Objective To discuss the interactive management mode (IMM) of preventive treatment on osteoporosis self-rehabilitation of rural elderly residents.Methods IMM was used to manage osteoporosis patients in the community of Changshu,and general self-efficacy scale was adopted for evaluation.Results Self-efficacy score (34.2) increased comparing with before(23.5 ) the medical management,the difference was statistically significant ( P＜0.05 ).Conclusion IMM of preventive treatment can effectively improve the rural community general self-efficacy level.

Objective To investigate the changes in nunmber and function of natural killer ( NK ) cells in patients with newly-diagnosed type 1 diabetes mellitus.Methods Cell courning was performed in peripheral blood mononuclear cell ( PBMC ) subsets in 43 cases with newly diagnosed type 1 diabetes ( T1D ),14 cases with newly diagnosed type 2 diabetes( T2D ) and 21 cases of normal controls by flow cytometry sorting.And then,isolating and collecting NK cells were performed in T1D patients and normal controls.Real time PCR was performed to evaluate the mRNA expression levels of NK cell activity related genes IFN-γ,perforin,NKp46,and NKp30 in NK cells.Results Compared to normal controls,both the proportion and the absolute counting of NK cells in PBMC from patients with T1D were significantly decreased [( 102±86 )/μl vs ( 355±264 )/μ1,P＜0.01],while only the proportion of CD4+ cell were slightly increased( P＜0.05 ).No statistical difference was observed regarding CD8+ T cells ( P＞0.05 ).mRNA expression levels of NK cell activity related genes perforin and NKp46 in NK cells were remarkably down-regulated ( P＜0.05 ),while IFN-γ and NKp30 were not changed compared with normal controls.Conclusions The reduced number and functional deficiency of NK cells may lead to the immune dysfunction in T1D and play an important role in the development of T1D.

Pleomorphic adenoma (PA) is the most common benign tumour in the salivary gland and has high morphological complexity. However, the origin and intratumoral heterogeneity of PA are largely unknown. Here, we constructed a comprehensive atlas of PA at single-cell resolution and showed that PA exhibited five tumour subpopulations, three recapitulating the epithelial states of the normal parotid gland, and two PA-specific epithelial cell (PASE) populations unique to tumours. Then, six subgroups of PASE cells were identified, which varied in epithelium, bone, immune, metabolism, stemness and cell cycle signatures. Moreover, we revealed that CD36⁺ myoepithelial cells were the tumour-initiating cells (TICs) in PA, and were dominated by the PI3K-AKT pathway. Targeting the PI3K-AKT pathway significantly inhibited CD36⁺ myoepithelial cell-derived tumour spheres and the growth of PA organoids. Our results provide new insights into the diversity and origin of PA, offering an important clinical implication for targeting the PI3K-AKT signalling pathway in PA treatment.
Humans ; Adenoma, Pleomorphic/genetics* ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; Transcriptome ; Myoepithelioma

Diabetic neuropathic pain (DNP) is the most common disabling complication of diabetes. Emerging evidence has linked the pathogenesis of DNP to the aberrant sprouting of sensory axons into the epidermal area; however, the underlying molecular events remain poorly understood. Here we found that an axon guidance molecule, Netrin-3 (Ntn-3), was expressed in the sensory neurons of mouse dorsal root ganglia (DRGs), and downregulation of Ntn-3 expression was highly correlated with the severity of DNP in a diabetic mouse model. Genetic ablation of Ntn-3 increased the intra-epidermal sprouting of sensory axons and worsened the DNP in diabetic mice. In contrast, the elevation of Ntn-3 levels in DRGs significantly inhibited the intra-epidermal axon sprouting and alleviated DNP in diabetic mice. In conclusion, our studies identified Ntn-3 as an important regulator of DNP pathogenesis by gating the aberrant sprouting of sensory axons, indicating that Ntn-3 is a potential druggable target for DNP treatment.
Mice ; Animals ; Diabetes Mellitus, Experimental/metabolism* ; Axons/physiology* ; Diabetic Neuropathies ; Sensory Receptor Cells/metabolism* ; Neuralgia/metabolism*