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Background: Conventional MR imaging has limited value in identifying H3 K27M mutations. We aimed to investigate the capacity of quantitative MR imaging variables in identifying the H3 K27M mutation status of diffuse midline glioma. Materials and Methods: Twenty-three patients with H3 K27M mutation and thirty-two wild-type patients were recruited in this retrospective study, all of whom underwent multimodal MR imaging. Clinical data and quantitative MR imaging variables were explored by subgroup analysis stratified by age (juveniles and adults). Then, a logistic model for all patients was constructed to identify potential variables for predicting K27M mutation status. Besides, a retrospective validation set including 13 patients was recruited. The C-index and F1 score were used to evaluate the performance of the prediction model. Results: It turned out that patients with H3 K27M mutation were younger in the adult subgroup. In the mutation group, some relative apparent diffusion coefficient (rADC) histogram parameters and myo-inositol/creatine plus phosphocreatine (Ins/tCr) ratio were lower than in the wild-type group of both juveniles and adults (p < 0.05). After nested cross-validation and LASSO algorithm, the age, Ins/tCr, and rADC_15th were selected as potential predictors for H3 K27M mutation in the model. The nomogram model showed good diagnostic power with a validated C-index of 0.884. In addition, the area under the curve (AUC) was 0.898 (0.976 in validation set) and the F1 score was 0.732. Conclusions: In conclusion, age, rADC_15th, and Ins/tCr values were helpful in identifying H3 K27M mutations in midline gliomas. [ABSTRACT FROM AUTHOR]

Aim: Many strategies are explored to ameliorate kidney allograft tubular atrophy and interstitial fibrosis (TA/IF), but little progress has been achieved. The latest evidence suggested that CD133+ cell in kidney represent a potential multipotent adult resident stem cell population that may contribute to the renal injury repair. Here we investigate whether the CD133+ cells exist in transplanted renal and exert a growth and self-repair procedure in TA/IF. Methods: Allografts from rat kidney transplant models were harvested at 4 weeks, 8 weeks and 12 weeks post transplantation. We performed immunohistochemistry to detect the CD133+ cells and immunofluorescence to detect the co-expression of CD133 or Pax-2 with Ki-67. We furthermore analysed the E-cadherin using serial sections. Results: CD133+ cells were seldom seen in control kidney, but distributed sporadically in the cortex parenchyma along with the deterioration of TA/IF. The number of CD133+ cell increased after 4 weeks and reached the peak at 8 weeks, then decreased at 12 weeks. From 8 weeks, some new tubules expressing E-cadherin were constructed with CD133+ cells. Almost all the CD133+ cells were Ki-67-positive, but not all the Ki-67+ cells expressed CD133. The rest Ki-67+ cells almost expressed Pax-2. Conclusion: Our study reveals that when majority of the tubules are damaged, a self-repair mechanism is evoked by potential adult stem cells to compensate the renal function. Thus, potential adult resident stem cells offer a new avenue for autologous cell therapies in TA/IF. [ABSTRACT FROM AUTHOR]