BACKGROUND: Bone cement coated by different materials has various characteristics and causes varying therapeutic effects. OBJECTIVE: By comparing characteristics of CPC, CPC/D, and CPC/M/D3 to investigate the preparation of doxorubicin microspheres-coated bone cement. METHODS: Doxorubicin microspheres were prepared with multiple emulsion solvent volatilixation method. Doxorubicin microspheres were mixed with CPC as the ratio of 3:7 to prepare doxorubicin microspheres-coated bone cement. The samples were randomly divided into three groups: CPC group, containing bone cement alone; CPC/D group, containing doxorubicin;CPC/M/D group, containing doxorubicin microspheres. Scanning electron microscope at varying magnification was used to observe structural characteristics and measure the diameter of microspheres. X-ray diffraction was used to estimate the extent of CPC and CPC/M/D samples. The initial and final setting time of cement samples in the three different groups was measured at 25 ℃ and 37℃ respectively. The injectability and interval porosity of different samples were tested. The compressive strength of the specimens was measured using a universal material testing machine to record the maximal compressive strength and breaking strength. RESULTS AND CONCLUSION: PLGA microspheres (100-150 μm) were globular and the surface was slick and sly. Micrestructure of bone cement was not obviously changed following mixing with drugs, thus the location and characteristics of drugs in bone cement were not determined. Micrespheres-coated bone cement (100-150 μm) was distributed among CPC powder. All the X-ray diffraction pattern of three different samples was in coincidence with standard X-ray diffraction pattern of hydroxyapatite, i.e., the major peak was located near 32°. Additional drugs and microspheres did not cause new phases. Obvious collapsing was not observed in the three samples following immediately adding in saline, but the collapsing appeared in both CPC/D and CPC/M/D samples after 24 hours. The setting-up time of CPC/M/D was the longest, but that of CPC was the shortest. On the other hand, the setting-up time was the longest at 37℃. The final setting-up time of CPC/M/D group was 45 minutes. The doxorubicin microspheres-coated bone cement showed the best property of injectability among the three kinds of cement. The interval porosity was the highest in the CPC/M/D group but the lowest in the CPC group. Interval porosity of doxorubicin microspheres-coated bone cement was up to 61.67%. The yield stress was the strongest in the CPC group but the weakest in the CPC/M/D group. Additionally, the yield stress of calcium phosphate cement dramatically decreased while doxrorubicin microspheres were coated. However, there was no significant difference between them. The preparation of doxorubicin microspheres-coated bone cement was reliable and the product had good structures and properties.

Objective To study the value of three dimensional dynamic contrast and digital subtraction MRI in diagnosing breast cancer.Methods 52 patients with breast diseases were enrolled in this study,including 27 malignant lesions and 36 benign lesions verified by histopathology.the morphologic features and enhancement kinetics of breast lesion on MRI were observed.The morphologic manifestation,early-phase enhancement rate,peak enhancement rate,peak time and time-signal intensity curve were evaluated.Results The benign lesions were mainly characterized by regular mass,well-defined border,internal septation,homogeneous enhancement,and the malignant lesions by irregular shape,speculated margin,rim enhancement,inhomogeneous enhancement.The early-phase enhancement rate,peak time and curve type were significantly different between breast benign and malignant lesions(P

Objective To discuss the effect of H2 on osteoclast differentiation of RAW264.7 cells induced by RANKL and RANKL/TNF-α.MethodsRAW264.7 cells were treated with H2 in the presence of RANKL and RANKL/TNF-α.RAW264.7 cells viability was assessed by CCK-8.Test the Oxidative Stress of the induced RAW264.7.The number of TRAP-positive cells were counted under light microscopy.The levels of cathepsin K (CTK) and matrix metalloprotein-9(MMP-9) mRNA were analyzed by real-time PCR.ResultsH2 can not influence the RAW264.7 cell viability but can lower oxidative stress.The significant difference(P<0.05) indicated that H2 could significantly decrease the number of TRAP-positive MNCs.The significant difference among the 4 groups in CTK and MMP-9 genes (P<0.05) indicated that H2 could down-regulate their mRNA expression.ConclusionH2 can reduce the oxidative stress and inhibit differentiation of RAW264.7 cells into osteoclasts.

Objectve To study the effect of interaction between ADIPOQ 11377C/G (rs266729) gene polymorphism and physical activity in metabolic syndrome in children. Methods We conducted a case-control study in 114 cases and 114 controls. The genotype of ADIPOQ 11377C/G had been detected in direct sequenc-ing. The effect of interaction between gene polymorphism and physical activity was evaluated by a crossover analysis. Results Efficient physical activity was a protective factor (OR = 0.14); there was interaction between inefficient physical activity and CC genotype of 11377C/G which was a risk factor for metabolic syndrome in children. Conclusion Efficient physical activity can reduce the risk of metabolic syndrome in children. There was interaction between 11377C/G (rs266729) polymorphism and physical activity.

OBJECTIVE: To assess the long-term clinical efficacy of endoscopic surgery of primary sinonasal malignant neoplasms and find out the potential postoperative prognostic factors. METHOD: Forty-three clinical cases of primary sinonasal malignant neoplasms treated under endoscopy were analyzed retrospectively. RESULT: Fifteen patients died. The 1-year, 2-year, 3-year and 5-year survival rates were 83. 7% (36/43), 74. 4% (32/43), 69. 8% (30/43) and 65. 1% (28/43), respectively. Kaplan-Meier single-variable analysis showed that gender, T grade, TNM stage and pathological types of olfactory neuroblastoma were statistically significant prognostic factors (P< 0. 05). COX Pro-Portional hazard models showed that TNM stage was an independent prognostic factors. CONCLUSION Endoscopic surgery for primary sinonasal malignant neoplasms is a safe and effective minimally invasive surgical treatment, and it is an important supplement to the traditional surgery. Gender, T grade, TNM stage and pathological types of olfactory neuroblastoma might be significant prognostic factors.
Endoscopy ; Esthesioneuroblastoma, Olfactory ; surgery ; Humans ; Nasal Cavity ; pathology ; surgery ; Nose Neoplasms ; surgery ; Proportional Hazards Models ; Retrospective Studies ; Survival Rate ; Treatment Outcome

Objective: The study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins. Methods: An SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs. Results: In the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test. Conclusion STM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.

Objective: The study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins. Methods: An SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs. Results: In the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test. Conclusion STM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.

Objective: The study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins. Methods: An SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs. Results: In the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test. Conclusion STM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.

Objective: The study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins. Methods: An SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs. Results: In the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test. Conclusion STM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.

Objective: The study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins. Methods: An SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs. Results: In the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test. Conclusion STM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.