Objective To evaluate the dosimetric characteristics of base dose plan compensation (BDPC) optimization method applied on the intensity-modulated radiotherapy (IMRT) for upper esophageal carcinoma,based on the Eclipse treatment planning system.Methods Nineteen patients were included.For each case initial IMRT plan was generated and further optimized respectively by the two following methods:the BDPC method and hot and cold spot control (HCSC) method.Then the BDPC and HCSC plans were compared concerning planning-target-volume (PTV) coverage,conformity index (CI),and homogeneity index (HI),as well as organ-at-risk (OAR) sparing,planning time,monitor unit (MU) and delivery time.Results Compared with the HCSC plans,the BDPC plans provided superior CI and HI (Z =-3.662,-3.745,P ＜ 0.05),as well as lower D2％ (near-maximum dose) (Z =-3.823,P ＜ 0.05) and comparable D98％ (near-minimum dose) (P ＞ 0.05) for PTV64 (high-risk PTV),and provided superiorCI (Z=-3.340,P＜0.05),lower D95％ and D98％ (Z=-3.582,-2.616,P＜0.05) for PTV54 (low-risk PTV).The BDPC plans also provided slightly lower doses to the spinal cord and lung compared with the HCSC plans (Z =-3.625--3.369,P ＜ 0.05).Moreover,the planning time [(26.05 ±0.88) min] for BDPC plans was less than that of the HCSC plans [(33.73 ± 3.24) min] (Z =-3.823,P ＜0.05).The MU of the BDPC plans (1 019 ± 167) was higher than that of the HCSC plans (1 003 ±159) (Z=-2.616,P＜0.05),while the delivery time [(3.52 ±0.29) min] was more than that of the HCSC plans [(3.50±0.28) min] (Z=-2.548,P＜0.05).Conclusions The BDPC optimization method can significantly improve target dose homogeneity and conformity with effective reduction of the dose to OARs for upper esophageal carcinoma.Moreover,it is simple and can improve the treatment planning efficiency.

Objective:To observe the effect of mirror visual feedback training on upper limb function and muscle tension in children with spastic hemiplegia resulting from cerebral palsy (SHCP).Methods:Seventy-six children aged 2-5 with SHCP were randomly divided into a control group of 33 and a treatment group 34. All were given routine occupational therapy, physical therapy, massage and physical agents. Each therapy session lasted 30 minutes daily, 5 times a week over 3 weeks as a course of treatment. There was a one week interval after each of 6 courses, so the total treatment lasted 6 months. The treatment group was additionally trained with mirror visual feedback with the same schedule. Before, as well as after 3 and 6 months of treatment, each patient′s upper limb motor function, fine motor function and muscle tone were evaluated using the Fugl-Meyer motor function assessment scale (FMA), the Peabody fine motor development scales (PDMS-FM), the modified Ashworth scale (MAS) and integrated electromyograms (iEMGs).Results:There were no significant differences between the two groups before treatment. After both 3 and 6 months significant improvement was observed in both groups′ average FMA score, PDMS-FM total score, grip, and visual motor integration. At both points the treatment group′s averages were significantly better than those of the control group. The average MAS and iEMG results, however, were not significantly different at either time point.Conclusions:For children with spastic hemiplegia caused by cerebral palsy, mirror visual feedback training can effectively improve upper limb functioning, but it cannot reduce their muscle tone.

Implant dentures have become the main method for the treatment of dentition defects or complete edentulism. However, due to the lack of periodontal ligament and periodontal ligament proprioceptors, implant dentures have very limited cushioning and sensing capabilities and are prone to occlusal overload. As a risk factor for peri-implantitis, occlusal overload seriously threatens the stability and success rate of implant dentures. This paper reviews the occlusal overload of implant dentures, the causal relationship between occlusal overload and plaque biofilms in peri-implantitis, the mechanism by which occlusal overload promotes peri-implantitis, and the effect of reasonable clinical occlusal adjustment on healing. This review shows that occlusal overload is closely related to the occurrence of peri-implantitis. Occlusal overload can promote the process of peri-implantitis by increasing the release of inflammatory factors and mechanical transduction mechanisms. The intervention of the patients’ bad bite habits and occlusal adjustment can promote the healing of peri-implantitis. At present, there is no uniform standard ideal experimental model for occlusal overload. The phenomenon and mechanism of bone resorption around the implant caused by overload force still need further observation and research, which will help determine the intensity, direction and timing of occlusal loading to guide clinical occlusal adjustment.

Objective: To investigate the expression and role of LINC00052 during glycidyl methacrylate (GMA) -induced malignant transformation of 16HBE cells. Methods: Human bronchial epithelial (16HBE) cells were divided into GMA transformation group and corresponding DMSO control group, and the 10th, 20th and 30th generation cells of each group were collected LncRNA microarrays were used to analysis expression of LINC00052 in different stage of malignant transformation. Bioinformatics analysis was applied and the relative expression of LINC00052 and its potentially target genes was detected by real-time quantification PCR (qPCR) . Results: The results of microarray analysis showed that LINC00052 was up-regulated by 1.32-fold, down-regulated by 1.64-fold and down-regulated by 4.92-fold in the malignant transformation early (P10) , middle term (P20) and late (P30) , respectively, The results of qPCR showed that compared with the DMSO control group, the expression of LINC00052 was up-regulated by 1.55 times, down-regulated by 1.20 times and down-regulated by 2.35 times in P10, P20 and P30, respectively, and the difference was statistically significant (P<0.05) . There was a statistically significant difference in the relative expression of NTRK3 between the GMA transformation group of P10 and P30 generations with the corresponding DMSO control group (P<0.05) . Conclusion LINC00052 is highly expressed in early time of GMA-induced malignant transformation of 16HBE, and down-regulated in the middle and last stage of malignant transformation and may play a protective role in GMA-induced malignant transformation of 16HBE by influencing the expression of its target gene NTRK3.

Pancreatic ductal adenocarcinoma (PDAC) is characterized by the highest mortality among carcinomas. The pathogenesis of PDAC requires elevated autophagy, inhibition of which using hydroxychloroquine has shown promise. However, current realization is impeded by its suboptimal use and unpredictable toxicity. Attempts to identify novel autophagy-modulating agents from already approved drugs offer a rapid and accessible approach. Here, using a patient-derived organoid model, we performed a comparative analysis of therapeutic responses among various antimalarial/fungal/parasitic/viral agents, through which econazole (ECON), an antifungal compound, emerged as the top candidate. Further testing in cell-line and xenograft models of PDAC validated this activity, which occurred as a direct consequence of dysfunctional autophagy. More specifically, ECON boosted autophagy initiation but blocked lysosome biogenesis. RNA sequencing analysis revealed that this autophagic induction was largely attributed to the altered expression of activation transcription factor 3 (ATF3). Increased nuclear import of ATF3 and its transcriptional repression of inhibitor of differentiation-1 (ID-1) led to inactivation of the AKT/mammalian target of rapamycin (mTOR) pathway, thus giving rise to autophagosome accumulation in PDAC cells. The magnitude of the increase in autophagosomes was sufficient to elicit ER stress-mediated apoptosis. Furthermore, ECON, as an autophagy inhibitor, exhibited synergistic effects with trametinib on PDAC. This study provides direct preclinical and experimental evidence for the therapeutic efficacy of ECON in PDAC treatment and reveals a mechanism whereby ECON inhibits PDAC growth.