RESUMEN
@#Maintaining bone homeostasis relies on the balance between bone remodeling involving bone resorption by osteoclasts and bone formation by osteoblasts under physiological conditions. An increasing number of studies have shown that the ubiquitin-proteasome system plays an important role in bone remodeling. The ubiquitination process is reversible through the action of deubiquitinase (DUB), and ubiquitin-specific proteases (USPs) are the largest of the DUB families. This article summarizes the mechanisms by which USPs regulate bone homeostasis, including USP4 and USP7, by affecting bone formation through signaling pathways such as Wnt/β-catenin and cylindromatosis (CYLD) and regulating bone resorption through signaling pathways such as nuclear factor-kappa B (NF-κB). In addition to affecting bone resorption and bone formation during bone reconstruction, the effect of USPs on bone is also reflected in the osteogenic differentiation of human periodontal membrane stem cells and implant bone binding. Future research should determine whether USPs have a greater regulatory effect on bone reconstruction and the specific mechanism of their regulatory effect to provide more approaches for the treatment of bone diseases.
RESUMEN
Background/Aims@#This study compared long-term clinical outcomes between male and female acute myocardial infarction (AMI) patients with and without diabetes mellitus (DM). @*Methods@#From November 2011 to December 2015, 13,104 patients with AMI were enrolled in the Korea Acute Myocardial Infarction Registry National Institutes of Health (KAMIR-NIH) (4,458 diabetic patients and 8,646 non-diabetic patients). Propensity score matching (PSM) was used to reduce bias due to confounding variables. Following PSM, 2,046 diabetic patients, 1,023 males (69.8 ± 9.4 years) and 1,023 females (69.9 ± 9.4 years); and 3,412 non-diabetic patients, 1,706 males (70.0 ± 10.4 years) and 1,706 females (70.4 ± 10.8 years) were analyzed. Clinical outcomes were compared between male and female patients with and without diabetes over a 3-year clinical follow-up. @*Results@#In diabetic patients, mortality (21.1% vs. 21.5%, p = 0.813) and major adverse cardiac events (MACE) (30.6% vs. 31.4%, p = 0.698) were not significantly different between males and females. However, mortality (15.8% vs. 12.0%, p = 0.002) and MACE (20.8% vs. 15.6%, p < 0.001) were significantly higher in male non-diabetic patients than in female non-diabetic patients. The predictors of mortality for both males and females in the diabetic and non-diabetic groups were old age, heart failure, renal dysfunction, anemia, and no percutaneous coronary intervention. @*Conclusions@#The long-term clinical outcomes in AMI patients with DM did not significantly differ by sex. However, the mortality and MACE in non-diabetic male patients were higher than those in females.
RESUMEN
BACKGROUND@#Although percutaneous coronary intervention (PCI) had become widely employed therapeutic procedure for coronary artery disease, stent restenosis limited the benefits of this revascularization and the question how to prevent such events remained unresolved. While numerous empirical observations suggested Tongguan Capsules (), a patented Chinese Medicine, could decrease frequency and duration of angina pectoris attacks, evidence supporting its efficacy on restenosis remained inadequate.@*OBJECTIVE@#This trial was designed to determine whether Tongguan Capsules would reduce restenosis rate in patients after successful stent implantation.@*METHODS@#Approximately 400 patients undergoing percutaneous coronary stent deployment were enrolled and randomized to control group or Tongguan Capsules (4.5 g/d) for 3 months. All patients received standard anti-platelet, anti-coagulation and lipid-decreasing treatments, concurrently. The primary clinical endpoint was the 12-month incidence of the major adverse cardiovascular events (defined as cardiac death, myocardial infarction, and recurrence of symptoms requiring additional revascularization). The angiographic end point was restenosis rate at 6 months.@*CONCLUSION@#This study would provide important evidence for the use of Tongguan Capsules in patients after stent implantation in combination with routine therapies, which may significantly reduce incidence of the restenosis so as to potentially improve the clinical outcomes. (registration number: ChiCTR-TRC- ChiCTR-IIR-17011407).
RESUMEN
Objective@#Yingying, Email: yywdentist@163.com, Tel: 86⁃28⁃85503579 【Abstract】 Objective To explore the effect of 1,25(OH) 2 D 3 on the regulation of bone metabolism in a high⁃glucose environment and to provide evidence for the possible regulatory mechanism of 1,25(OH) 2 D 3 on osteoblasts in a high⁃glu⁃ cose environment.@* Methods@#The osteoblast cell line MC3T3⁃E1 was cultured in 3 groups: ① control group, cultured in low⁃glucose (5.5 mmol/L) DMEM; ② high⁃glucose group: cultured in high⁃glucose (22 mmol/L) DMEM; ③ high⁃glu⁃ cose +1,25(OH) 2 D 3 group: high⁃glucose DMEM + 1,25(OH) 2 D 3 medium culture. The CCK⁃8 method was used to detect cell proliferation in each group; Annexin V and FITC apoptosis kits were used to detect apoptosis; Alizarin red was used to semiquantitatively analyze cell differentiation; qRT⁃PCR was used to detect forkhead transcription factor⁃1 (forkhead transcription factor 1, FoxO1) mRNA expression. Immunofluorescence was used to observe the changes in FoxO1 pro⁃ tein expression and its relative position in the nucleus.@* Results@#ence was used to observe the changes in FoxO1 pro⁃ tein expression and its relative position in the nucleus. Results Our analysis showed that compared with those in the control group, the osteoblast apoptosis and proliferation in the high⁃glucose group were improved, while differentiation was inhibited (P < 0.05); at the same time, the mRNA expression of FoxO1(P = 0.006) was reduced. The immunofluores⁃ cence results showed that more FoxO1 was inside the nucleus (P < 0.001). Compared with those in the high⁃glucose group, excessive proliferation was inhibited, apoptosis was reduced, and osteogenic differentiation was improved in the high⁃glucose +1,25(OH) 2 D 3 group (P < 0.05); furthermore, FoxO1 mRNA was decreased (P = 0.006), and the transfer of FoxO1 protein was blocked (P < 0.001).@* Conclusion @#re, FoxO1 mRNA was decreased (P = 0.006), and the transfer of FoxO1 protein was blocked (P < 0.001). Conclusion We found that 1,25(OH) 2 D 3 may prevent the transfer of FoxO1 to the cell nucleus, inhibit the abnormal proliferation and apoptosis of osteoblasts in a high⁃glucose environment, and re⁃ verse the inhibitory effect of high glucose on the differentiation of osteoblasts.
RESUMEN
AIM:To study the effect of microRNA-7 (miR-7) knockdown (KD) on concanavalin A (ConA)-induced acute liver injury (ALI) in mice.METHODS:Wild type (WT) mice and miR-7KD mice were received ConA (30 mg/kg) to induced acute liver injury model by intraperitoneal injection,and the morphological changes,liver weight and weight index were measured 48 h later.The pathological changes of the liver tissues were observed by HE staining.The levels of serum alanine aminotransferase (ALT),IL-4 and IFN-γ were detected by ELISA.The proportional changes of CD4 + T cells and the relative levels of IL-4 and IFN-γwere analyzed by flow cytometry.RESULTS:The color of the liver tissue became lighter,and the weight and weight index were changed significantly in miR-7KD mice compared with control group (P ＜ 0.05).HE staining showed that the inflammatory cell infiltration was increased in the liver of miR-7KD mice.Moreover,the level of serum ALT was significantly increased (P ＜ 0.05).The serum level of IFN-γelevated significantly (P ＜ 0.01),while the IL-4 levels decreased significantly (P ＜ 0.01) in the serum of miR-7KD mice.Furthermore,the proportion of CD4 + T cells and relative IFN-γcells increased obviously (P ＜ 0.01).CONCLUSION:miR-7 knockdown promotes the pathogenesis of the ConA-induced acute liver injury in mice.
RESUMEN
AIM:To study the effect of microRNA-7 (miR-7) knockdown (KD) on concanavalin A (ConA)-induced acute liver injury (ALI) in mice.METHODS:Wild type (WT) mice and miR-7KD mice were received ConA (30 mg/kg) to induced acute liver injury model by intraperitoneal injection,and the morphological changes,liver weight and weight index were measured 48 h later.The pathological changes of the liver tissues were observed by HE staining.The levels of serum alanine aminotransferase (ALT),IL-4 and IFN-γ were detected by ELISA.The proportional changes of CD4 + T cells and the relative levels of IL-4 and IFN-γwere analyzed by flow cytometry.RESULTS:The color of the liver tissue became lighter,and the weight and weight index were changed significantly in miR-7KD mice compared with control group (P ＜ 0.05).HE staining showed that the inflammatory cell infiltration was increased in the liver of miR-7KD mice.Moreover,the level of serum ALT was significantly increased (P ＜ 0.05).The serum level of IFN-γelevated significantly (P ＜ 0.01),while the IL-4 levels decreased significantly (P ＜ 0.01) in the serum of miR-7KD mice.Furthermore,the proportion of CD4 + T cells and relative IFN-γcells increased obviously (P ＜ 0.01).CONCLUSION:miR-7 knockdown promotes the pathogenesis of the ConA-induced acute liver injury in mice.
RESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of cerebral X-ray irradiation on learning and memory function in young rats.</p><p><b>METHODS</b>Fifty-four SD rats aged 35 d were randomly divided into 3 groups with 18 in each group: rats in 3-d group and 7-d group received X-ray irradiation with a dose of 28.5 mGy/d for 3 d and 7 d, respectively; rats in control group received sham X-ray irradiation. Morris water maze (MWM) was tested when animals at age of 60 d; then the animals were sacrificed and brain samples were taken. The neurodegeneration was observed by Fluro-Jade B staining; the expression of N-methyl-aspartate (NMDA) receptors subunit 2B (NR2B) and postsynaptic density protein-95 (PSD-95) in the hippocampus were analyzed by immunofluorescence and Western blot methods, respectively, and ultrastructure of CA1 region was observed with electron microscopy.</p><p><b>RESULTS</b>No significant difference in 1-4 d escape latency as shown in MWM test was noted between 3d group and control group (P>0.05); while the escape latency in 7d group was significantly longer than that in control group (P<0.01). No significant differences in lingering in the quadrant and the frequency of passing through the original platform between 3-d group and control group (P>0.05), while those in 7-d group were significantly lower than those in control group (P<0.01). Compared to control group, the number of FJB positive cells in 7-d group was increased (P<0.01); the expressions of NR2B and PSD-95 in hippocampus CA1 region were also increased (P<0.05). The ultrastructure observation in 7-d group showed that the synapse structure of some neurons was impaired.</p><p><b>CONCLUSION</b>X-ray irradiation may affect learning and memory function of young rats, which is associated with overexpression of NR2B and PSD-95 in hippocampal regions.</p>