How to form shared objects to enhance university-school collaboration? A cultural-historical activity theory perspective.

Introduction: University-school (U-S) collaboration has proven to be an effective approach for teacher professional development, but it could be hampered by the lack of shared objects. To understand how shared objects are formed in U-S collaboration, this research established a university-school collaborated Change Laboratory in W primary school based on cultural-historical activity theory, which is under the background of Chinese teaching research activity. Methods: Recordings of meetings throughout the year were transcribed into texts and coded, and then analyzed via the method of grounded theory and contradiction analysis. Results: The findings reveal that, in comparison to previous studies regarding shared object formation process, this study identified an special phase named "experimental object," which highlights the significance of experimentation in U-S collaboration. Also, multiple contradictions are recognized as the driving force for shared object formation which would gradually transform into fundamental conflicts between tools. The main contradictions identified include those between scientific and daily concepts, university culture and school culture, as well as new experiment and old routine. Discussion: The current study implicates that U-S collaboration is an expansive learning process to acquire unknown knowledge, which necessitates both parties engaging in exploration and experimentation together. Furthermore, shared object formation within U-S collaboration requires participants to focus on developing teaching tools while consciously undergoing changes in aspects such as logic of thinking, culture and routine.

Correlation of Serum M-CSF, CER, and TIMP-1 Levels with Liver Fibrosis in Viral Hepatitis.

Objective: This research is aimed at investigating the relationship between liver fibrosis in viral hepatitis and macrophage colony-stimulating factor (M-CSF), tissue inhibitor of matrix metalloproteinase (TIMP-1), and ceruloplasmin (CER) in serum level. Methods: Patients were randomly selected among those admitted to our hospital, and 60 healthy volunteers were chosen to serve as control participants. The levels of serum M-CSF, CER, and TIMP-1 were compared. According to the severity of their liver fibrosis, patients with CHB were separated into four groups: S1, S2, S3, and S4. Serum levels of M-CSF, CER, and TIMP-1 were correlated with liver fibrosis and hepatitis markers, and the diagnostic usefulness of the three indices was assessed with liver cirrhosis patients. Results: Increases in M-CSF and TIMP-1 in the CHB group but decreases in CER were statistically significant (P < 0.05). Serum levels of M-CSF, CER, TIMP-1, HA, PC-III, C-IV, and LN differed significantly across the four study groups (P < 0.05). Over time, as liver fibrosis worsened, we observed a progressive uptick in M-CSF, TIMP-1, LN, HA, C-IV, and PC-III levels and a progressive downtick in CER levels, with significant (P < 0.05) differences between the groups. There was a significant positive correlation between liver fibrosis and serum M-CSF, PC-III, TIMP-1, HA, LN, and C-IV levels in the CHB group (P < 0.05) and a significant negative correlation between serum CER and these same factors (P < 0.05). The AUC of 0.956 for diagnosing the S4 stage was greater than that of 0.857, 0.851, and 0.817 for M-CSF, CER, and TIMP-1, respectively. Conclusions: In CHB patients, the liver fibrosis degree is associated with the M-CSF, CER, and TIMP-1 levels, and the combined clinical detection of these three markers has better diagnostic significance.

Human umbilical cord mesenchymal stem cells inhibit proliferation of hepatic stellate cells in vitro.

The effect of human umbilical cord mesenchymal stem cells (hUC-MSCs) on the proliferation of hepatic stellate cells (HSCs) is largely unknown. The purpose of this study was to explore the mechanism of action of hUC­MSCs on the proliferation of HSCs in vitro. The upper and lower double-cell co-culture system was established between hUC­MSCs and HSCs in the experimental group. HSCs were cultured alone as a negative control group. Cell proliferation and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Cell supernatants were harvested to determine the concentration of transforming growth factor-ß1 (TGF-ß1) by ELISA. mRNA and protein of TGF-ß1, Smad3 and Smad7 in HSCs were determined by reverse transcription-polymerase chain reaction and western blotting, respectively. In the co-culture group, the proliferation of HSCs was significantly inhibited compared with the negative control group at 24 and 48 h (p<0.05). Apoptosis of HSCs in the co-culture group increased compared with that in the negative control group, which was more obvious at 48 h (p<0.05). The concentration of TGF-ß1 in the co-culture group was significantly lower than in the HSCs cultured alone (p<0.05). After HSCs were co-cultured with hUC­MSCs for 48 h, expression of TGF-ß1 and Smad3 mRNA and protein was reduced and expression of Smad7 mRNA and protein was increased compared with the negative control group (p<0.05). hUC­MSCs inhibited proliferation of HSCs, possibly through inhibiting TGF-ß1 and Smad3 expression and increasing Smad7 protein expression.

Bone marrow-derived mesenchymal stem cells inhibit the proliferation of hepatic stellate cells by inhibiting the transforming growth factor ß pathway.

Bone marrow-derived mesenchymal stem cells (BM-MSCs) are considered to be a potential therapy for end-stage liver disease. However, the therapeutic mechanism of BM-MSCs remains unclear. The aim of the current study was to investigate the role of paracrine signaling in BM­MSCs in liver cirrhosis in vitro. Human BM­MSCs and hepatic stellate cells (HSCs) were cultured using a vertical double cell co­culture system. Groups were divided into HSCs alone (control group) and the co­culture system of BM­MSCs with HSCs (experimental group). HSC morphology was observed by inverted phase contrast microscopy. The proliferative capacity of HSCs was measured with the MTT assay and flow cytometry. Hoechst staining was performed to examine the apoptosis of HSCs. Transforming growth factor (TGF)­ß1 and Smad7 mRNA expression were detected by reverse transcription­quantitative polymerase chain reaction and western blotting. BM­MSCs did not inhibit the proliferation of HSCs at 24 h, however significantly inhibited the proliferation of HSCs at 48 and 72 h. BM­MSCs additionally induced the apoptosis of HSCs at 48 h. The concentration of TGF­ß1 in the supernatant at 24 h and 48 h in the co­cultured system was observed to be significantly lower than in the control group (P<0.05). The level of TGF­ß1 mRNA in the experimental group at 48 h was significantly lower than the control group, however Smad7 mRNA levels were significantly greater than in the control group. Additionally, TGF­ß1 protein levels were significantly lower than in the control group, however levels of Smad7 were greater than the control group. It was concluded that BM­MSCs are able to inhibit the proliferation and promote the apoptosis of HSCs. In addition, the mechanism may be associated with inhibition of the TGF-ß1/Smad pathway in HSCs.