could be produced in higher amounts in LUAD cells due to miR-186-5p. Overexpression of miR-186-5p and knockdown PRKAA2 up-regulated MDA content and reduced GSH content in LUAD cells, respectively. miR-186-5p could increase the content of L-ROS and promote the ferroptosis sensitivity of LUAD cells by targeting PRKAA2. CONCLUSIONS miR-186-5p promotes ferroptosis of LUAD cells through targeted regulation of PRKAA2, thus inhibiting the proliferation, invasion and migration of LUAD.
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Humans ; Lung Neoplasms/genetics* ; Carcinoma, Non-Small-Cell Lung ; Ferroptosis/genetics* ; Reactive Oxygen Species ; Adenocarcinoma of Lung/genetics* ; MicroRNAs/genetics* ; 3,4-Methylenedioxyamphetamine ; Cell Proliferation/genetics* ; Cell Movement/genetics* ; Gene Expression Regulation, Neoplastic ; Cell Line, Tumor ; AMP-Activated Protein Kinases

Objective To evaluate the diagnostic value of shear wave elastography on deep venous thrombosis in different stage.Methods Models of rabbits'deep venous thrombosis have been established to noninvasively measure Young's moduli of thrombosis in day 1 ,4,7,10 and 14 respectively by shear wave elastography.Results The elastic modulus of thrombosis increased with increment of the stages of thrombosis.Specifically,the mean Young's moduli of thrombosis increased from (4.0±1 .42)kPa (day 1)to (25.71 ±6.09)kPa (day 14),with statistical differences between each two observation time points (P <0.05).Conclusions Shear wave elastography can effectively reflect the elasticity of thrombosis in different stages,and the stage of thrombosis can be estimated judging by quantitative ultrasound elasticity preliminarily.

Objective To investigate the detection of human bocavirus (HBoV) in children with acute respiratory infection and to explore the relationship between viral load and clinical characteristics of acute respiratory infection in children.Methods A total of 4 501 nasopharyngeal secretion samples were collected from hospitalized children with acute respiratory infection from January 2013 to June 2013.HBoV-positive children were divided into simple infection group and mixed infection group.Children with HBoV DNA≥1 × 104 copy/mL were categorized into high viral load group,while those with HBoV DNA ＜1 × 104 copy/mL were categorized into low viral load group.HBoV was determined by fluorescence quantitative polymerase chain reaction (PCR).Respiratory syncytial virus (RSV),influenza virus (Inf)-A,Inf-B,parainfluenza virus (Pinf)-Ⅰ 、Pinf-Ⅱ 、Pinf-Ⅲ and adeno virus antigen were detected by direct antigen-specific immunofluorescence assays.Mycoplasm Pnuemonia was detected by real-time fluorescence quantitative PCR.Serum mycoplasma antibodies were detected by enzyme-linked immunosorbent assay (ELISA).Bacteria was detected by sputum culture.Over the same period,23 children undergoing elective inguinal hernia operation with no respiratory infection or fever were considered as control group.The percentage of peripheral blood T lymphocyte subsets were tested by flow cytometry.Inter-group differences were compared using Chi-square test or Fisher exact test.Viral loads were compared using Mann-Whitney test.Results Two hundred and twenty-two HBoV-positive cases were detected with a positive rate of 5.41％ (222/4 105),33.33％ (74/222) of which were with high viral load and 66.67％ (148/222) were with low viral load.There was a high incidence in the age group of 1-2 years.The simple HBoV infection accounted for 24.32％,including 26 cases with high viral load and 28 cases with low viral load.Wheezing was more common in patients with high viral load than those with low viral load,and the difference was statistically significant (88.46 ％ vs 42.86 ％,x2 =12.295,P=0.001).Among the 222 HBoV-positive cases,the median viral load of HBoV in simple infection group was 3.86 × 103 copy/mL,and 1.0× 103 copy/mL in mixed infection group.The difference of the viral load between these two groups was statistically significant (Z =2.906,P =0.004).Mycoplasma and Streptococcus pneumonia were most commonly detected in the 168 patients with mixed infection.Percentages of CD3+ and CD3+/CD8+ subsets were significantly lower in HBoV simple infection group and mixed infection group,compared to control group (both P＜0.05).However,percentages of CD3 /CD19+,CD19+/ CD23+ subsets were significantly higher in HBoV simple infection group and mixed infection group,compared to control group (both P＜0.05).Conclusions HBoV is one of the pathogens causing acute respiratory tract infection in children,which lead to cellular immunity dysfunction in children.Moreover,children with higher HBoV load are more likely to develop wheezing.Co-infection with other pathogens should be considered in children with low HBoV load.

Objective: To explore the relevant factors of work-related musculoskeletal disorders (WMSDs) among dentists through Meta analysis, providing a basis for the prevention and control of WMSDs among dentists. Methods: In April 2022, cross-sectional research literatures on the prevalence correlation of WMSDs among Chinese dentists were searched in databases such as China National Knowledge Infrastructure, Wanfang, VIP, PubMed, Web of Science, and Em Base database. The search was conducted from the establishment of the database until April 2022, literatures were selected using keywords such as musculoskeletal disorders and dentists. To extract gender, age, length of service, disease classification and other related influencing factors as indicator, and prevalence was selected as the outcome indicator. After evaluating the quality of the literatures, RevMan 5.3 software was used to calculate the combined RD (95%CI) values of the included literatures. Results: A total of 15 articles were included, with a total sample size of 3646 people. Meta analysis results showed that the prevalence of WMSDs among dentists in China was 80%, and the top three parts of the incidence rates were 65% of the waist, 58% of the neck, and 50% of the back. Gender, age, length of service, region and disease classification all increased the risk of WMSDs, and the combined effect size were 75%, 78%, 71%, 77% and 82% respectively (P<0.05) . Conclusion: The occurrence of WMSDs among dentists in China is related to multiple factors such as gender, age, length of service and disease classification. The above risk factors should be taken into account in the workplace and preventive measures should be actively implemented to prolong the working life of dentists.
Humans ; Prevalence ; Cross-Sectional Studies ; Occupational Diseases/epidemiology* ; Surveys and Questionnaires ; Musculoskeletal Diseases/epidemiology* ; Risk Factors ; China/epidemiology* ; Dentists