Objective To investigate the effect of sensory and motor nerve homogenates at different concentrations on the proliferation and osteogenesis differentiation of bone marrow mesenchymal stem cells (BMSCs) in rats.Methods The saphenous nerve and the muscle branch of the sciatic nerve in rats were extracted surgically as sensory and motor nerve tissues,respectively.The primary nerve homogenates (10 mg/mL) were prepared as per 10 mg tissue with 1 mL osteoblast inducing conditional media,and 10 times diluted after filtration purification to prepare sensory and motor nerve homogenates at concentration gradients of 1.0,0.1,0.01,0.001 and 0.0001 mg/mL.Cultivation GFP ± rat pups BMSCs in vitro were trained to P3 generation.The experiment was carried out in 3 groups.The sensory and motor nerve homogenates of 500 μL at the above 6 concentration gradients were added during cultivation respectively in the sensory nerve group (n =18) and the motor nerve group(n =18) while 500 μL of osteoblast inducing conditional media was added in the control group(n =3).Cell proliferation quantity detection and alkaline phosphatase (ALP) staining were used to assess the proliferation and differentiation of BMSCs after 14 days.Results According to the results of CCK-8,the cellular absorbance values at concentrations of 1.0 and 0.1 mg/mL homogenate in the sensory nerve group (1.957 ±0.065 and 1.751±0.073) were significantly greater than in the control group (1.145±0.087) while the cellular absorbance value at concentration of 10.0 mg/mL homogenate in the motor nerve group (0.304 ± 0.619) was significandy smaller than in the control group (1.145 ± 0.087) (P ＜ 0.05).According to the ALP staining,the amounts of cellular calcium nodules in the sensory and motor nerve groups (2.667 ± 0.816 and 3.000 ± 0.632,respectively) were significantly smaller than in the control group (11.833 ± 1.471) (P ＜ 0.05).Conclusion Sensory nerve homogenate is different from motor nerve homogenate in that it may promote proliferation of BMSCs and inhibit osteogenesis differentiation of BMSCs in a certain rage of concentrations.

Objective To investigate the effect of prevascularized tissue-engineered bone graft on regeneration of femoral bone defects in rats.Methods Models of femoral bone defect were created at the bilateral hind limbs of 20 healthy female 10 week-old rats which were divided into 2 even groups randomly (n =10).In group A,conventional tissue-engineered bone grafts were transplanted into the femoral bone defects;in group B,tissue-engineered bone grafts and vascular bundles were implanted into the femoral defects.At 1,4 and 8 weeks after operation,3 rats were sacrificed each time in each group to harvest samples.The remaining one in each group served as a spare animal.Regeneration of bone defects and degradation of scaffolds were assessed by radiologic modality and hematein eosin staining.Results At week 1,the new bone ratio (BV/TV) was 5.47％ ± 1.90％ in group A and 8.49％ ± 1.26％ in group B,showing no significant difference (P ＞ 0.05);at weeks 4 & 8,the BV/TV were 17.54％ ±2.04％ and 39.73％ ± 4.01％ in group A,significantly lower than those in group B (25.32％ ± 2.15％ and 53.22％ ± 2.94％) (P ＜ 0.05).At weeks 1 & 4,the scaffold degradation ratios (RSV/SV) were 97.33％ ± 2.52％ and 80.60％ ±4.00％,showing no significant differences from those in group B (95.67％ ±3.51％ and 75.22％ ±6.20％) (P ＞ 0.05).At week 8,the scaffold degradation ratio in group A (65.46％ ±4.51％) was significantly higher than that in group B (50.19％ ±4.91％) (P ＜ 0.05).At week 8,hematein eosin staining showed better integration of scaffolds with the femur,faster degradation of the interior scaffolds and greater osteogenetic activity in group B.Conclusion Prevascularization of tissue-engineered bone graft may increase new bone volume and scaffold degradation rate,promoting repair of femoral bone defects in rats.

Objective:To investigate the clinical features,differential diagnosis and treatment of intravascular NK/T cell lymphoma.Methods:The clinical data and diagnosis and treatment process of 2 patients with intravascular NK/T cell lymphoma admitted to Chongqing University Cancer Hospital were retrospectively analyzed, and related literatures were reviewed.Results:Both patients were initially presented with cutaneous symptoms. Patient 1 was diagnosed with intravascular NK/T cell lymphoma, and received 4 courses of programmed-death receptor 1 (PD-1) inhibitor toripalimab + P-Gemox (pegaspargase + gemcitabine + oxaliplatin) regimen, 1 course of PD-1 + ME (toripalimab + mitoxantrone + etoposide) regimen and then underwent autologous hematopoietic stem cell transplantation; patient 2 was diagnosed with intravascular NK/T cell lymphoma involving the nasal cavity, and received 4 courses of P-Gemox regimen, and then received autologous hematopoietic stem cell transplantation in the other hospital. Both patients achieved good therapeutic efficacy.Conclusions:Intravascular NK/T cell lymphoma is very rare, frequently involving the skin and central nervous system. Intravascular growth of tumor cells derived from NK cells is the key point of diagnosis and differential diagnosis. P-Gemox regimen and hematopoietic stem cell transplantation could bring better curative effect.

Gene therapy represents a promising treatment for the Alzheimer׳s disease (AD). However, gene delivery specific to brain lesions through systemic administration remains big challenge. In our previous work, we have developed an siRNA nanocomplex able to be specifically delivered to the amyloid plaques through surface modification with both CGN peptide for the blood-brain barrier (BBB) penetration and QSH peptide for -amyloid binding. But, whether the as-designed nanocomplex could indeed improve the gene accumulation in the impaired neuron cells and ameliorate AD-associated symptoms remains further study. Herein, we prepared the nanocomplexes with an siRNA against -site amyloid precursor protein-cleaving enzyme 1 (BACE1), the rate-limiting enzyme of A production, as the therapeutic siRNA of AD. The nanocomplexes exhibited high distribution in the A deposits-enriched hippocampus, especially in the neurons near the amyloid plaques after intravenous administration. In APP/PS1 transgenic mice, the nanocomplexes down-regulated BACE1 in both mRNA and protein levels, as well as A and amyloid plaques to the level of wild-type mice. Moreover, the nanocomplexes significantly increased the level of synaptophysin and rescued memory loss of the AD transgenic mice without hematological or histological toxicity. Taken together, this work presented direct evidences that the design of precise gene delivery to the AD lesions markedly improves the therapeutic outcome.