Pulpitis is a common infective oral disease in clinical situations. The regulatory mechanisms of immune defense in pulpitis are still being investigated. Osteomodulin (OMD) is a small leucine-rich proteoglycan family member distributed in bones and teeth. It is a bioactive protein that promotes osteogenesis and suppresses the apoptosis of human dental pulp stem cells (hDPSCs). In this study, the role of OMD in pulpitis and the OMD-induced regulatory mechanism were investigated. The OMD expression in normal and inflamed human pulp tissues was detected via immunofluorescence staining. Intriguingly, the OMD expression decreased in the inflammatory infiltration area of pulpitis specimens. The cellular experiments demonstrated that recombined human OMD could resist the detrimental effects of lipopolysaccharide (LPS)-induced inflammation. A conditional Omd knockout mouse model with pulpal inflammation was established. LPS-induced inflammatory impairment significantly increased in conditional Omd knockout mice, whereas OMD administration exhibited a protective effect against pulpitis. Mechanistically, the transcriptome alterations of OMD overexpression showed significant enrichment in the nuclear factor-κB (NF-κB) signaling pathway. Interleukin-1 receptor 1 (IL1R1), a vital membrane receptor activating the NF-κB pathway, was significantly downregulated in OMD-overexpressing hDPSCs. Additionally, the interaction between OMD and IL1R1 was verified using co-immunoprecipitation and molecular docking. In vivo, excessive pulpal inflammation in Omd-deficient mice was rescued using an IL1R antagonist. Overall, OMD played a protective role in the inflammatory response via the IL1R1/NF-κB signaling pathway. OMD may optimize the immunomodulatory functions of hDPSCs and can be used for regenerative endodontics.
Pulpitis/metabolism* ; NF-kappa B/metabolism* ; Animals ; Signal Transduction ; Humans ; Mice ; Mice, Knockout ; Dental Pulp/metabolism* ; Disease Models, Animal ; Lipopolysaccharides

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

Objective To evaluate the efficacy and safety of Paclitaxel drug coated balloon (DCB) (SeQuent Please) in an elderly patients with de novo coronary disease.Methods We performed a retrospective study of 158 consecutive patients (63 patients aged ≥65 yrs and 95 patients aged ＜65 yrs) received DCB therapy in Cath Lab of Beijing Hospital.Clinical characteristic was recorded and coronary angiography was analyzed with quantitative coronary angiography (QCA) software.Results In elderly group,more patients have hypertension (65.1％ vs.56.8％),atrial fibrillation (7.9％ vs.2.1％),previous percutaneous coronary intervention (PCI) history (44.4％ vs.23.2％,P＜0.01) and non ST-elevated myocardial infarction (NSTEMI) (14.3％ vs.4.2％,P ＜0.05).In non-elderly group,more patients were male (71.6％ vs.50.8％,P＜0.05) and current smoker (52.3％ vs.30.2％,P＜ 0.01).Old patients had more complicated lesions,especially calcified lesions (36.8％ vs.14.0％,P＜0.01).Despite of that,our study showed a higher success rate of PCI in elderly group.Both groups of patients showed significant acute gain in minimal lumen diameter (MLD) after DCB released.At 4 days post-operation,there was one case that underwent acute myocardial infarction requiring emergent target lesion revascularization (TLR) in non-elderly group.No major adverse cardiac event (MACE) was observed in the elderly group during hospitalization.Twenty-one patients underwent coronary angiographic followed up at average 9 months post PCI.The QCA analysis showed that MLD of lesions treated with DCB had mildly increased [(2.00±0.67) mm vs.(1.91 ± 0.47) mm,P＞0.05],the late lumen loss (LLL) was (-0.09±0.50) mm.At 9 months follow-up,the MACE rate in the elderly group was 1.6％ and 1.1％ in non-elderly group,with TLR rates at 0.0％ and 1.1％ respectively (both P＞0.05).No death was observed in either group.Conclusions The efficacy and safety of DCB on the elderly patients with de novo lesions is as good as non-elderly patients despite more complex anatomy and comorbidities.

Objective To evaluate the surgical characteristics and clinical effect of percutaneous reduction with kirachner wire assisted by a small lateral incision approach for poking reduction and allngraft bone transplantation in treating compressive intra-articular calcaneal fractures. Methods A retrospective analysis was performed among 17 patients with compressive intra-articular calcaneal fractures (Sanders Ⅱ to Ⅲ ) treated by percutaneous reduction with kirachner wire assisted by a small lateral incision approach for poking reduction and allograft bone transplanta-tion. Results All the patients were followed-up for an average time of 13.5 months. The wound of 15 feet achieved primary healing, the acute rejection was found in 2 patients. The Bohler's angle was (9.58±5.25)° and Gissane an-gle was (101.15±13.83)° preoperation and was (33.55±4.17)° and (113.25±12.17)° immediate postopera-tion, showing statistically significant differences pre-and postoperation(P < 0.05). By the lately follow-up, the Bohler angle was (31.65±7.72)° and Gissane angle was (111.15±8.68)°, also showing statistically significant differ-ences when compared to preoperation (P < 0.05), there was no statistically significant differences (P > 0.05) when compared with normal X-ray. Conclusion That percutaneous reduction with kirschner wire assisted by a small lateral incision approach for poking reduction and allograft bone transplantation in treating the compressive intra-articular cal-caneal fractures (Sanders Ⅱ to Ⅲ) is minimally invasive, less complication, and it enables satisfactory recoastruc-tion of bone defects and allows metanatomic reduction and functional recovery, also maintaining restoration of calcane-al height and anatomic reduction of the posterior facet.

Objective To observe the changes of serum soluble CD40 ligand (sCD40L) and fibrinogen in acute myocardial infarction (AMI) patients and to investigate the clinical predictive value of increased serum sCD40L and fibrinogen. Methods Serum sCD40L level of 60 AMI patients was determined by enzyme-linked im-munosorbent assay (ELISA). Plasma level of fibrinogen was measured. The patients were followed up for 2 years af-ter discharge from the hospital and were observed for cardiovascular event. Results AMI patients had higher sCD40L and fibrinogen levels than those of controls [(15.36±7.32) μg/L vs. (5.79±2.78) μg/L, (4.60±1.37)g/L vs. (3.03±0.82) g/L,P<0.001] ,which were significantly higher in the patients experiencing cardio-vascular event than those without cardiovascular event [(18.14±6.34) μg/L vs. (14.38±6.67) μg/L and (4.97±1.33)g/L vs. (4.20±1.24} g/L] (P<0.05). The patients with sCD40L≥14.5 μg/L or fibrinogen≥ 4.4 g/L experienced increased risk of adverse cardiovascular events (P<0.05). In AMI patients, sCD40L level was significantly higher in patients with diabetes than in nondiabetics [(18.38±6.71) μg/L vs. (14.46±6.48) μg/L, P<0.05)]. Fibrinogen level was related to sCD40L (r=0.27, P<0.05) and LVEF(r=-0.319, P<0.05). Conclusion Increased sCD40L and fibrinogen levels,which maybe related to the pathogenesis of AMI,can be found in AMI patients and can indicate an independent increased risk of major adverse cardiovascular events. Diabetes is independently associated with elevated sCD40L level in AMI patients.