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.

Objective To compare the levels of indoleamine 2,3-dioxygenase (IDO) in the peripheral blood mononuclear cells(PBMCs) from HIV-1 infected and HIV-1 negative individuals and in human tumor cells in the presence or absence of TLR ligand stimulation.Methods TaqMan probe real-time RT-PCR method for human IDO mRNA was established; IDO mRNA levels in the PBMCs from HIV-1+ and HIV-1-individuals were tested; IDO mnRNA levels in mucosal origin(T84,Caco-2,Hela) and leukocyte origin(THP-1,MT-4) tumor cells before and after exposure to agonists for TLR4,TLR7/8 and TLR9 were examined.Results It was found that a high level of IDO mRNA could be found in HIV-1+ individuals( 103.42 copy IDO mRNA/106 copy GAPDH mRNA) ; however,some high risk HIV-1-individuals may have also a high level of IDO mRNA.Some of the tumor cells could express higher level of IDO mRNA after exposure to TLR agonist.Conclusion This study indicated a role for IDO in the viral persistence and tumor formation in HIV/AIDS and further studies were warranted.

Diabetic kidney disease (DKD) is a primary cause of chronic kidney disease and end-stage renal disease, as well as one of the most common microvascular consequences of diabetes mellitus. Obesity, as a metabolic disease, has a substantial impact on the onset and progression of DKD. Epidemiological studies have revealed obesity is a risk factor of DKD and end-stage renal disease, which can promote the occurrence and progression of DKD through various mechanisms, including alterations in hemodynamics, metabolic regulation, and chronic inflammation. Clinical researches also have demonstrated the importance of various weight loss interventions in the prevention and management of DKD. Therefore, gaining a deeper understanding of the correlation between obesity and DKD will contribute to improving the prognosis and quality of life of individuals with diabetes mellitus. The paper reviews the relationship between obesity and DKD on the epidemiological characteristics of obesity and DKD, the potential mechanism of obesity affecting DKD and the influence of obesity intervention on DKD.

Objective To analyze and evaluate the CT and MRI features of synovial sarcoma (SS).Methods Clinical and imaging data of 25 cases with SS confirmed by pathology were retrospectively analyzed.1 5 cases with CT scan,including 1 1 contrastGenhanced CT scan,and 1 2 cases with MRI scan,including 8 contrastGenhanced MRI scan.Results Among 25 cases,1 8 were located in the lower extremities,2 in the upper extremities and in the chest wall respectively,1 case in the lung parenchyma,mediastinum and spine respectively.1 8 cases were deep seated,while 1 9 cases were lobulated.On CT image,most of the lesions were isodense or hypodense to muscle,while 3 cases presented peripheral calcification,and 9 cases showed progressive enhancement.On MRI,10 cases were isointense or slight hypointense on T1 WI,while 9 cases presented hyperintense or slight hyperintense on T2 WI.9 cases showed cystic change (7 of them located in the periphery),and 8 cases showed short T1 signal.3 cases demonstrated "fluidGfluid levels",and 9 cases exhibited hypointense septa.7 cases revealed "triple sign"on T2 WI and 7 cases showed obviously heterogenous enhancement.Conclusion Synovial sarcomas are mostly located in the lower extremities,with clear margins,peripheral cystic changes,intramural hemorrhage,"triple sign"on T2 WI and progressive enhancement.

Distal junctional problem (DJP) is one of the severe complications after spinal correction, fixation and fusion. As the number of patients receiving spinal surgery increased recently, the incidence of DJP also increased dramatically. Compared with proximal junctional problem, the incidence of DJP is low. However, the clinical symptoms are severe, and the rate of surgical revision is high in patients with distal junctional problems. DJP include distal junctional kyphosis (DJK) and distal junctional failure(DJF). The definition of DJK is confusing, however, and the most commonly used was that the distal junction Angle at the last follow-up was greater than 10° and increased by 10° compared with that before surgery. There are 6 DJF modes: progressive loss of lumbar lordosis,acute wedging in the disc below the instrumentation, fracture of LIV, osteoporotic fracture below the long rigid fixation, failure of the instrumentation at LIV, spinal stenosis and or segmental instability underneath the instrumentation. Possible risk factors for DJP include weight, age, type of spinal deformity, osteoporosis, choice of LIV, hip disease, deformity location, surgical approach, surgical procedure, fusion segments, fixation devices, LIV at L5, fixed to S1 with no iliac screws, poor restoration of spinal alignment, et al. Currently, there are some controversies in DJP, mainly including the incidence, risk factors whether needs to and how to revise. The review intends to conduct a simple literature review of the current DJP diagnostic criteria, incidence, risk factors, and other research progress, in order to improve the understanding of the distal junction problem.

Background::The risk for chronic kidney disease (CKD) is influenced by genetic predisposition, sex, and lifestyle. Previous research indicates that coffee is a potentially protective factor in CKD. The current study aims to investigate whether sex disparity exists in the coffee–CKD association, and whether genetic risk of CKD or genetic polymorphisms of caffeine metabolism affect this association.Methods::A total of 359,906 participants from the UK Biobank who were enrolled between 2006 and 2010 were included in this prospective cohort study, which aimed to estimate the hazard ratios for coffee intake and incident CKD using a Cox proportional hazard model. Allele scores of CKD and caffeine metabolism were additionally adjusted for in a subsample with qualified genetic data ( n = 255,343). Analyses stratified by genetic predisposition, comorbidities, and sex hormones were performed. Tests based on Bayesian model averaging were conducted to ascertain the robustness of the results. Results::Coffee was inversely associated with CKD in a dose-dependent manner. The effects of coffee did not differ across different strata of genetic risk for CKD, but were more evident among slower genetically predicted caffeine metabolizers. Significant sex disparity was observed ( P value for interaction = 0.013), in that coffee drinking was only associated with the risk reduction of CKD in females. Subgroup analysis revealed that testosterone and sex hormone-binding globulin (SHBG), but not estradiol, modified the coffee–CKD association. Conclusions::In addition to the overall inverse coffee–CKD association that was observed in the general population, we could also establish that a sex disparity existed, in that females were more likely to experience the benefit of the association. Testosterone and SHBG may partly account for the sex disparity.

A 63-year-old maintenance hemodialysis patient with diabetic nephropathy was reported. The patient was incapacitated, with systemic edema, heart failure, severe anemia, malnutrition, gastrointestinal bleeding, and intractable hypertension. We adopted integrated management methods such as "multidisciplinary collaboration" and "doctor-patient collaboration": by accurately controlling the volume load to protect the residual renal function, taking into account the treatment of underlying diseases and complications, integrating the clinical parameters of dialysis and the interdialysis period, and combining the subjective clinical symptom score with the objective index analysis, the objectives of effectively controlling the dry weight of patients, alleviating complications, improving nutrition and protecting the residual renal function were finally achieved. The quality of life of the patient had been significantly improved.

Asians ; China/epidemiology* ; Humans ; Patient Discharge ; Patient Readmission

Objective:To investigate the effects and possible mechanisms of caffeic acid phenethyl ester (CAPE) on the replication, amplification, and fibre formation of prions (PrP Sc). Methods:The CCK8 assay was used to detect the cell viability of the prion-infected cell model SMB-S15 after CAPE treatment for 3 days and 7 days and the maximum safe concentration of CAPE for SMB-S15 was obtained. The cells were treated with a concentration within a safe range, and the content of PrP Sc in the cells before and after CAPE treatment was analyzed by western blot. Protein misfolding cycle amplification (PMCA) and western blot were used to assess changes in PrP Sc level in amplification products following CAPE treatment. Real-time-quaking induced conversion assay (RT-QuIC) technology was employed to explore the changes in fibril formation before and after CAPE treatment. The binding affinity between CAPE and murine recombinant full-length prion protein was determined using a molecular interaction assay. Results:CCK8 cell viability assay results demonstrated that treatment with 1 μmol/L CAPE for 3 and 7 days did not exhibit statistically significant differences in cell viability compared to the control group (all P<0.05). However, when the concentration of CAPE exceeded 1 μmol/L, a significant reduction in cell viability was observed in cells treated with CAPE for 3 and 7 days, compared to the control group (all P<0.05). Thus, 1 μmol/L was determined as the maximum safe concentration of CAPE treatment for SMB-S15 cells. The western blot results revealed that treatment with CAPE for both 3 and 7 days led to a detectable reduction in the levels of PrP Sc in SMB-S15 cells (all P<0.05). The products of PMCA experiments were assessed using western blot. The findings revealed a significant decrease in the levels of PrP Sc (relative grey value) in the PMCA amplification products of adapted-strains SMB-S15, 139A, and ME7 following treatment with CAPE, as compared to the control group (all P<0.05). The RT-QuIC experimental results demonstrated a reduction in fibril formation (as indicated by ThT peak values) in CAPE-treated mouse-adapted strains 139A, ME7, and SMB-S15, as well as in SMB-S15 cells infected with prions. Furthermore, CAPE exhibited varying degrees of inhibition towards different seed fibrils formation, with statistically significant differences observed (all P<0.05). Notably, CAPE exhibited a more pronounced inhibitory effect on ME7 seed fibrils. Molecular interaction analyses demonstrated significant binding between CAPE and murine recombinant prion protein, and the association constant was (2.92±0.41)×10 -6 mol/L. Conclusions:CAPE inhibits PrP Sc replication, amplification, and fibril formation in vitro possibly due to specific interactions with the prion protein at the molecular level.

Objective:To investigate the effects and possible mechanisms of caffeic acid phenethyl ester (CAPE) on the replication, amplification, and fibre formation of prions (PrP Sc). Methods:The CCK8 assay was used to detect the cell viability of the prion-infected cell model SMB-S15 after CAPE treatment for 3 days and 7 days and the maximum safe concentration of CAPE for SMB-S15 was obtained. The cells were treated with a concentration within a safe range, and the content of PrP Sc in the cells before and after CAPE treatment was analyzed by western blot. Protein misfolding cycle amplification (PMCA) and western blot were used to assess changes in PrP Sc level in amplification products following CAPE treatment. Real-time-quaking induced conversion assay (RT-QuIC) technology was employed to explore the changes in fibril formation before and after CAPE treatment. The binding affinity between CAPE and murine recombinant full-length prion protein was determined using a molecular interaction assay. Results:CCK8 cell viability assay results demonstrated that treatment with 1 μmol/L CAPE for 3 and 7 days did not exhibit statistically significant differences in cell viability compared to the control group (all P<0.05). However, when the concentration of CAPE exceeded 1 μmol/L, a significant reduction in cell viability was observed in cells treated with CAPE for 3 and 7 days, compared to the control group (all P<0.05). Thus, 1 μmol/L was determined as the maximum safe concentration of CAPE treatment for SMB-S15 cells. The western blot results revealed that treatment with CAPE for both 3 and 7 days led to a detectable reduction in the levels of PrP Sc in SMB-S15 cells (all P<0.05). The products of PMCA experiments were assessed using western blot. The findings revealed a significant decrease in the levels of PrP Sc (relative grey value) in the PMCA amplification products of adapted-strains SMB-S15, 139A, and ME7 following treatment with CAPE, as compared to the control group (all P<0.05). The RT-QuIC experimental results demonstrated a reduction in fibril formation (as indicated by ThT peak values) in CAPE-treated mouse-adapted strains 139A, ME7, and SMB-S15, as well as in SMB-S15 cells infected with prions. Furthermore, CAPE exhibited varying degrees of inhibition towards different seed fibrils formation, with statistically significant differences observed (all P<0.05). Notably, CAPE exhibited a more pronounced inhibitory effect on ME7 seed fibrils. Molecular interaction analyses demonstrated significant binding between CAPE and murine recombinant prion protein, and the association constant was (2.92±0.41)×10 -6 mol/L. Conclusions:CAPE inhibits PrP Sc replication, amplification, and fibril formation in vitro possibly due to specific interactions with the prion protein at the molecular level.