Objective To explore ways to improve effect of antiretroviral therapy in acquired immune defi-ciency syndrome patients with comorbid malnutrition, in an effort to enhance quality of life and reduce cost. Methods 126 AIDS patients with comorbid malnutrition were randomly divided into treatment group ( n=63) and control group (n=63). Patients in the treatment group were given nutrition support besides antiretroviral ther-apy (ART), while those in the control group only received ART. After 3 months, the two groups were compared in terms of body mass index, skinfold thickness, CD4+T cell count and human immunodeficiency virus load. Re-sults The two groups were comparable before treatment in BMI, skinfold thickness, CD4+T cell count and HIV load (P>0. 05). After treatment, the treatment group, compared with the controls, had higher BMI [ (23. 23± 3. 15) kg/m2vs. (17. 25±1. 83) kg/m2], thicker skinfold [ (42. 9±6. 8) mm vs. (34. 5±5. 2) mm in males;(97. 6±17. 4) mm vs. (92. 3±14. 7) mm in females], higher CD4+T cell count (χ2=12. 573, P<0. 01), and lower HIV load (χ2=8. 683, P<0. 01). Conclusion Nutrition support may improve treatment of AIDS patients with comorbid malnutrition, as manifested in better BMI, skinfold thickness, CD4+T cell count and HIV load.

Ameloblastoma is a benign tumor characterized by locally invasive phenotypes,leading to facial bone destruction and a high recurrence rate.However,the mechanisms governing tumor initiation and recurrence are poorly understood.Here,we uncovered cellular landscapes and mechanisms that underlie tumor recurrence in ameloblastoma at single-cell resolution.Our results revealed that ameloblastoma exhibits five tumor subpopulations varying with respect to immune response(IR),bone remodeling(BR),tooth development(TD),epithelial development(ED),and cell cycle(CC)signatures.Of note,we found that CC ameloblastoma cells were endowed with stemness and contributed to tumor recurrence,which was dominated by the EZH2-mediated program.Targeting EZH2 effectively eliminated CC ameloblastoma cells and inhibited tumor growth in ameloblastoma patient-derived organoids.These data described the tumor subpopulation and clarified the identity,function,and regulatory mechanism of CC ameloblastoma cells,providing a potential therapeutic target for ameloblastoma.