Objective To examine the possible effect of ionizing radiation on thyroid function among medical workers in the department of cardiovascular medicine. Methods Forty-six medical workers in the department of cardiovascular medicine with exposure to ionizing radiation were enrolled as the study subjects. Subjects’ demographic features were collected. Serum free triiodothyronine (fT3), free thyroxine (fT4), and thyroid-stimulating hormone (TSH) levels were measured using chemiluminescence assay, and the annual personal dose equivalent (Hp (10)) received in 2019 and the fiver-year cumulative Hp (10) from 2015 to 2019 were measured using a thermoluminescent personal dosimeter. The associations of altered thyroid functions with subjects’ age, sex, previous history of thyroid diseases, family history of thyroid diseases, working post, work seniority, and previous history of exposure to ionizing radiation were evaluated using an exact logistic regression model. Results The incidence of subclinical hypothyroidism (elevated serum TSH level without alteration in fT3 or fT4 level) was 6.5% among the study subjects. The Hp (10) was 0 to 4.5 mSv among the subjects in 2019, with a mean dose of (0.2 ± 0.7) mSv and a median dose of 0 mSv, and the five-year cumulative Hp (10) from 2015 to 2019 was 0 to 11.6 mSv, with a mean dose of (0.8 ± 2.3) mSv and a median dose of 0 mSv. The exact logistic regression analysis showed that the altered thyroid functions were not significantly associated with age, sex, previous history of thyroid diseases, family history of thyroid diseases, working post, work seniority, or previous history of exposure to ionizing radiation (all P > 0.05). Conclusion Long-term exposure to low-dose ionizing radiation may be associated with an increased risk of subclinical hypothyroidism among medical workers in the department of cardiovascular medicine.

It has been recognized that long-term exposure of the heart to high-dose ionizing radiation can result in cardiac injury. Nevertheless, recent epidemiological, experimental, and clinical studies have demonstrated that exposure to low-dose ionizing radiation may also cause cardiovascular injury via various mechanisms. This article reviews the cardiac injury and potential cardiovascular risk caused by ionizing radiation, summarizes the currently available non-invasive approaches used for detecting radiation-induced cardiac injury, and proposes interventions to prevent and alleviate it, with the hope of providing a reference for early identification and interventions for radiation-induced cardiac injury.

Objective To examine the effects of ionizing radiation on blood pressure and electrocardiography among healthcare workers in department of cardiovascular diseases, and to provide a reference for formulating the protective interventions against radiation exposure. Methods A total of 127 healthcare workers with radiation exposure in the Department of Cardiovascular Diseases of The 904th Hospital of the Joint Logistics Support Force of the PLA from 2018 to 2022 were included in the observation group. Meanwhile, 127 age- and gender-matched healthcare workers without radiation exposure in the same department during the same study period were included in the control group. The systolic blood pressure, diastolic blood pressure, heart rate, and the detection rates of hypertension and abnormal electrocardiography were compared between groups. Results There were no significant differences between groups in mean age (t = 0.77, P > 0.05), sex (χ² = 0.02, P > 0.05), prevalence of smoking (χ² = 0.28, P > 0.05), and alcohol consumption (χ² = 0.02, P > 0.05). There were significant differences between the observation and control groups in systolic blood pressure [(127.77 ± 15.43) mmHg vs. (111.23 ± 19.10) mmHg; t = 4.21, P < 0.05], diastolic blood pressure [(79.32 ± 8.23) mmHg vs. (69.91 ± 10.21) mmHg; t = 4.09, P < 0.05], prevalence of hypertension [17.32% (22/127) vs. 8.66% (11/127); χ² = 4.21, P < 0.05], heart rate [(81.10 ± 11.27) beats/min vs. (70.45 ± 10.55) beats/min; t = 4.33, P < 0.05], and abnormal rate of electrocardiography [21.26% (27/127) vs. 10.24% (13/127); χ² = 5.82, P < 0.05]. Conclusion Ionizing radiation affects blood pressure and electrocardiography among healthcare workers in department of cardiovascular diseases. The prevention and monitoring of radiation exposure and occupational physical examination should be improved among healthcare workers with exposure to radiation in the department of cardiovascular diseases, with aims to reduce the hazard of radiation exposure and protect the health of healthcare workers.

The thyroid gland is highly sensitive to the carcinogenic effects of radiation exposure during childhood and adolescence. Epidemiological data have shown that exposure to ionizing radiation during childhood and adolescence results in an increased risk of thyroid cancer, and most cases of radiation-induced thyroid cancer are diagnosed with papillary thyroid carcinoma. The risk of radiation-induced thyroid cancer is affected by radiation dose, age, latency period, iodine status, chemotherapy, and body mass index. Therefore, proper use of physical shielding and prompt administration of stable iodine can be adopted to minimize the risk of radiation-induced thyroid cancer.

BACKGROUND:Previous studies have found that qi deficiency and blood stasis syndrome is the main syndrome among various TCM syndromes of cervical spondylotic myelopathy.However,there is no report on proteomic markers as early diagnosis indicators for the transformation of developmental cervical spinal stenosis with qi deficiency and blood stasis syndrome to cervical spondylotic myelopathy. OBJECTIVE:To explore serum proteomics difference between developmental cervical spinal stenosis and cervical spondylotic myelopathy and to find and identify the potential serum biomarkers between them. METHODS:Serum samples of nine patients with cervical spondylotic myelopathy of qi deficiency and blood stasis syndrome(experimental group)and nine patients with developmental cervical spinal stenosis of qi deficiency and blood stasis syndrome(control group)were collected.The proteomic analysis was carried out by Tandem Mass Tag combined with liquid chromatography tandem mass spectrometry,so as to find and identify differentially expressed proteins. RESULTS AND CONCLUSION:A total of 1027 significantly differential proteins were initially screened by TMT technology and 89 significantly differential proteins were finally identified(P<0.05).Compared with the control group,there were 45 up-regulated proteins in the experimental group,such as α-actinin-4,α-actinin-1,cell division control protein 42 homolog,integrin-linked protein kinase and B-actin.Conversely,there were 44 down-regulated proteins in the experimental group compared with the control group,such as fibronectin,fibrinogen γ chain,fibrinogen α chain,fibrinogen β chain.Gene ontology enrichment analysis indicated that these differential proteins were involved in signal receptor binding,kinase binding,protein kinase activity,integrin binding,actin filament binding and other molecular functions.Based on the Kyoto Encyclopedia of Genes and Genomes pathway analysis,20 common differential signal/metabolic pathways were identified,including Rap1 signaling pathway,adherens junction,tight junction,platelet activation,and regulation of actin cytoskeleton.Protein-protein interaction analysis showed that ILK,FGA,FGB,FGG,FN1,Cdc42,ACTN1,ACTN4 and ACTB were located at the nodes of protein-protein interaction network and were closely related to bone formation and destruction system,nervous system,coagulation system,cellular inflammation and other systems.To conclude,the serum differentially expressed proteins between developmental cervical spinal stenosis and cervical spondylotic myelopathy can be successfully screened by Tandem Mass Tag combined with liquid chromatography tandem mass spectrometry.ILK,FN1,CDC42 and ACTN 4 are identified as specific markers for the transformation of developmental cervical spinal stenosis with qi deficiency and blood stasis syndrome into cervical spondylotic myelopathy.These findings provide a basis for further clarifying the transformation mechanism.

BACKGROUND:Serum-specific biomarkers between normal healthy individuals and populations with developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome)have not been fully defined. OBJECTIVE:To screen and identify the potential biomarkers of developmental cervical canal stenosis with Qi deficiency and blood stasis. METHODS:Serum samples were collected from nine patients with developmental cervical canal stenosis with Qi deficiency and blood stasis and eight healthy people.Differentially expressed proteins in serum were screened and identified using isotope relative labeling and absolute quantification combined with liquid chromatography tandem mass spectrometry.Western blot was used to verify some significant differentially expressed proteins. RESULTS AND CONCLUSION:A total of 61 differentially expressed proteins(P<0.05)were identified using tandem mass spectrometry techniques.Compared with the healthy normal population group,14 differentially expressed proteins such as complement component C1q receptor,apolipoprotein A4,and C-C motif chemokine ligand 18 were significantly upregulated,while 47 differentially expressed proteins such as myosin light chain 3,mitochondrial translation elongation factor,and nucleolar phosphoprotein 1 were significantly downregulated.The results of gene ontology enrichment analysis indicated that these differentially expressed proteins might participate in molecular functions such as regulation of chromosomal tissue,mitochondrial membrane tissue,and muscle system processes.Protein-protein interaction network analysis showed that 38 common differential proteins,including complement component C1q receptor,apolipoprotein A4,C-C motif chemokine ligand 18,myosin light chain 3,mitochondrial translation elongation factor,and nucleolar phosphoprotein 1,were located at functional network nodes between healthy normal individuals and those with developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome),and were closely related to the local energy metabolism of the cervical spine,the production of cervical vertebral osteocytes,and the formation of osteoclasts.The main differentially expressed protein myosin light chain 3 was validated using western blot assay,and the validation results were consistent with the proteomic results.To conclude,the preliminary discovery of differentially expressed proteins in serum between healthy normal individuals and those with developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome)through absolute quantitative technology combined with liquid chromatography tandem mass spectrometry technology suggests that myosin light chain 3 may be a specific serum marker for developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome).

As confusion mounts over RNA isoforms involved in phenotypic plasticity, aberrant CpG methylation-mediated disruption of alternative splicing is increasingly recognized as a driver of intratumor heterogeneity (ITH). Protease serine 3 (PRSS3), possessing four splice variants (PRSS3-SVs; PRSS3-V1-V4), is an indispensable trypsin that shows paradoxical effects on cancer development. Here, we found that PRSS3 transcripts and their isoforms were divergently expressed in lung cancer, exhibiting opposing functions and clinical outcomes, namely, oncogenic PRSS3-V1 and PRSS3-V2 versus tumor-suppressive PRSS3-V3, by targeting different downstream genes. We identified an intragenic CpG island (iCpGI) in PRSS3. Hypermethylation of iCpGI was mediated by UHRF1/DNMT1 complex interference with the binding of myeloid zinc finger 1 (MZF1) to regulate PRSS3 transcription. The garlic-derived compound diallyl trisulfide cooperated with 5-aza-2'-deoxycytidine to exert antitumor effects in lung adenocarcinoma cells through site-specific iCpGI demethylation specifically allowing MZF1 to upregulate PRSS3-V3 expression. Epigenetic silencing of PRSS3-V3 via iCpGI methylation (iCpGIm) in BALF and tumor tissues was associated with early clinical progression in patients with lung cancer but not in those with squamous cell carcinoma or inflammatory disease. Thus, UHRF1/DNMT1-MZF1 axis-modulated site-specific iCpGIm regulates divergent expression of PRSS3-SVs, conferring nongenetic functional ITH, with implications for early detection of lung cancer and targeted therapies.