BACKGROUND:Different mechanical stimulations may have an effect on the level of metabolism of chondrocytes, but the effect is not clear.
OBJECTIVE:To investigate expression level changes in metabolic genes that participate in cartilage cel decomposition and synthesis under compressive stress and tensile stress conditions.
METHODS:We obtained articular chondrocytes from 2-week-old Sprague-Dawley rats. Primary cultured chondrocytes were identified. Passage one chondrocytes received cyclic tensile stress and cyclic compressive stress of 3%and 7%, respectively, so as to measure articular changes in chondrocytes-related genes.
RESULTS AND CONCLUSION:When chondrocytes were subjected to cyclic tensile stress of 3%, synthetic metabolic gene col agen types I and II and proteoglycan mRNA expression levels were decreased. If 3%cyclic compressive stress was applied, proteoglycan mRNA expression levels were increased, and type I col agen mRNA expression levels were decreased (P<0.001), and matrix metal oproteinase-13 mRNA expression levels were reduced (P<0.01). When strain reached 7%, cyclic tensile stress and compressive stress could lead to a general decrease in anabolism-related genes. The former could also make matrix metal oproteinase-13 mRNA expression levels increased (P<0.05). 3%cyclic compression ratio and 3%cyclic stretch made cytoskeleton become oval. These results indicated that in vitro, proper cyclic compressive stress is beneficial to maintain the growth characteristics of articular chondrocytes in rats. Smal tensile stress can decrease the synthesis ability of chondrocytes. The effect of stress may be caused by changing the cytoskeleton.

BACKGROUND:It is wel-known that mechanical stimulation could promote fracture healing. However, what kind of mechanical stimulation induced by treadmil exercise can increase the bone conductibility of bone material and promote the healing of bone defect is stil unclear.
OBJECTIVE:To evaluate the influence of indirect mechanical stimulation produced by treadmil exercise on bone defect healing and osteogenesis of bone materials.
METHODS:Sprague-Dawley rats at 12 weeks old were used in this study to establish a bone defect of 3 mm in diameter and height at the left distal femur. Afterwards, calcium sulphate scaffolds were implanted into the defects. The rats were divided into treadmil exercise group and control group. Treadmil exercise was began at 1 week postoperatively, 10 m/min, 45 minutes per day, 5 days per week, for 3 weeks. Control group did not receive any exercise. Micro-computed tomography was used to determine bone formation in the bone defects at 1, 2, 3, and 4 weeks after surgery. The sections of left distal femur were subject to hematoxylin-eosin staining, the new bone formation and degradation of bone materials in the bone defects were observed.
RESULTS AND CONCLUSION:Micro-CT analysis showed that, a smal amount of new bone formed in both treadmil exercise group and control group at 1 week after surgery. In treadmil exercise group, new bone formation was significantly higher than the control group at 2, 3, 4 weeks (P<0.05). At 4 weeks, histological results also confirmed the difference of new bone formation in bone defect between treadmil exercise group and control group. In addition, bone mineral density of treadmil exercise group was higher than that of control group at 2, 3, 4 weeks, but no significant difference was found (P>0.05). The results suggest that moderate treadmil exercise could promote bone defect healing and enhance osteoconductivity of bone substitute.

Objective To study the closure time of neonatal ductus venosus and the Z score regression equation, and to explore the variation of closure time of neonatal ductus venosus with gestationalage.Methods Color doppler ultrasound was applied to detect the closure time of neonatal ductus venosus in normal newborns, Z score regression equation ( lnY =a +bX +cX2 ) for the closure time of neonatal ductus venosus ( Y ) was developed by regression analysis which used gestational age ( X) as an independent variable. The Z scores of the closure time of neonatal ductus venosus in different gestational age were calculated by the formula [ Z = ( M - Y )/S x , M for observation value, Y for predictivevalue].Results There were 432 cases in our study.The closure time of neonatal ductus venosus was negatively related to gestational age ( r = -0. 938 , P <0. 001 ) . The nonlinear regression equation was lnY= -5. 228+0. 089X-0. 000228X2, R2 =0. 854, Sx =0. 214(P<0. 001). Based on the predicted mean of the closure time and Sx related to different gestational age, Z scores for specific closure time of neonatal ductus venosus could be calculated by the formula [ Z =( M -Y)/Sx ] . The Z scores were normally distributed,and did not change with gestational age.Conclusions Theclosure & nbsp;time of neonatal ductus venosus is negatively related to gestational age. The Z scores obtained by the predicted nonlinear regression equation are normally distributed.

Objective Definition Chiasm of crus penis and discuss its possible role in penile erection. Methods Penile samples were acquired from 15 formalin preserved corpses.The structure located among crus penises were observed.The information about the structure located in crus penises with the nerve and blood vessel structure were recorded and analyzed. Results There was a structure of muscle fiber of ischiocavernosus among the crus penises.These muscle fiber through muscle bundle and tendon reach albuginea of cavernous body of the penis.There was long muscle fiber in the lateral surface of crus penises.While the muscle bundles were interlaced with each other with opposite side homonymous muscle and were encased with connective tissue when it reach to the back side of cavernous body of the penis.There were nerves and blood vessels observed in and out of the cavernous body of the penis and through the above structure in the crus penises. Conclusions Chiasm of crus penis was named as a structure of muscle fiber coming from two sides of the ischiocavernosus in crus penises.The structure of Chiasm of crus penis may provide an internal connection for the role of controlling the erection of the penis.

BACKGROUND:Traction is clinically used for the early treatment of intervertebral disc degeneration,but its effect on the normal intervertebral disc remains unknown.Whether it directly causes intervertebral disc degeneration or has a positive effect is the key point of this study. OBJECTIVE:To design a static traction model and observe the effect of static traction on the nucleus pulposus and annulus fibrosus of the intervertebral disc METHODS:Twenty Sprague-Dawley rats,3 months of age,were included in the study.The intervertebral disc spaces between 7/8,8/9 and 9/10 were stretched by 1 mm,and the intervertebral disc spaces between 6/7 and 10/11 were used as control.Five rats were randomly selected at 2,4,6,and 8 weeks of traction to perform MRI T2-weighted scans of the caudal vertebra,tissue section staining,and RT-PCR gene assays for anabolic metabolism to observe the effects of static traction on the nucleus pulposus and annulus fibrosus of the intervertebral disc. RESULTS AND CONCLUSION:After short-term static traction of the rat caudal vertebra,the T2-weighted image signal in the nucleus pulposus region was enhanced.During the traction period,nucleus pulposus cells grew well,the intercellular matrix was abundant,and the annulus fibrosus arranged regularly.The RT-PCR results showed that after traction,the mRNA expression of proteoglycan increased,the expression of matrix metalloproteinase-3 decreased,the expression of type Ⅰ and Ⅱ collagen decreased,and the expression of matrix metalloproteinase-13 increased and tissue inhibitor of matrix metalloproteinase 1 increased.These gene results also indicated that traction made proteoglycan more inclined to an anabolic state,and type Ⅰ and Ⅱ collagen more inclined to a catabolic state.To conclude,static traction promotes proteoglycan anabolism making the nucleus pulposus moist.

BACKGROUND:Many factors can cause disc degeneration,including aging,nutritional deficiency,and mechanical factors.The mechanical load is considered to be a very important factor,but its mechanism is still unclear. OBJECTIVE:To investigate the role of sclerostin(SOST)and Wnt/β-catenin signaling pathways in inducing degeneration of endplate cartilage. METHODS:Cartilage endplate cells were extracted from 4-week-old male Sprague-Dawley rats.Compressive stress was applied to endplate chondrocytes in vitro using a mechanical loading apparatus,and the cell viability was determined by the cell counting kit-8 assay at 1,3,5,and 7 days after compression.Western blot,reverse transcription quantitative PCR,and cellular immunofluorescence techniques were employed to examine intracellular cartilage markers(Aggrecan and type Ⅱ collagen)as well as calcification-related factors(Runx2 and osteocalcin).The expression of extracellular matrix degradation enzyme and genes related to the signaling pathway(SOST and β-catenin)was also analyzed. RESULTS AND CONCLUSION:Under compressive stress,the cell activity of endplate chondrocytes increased with both the duration and intensity of stress.Furthermore,the expression levels of Aggrecan and type Ⅱ collagen decreased in endplate cells under compressive stress,while those of calcification-related factors(Runx2 and osteocalcin)increased.Additionally,compressive stress promoted extracellular matrix degradation in endplate chondrocytes,leading to an increase in matrix metalloproteinase 3 and matrix metalloproteinase 13 expression.Abnormalities were observed in the Wnt/β-catenin signaling pathway within these cells under compressive stress,characterized by a decrease in specific inhibitory factor SOST expression accompanied by abnormal accumulation of β-catenin.To conclude,decreased SOST expression in endplate chondrocytes under compressive stress activates the Wnt/β-catenin signaling pathway,thereby promoting calcification,degeneration and extracellular matrix degradation in the cartilage endplate.

BACKGROUND:Numerous studies have shown that mechanical stimulation is essential for the lineage-specific differentiation of bone marrow mesenchymal stem cells.However,osteogenic differentiation of bone marrow mesenchymal stem cells on surfaces with different roughnesses under mechanical stretching conditions is unknown. OBJECTIVE:To investigate the effects and action mechanisms of different roughness surfaces of polydimethylsiloxane(PDMS)on osteogenic differentiation of bone marrow mesenchymal stem cells under stretching conditions. METHODS:Three morphologies with different roughnesses(PDMS-120M,PDMS-1000M,and PDMS-10000M)were constructed on PDMS surfaces by means of different grits of sandpaper(120 grits,1 000 grits and 10 000 grits),and PDMS surfaces in contact with air served as a control group.With different amplitudes of 0%,2%,4%,and 6%,osteogenesis-related gene expression of bone marrow mesenchymal stem cells on different PDMS surfaces under static and stretching conditions was detected by RT-qPCR.RT-qPCR and western blot assay were used to detect the expression of SIRT1 gene and protein as well as osteogenesis-related genes and proteins in bone marrow mesenchymal stem cells on different roughness surfaces under 2%stretching conditions.Alkaline phosphatase staining and alizarin red staining were further used to observe the osteogenic differentiation ability of bone marrow mesenchymal stem cells on different PDMS surfaces under 2%stretching conditions. RESULTS AND CONCLUSION:(1)Bone marrow mesenchymal stem cells on the PDMS-1000M surface with a roughness of(13.51±2.11)μm had better osteogenic gene expression under static conditions.(2)Bone marrow mesenchymal stem cells on the PDMS surface in contact with air had better osteogenic differentiation under 4%stretching conditions,while bone marrow mesenchymal stem cells on the PDMS-1000M surface had better osteogenic differentiation under 2%stretching conditions.(3)Bone marrow mesenchymal stem cells on the PDMS-1000M surface with a roughness of(13.51±2.11)μm had better osteogenic differentiation under 2%stretching conditions,which may be related to activation of SIRT1 signaling pathway.