BACKGROUND:Radiotherapy significantly improves survival rates in patients with various malignant tumors.However,with prolonged post-treatment survival,many patients face the risk of radiation-related cardiac toxicity.This is especially true after chest radiotherapy,where the risk of radiation-induced heart disease significantly increases,becoming one of the most severe complications affecting prognosis survival.OBJECTIVE:To identify diagnostic markers of endothelial cellular senescence in radiation-induced heart disease through systematic transcriptomic analysis.METHODS:Firstly,genes associated with cellular senescence were screened from the CellAge database and intersected with the transcriptomic training dataset of a mouse model of radiation-induced heart disease to identify differentially expressed senescence-related genes.Secondly,weighted gene co-expression network analysis and machine learning were used to identify key hub genes that play critical roles in radiation-induced heart disease.The expression of these genes was validated using a dataset of radiation-induced endothelial injury.Additionally,the quanTlseq method was employed to assess the immune infiltration status related to radiation-induced heart disease.The expression levels of key genes and their association with survival in esophageal squamous cell carcinoma patients receiving chest radiotherapy were explored through the analysis of The Cancer Genome Atlas database.RESULTS AND CONCLUSION:(1)Systematic transcriptomic analysis identified CCND1 as the core gene of endothelial cellular senescence in radiation-induced heart disease,and this finding was validated in the mouse model of radiation-induced heart disease.(2)The diagnostic model constructed from these data indicated that CCND1 had high specificity and sensitivity for diagnosing radiation-induced heart disease.(3)Immune infiltration analysis revealed significant immune response dysregulation in the mouse model of radiation-induced heart disease,and CCND1 was closely related to various immune cells.(4)Kaplan-Meier survival analysis showed that CCND1 was associated with poorer disease-specific survival in esophageal squamous cell carcinoma patients receiving chest radiotherapy.This study systematically uncovers,for the first time,the pivotal role of CCND1 in endothelial cell senescence associated with radiation-induced heart disease.CCND1,a gene integral to cell cycle regulation,can induce cellular senescence when abnormally expressed.Furthermore,the findings highlight its potential as an early diagnostic marker.

BACKGROUND:Radiotherapy significantly improves survival rates in patients with various malignant tumors.However,with prolonged post-treatment survival,many patients face the risk of radiation-related cardiac toxicity.This is especially true after chest radiotherapy,where the risk of radiation-induced heart disease significantly increases,becoming one of the most severe complications affecting prognosis survival.OBJECTIVE:To identify diagnostic markers of endothelial cellular senescence in radiation-induced heart disease through systematic transcriptomic analysis.METHODS:Firstly,genes associated with cellular senescence were screened from the CellAge database and intersected with the transcriptomic training dataset of a mouse model of radiation-induced heart disease to identify differentially expressed senescence-related genes.Secondly,weighted gene co-expression network analysis and machine learning were used to identify key hub genes that play critical roles in radiation-induced heart disease.The expression of these genes was validated using a dataset of radiation-induced endothelial injury.Additionally,the quanTlseq method was employed to assess the immune infiltration status related to radiation-induced heart disease.The expression levels of key genes and their association with survival in esophageal squamous cell carcinoma patients receiving chest radiotherapy were explored through the analysis of The Cancer Genome Atlas database.RESULTS AND CONCLUSION:(1)Systematic transcriptomic analysis identified CCND1 as the core gene of endothelial cellular senescence in radiation-induced heart disease,and this finding was validated in the mouse model of radiation-induced heart disease.(2)The diagnostic model constructed from these data indicated that CCND1 had high specificity and sensitivity for diagnosing radiation-induced heart disease.(3)Immune infiltration analysis revealed significant immune response dysregulation in the mouse model of radiation-induced heart disease,and CCND1 was closely related to various immune cells.(4)Kaplan-Meier survival analysis showed that CCND1 was associated with poorer disease-specific survival in esophageal squamous cell carcinoma patients receiving chest radiotherapy.This study systematically uncovers,for the first time,the pivotal role of CCND1 in endothelial cell senescence associated with radiation-induced heart disease.CCND1,a gene integral to cell cycle regulation,can induce cellular senescence when abnormally expressed.Furthermore,the findings highlight its potential as an early diagnostic marker.

Objective To analyze the epidemiological characteristics and risk factors of an outbreak of influenza A H1N1 in a specialized psychiatric hospital in Shantou City,Guangdong Province,provide scientific basis for the pre-vention and control of respiratory infectious diseases in psychiatric health institutions.Methods Data of infection cases in this hospital in May 1-27,2024 were collected with on-site epidemiological investigation method,and were analyzed with descriptive epidemiological methods.The specimens of the cases were performed nucleic acid testing by reverse transcription polymerase chain reaction(RT-PCR)method.Results A total of 43 influenza-like cases in this outbreak have been reported,with an incidence of 16.67％,including 42 hospitalized patients and 1 healthcare worker.Among the 42 hospitalized patients,there were 41 males,with an incidence of 35.04％and 1 female with an incidence of 2.22％,there was a statistically significant difference in incidence between hospitalized patients of different genders(x2=18.23,P＜0.001).The epidemic curve shows that after the first case appeared on May 8,2024,the number of cases increased significantly from May 13,and reached its peak on May 17(n=17).31 pa-tients' throat swab specimens were collected,out of which 29(93.55％)were positive for influenza A H1N1 virus nucleic acid and 2(6.45％)were negative.Conclusion This epidemic is an outbreak of influenza A H1N1 in a psy-chiatric health institution,the epidemic curve shows a point source human-to-human transmission mode.Failure to effectively identify and isolate cases in the early stage can lead to the spread of the epidemic across floors and wards.It is necessary to regularly organize hospitalized patients and healthcare workers to receive influenza vaccines,strict-ly implement the health monitoring system,strengthen the control of external personnel,and enhance the early de-tection and emergency response capabilities for infectious disease outbreaks.

Arginine methylation is a critical post-translational modification that plays multifaceted biological functions. However, the manipulation of protein arginine methylation largely depends on genetic or pharmaceutic inhibition of the regulatory enzymes, protein arginine methyltransferases (PRMTs), or non-methylation substitution of corresponding arginine residue to lysine or alanine of protein of interest (POI), which inevitably affects other substrates, or disrupts the structure of POI. Thus, it urges an approach to specifically modulate the arginine methylation of a POI under physiological conditions. To this end, we report the discovery of a methylation tagging system (MeTAG), that enables targeted modification of protein arginine methylation. Through bridging the methyltransferase PRMT5 proximity to a POI, MeTAG facilitates the arginine methylation of POIs, including known arginine methylated proteins, androgen receptor (AR) and protein kinase B (AKT), as well as a neo-substrate E1A binding protein (p300), in a reversible and PRMT5-dependent manner. Moreover, MeTAG can regulate downstream signaling in a methylation dependent manner, leading to downregulation of PSMA mRNA level and activation of AKT. Therefore, MeTAG represents a feasible approach to modulate protein methylation and thereby perturbs protein function in biological and therapeutic contexts.

Objective To analyze the epidemiological characteristics and risk factors of an outbreak of influenza A H1N1 in a specialized psychiatric hospital in Shantou City,Guangdong Province,provide scientific basis for the pre-vention and control of respiratory infectious diseases in psychiatric health institutions.Methods Data of infection cases in this hospital in May 1-27,2024 were collected with on-site epidemiological investigation method,and were analyzed with descriptive epidemiological methods.The specimens of the cases were performed nucleic acid testing by reverse transcription polymerase chain reaction(RT-PCR)method.Results A total of 43 influenza-like cases in this outbreak have been reported,with an incidence of 16.67％,including 42 hospitalized patients and 1 healthcare worker.Among the 42 hospitalized patients,there were 41 males,with an incidence of 35.04％and 1 female with an incidence of 2.22％,there was a statistically significant difference in incidence between hospitalized patients of different genders(x2=18.23,P＜0.001).The epidemic curve shows that after the first case appeared on May 8,2024,the number of cases increased significantly from May 13,and reached its peak on May 17(n=17).31 pa-tients' throat swab specimens were collected,out of which 29(93.55％)were positive for influenza A H1N1 virus nucleic acid and 2(6.45％)were negative.Conclusion This epidemic is an outbreak of influenza A H1N1 in a psy-chiatric health institution,the epidemic curve shows a point source human-to-human transmission mode.Failure to effectively identify and isolate cases in the early stage can lead to the spread of the epidemic across floors and wards.It is necessary to regularly organize hospitalized patients and healthcare workers to receive influenza vaccines,strict-ly implement the health monitoring system,strengthen the control of external personnel,and enhance the early de-tection and emergency response capabilities for infectious disease outbreaks.

OBJECTIVE To investigate the inhibitory effects of ursolic acid on interleukin-6 （IL-6）-mediated invasion and migration of breast cancer MDA-MB-231 cells （hereinafter referred to as “231 cells”）. METHODS The effects of 20， 40， 80， 160 and 320 µmol/L ursolic acid on the proliferation rate of 231 cells were measured by CCK-8 method. The breast cancer 231 cells were divided into control group， model group and administration group. The migration and invasion abilities of cells were detected by scratch assay and Transwell assay. Real-time quantitative polymerase chain reaction （q-PCR） assay and Western blot assay were used to detect the mRNA and protein expressions of epithelial-mesenchymal transition-related makers such as E cadherin （E-cad）， matrix metalloprotein 2 （MMP2）， MMP9， vimentin （Vim）， CD44 molecule （CD44） and aldehyde dehydrogenase 1 family member A1 （ALDH1A1）. The phosphorylation levels of JAK2 and STAT3 in the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway （in terms of p-JAK2/JAK2 ratio and p-STAT3/STAT3 ratio） were detected by Western blot assay. RESULTS A low concentration of ursolic acid of 20 µmol/L （no significant inhibitory effect on cell proliferation ability） was selected as the subsequent administration concentration. Compared with the control group， the migration and invasion abilities of cells in the model group were significantly enhanced （P＜0.05）； compared with the model group， the migration and invasion abilities of cells in the administered group were significantly reduced （P＜0.05）. Compared with the control group， the relative mRNA and protein expressions of epithelial-mesenchymal transition-related markers MMP9， MMP2， Vim， ALDH1A1 and CD44 were all elevated to different extents， and the mRNA and protein expressions of E-cad were all decreased to different extents in the model group cells， and part of the differences had statistical significance （P＜0.05）， the p-JAK2/JAK2 ratio and p-STAT3/STAT3 ratio were significantly increased in the model group （P＜0.05）； compared with the model group， the expressions of the above indicators were reversed to some extent in the administration group. CONCLUSIONS Ursolic acid blocks the activation of JAK2/STAT3 signaling pathwby the inflammatory factor IL-6， which ultimately interrupts the invasion and metastasis of breast cancer cells.

Objective:To evaluate the optimized efficacy of erector spinae plane block (ESPB) with high volume of ropivacaine combined with general anesthesia for patients undergoing thoracoscopic pulmonary surgery.Methods:Sixty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes, aged 18-64 yr, with body mass index of 18-24 kg/m 2, scheduled for elective thoracoscopic pulmonary surgery, were divided into 2 groups ( n=30 each) using a random number table method: ESPB with high volume (40 ml) of 0.4% ropivacaine combined with general anesthesia group (E40 group) and ESPB with conventional volume (20 ml) of 0.4% ropivacaine combined with general anesthesia group (E20 group). Ultrasound-guided ESPB was performed on the operated side before general anesthesia induction in both groups.In E40 group, 0.4% ropivacaine 40 ml was injected.In E20 group, 0.4% ropivacaine 20 ml was injected.Total intravenous anesthesia was applied in both groups.Sufentanil was used for patient-controlled intravenous anesthesia (PCIA) after the end of operation.The PCIA pump was set up with a 2 ml bolus dose (0.04 μg/kg), a 10 min lockout interval and background infusion at a rate of 0.05 μg·kg -1·h -1.The analgesia lasted for 48 h after operation, and the numeric rating scale (NRS) score was maintained ≤ 3.When NRS score ≥ 4, morphine 5 mg was intravenously injected for rescue analgesia.The onset time of block, intraoperative consumption of propofol and remifentanil, time to first pressing the analgesia pump, the first requirement for morphine and the ratio of patients using morphine within 48 h after surgery were recorded.The cumulative consumption of requirement for opioids (effective pressing dose of analgesic pump+ consumption of requirement for morphine) within 12, 24, 36 and 48 h after surgery and satisfaction with analgesia were recorded.The extubation time, length of ICU stay, the first postoperative off-bed time, the chest tube removal time and duration of stay in hospital were recorded.The incidence of intraoperative adverse events (hypertension and hypotension) and postoperative adverse events (dizziness, nausea and vomiting) were recorded. Results:Compared with E20 group, the onset time of block was significantly shortened, the cumulative consumption of requirement for opioids within 24, 36 and 48 h after surgery was decreased, the ratio of paitents using morphine within 48 h after surgery was decreased, time to first pressing the analgesia pump and the first requirement for morphine were prolonged, satisfaction with analgesia score was increased, and the first postoperative off-bed time and the chest tube removal time were shortened in group E40 ( P<0.05). There was no significant difference in the incidence of adverse events between the 2 groups ( P>0.05). Conclusion:Compared with ESPB with the conventional volume of ropivacaine combined with general anesthesia, ESPB with the high volume of ropivacaine combined with general anesthesia can reduce the postoperative consumption of opioids, and prolong the duration of effective analgesia, which are helpful for postoperative rapid recovery without increasing the development of adverse events in patients undergoing thoracoscopic pulmonary surgery.

Objective:To explore the application of nursing of theory education combined with experience education in the rehabilitation of patients with idiopathic pulmonary artery hypertension (IPAH) .Methods:Nursing of theory education combined with experience education was carried out in Department of Respiratory Medicine in Affiliated Hospital of Jining Medical University in December 2017. Using the convenient sampling method, 53 patients with IPAH who were admitted from August 2016 to December 2017 were selected as the control group and they were given routine nursing. A total of 53 IPAH patients who were admitted from January 2018 to May 2019 were selected as the research group, and they were given nursing of theory combined with experience education at basis of the control group. Before the intervention and 1 month after discharge from the hospital, patients in two groups were assesses by Exercise of Self-Care Agency (ESCA) scale, the MOS 36-item Short-Form Health Survey (SF-36) , 6 minutes walking distance (6MWD) and Borg Scale (BS) , and the occurrence of complications in the two groups during hospitalization and discharge for 1 month was recorded.Results:After 1 month of discharge, scores of self-care skills, self-care concept, self-care responsibilities and health knowledge and the total self-care score of ESCA were respectively (35.52±2.16) , (22.32±1.55) , (27.15±2.02) , (48.67±2.85) and (130.67±3.38) . Scores of physical functioning, role-physical, vitality, role-emotional, social functioning and mental health and overall health score of SF-36 were respectively (74.73±12.83) , (71.79±11.31) , (72.06±11.43) , (69.67±10.54) , (71.23±10.72) , (72.43±13.30) and (65.45±14.27) . The 6MWD distance was (512.67±86.85) m, and BS score was (3.79±0.85) . Compared with the control group, the differences were statistically significant ( P<0.01) . During hospitalization and one month after discharge, the complication rate of the research group was lower than that of the control group, and the difference was statistically significant ( P<0.05) . Conclusions:Nursing of theory education combined with experience education can improve the self-care ability of IPAH patients, improve their quality of life, and reduce the incidence of complications, which is worthy of clinical application.

Autonomic Nervous System ; physiopathology ; Blood Pressure ; physiology ; Cardiovascular Diseases ; therapy ; Cardiovascular System ; physiopathology ; Diabetic Neuropathies ; therapy ; Humans

Excessive reactive oxygen species (ROS) (such as the superoxide radical) are commonly associated with cardiac autonomic dysfunctions. Though superoxide dismutase 1 (SOD1) overexpression may protect against ROS damage to the autonomic nervous system, superoxide radical reduction may change normal physiological functions. Previously, we demonstrated that human SOD1 (hSOD1) overexpression does not change baroreflex bradycardia and tachycardia but rather increases aortic depressor nerve activity in response to arterial pressure changes in C57B6SJL-Tg (SOD1)2 Gur/J mice. Since the baroreflex arc includes afferent, central, and efferent components, the objective of this study was to determine whether hSOD1 overexpression alters the central and vagal efferent mediation of heart rate (HR) responses. Our data indicate that SOD1 overexpression decreased the HR responses to vagal efferent nerve stimulation but did not change the HR responses to aortic depressor nerve (ADN) stimulation. Along with the previous study, we suggest that SOD1 overexpression preserves normal baroreflex function but may differentially alter the functions of the ADN, vagal efferents, and central components. While SOD1 overexpression likely enhanced ADN function and the central mediation of bradycardia, it decreased vagal efferent control of HR.
Animals ; Baroreflex ; physiology ; Blood Pressure ; physiology ; Bradycardia ; metabolism ; Heart Rate ; physiology ; Humans ; Mice, Transgenic ; Superoxide Dismutase-1 ; metabolism ; Vagus Nerve ; metabolism