CT laser simulation positioning system is a necessary auxiliary device for radiotherapy. Its main purpose is to position patients by simulating different kinds of treatment machine. In order to demarcate the mark of the iso-center, it is common to use the laser positioning device to indicate the iso-center. The kernel technology of the laser positioning system is the controlling of the step progress motor by using the MCS, which is to control the movement of step progress motor using the wheel of the motor. This design uses MCS-51 to control step progress motor by the way of exporting the rectangle wave form through I/O port of 8255 chip. The system configuration is simple, the operation is convenient and the positioning is precise.

Purpose To evaluate the consistency and repeatability of cerebral blood flow(CBF)values measured by automatic segmentation of region of interest(ROI)and arterial spin labeling(ASL)functional image fusion in hippocampal sclerosis patients with medial temporal lobe epilepsy.Materials and Methods From January 2021 to October 2022,a total of 52 patients with medial temporal lobe epilepsy confirmed by MRI or pathology in General Hospital of Ningxia Medical University were retrospectively collected.All subjects were scanned on 3.0T MRI to obtain axial T1 weighted three-dimensional magnetization reserve gradient echo(3D-T1W1-MPGAGE)sequence and three-dimensional pseudo continuous ASL sequence.The 3D-T1W1-MPGAGE imaging were automatically segmented.Two physicians used the freeview visualization interface of freeSurfer software to fuse the ROI and ASL functional images of the hippocampal subregions and to measure the CBF values.The intra-observer and inter-observer consistency and repeatability were evaluated and analyzed.The consistency analysis and repeatability evaluation were performed via intraclass correlation coefficient(ICC),Bland-Altman diagram and Wilcoxon rank sum test.Results The ICC of CBF values measured by two physicians were all>0.750,with an average of 0.868±0.095.The ICC of left and right hippocampal subregions were as follows:subiculum(SUB):0.818/0.801,cornu ammonis(CA)1:0.920/0.907,CA2-3:0.759/0.978,CA4:0.757/0.758 and dentate gyrus(DG):0.990/0.991;The ICC delineated by the same physician's ROI were all>0.990 with an average of 0.994±0.002.The ICC of left and right hippocampal subregions were as follows:SUB:0.993/0.993,CA1:0.996/0.995,CA2-3:0.989/0.994,CA4:0.992/0.995 and DG:0.993/0.996.The Bland-Altman diagram showed the scatter distribution and consistency,and the coefficient of repeatability was obtained.The same observer had certain repeatability for the fusion measurement of automatic segmentation ROI and ASL functional images.Conclusion The CBF values measured by fusing ROI and ASL functional images of automatically segmented hippocampal subregion have higher consistency and repeatability.

Objective: To observe the effect of meisoindigo on apoptosis and proliferation of JAK2/V617F heterozygous mutation cell line-SET2 cell line to further explore the role of JAK-STAT pathway in this effect. Methods: Cell apoptosis after treated with different concentration of meisoindigo (0, 5, and 10 μmol/L) was evaluated by flow cytometry at different time points (24, 48, 72 h). Cell proliferation with CCK8 test was evaluated at different time points (24, 48, 72, 96 h) after administered with different concentration of meisoindigo (0, 5, 10, and 20 μmol/L). After treatment with different concentration of meisoindigo (0, 5, 10, and 20 μmol/L), SET2 cells were collected after 12 h, and then cultured in incomplete methylcellulose-based medium for clone formation. JAK-STAT signaling pathway and apoptosis related protein by Western blot test were evaluated 12 h after administered with different concentration of meisoindigo (0, 5, 10, and 20 μmol/L). Results: At different time points after treated with meisoindigo, the apoptosis rate of SET2 cell lines increased (P<0.01) with the inhibited proliferation (P<0.01), and the decreased clone formation rate of SET2 cell lines [0 μmol/L meisoindigo: (4.48±1.19)%, 20 μmol/L meisoindigo: (2.55±0.36)%; Dunnett P=0.020] in the presence of augmented concentrations of meisoindigo. At 12 hours after administration with meisoindigo, the reduced expressions of JAK2, P-JAK2, P-STAT1, P-STAT3, P-STAT3, STAT5, the decreased anti-apoptosis proteins BCL-2, BCL-XL and the increased pro-apoptosis protein BID, BIM were observed in the presence of increased concentrations of meisoindigo. Conclusion Meisoindigo played an important role during the apoptosis and the inhibition of proliferation in ph-negative myeloproliferative neoplasm cell-SET2 cell lines, which might be related to the inhibition of JAK-STAT signaling pathway with up-regulation of pro-apoptosis protein and down-regulation of anti-apoptosis protein.

Objective: To explore the effects and molecular mechanism of the selective JAK1inhibitor SHR0302 and Ruxolitinib on myeloproliterative neoplasms (MPN) cell line SET2 and primary cells in vitro. Methods: Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colony formation unit (BFU-E) of primary cells from MPN patients. Multi-factor kits were used to detect six inflammatory cytokines. Phosphorylated proteins of Jak-Stat signaling pathway were tested by Western blot. Results: At different time points after treated with SHR0302 and Ruxolitinib, the inhibition of cell proliferation was dose dependent by both drugs (P<0.01) . The inhibitory rates of 2.5 μmol/L SHR0302 and 0.1 μmol/L Ruxolitinib on SET2 cells for 72 h were comparable, i.e. (59.94±0.60) % and (64.00±0.66) %, respectively, suggesting that the inhibitory effect of SHR0302 was weaker than that of Ruxolitinib. Similarly, both SHR0302 and Ruxolitinib inhibited BFU-E in primary marrow cells from MPN patients in a dose-dependent manner. SHR0302 1.0 μmol/L produced similar degree of inhibition compared to Ruxolitinib 0.2 μmol/L. Except IL-12, the expression of other 5 cytokines (IL-6, TNF-α, IL-1β, IL-2, IL-8) was significantly inhibited by 1.6 μmol/L SHR0302 in SET2 cells at 24 h (P<0.01) , while Ruxolitinib 1.0 μmol/L had the same effect. Several phosphorylated molecules of Jak-Stat signaling pathway were significantly inhibited by SHR0302 in SET2 cells only for 3 h. P-stat1 (Tyr701) , p-stat3 (Tyr705) were down-regulated when treated with SHR0302 1.0 μmol/L (P<0.05) , p-jak1 (tyr1022/1023) and p-stat5 (Tyr694) were inhibited at 5.0 μmol/L (P<0.05) . Ruxolitinib significantly inhibited the downstream STAT protein at 0.1 μmol/L. Again, the inhibitory effect of SHR0302 on protein expression was weaker than that of Ruxolitinib. Conclusion SHR0302 can effectively inhibit the proliferation of MPN cell line and patients' primary cells, as well as the expression of inflammatory factors. The molecular mechanism is possibly related to the down-regulation of phosphorylated proteins of Jak-Stat signaling pathway. Overall, the anti-proliferative and anti-inflammatory effects of SHR0302 are weaker than those of Ruxolitinib.