Objective:To systematically evaluate the intervention effect of acceptance commitment therapy on anxiety disorder.Methods:The full-text databases of Web of Science Core Collection, MEDLINE, KCI-Korean Journal Database, SciELO Citation Index, SpringerLink, Pubmed, EMBASE, Cochrane Library, CNKI Wanfang and Weipu were searched and randomized controlled studies related to acceptance commitment therapy for patients with anxiety disorder were collected.All randomized controlled studies met the criterion were included.Meanwhile, the literature quality of the included literatures was evaluated.The outcome indicators such as anxiety index, psychological flexibility and quality of life index were selected, and RevMan 5.3 software was used to analyze the literature data that met the inclusion criteria.Results:A total of 12 studies with 1 062 patients were included, including 513 cases in ACT group and 549 cases in control group.Meta analysis showed that ACT can effectively reduce anxiety level of patients with anxiety disorder (MD=-0.58, 95% CI: -0.85- -0.32, P<0.001), anxiety level in follow-up period (MD=-0.42, 95% CI: -0.75- -0.08, P=0.01), improving psychological flexibility (MD=0.46, 95% CI: 0.24~0.68, P<0.001); In the study of CBT(cognitive behavioral therapy) as the control group, there was no significant difference between ACT group and control group, among which after intervention (MD =-0.06, 95% CI: -0.47- 0.36, P=0.79), follow-up period (MD = 0.17, 95% CI: -0.07-0.41, P=0.16) .In the study with the control group as the blank control, ACT can reduce the anxiety level of patients with anxiety disorder (MD =-0.76, 95% CI: -0.97- -0.56, P<0.001), and the difference is statistically significant.Excluding the non-blank control study, ACT can reduce the anxiety level of patients with anxiety disorder (MD =-0.82, 95% CI: -1.09--0.55, P<0.001) in the studies where the proportion of women is greater than or equal to 70%.In the study of 50%-70% females, ACT can reduce the anxiety level of patients with anxiety disorder (MD =-0.68, 95% CI: -1.09 --0.28, P=0.01). All the differences were statistically significant.There was no significant difference between ACT and the control group for quality of life(MD=0.24, 95% CI: -0.01-0.49, P=0.06). Conclusion:ACT has a certain effect on patients with anxiety disorder, which not only improves the anxiety level of patients, but also keeps the effect of anxiety improvement during the follow-up period, and the improvement of psychological flexibility has also been verified.The immediate and long-term efficacy of ACT is similar to that of CBT, which further improve the reliability of ACT curative effect.Gender difference has not been confirmed for the therapeutic effect.ACT has no obvious improvement on the quality of life, and the conclusion of this study needs more randomized controlled studies with large samples and high quality to verify it.

To evaluate five methods in the estimation on the rate of case fatality during the epidemics of diseases based on the summarizing data. Case fatality rates,derived from the simulation data,2003 SARS epidemic data in Hong Kong,Singapore Beijing and the 2013 H7N9 epidemic data in mainland China were analyzed,using these 5 methods. Results from the simulation analysis discovered that the relative errors and the standard deviations of the Chen[7,8] (method 3),Chen[9] (method 4) were minor with high accuracy. Data from the analysis on 2003 SARS epidemic was noticed that the estimation from method 3,4 in Hong Kong and Singapore both showing high veracities. Since the case fatality rate reported in Beijing was not a constant value,method 5 showed low accuracy even though it was close to the final case fatality rate. Data from the 2013 H7N9 epidemic showed that the estimations of method 1,2,3,4 were all higher than that in the method 5, suggesting that method 3,4 could be used to estimate the case fatality rates of epidemics more precisely.

Due to the limited number of cases, conducting large-scale clinical trials for rare diseases is challenging. This review introduces several small sample statistical designs tailored for rare diseases, including crossover design, n-of-1 design, randomized placebo-phase design, randomized withdrawal design, group sequential design, and adaptive design. It discusses the advantages, disadvantages, and application scenarios of these designs. Additionally, it explores the benefits of Bayes decision-making in clinical trials for rare diseases. The aim is to provide a reference for designing and implementing small sample clinical trials for rare diseases.

Objective To explore the role of zinc finger protein 36 (ZFP36) in regulating osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and preosteoblasts. Methods ZFP36 expression was observed in primary mouse BMSCs and mouse preosteoblasts (MC3T3-E1 cells) during induced osteogenic differentiation. Zfp36-deficient cell models were constructed in the two cells using RNA interference technique and the changes in differentiation capacities of the transfected cells into osteoblasts were observed. Transcriptome sequencing was used to investigate the potential mechanisms of ZFP36 for regulating osteoblast differentiation of the two cells. U0126, a ERK/MAPK signal suppressor, was used to verify the regulatory mechanism of Zfp36 in osteogenic differentiation of Zfp36-deficient cells. Results During the 14-day induction of osteogenic differentiation, both mouse BMSCs and MC3T3-E1 cells exhibited increased expression of ZFP36, and its mRNA expression reached the peak level on Day 7 (P<0.0001). The Zfp36-deficient cell models showed reduced intensity of alkaline phosphatase (ALP) staining and alizarin red staining with significantly lowered expressions of the osteogenic marker genes including Alpl, Sp7, Bglap and Ibsp (P<0.01). Transcriptome sequencing verified the reduction of bone mineralization-related gene expressions in Zfp36-deficient cells and indicated the involvement of ERK signaling in the potential regulatory mechanism of Zfp36. Immunoblotting showed that pERK protein expression increased significantly in Zfp36-deficient cells compared with the control cells. In Zfp36-deficient MC3T3-E1 cells, inhibition of activated ERK/MAPK signaling with U0126 resulted in obviously enhanced ALP staining and significantly increased expressions of osteoblast differentiation markers Runx2 and Bglap (P<0.05). Conclusions ZFP36 is involved in the regulation of osteoblast differentiation of mouse BMSCs and preosteoblasts, and ZFP36 deficiency causes inhibition of osteoblast differentiation of the cells by activating the ERK/MAPK signaling pathway.

Objective To explore the role of zinc finger protein 36 (ZFP36) in regulating osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and preosteoblasts. Methods ZFP36 expression was observed in primary mouse BMSCs and mouse preosteoblasts (MC3T3-E1 cells) during induced osteogenic differentiation. Zfp36-deficient cell models were constructed in the two cells using RNA interference technique and the changes in differentiation capacities of the transfected cells into osteoblasts were observed. Transcriptome sequencing was used to investigate the potential mechanisms of ZFP36 for regulating osteoblast differentiation of the two cells. U0126, a ERK/MAPK signal suppressor, was used to verify the regulatory mechanism of Zfp36 in osteogenic differentiation of Zfp36-deficient cells. Results During the 14-day induction of osteogenic differentiation, both mouse BMSCs and MC3T3-E1 cells exhibited increased expression of ZFP36, and its mRNA expression reached the peak level on Day 7 (P<0.0001). The Zfp36-deficient cell models showed reduced intensity of alkaline phosphatase (ALP) staining and alizarin red staining with significantly lowered expressions of the osteogenic marker genes including Alpl, Sp7, Bglap and Ibsp (P<0.01). Transcriptome sequencing verified the reduction of bone mineralization-related gene expressions in Zfp36-deficient cells and indicated the involvement of ERK signaling in the potential regulatory mechanism of Zfp36. Immunoblotting showed that pERK protein expression increased significantly in Zfp36-deficient cells compared with the control cells. In Zfp36-deficient MC3T3-E1 cells, inhibition of activated ERK/MAPK signaling with U0126 resulted in obviously enhanced ALP staining and significantly increased expressions of osteoblast differentiation markers Runx2 and Bglap (P<0.05). Conclusions ZFP36 is involved in the regulation of osteoblast differentiation of mouse BMSCs and preosteoblasts, and ZFP36 deficiency causes inhibition of osteoblast differentiation of the cells by activating the ERK/MAPK signaling pathway.

To evaluate five methods in the estimation on the rate of case fatality during the epidemics of diseases based on the summarizing data. Case fatality rates, derived from the simulation data, 2003 SARS epidemic data in Hong Kong, Singapore Beijing and the 2013 H7N9 epidemic data in mainland China were analyzed, using these 5 methods. Results from the simulation analysis discovered that the relative errors and the standard deviations of the Chen [7, 8] (method 3), Chen [9] (method 4)were minor with high accuracy. Data from the analysis on 2003 SARS epidemic was noticed that the estimation from method 3, 4 in Hong Kong and Singapore both showing high veracities. Since the case fatality rate reported in Beijing was not a constant value, method 5 showed low accuracy even though it was close to the final case fatality rate. Data from the 2013 H7N9 epidemic showed that the estimations of method 1, 2, 3, 4 were all higher than that in the method 5, suggesting that method 3, 4 could be used to estimate the case fatality rates of epidemics more precisely.
China ; epidemiology ; Hong Kong ; epidemiology ; Humans ; Influenza A Virus, H7N9 Subtype ; Influenza, Human ; mortality ; Regression Analysis ; Severe Acute Respiratory Syndrome ; mortality