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.

Autologous blood patch pleurodesis (ABPP) was first proposed in 1987. Now it is mainly used to treat intractable pneumothorax and persistent air leakage after pneumonectomy, and also used to treat pneumothorax in children and other rare secondary pneumothorax. Persistent air leakage and pneumothorax of various causes are essentially alveolar pleural fistula. It can usually be treated by closed thoracic drainage, continuous negative pressure suction and surgery. Pleurodesis is a safe and effective alternative to surgery for patients who have failed conventional conservative treatment and can not receive operations. Compared with other pleurodesis adhesives, autologous blood (ABPP) is safer and more effective, and it is simple, painless, cheap and easy to be accepted by patients. But in the domestic and foreign researches in recent years, many details of ABPP treatment have not been standardized. For further research and popularization of ABPP, this article reviews the detailed regulations, efficacy and safety of this technology.

Objective To investigate the effect of great omentum combined with medical obturation glue on preventing thoracic cavity anastomotic leakage.Methods From August 2008 to September 2012,560 patients with esophageal gastric cardial carcinoma were enrolled and divided into two groups:the regular group (n =280) and the experimental group (n =280).In the regular group,anastomosis was reinforced with interrupted mattress sutures after esophageal gastric anastomosis was stapled.In the experimental group,anastomosis was covered with great omentum and medical obturation glue was sprayed to conglutinate after reinforced with interrupted mattress sutures.After that,gastric corpus was fixed upon the thoracic aorta and posterior chest wall.The clinical effects of the two groups were compared.Results Intrathoracic anastomotic leakage occurred in 8 cases (2.86％(8/280)) of the regular group,including 7 cases with symptomatic leakage and 1 case with asymptomatic loculate leakage.Seven patients were cured with conservative treatment and 1 patient with severe infection left hospital without cure.Average length of hospital stay was (55.6 ± 30.5) days postoperatively.Anastomotic stenosis occurred in 11 patients (3.93％,11/280).In the experimental group,one patient (0.36％,1/280) with asymptomatic loculate leakage was hospitalized for 20 days,and finally cured and discharged.8 cases with anastomotic stenosis occurred in the experimental group (2.86％,8/280).There was statistic difference in the rate of intrathoracic anastomotic leakage between the two groups (P =0.044),but there was no statistic difference in anastomotic stenosis between the two groups (P =0.484).Conclusion The technique of great omentum combined with medical obturation glue for preventing thoracic cavity anastomotic leakage,which is easy to perform,can obviously decrease the occurrence and attenuate the symptom of intrathoracic anastomotic leakage,and anastomotic stenosis increases unobviously.It also can shorten the length of hospital stay and is worthy of clinical promotion.