CD133 has been confirmed as a stem cell surface marker in a variety of tumors.Specific markers of cancer stem cells in the thyroid cancer are not yet clear.Results of some studies showed that expression of CD133 was found in undifferentiated thyroid cancer cells which had the characteristics of stem cells.Those cells had the ability to self-renewal,multi-directional differentiation,potential development to cancer,and radio-and chemotherapy resistance.This article mainly views the progresses of CD133 in thyroid cancer research.

Objective To evaluate the efficacy of 90Sr-90Y applicator treatment for hemangioma by superficial ultrasound.Methods A total of 94 infants with hemangioma were retrospectively analyzed,including 37 males and 57 females (age range:1-12 months,mean =4.5 months).Thickness of hemangioma was measured by superficial ultrasound on the day before 90Sr-90Y applicator treatment,10 d and 3 months after treatment.Paired t test and x2 test were used to analyze data.ROC curve was analyzed to determine the tumor thickness which could be cured by one-cycle of treatment.Results Sixty-two cases were cured,29 cases had partial response and 3 cases had treatment failure.Thickness of hemangioma was (0.38 ±0.28)cm before treatment and (0.16±0.35) cm 3 months post-treatment and the difference was statistically significant (t=7.377,P＜0.05).The treatment effect of 90Sr-90Y applicator was not influenced by gender.According to the site of hemangioma,the curative rates were 20/38 in head & neck,22/33 in chest,20/23 in limbs.Only the difference between the curative rates in head & neck and limbs was statistically significant (x2 =7.478,P＜0.05).The treatment effect of 90Sr-90Y applicator was evaluated by the thickness of hemangioma under the skin at 3 months post-treatment and the area under the ROC was 0.93.The threshold of the thickness of hemangioma which could be cured by one-cycle of treatment was 0.32 cm with the sensitivity of 93.8％ and specificity of 85.5％.Conclusions The 90Sr-90Y applicator had a good treatment effect on pure hemangioma in infants,especially for those located in limbs and torso.The lesion with thickness less than 0.32 cm had a higher chance to be cured by one-cycle of treatment.

Objective To investigate the mechanism and role of ?-ray of 103Pd in the treatment of biliary duct cancer.Methods A series of biliary duct cancer cells were treated with different ?-ray dose,and MTT [3-(4,5-dimethy thiazol-2-yl)-2,5-diphenyl terazolium-bromide] technique was used to determine the inhibition rate of ?-ray of 103Pd on the biliary duct cancer cells;and electron micro-technique,DNA agarose gel electrophoresis and flow cytometry to evaluate the morphological characteristics and apoptosis rate of the biliary duct cancer cells were also used.Results The ?-ray radiation of 103Pd resulted in significant inhibition of the biliary duct cancer cells.The features of biliary duct cancer cells apoptosis(e,g:apoptic bodies,DNA ladders band hypodiploid DNA peak) could be seen in the group with lower dosage(5.333mci),and cell necrosis was seen in higher dosage(more than 6.645 mci).Conclusions The ?-ray radiation could induce apoptosis of the biliary duct cancer cells,but with dose dependence,and apoptosis can be an important mechanism for radiation treatment of biliary duct cancer.

Objective To study the effect of BCL-2 ?-radiation on BCL-2 gene in dogs, and its relationship and signifcane on apoptosis of proliferated smooth muscle cells of bile duct wall. Methods The ~(103)Pd (radioactivity) stent(experiment group) or ordinary stent(control group) was positioned into the target segment of bile duct. The injured bile duct segments were dissected free from the dogs, and BCL-2 gene in the (control) and r-radiation-induced apoptotic smooth mucle cells of bile duct wall was analysed by using (immuno-histochemical) technique. The number of apoptotic cells was counted, and size of lumen of bile duct in both groups was measured by a computerized imaging system.Results BCL-2 gene expression was weaker in the ~(103)Pd radioactive stent group than in the ordinary stent group. The group of dogs with low expression of BCL-2 genes showed marked apoptosis of proliferated smooth mucle cells of bile duct and there was no overt stenosis of extrahepatic bile ducts. The group that showed high expression of BCL-2 gene did not show marked apoptosisi of proliferated smooth muscle cells of bile duct, and there was marked stenosis of extrahepatic bile duct.Conclusions The expression level of BCL-2 in experimental dogs is related to the develoment of (cellular) apoptosis and to radiation sensitivity of the cells. ~(103)Pd radioactive stent can reduce the expression of BCL-2 gene, promote apoptosis of proliferated smooth muscle cells of bile duct, and suppress stricture (formation) of extrahepatic bile duct.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.