OBJECTIVE To determine the optimal therapeutic plan for metastatic hormone-sensitive prostate cancer （mHSPC）， and to provide reference for clinical decision-making. METHODS Retrieved from Medline， Embase， BIOSIS preview， the Cochrane Library and ClinicalTrials. gov systematically， randomized controlled trials about mHSPC therapy， with overall survival （OS） and radiographic progression-free survival （rPFS） as efficacy outcomes and the incidence of serious adverse events （SAEs） as safety outcome， were collected during the inception-Mar. 2022. Two researchers independently screened the literature， extracted data， and evaluated the risk of bias for the included study before conducting a Bayesian network meta-analysis. RESULTS Eight studies with 9 437 patients were finally included. The effectiveness and safety of 7 therapy plans were compared [abiraterone acetate， apalutamide， darolutamide+docetaxel， docetaxel， enzalutamide， standard non-steroidal antiandrogen （SNA） in addition to ADT， and ADT alone]. In terms of efficacy index， the most beneficial regimen （except for ADT+SNA） for OS was ADT+darolutamide+docetaxel （HR＝0.54， 95%CI of 0.44-0.66）， followed by ADT+abiraterone acetate （HR＝0.64，95%CI of 0.57- 0.71）， apalutamide （HR＝0.65， 95%CI of 0.53-0.79）， enzalutamide （HR＝0.66， 95%CI of 0.53-0.82）； the least beneficial regimen for OS was ADT+docetaxel （HR＝0.79， 95%CI of 0.71-0.88）. The most beneficial regimen （except for ADT+SNA） for rPFS was ADT+enzalutamide （HR＝0.39， 95%CI of 0.30-0.50）， followed by ADT+apalutamide （HR＝0.48， 95%CI of 0.39- 0.60）， abiraterone acetate （HR＝0.57， 95%CI of 0.51-0.64）， docetaxel （HR＝0.62， 95%CI of 0.56-0.69）. The results of the tumor- loading subgroup analysis were the same. In terms of safety， ADT+darolutamide+docetaxel （OR＝25.86， 95%CI of 14.08-51.33）， and ADT+docetaxel （OR＝23.35， 95%CI of 13.26-44.81） were associated with markedly increased SAEs； the incidence of SAEs caused by ADT+abiraterone acetate （OR＝1.42，95%CI of 1.10-1.82） was slightly increased， and those of other therapy plans had no significant difference. CONCLUSIONS Compared with ADT alone， ADT+ darolutamide+docetaxel may provide the most significant OS benefit， but the incidence of SAEs is increased greatly； compared with ADT+docetaxel， ADT+abiraterone acetate， apalutamide or enzalutamide provide more OS benefits. ADT+enzalutamide provide optimal rPFS benefits with no increased SAEs.

As an important branch of artificial intelligence,machine learning meets the demand for digital intelligence in prosthodon-tics with the rapid development and application of its algorithm.This review provides an overview of the application of machine learning algorithms in dental restoration,including the design of dental prostheses,tooth shade selection,and tooth preparation line detection.Additionally,this paper also briefly analyzes the merits of machine learning and discusses the challenges and issues in current re-search,to provide references for research on machine learning algorithms in prosthodontics.

BACKGROUND: Scar hypertrophy is always followed by the wound healing in burn and trauma. Endothelial cells play a key role in scar hypertrophy, so inhibitory growth of endothelial cells can relieve scar hypertrophy to a certain degree. OBJECTIVE: To construct a recombinant adenovirus vector expressing human endostatin (Ad/hEnd), and to investigate the cooperative effect of Ad/hEnd and keratinocyte on endothelial cell proliferation. DESIGN, TIME AND SETTING: Observational study, which was performed in the State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital of the Third Military Medical University of Chinese PLA between September 2006 and May 2007. MATERIALS: pAdTrack-CMV and pAdEasy-1 were obtained from Stratagene Company, USA; 293 cell and Ecoli.DH5α were stored in our laboratory. METHODS: The endostatin gene sequence was obtained by reverse transcription-polymerase chain reaction (RT-PCR) and polymerase chain reaction (PCR) based on mRNA of human fetal hepatic tissue and inserted into the adenovims shuttle plasmid pAdTrack-CMV to obtain recombinant plasmid pAdTrack-ES. After identification, positive recon was transformed into pAdeasy 1 recipient virus to screen positive clones. The adenovirus Ad/hEnd was generated from 293 cells and identified by PCR and fluorescence microscope. Then the keratinocytes were infected with Ad/hEnd, and co-cultured with endothelial cells by nest dish culture method. The content of endostatin was detected, and the non-transfection keratinocytes were used as the controls. MAIN OUTCOME MEASURES: Homologous recombination and identification of pAd/hEnd; generation and identification of Ad/hEnd; endostatin expression after 293 cell transfection; purification and titer measurement of Ad/hEnd; content of endostatin in culture solution; apoptotic percentage of endothelial cells; inhibitory ratio of endothelial cells. RESULTS: Ad/hEnd was constructed and the virus titer was generally up to 1.65×1012 PFU/L. Ad/hEnd-infected keratinocytes could effectively express and secrete endostatin of which the content reached 226 μg/L after 3 days of co-culture. The apoptotic percentage and inhibitory ratio of the endothelial cells co-cultured with Ad/hEnd-infected keratinocytes were significantly higher than those in control group (P<0.05). CONCLUSION: Ad/hEnd-infected keratinocytes co-cultured with endothelial cells can promote apoptosis and inhibit proliferation of endothelial cells through excretion of endostatin.

AIM：To investigate the change in myocardial mitochondrial Ca2＋ concentration (［Ca2+］m) and its mechanism in the early stage of severe burn. METHODS：An experimental model of 30%TBSA full-thickness skin scalding was reproduced in rats. ［Ca2+］m, cytosolic Ca2＋ concentration (［Ca2＋］c) and mitochondrial Ca2＋ transport velocity were determined. RESULTS: ① ［Ca2+］m increased evidently at 1st hour postburn, and continuously at 3rd hour, reached the peak at 6th hour postburn, then, it decreased at 12th and 24th hour, but remained in higher level than that of the control. ② There was no significant difference in ［Ca2＋］c between 1st hour postburn and the control, but ［Ca2＋］c increased evidently at 3rd, 6th, 12th, 24th hour postburn. ③ mitochondrial Ca2＋ uptake velocity at 1st hour postburn was higher than that of control, and Ca2＋ release velocity didn't change obviously, but both of them were decreased at 3rd, 6th, 12th, 24th hour postburn. ④ ［Ca2+］m was positive correlated with ［Ca2＋］c after burn, and negative correlated with mitochondrial Ca2＋ release velocity at 3rd, 6th, 12th, 24th hour postburn, respectively. CONCLUSION: There was obvious Ca2＋ overload in myocardial mitochondria after severe burn, the mechanism of which might include ascent of ［Ca2＋］c and disorder of Ca2＋ transport in mitochondria.

AIM: To study the role of mitochondrial nitric oxide synthase (mtNOS) in the damages of myocardial mitochondria during the early stage after severe burns.METHODS: An experimental model of 30% TBSA full-thickness skin scalding was reproduced in rats. Myocardial mitochondria were isolated from control and burned rats at 1, 3, 6, 12 and 24 h postburn. The mitochondrial respiratory function, content of mitochondrial calcium([Ca 2+ ] m) and activities of mtNOS and cytochrome c oxidase were determined. RESULTS: (1) Myocardial mitochondrial respiratory control rate(RCR) at 1 h was evidently higher than that of control, but at 3, 6, 12 and 24 h postburn, it was significantly lower than that of the control. The changes in ST 3 is parallel to those of RCR, and ST 4 was evidently increased only at 3 h postburn. (2) [Ca 2+ ] m was higher at all time points postburn and the activity of mtNOS was higher significantly only at 3, 6, 12 and 24 h than that of the control. The activity of cytochrome c oxidase at the 3, 6, 12 and 24 h was low comparing to the control. (3) After severe burns, RCR was negatively correlated with mtNOS activity( r=0.9347, P

AIM:To investigate the change in myocardial mitochondrial Ca 2+ concentration ([Ca 2+ ] m) and its mechanism in the early stage of severe burn. METHODS:An experimental model of 30%TBSA full-thickness skin scalding was reproduced in rats. [Ca 2+ ] m, cytosolic Ca 2+ concentration ([Ca 2+ ] c) and mitochondrial Ca 2+ transport velocity were determined. RESULTS: ① [Ca 2+ ] m increased evidently at 1st hour postburn, and continuously at 3rd hour, reached the peak at 6th hour postburn, then, it decreased at 12th and 24th hour, but remained in higher level than that of the control. ② There was no significant difference in [Ca 2+ ] c between 1st hour postburn and the control, but [Ca 2+ ] c increased evidently at 3rd, 6th, 12th, 24th hour postburn. ③ mitochondrial Ca 2+ uptake velocity at 1st hour postburn was higher than that of control, and Ca 2+ release velocity didn't change obviously, but both of them were decreased at 3rd, 6th, 12th, 24th hour postburn. ④ [Ca 2+ ] m was positive correlated with [Ca 2+ ] c after burn, and negative correlated with mitochondrial Ca 2+ release velocity at 3rd, 6th, 12th, 24th hour postburn, respectively. CONCLUSION: There was obvious Ca 2+ overload in myocardial mitochondria after severe burn, the mechanism of which might include ascent of [Ca 2+ ] c and disorder of Ca 2+ transport in mitochondria. [