Objective:To investigate the clinical value of three-dimensional arterial spin marker imaging(3D-ASL) for evaluating collateral circulation compensatory status in patients with cerebral infarction.Methods:A total of 24 patients with cerebral infarction who were treated at Wenzhou Hospital of Traditional Chinese Medicine Affiliated to Zhejiang University of Chinese Medicine from September 2017 to January 2019 were examined by 1.5-T high-field MR scanner.The changes of cerebral blood flow(CBF) between the infarcted area and the contralateral normal area were compared when the labeled delay time(PLD)=1.5s and PLD=2.5s, and the patients were divided into the group with strong collateral circulation compensation and the group with weak collateral circulation compensation according to the difference in lesion area measured by 3D-ASL(PLD=1.5s and 2.5s). The changes of national institutes of health stroke scale(NIHSS) score and Bathel index at admission and 15 days after admission were compared.Results:3D-ASL measurement of PLD=1.5s showed that the CBF value in the infarcted area was (33.70±20.83)mL/(100g×min), which was significantly lower than that in the contralateral normal area(PLD=1.5s)[(49.93±13.13)mL/(100g×min)]( t=3.229, P<0.05). When PLD=2.5s, ASL measurement results showed that the CBF value in the infarcted area increased significantly[(58.26±23.50)mL/(100g×min) vs.(33.70±20.83)mL/(100g×min)]( t=3.831, P<0.05), and the CBF value in the contralateral normal area also increased significantly[(68.29±14.03)mL/(100g×min) vs.(49.93±13.13)mL/(100g×min)]( t=4.681, P<0.05). At this time, the CBF value in the infarcted area was still significantly lower than that in the contralateral normal area[(58.26±23.50)mL/(100g×min) vs.(68.29±14.03)mL/(100g×min)]( t=1.795, P<0.05). On the day of admission, the BI index of patients in the weak collateral circulation compensation group(12 cases) was significantly higher than that in the strong collateral circulation compensation group(12 cases)[(90.42±10.50) vs.(67.92±27.57)]( t=2.642, P<0.05), and the NIHSS score was significantly lower than that in the strong collateral circulation compensation group[(1.25±1.01) vs.(3.83±3.62)]( t=2.378, P<0.05). After 15 d of admission, there were no significant differences in BI index and NIHSS score between the two groups(all P>0.05). Conclusion:3D-ASL with different delay time can effectively and intuitively reflect collateral circulation compensation of patients with cerebral infarction, and it has very important reference value for the evaluation of patients' disease and the formulation of clinical treatment plan.

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.