Oncolytic viruses (OVs) represent a promising immunotherapy for cancer treatment, though their clinical application is often limited by systemic toxicity and low immunogenicity. To address this, we developed NDV-GT, a genetically engineered Newcastle disease virus that encodes porcine α-1,3-galactosyltransferase. These epitopes are recognized by pre-existing natural antibodies, triggering a hyperacute rejection response characterized by complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC). Furthermore, NDV-GT modulates the tumor microenvironment by promoting T-cell infiltration and cytokine secretion, converting immunologically "cold" tumors into "hot" ones. Mechanistically, the virus inhibits PI3K/AKT and NF-κB signaling pathways, inducing apoptosis and suppressing tumor proliferation. In a preliminary clinical study of 20 patients with advanced refractory carcinomas, NDV-GT achieved a 90.0% disease control rate with no serious adverse events, underscoring its potential as a novel, safe, and effective oncolytic agent that elicits robust antitumor immunity.

BACKGROUND:Radiopharmaceuticals are being used more frequently to treat neuroendocrine tumors and advanced prostate cancer; however, their clinical application is associated with adverse drug reactions (ADRs) that may affect patient safety. Real-world data from spontaneous reporting systems such as the World Health Organization's (WHO's)-VigiAccess can aid in assessing safety after the drugs have been marketed. MATERIALS AND METHODS:A retrospective descriptive analysis was conducted using ADR reports from the WHO-VigiAccess database up to November 2024. Reports related to lutetium (177Lu) dotatate (Lutathera®), lutetium (177Lu) vipivotide tetraxetan (Pluvicto®), and radium (223Ra) dichloride (Xofigo®) were extracted and analyzed with respect to patient demographics, geographic distribution, and ADRs classified by MedDRA System Organ Class and Preferred Terms. Descriptive statistics were used to compare safety profiles. RESULTS:A total of 17,743 ADR reports were analyzed. Lutathera was predominantly associated with gastrointestinal disorders and skin or subcutaneous tissue reactions. In contrast, Pluvicto demonstrated a higher frequency of general systemic disorders and a disproportionately higher number of fatal outcomes, a finding consistent with its indication for the treatment of advanced prostate cancer. Xofigo was primarily linked to hematological and musculoskeletal toxicities. In addition to 169 ADRs that were common to all three agents, distinct drug-specific reaction patterns were also observed. CONCLUSIONS:WHO-VigiAccess data reveal clearly differentiated ADR profiles among Lutathera, Pluvicto, and Xofigo. These results highlight the necessity for individualized risk assessment, careful monitoring, and further prospective investigations to optimize the safe clinical application of radiopharmaceuticals.

High-dose ionizing radiation (IR), as encountered in radiotherapy-related and radiological emergency contexts, induces severe acute developmental and neurobehavioral toxicity. However, safe and effective natural radioprotective agents remain limited. Ferulic acid (FA), a natural phenolic compound widely found in medicinal and edible plants, possesses well-established antioxidant and anti-inflammatory properties. Nevertheless, its protective effects and underlying mechanisms against high-dose IR-induced acute in vivo injury remain largely unclear. This study aimed to evaluate the in vivo protective effects of FA against acute IR-induced developmental and neurobehavioral toxicity in zebrafish and to investigate the involvement of apoptosis-related pathways. An acute radiation injury model was established in zebrafish embryos subjected to 1-10 Gy IR treatment, and 2.5 Gy was selected for FA intervention based on the dose-response results. Developmental phenotyping, locomotor activity, and social behavioral assays were conducted to assess IR-induced toxicity. Transcriptomic profiling combined with GO and KEGG enrichment analyses, RT-qPCR validation, and acridine orange staining were performed to explore the potential molecular mechanisms. High-dose IR treatment induced dose-dependent developmental defects, increased mortality, and pronounced locomotor and social behavioral abnormalities in zebrafish larvae. FA treatment significantly alleviated IR-induced developmental toxicity and improved locomotor activity and light-dark transition responses. Transcriptomic analysis showed that FA was associated with broad modulation of IR-responsive gene expression changes, with apoptosis, organelle homeostasis, and cell cycle-related processes identified as major transcriptomic features. Four apoptosis-associated candidate genes (chchd10, dmtf1, rcn3, and nr3c2) were identified and validated under irradiated conditions. FA attenuated the aberrant expression of these genes and reduced excessive apoptosis-associated signals in vivo. Collectively, these findings demonstrate that FA confers significant protection against high-dose IR-induced acute in vivo toxicity, at least in part, in association with apoptosis-related transcriptional modulation and attenuation of apoptosis-associated signals. This study provides mechanistic insights supporting FA as a promising natural radioprotective agent for further evaluation in radiotherapy-related and radiological emergency contexts.

BackgroundKeratoconus is a diseased corneal dilation of unknown etiology. Studies have shown that inflammation may play a role in keratoconus. Inflammatory enteritis (IBD), including ulcerative colitis (UC), is a chronic, systemic inflammatory disease. We used Mendelian randomization to assess the causal relationship among IBD, UC and keratoconus.MethodsThe instrumental variable of IBD and UC was selected, the information of the instrumental variable in keratoconus outcome was extracted, and the causal relationship was assessed by the inverse variance weighted method by primary analysis, and its relevant sensitivity analysis.ResultsA causal relationship between IBD and keratoconus was observed significantly (P = 0.017, OR = 1.21, 95% CI = 1.03–1.41), and same as to UC and keratoconus (P = 0.038, OR = 1.25, 95% CI = 1.01–1.54).ConclusionIBD may play a causal role in the development of keratoconus, but the mechanism needs to be further elucidated.

Developing a rapid detection method of Cr(VI) and ascorbic acid (AA) is vital in the food and environmental fields. Herein, an anthrylimidazole-based fluorescent ionic liquid (AI-FIL) with the advantageous fluorescent properties was successfully prepared and used to construct a promising "on-off-on" fluoroprobe for rapid/sensitive Cr(VI) and AA detection. Cr(VI) could effectively quench the fluorescence of AI-FIL owing to the inner-filter effect and photoinduced electron-transfer process. However, the decreased fluorescence could be rapidly recovered by AA owing to the redox reaction between AA and Cr(VI). For Cr(VI) detection, a satisfactorily linear response (0.03-300 mu M) was achieved with the corresponding detection limit of 9 nM. For AA detection, a good linearity from 1 to 1000 mu M was obtained with the resultant detection limit of 0.3 mu M. Moreover, the AI-FIL based fluoroprobe was successfully utilized for Cr(VI) and AA detection in food and water samples with satisfactory accuracy and precision.

Introduction: Sepsis is a worldwide epidemic, with high morbidity and mortality. Cuproptosis is a form of cell death that is associated with a wide range of diseases. This study aimed to explore genes associated with cuproptosis in sepsis, construct predictive models and screen for potential targets. Methods: The LASSO algorithm and SVM-RFE model has been analysed the expression of cuproptosis-related genes in sepsis and immune infiltration characteristics and identified the marker genes under a diagnostic model. Gene -drug networks, mRNA-miRNA networks and PPI networks were constructed to screen for potential biological targets. The expression of marker genes was validated based on the GSE57065 dataset. Consensus clustering method was used to classify sepsis samples. Results: We found 381 genes associated with the development of sepsis and discovered significantly differentially expressed cuproptosis-related genes of 16 cell types in sepsis and immune infiltration with CD8/CD4 T cells being lower. NFE2L2, NLRP3, SLC31A1, DLD, DLAT, PDHB, MTF1, CDKN2A and DLST were identified as marker genes by the LASSO algorithm and the SVM-RFE model. AUC > 0.9 was constructed for PDHB and MTF1 alone respectively. The validation group data for PDHB ( P =0.00099) and MTF1 ( P =7.2e-14) were statistically significant. Consistent clustering analysis confirmed two subtypes. The C1 subtype may be more relevant to cellular metabolism and the C2 subtype has some relevance to immune molecules. The results of animal experiments showed that the gene expression was consistent with the bioinformatics analysis. Discussion: Our study systematically explored the relationship between sepsis and cuproptosis and constructed a diagnostic model. And, several cuproptosis-related genes may interfere with the progression of sepsis through immune cell infiltration.

OBJECTIVE:The cardiovascular system effects of environmental low-dose radiation exposure on radiation practitioners remain uncertain and require further investigation. The aim of this study was to initially investigate and explore the mechanisms by which low-dose radiation may contribute to atherosclerosis through a multi-omics joint comprehensive basic experiment. METHODS:We used WGCNA and differential analyses to identify shared genes and potential pathways between radiation injury and atherosclerosis sequencing datasets, as well as tissue transcriptome immune infiltration level extrapolation and single-cell transcriptome data correction using the CIBERSORT deconvolution algorithm. Animal models were constructed by combining a high-fat diet with 5 Gy γ-ray whole-body low-dose ionizing radiation. The detection of NETs release was validated by enzyme-linked immunosorbent assay. RESULTS:Analysis reveals shared genes in both datasets of post-irradiation and atherosclerosis, suggesting that immune system neutrophils may be a key node connecting radiation to atherosclerosis. NETs released by neutrophil death can influence the development of atherosclerosis. Animal experiments showed that the number of neutrophils decreased (P < 0.05) and the concentration of NETs reduced after low-dose radiation compared with the control group, and the concentration of NETs significantly increased (P < 0.05) in the HF group. Endothelial plaques were significantly increased in the high-fat feed group and significantly decreased in the low-dose radiation group compared with the control group. CONCLUSIONS:Long-term low-dose ionizing radiation exposure stimulates neutrophils and inhibits their production of NETs, resulting in inhibition of atherosclerosis.

BACKGROUND:The incidence of inflammatory bowel disease (IBD) is growing in the population. At present, the etiology of inflammatory bowel disease remains unclear, and there is no effective and low-toxic therapeutic drug. The role of the PHD-HIF pathway in relieving DSS-induced colitis is gradually being explored.METHODS:Wild-type C57BL/6 mice were used as a model of DSS-induced colitis to explore the important role of Roxadustat in alleviating DSS-induced colitis. High-throughput RNA-Seq and qRT-PCR methods were used to screen and verify the key differential genes in the colon of mice between normal saline (NS) and Roxadustat groups.RESULTS:Roxadustat could alleviate DSS-induced colitis. Compared with the mice in the NS group, TLR4 were significantly up-regulated in the Roxadustat group. TLR4 KO mice were used to verify the role of TLR4 in the alleviation of DSS-induced colitis by Roxadustat.CONCLUSION:Roxadustat has a repairing effect on DSS-induced colitis, and may alleviate DSS-induced colitis by targeting the TLR4 pathway and promote intestinal stem cell proliferation.

Despite the wide application of radiotherapy in HCC, radiotherapy efficacy is sometimes limited due to radioresistance. Although radioresistance is reported with high glycolysis, the underlying mechanism between radioresistance and cancer metabolism, as well as the role of cathepsin H (CTSH) within it, remain unclear. In this study, tumor-bearing models and HCC cell lines were used to observe the effect of CTSH on radioresistance. Proteome mass spectrometry, followed by enrichment analysis, were used to investigate the cascades and targets regulated by CTSH. Technologies such as immunofluorescence co-localization flow cytometry and Western blot were used for further detection and verification. Through these methods, we originally found CTSH knockdown (KD) perturbed aerobic glycolysis and enhanced aerobic respiration, and thus promoted apoptosis through up-regulation and the release of proapoptotic factors such as AIFM1, HTRA2, and DIABLO, consequently reducing radioresistance. We also found that CTSH, together with its regulatory targets (such as PFKL, HK2, LDH, and AIFM1), was correlated with tumorigenesis and poor prognosis. In summary, our study found that the cancer metabolic switch and apoptosis were regulated by CTSH signaling, leading to the occurrence of radioresistance in HCC cells and suggesting the potential value of HCC diagnosis and therapy.

Abstract Background Aberrant splice variants play different roles in the formation of tumors. We observed the splice isoform of Protein arginine methyltransferase 5 (PRMT5-ISO5) increases in HCC patients undergoing stereotactic body radiotherapy, which is associated with improvement of poor prognosis. However, the mechanism of alternative splicing of PRMT5-ISO5 induced by ionizing radiation (IR) is still unclear. Methods The transcriptional changes of PRMT5-ISO5 induced by IR were validated by reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay. Bioinformatic analyses were performed to identify potential splicing factors involved in regulating PRMT5 splicing. Small interferring RNA and overexpressing plasmids for SRSF3 and HNRNPH1 were introduced into HCC cell lines, followed by in vitro functional experiments in regulating PRMT5 splicing by RT-qPCR, western blot and RNA-immunoprecipitation assay in vitro. The roles of IR-induced PRMT5-ISO5 and hepatocyte-specific Prmt5 knockout on HCC progression were evaluated in vivo. Results we indicated IR could induce PRMT5-ISO5 transcript in HCC cells by virtue of splicing factors SRSF3 and HNRNPH1. Mechanistically, HNRNPH1 silencing resulted in the decrease of PRMT5-ISO5 while SRSF3 silencing led to the increase of PRMT5-ISO5. In addition, both SRSF3 and HNRNPH1 bound to PRMT5 precursor mRNA on the region around 3' splicing site of intron 2 and alternative 3’ splicing site on exon 4, leading to their opposite functions on regulating PRMT5 splicing. In vivo, the increase of PRMT5-ISO5 induced by IR led to tumor regression, and liver-specific Prmt5 depletion decelerated the progression of Akt/N-Ras-derived spontaneous HCC. Conclusion Our study not only provides mechanistic views that IR-induced SRSF3 downregulation leads to the imbalance of SRSF3 and HNRNPH1 in regulating PRMT5-ISO5 transcript, but also indicates a potential radiotherapeutic of PRMT5-ISO5 in HCC formation since liver-specific Prmt5 knockout inhibits spontaneous HCC tumorigenesis.

Ferroptosis is the name given to the type of non-apoptotic cell death that is caused by iron accumulation and subsequent lipid peroxidation. However, how ionizing radiation (IR)-induced ferroptosis is regulated in estrogen receptor-positive (ER+) breast cancer cells remains unclear. To attempt to resolve this issue, bioinformatics analysis was performed to evaluate the prognostic value of estrogen receptor 1 (ESR1) in breast cancer tissues. A total of four breast cancer cell lines and an MCF10A non-malignant counterpart were used. Western blotting was used to analyze the levels of protein expression, whereas immunoprecipitation (IP) and ubiquitination experiments were used to test protein binding and ubiquitination levels, respectively. Flow cytometry was subsequently used to analyze cell death and lipid peroxidation levels. The results showed that a high expression level of ESR1 was significantly correlated with poor overall survival in breast cancer. ESR1 knockdown significantly enhanced IR-induced ferroptosis and increased the CD71 protein level. The IP results showed that ESR1 enhanced the binding of the E3 ubiquitin ligase NEDD4L to CD71, promoting the ubiquitination and degradation of CD71, suggesting that CD71 expression was regulated by both ESR1 and NEDD4L. Taken together, the findings in the present study have demonstrated a regulatory relationship between ESR1 and NEDD4L/CD71 in IR-induced ferroptosis. In addition, the ESR1/NEDD4L/CD71 axis may be a potential target for the radiotherapy of breast cancer.

Herein, glutathione-capped copper nanoclusters (CuNCs) and graphitic carbon nitride nanosheets (g-C3N4 NSs) were synthesized by a facile one-pot chemical reduction and directly thermal pyrolysis following ultrasonic exfoliation approaches, respectively. The introduction of Ce(III) (Ce3+) played dual functions in constructing a fluorescence-enhanced ratiometric nanoprobe (g-C3N4 NSs-Ce3+-CuNCs), i.e., triggering aggregation-induced emission of CuNCs and conjugating g-C3N4 NSs with CuNCs by virtue of electrostatic and coordination interactions. The as-fabricated nanohybrid displayed 460 and 625 nm dual-emitting peaks, attributing to the emission of g-C3N4 NSs and CuNCs, respectively. Upon addition of H2O2, the 625 nm emission was dramatically quenched, whereas the 460 nm emission remained nearly unchanged, thereby causing obvious color changes from purple to blue under a 365-nm UV lamp. A ratiometric fluorescent assay, based on g-C3N4 NSs-Ce3+-CuNCs, was devised for sensitive and visual detection of H2O2, which spanned the linear range of 2-100 mu M with a detection limit of 0.6 mu M. In the presence of glucose oxidase, the ratiometric nanoprobe could be simultaneously employed to detect glucose across the linear range of 1.6-320 mu M with a detection limit of 0.48 mu M. In milk and human serum samples, the fortified recoveries for H2O2 and glucose by the nanoprobe were in the range of 95.5-103.6% with RSDs < 3.8%. The real detection levels for glucose are consistent with those by a standard glucometer. As such, the ratiometric nanoprobe offers a promising methodology for several practical applications, such as point-of-care diagnosis and workplace health evaluations.

A novel ratiometric fluorescent probe was constructed for sensitive assay of hydrogen peroxide (H2O2) and glucose, which utilized the synergistically enhanced effects of Ce3+ and Fe2+ on copper nanoclusters (CuNCs) and coumarin. In the CuNCs-Ce3+/Fe2+-coumarin system, Ce3+ triggered the aggregation-induced emission phe-nomenon of CuNCs, and Fe2+ catalyzed the Fenton reaction to efficiently yield hydroxyl radical (center dot OH). In the presence of H2O2, the 625-nm red fluorescence of CuNCs was sharply quenched owing to the oxidation of CuNCs to Cu(II) by center dot OH, but the 460-nm blue fluorescence of 7-hydroxycoumarin from the oxidation of coumarin by center dot OH dramatically increased. Based on the reversible changes in two fluorescence signals, a satisfactorily ratio -metric probe was constructed for H2O2 assay with a detection limit (LOD) of 0.6 mu M accompanied by a visual color variation from red to blue. For glucose assay, this ratiometric probe gave a linear range of 3.2-160 mu M and LOD of 0.96 mu M owing to the oxidization of glucose to yield H2O2 in the presence of glucose oxidase and O2. Overall, the newly developed ratiometric probe shows a great prospect in real applications for visual assay of H2O2 and glucose by our naked eyes.

BackgroundThe application of high-energy medical electron accelerators in the radiotherapy becomes more and more widespread. Study of the radiation source and shielding of high-energy medical electron accelerators has been the focus of attention.PurposeThis study aims to simulate 15 MV X-ray beam of Clinac 23EX medical linear accelerator by using Monte Carlo method.MethodsFirst of all, a fine geometric model of the accelerator head in X-ray mode was constructed according to the material composition and geometric dimensions of the internal parts of the head provided by the manufacturer. Then the Monte Carlo N-Particle Transport Code (MCNP) software was applied to the calculation of the percentage depth dose (PDD) curves and profile curves of the X-ray beam under different irradiation fields. Comparisons of those results with that of measured results at the same conditions in the three-dimensional (3D) water model were performed. In addition, the effects of different components on the X-ray energy spectrum and penetration ability were analyzed.ResultsThe simulation results of the PDD curves and profile curves are in good agreement with the measured results of 3D water tank. The relative deviation of PDD curves is in the range of 0.62% to 1.34%, and the relative deviations of profile curves are between 0.35% and 2.76% in high dose area and 0.48% to 5.86% in low dose area, respectively.ConclusionsIt is confirmed that the detailed model of the accelerator head established in this study is accurate and reliable, hence appliable to the subsequent analysis of various source items. The effects of different components of accelerator on the X-ray energy spectrum and penetration ability provide references for optimizing shielding design and radiotherapy plan.

Objective:To summarize the research progress on tissue damage, poisoning mechanism and treatment measures for the injury caused by liquid rocket propellant nitrogen tetroxide (N 2O 4) in China and foreign copuntries. Literature resource and selection The literatures published in the related fields at home and abroad. Literature quotation Fifty-one references were cited. Literature synthesis N 2O 4 is currently a commonly used liquid rocket propellant, which is a colorless gas or liquid and easy decomposition into nitrogen dioxide. It has the characteristics of flammability, explosive, strong oxidation and toxicity. In the process of propellant transportation and usage, poisoning and explosion accidents caused by N 2O 4 leakage occurred from time to time, which seriously threatened the physical and mental health of employees. Early inhalation of N 2O 4 may cause eye and respiratory tract irritation, and severe ones included pulmonary edema and acute respiratory distress syndrome. Long-term exposure may lead to idiopathic pulmonary fibrosis, and the difficulty of treatment N 2O 4 for poisoning patients was increasedwheninjured by the blast of the explosion at the same time. A large number of experimental studies have shown that vitamins E and radix salviaemiltiorrhizae (RSM) can reduce oxidative stress and inflammatory responses induced by N 2O 4. However, due to the lack of specific antidotes in actual treatment, symptomatic treatments such as oxygen administration and correction of pulmonary edema were often used. Conclusions:N 2O 4 poisoning can cause acute respiratory system damage, such as respiratory tract inflammation and pulmonary edema and also lead to chronic diseases, such as fibrosis or other organ damages. Symptomatic and supported treatment is often used in the process of treatment. It indicated that further study of N 2O 4is needed to clarify the molecular mechanism of its action, so as to provide help for clinical treatment.

目的 分析HPV联合TCT检查在宫颈癌及宫颈高度病变中的筛查效果.方法 本次研究对象选取2019年9月-2019年12月期间60例宫颈癌及宫颈高度病变患者作为研究对象,60例人员全部接受高危型HPV检测及TCT检查.结果 联合实施该检测后的敏感度及特异性显著比单独实施效果理想,有统计学意义(P<0.05).结论 在宫颈癌及宫颈高度病变的患者中运用HPV联合TCT检查,可以有效的提高筛查结果,可以有效的帮助患者及时的治疗,具有临床推广应用价值.

Abstract Background: To investigate the prevalence and distribution of employees with fatty liver disease (FLD) and assess the risk factors associated with diseases and biochemical markers. Methods: Disease risk markers, and the levels of biochemical markers of 2541 participants from an Institute of Scientific Research in Beijing, were assessed according to standard methods and FLD was diagnosed by abdominal ultrasonography. Chi-square test was used to compare the results between participants with and without FLD. Results: The prevalence of FLD, based on abdominal ultrasonography examination, was 43.5% (1105/2541) in this population. The overall prevalence increased with age, and it was substantially higher in males (50.0% vs females: 34.6%, P < 0.001). The gender and age distributions were significantly different between the two groups (χ2=59.8 for gender and t= -15.2 for age or χ2=205.6 for age group, P < 0.05). Chi-square test results revealed statistically significant differences in the BMI, prehypertension, hypertension, prediabetes, diabetes, hyperlipidemia, mixed type hyperlipidemia, hypertriglyceridemia, and the rise of GGT, ALT, AST, total bilirubin and indirect bilirubin between populations with and without FLD (P < 0.05). The risk of disease and biochemical markers contributing to the development of FLD was assessed by calculating the odd ratio (OR) and 95% confidence interval (95% CI), and the results are ordered as follows: overweight and obesity [6.85 (5.54-8.48)], diabetes [6.00 (3.66-9.82)], prediabetes [5.06 (3.10-8.26)], ALT rise [4.67 (3.58-6.10)], GGT rise [4.01 (3.03-5.30)]. Multiple factors analysis was conducted to further compare those identified risk factors of FLD, which showed statistically significant differences in age, overweight and obesity, prediabetes, diabetes, mixed type hyperlipidemia, hypertriglyceridemia and ALT rise by Logistic regression analysis (P < 0.05). Conclusions: Chronic disease, especially FLD, can be easily ignored during health assessment, although it is as important health risk factor as overweight and obesity, hypertension and diabetes. Physical examination is a practical approach to detect FLD in the process of control and prevention.

新型冠状病毒肺炎的疫情发生以及快速传播,使公共卫生应急管理再次引起人们的关注.这次疫情既展现了公共卫生应急管理的重要性,也暴露了防治过程中存在的弊端.本文围绕公共卫生应急管理通过法律法规手段、行政管理手段、医疗技术手段、预防宣教手段在新型冠状病毒肺炎疫情中的应用,提出公共卫生应急管理优化策略,助力全国各省疫情防控工作,科学精准打赢疫情持久战,推进我国公共卫生应急管理事业的发展.

Background: Since the outbreak in Wuhan China in December 2019, novel coronavirus pneumonia (COVID-19) has spread rapidly throughout the whole nation. Besides Wuhan, Wenzhou is the city with the most confirmed cases outside Hubei Province.Methods: We analyzed the epidemiological features of COVID-19, the control measures taken and their effects. The characteristic of temporal and spatial distribution were analyzed with Geographic Information System (GIS), the basic reproductive number (R0) was calculated with the improved SEIR model, trend of cumulative cases is analyzed with Logistic Regression model.Findings: The results showed that a large number of people poured into Wenzhou from Hubei Province, which is the main reason for the outbreak of COVID-19. Confirmed patients gather mostly at Yueqing, Ruian counties, and the incidence peak appeared on Jan.29 and Feb.3, imported cases from Hubei decreased on Jan.30. For the emergency preparedness the strong control measures based on the principle of "three-level prevention" has been launched, an obvious decrease of R 0 appeared from 29 Jan, 2020, the median interval between onset and diagnosis of patients shortened from 7 to 3 days. A downward-point was expected on Feb.10, 2020 based on the logistic model, which has been validated in line with the reality.Interpretation: For the outbreak of such infectious diseases as COVID-19, public health methods play greater roles in controlling the epidemic.Funding Statement: This study was supported by National Natural Science Foundation of China (81972969, 81872558, 81773363 and 81673092). Declaration of Interests: The authors declare that they have no competing interests.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的了解高血压家族史与超重/肥胖对高血压患病的交互作用,为高血压的防治提供参考依据。方法于2017年9—12月采用普查的方法对北京市某科研院所的1 250名在职职工进行问卷调查和体格检查;应用logistic回归模型分析高血压家族史和超重/肥胖与高血压发病风险的关联强度,并采用相加作用模型分析其交互作用。结果北京市某科研院所1 250名职工中,患高血压者273例,高血压患病率为21.84%;有60.80%（760/1 250）的职工有高血压家族史,有48.72%（609/1 250）的职工超重/肥胖。在调整了性别、年龄、文化程度、家庭月收入、吸烟、饮酒和睡眠时间等混杂因素后,多因素非条件logistic回归分析结果显示,有高血压家族史者患高血压的风险为无高血压家族史者的2.59倍（OR=2.59,95%CI=1.38～4.84）,超重/肥胖者患高血压的风险为正常体重者的3.21倍（OR=3.21,95%CI=1.66～6.21）,有高血压家族史且超重/肥胖者患高血压的风险为无高血压家族史且非超重/肥胖者的7.64倍（OR=7.64,95%CI=4.21～13.89）。交互作用分析结果显示,高血压家族史及超重/肥胖的交互作用超额相对危险度、交互作用归因比和交互作用指数分别为2.85（95%CI=0.35～5.35）、 0.37（95%CI=0.13～0.62）和1.75（95%CI=1.06～2.89）,纯交互作用归因比为42.8%,即高血压家族史和超重/肥胖对高血压患病具有相加交互作用。结论有高血压家族史和超重/肥胖均可增加高血压的患病风险,且两者的交互作用增加了患高血压的风险。</span>