Background Long-term exposure to ambient fine particulate matter (PM_2.5) is a significant risk factor for cardiometabolic disorders. However, the mechanisms of its interaction with the endogenous circadian system remain incompletely understood. Objective To investigate whether chronic PM_2.5 exposure interferes with the rhythmic expression of the cardiac circadian clock, thereby disrupting downstream antioxidant defenses and metabolic homeostasis, and ultimately driving cardiometabolic dysfunction. Methods Seventy-two male C57BL/6 mice were randomly divided into a PM_2.5 exposure group (PM group) and a filtered air control group (FA group). Whole-body exposure was conducted for 8 weeks in a meteorological environmental animal exposure system. Samples were collected at six distinct zeitgeber time (ZT) points post-exposure. The 24 h ambulatory blood pressure and serum lipid profiles were monitored. Rhythm parameters were derived via cosinor analysis to compare differences in Midline statistic of rhythm (Mesor), amplitude, and phase between the two groups. The rhythmic expression of core circadian clock genes and antioxidant genes in the myocardium was detected by quantitative polymerase chain reaction (qPCR). Myocardial reactive oxygen species (ROS) levels and downstream pathway protein expression were analyzed by immunofluorescence and Western blot (WB), respectively. The expression changes of the clock gene retinoic acid receptor-related orphan receptor α (RORα) were assessed at both the mRNA and protein levels. Finally, Spearman correlation analysis was used to explore the relationships among myocardial RORα expression, lipid profiles, and oxidative stress indicators. Results Compared to the FA group, mice in the PM group exhibited a blunted circadian rhythm in blood pressure, characterized by sustained elevation throughout the day. Chronic PM_2.5 exposure showed a significant interaction with ZT on systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) (F-interaction=9.11, 5.70, and 6.02, respectively; P<0.05), as well as on serum triglycerides (TG), total cholesterol (T-CHO), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) (F-interaction=16.32, 11.12, 15.39, and 28.09, respectively; P<0.05). Cosinor analysis further revealed that the Mesor values of T-CHO, TG, and LDL-C were significantly increased (P<0.05), while that of HDL-C was significantly decreased in the PM group (P<0.05). The oscillation amplitudes of SBP, DBP, and MAP showed a decreasing trend, whereas those of TG and LDL-C were significantly increased (P<0.05). Furthermore, SBP, T-CHO, and HDL-C all exhibited a significant phase delay (P<0.05). Mechanistically, PM_2.5 exposure significantly suppressed the expression of the positive circadian regulator RORα in the myocardium, leading to disordered rhythmic expression of core clock genes (Bmal1, Clock, Per1/2, and Cry1/2). This exposure also inhibited the rhythmic expression of antioxidant genes (GPX1, SOD2, and CAT), resulting in increased ROS generation and elevated expression of calcium/calmodulin-dependent protein kinase II (CaMKII) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) proteins. Correlation analysis further revealed that myocardial RORα expression level was negatively correlated with T-CHO, TG, and LDL-C (r=−0.55, −0.63, and −0.51, respectively; P<0.001), and positively correlated with HDL-C (r=0.37, P=0.010), and antioxidant genes GPX1, SOD2, and CAT expression (r=0.34, 0.35, and 0.56, respectively; P < 0.001). Conclusion Chronic PM_2.5 exposure induces cardiometabolic dysfunction by suppressing myocardial RORα expression. This suppression disrupts the cardiac circadian clock and the diurnal balance of oxidative stress, triggering oxidative damage and elevating expression of CaMKII/NADPH pathway proteins. Collectively, these alterations precipitate the loss of cardiac metabolic rhythms and subsequent functional impairment.

Objective To study the short-term efficacy and toxicity of intraperitoneal chemotherapy combined with thermotherapy in the treatment of malignant ascites.Methods A total of 60 patients were randomly divided into control group (30 cases) and study group (30 cases).The control group received intraperitoneal chemotherapy and was given chemotherapy drugs injecting after drainage of ascites,while the study group was given intraperitoneal chemotherapy combined with whole body thermal therapy.The short-term efficacy and toxicity were evaluated.Results The efficacy rate of life quality improvement in the study group was higher than that in the control group (90％ vs.60％,P ＜ 0.05).There was no significant difference between the two groups in toxicity (P ＞0.05).Conclusion Intraperitoneal chemotherapy combined with whole body thermal therapy in the treatment of malignant ascites has higher efficacy and tolerance than intraperitoneal chemotherapy alone.

Objective To study the short-term efficacy and toxicity of intraperitoneal chemotherapy combined with thermotherapy in the treatment of malignant ascites.Methods A total of 60 patients were randomly divided into control group (30 cases) and study group (30 cases).The control group received intraperitoneal chemotherapy and was given chemotherapy drugs injecting after drainage of ascites,while the study group was given intraperitoneal chemotherapy combined with whole body thermal therapy.The short-term efficacy and toxicity were evaluated.Results The efficacy rate of life quality improvement in the study group was higher than that in the control group (90％ vs.60％,P ＜ 0.05).There was no significant difference between the two groups in toxicity (P ＞0.05).Conclusion Intraperitoneal chemotherapy combined with whole body thermal therapy in the treatment of malignant ascites has higher efficacy and tolerance than intraperitoneal chemotherapy alone.

Objective To study the significance of treating advanced primary hepatic carcinoma by using the different methods combined with chemotherapy. Methods One hundred and fifteen cases with advanced primary hepatic carcinoma were divided into 5 groups by accepting different chemotherapy: the groups of interventional-chemotherapy (group A, 40 cases), whole body hyperthermia combined with chemotherapy (group B, 16 cases), only chemotherapy (group C, 9 cases), local heat chemotherapy (group D, 26 cases), symptomatic supportive (group E, 24 cases) for comparing response rate (RR) and survival time between each other. Results The RR in group A,B,C were 30.5 % (12/40), 12.5 % (2/16), 11.1 % (1/9) respectively, and there was no significant difference among three groups (P>0.05). The mid-survival time of five groups were 7.7, 9.2, 7.9, 6.0, 4.7 months, and there was significant difference between group B and group E (P<0.05). The 0.5-, 1-, 2-year survival rate in group B were higher than those in group E with significant difference (81.2%vs. 29.1%, 37.5%vs. 12.5%, 12.5%vs. 0, all P<0.05). Conclusions The RR of only routine chemotherapy is low, while the RR of interventional-chemotherapy and local heat chemotherapy is high with non-prolonged survival time. Whole body hyperthermia combined with chemotherapy have active effects in helping to improve the efficacy and prolong the survival time in retreatment patients with advanced hepatic tumor.