Finite element analysis of dynamic changes in spinal mechanics of osteoporotic lumbar fracture.

AIM: This study aims to explore the effects of finite element biomechanical properties of different methods in the treatment of osteoporotic thoracolumbar fractures. METHODS: Based on the ultra-thin computed tomography scan data of a volunteer's thoracolumbar spine, the finite element method was used to simulate the treatment of osteoporotic thoracolumbar fracture. Spiral computed tomography scanning was used to obtain images of the thoracolumbar region, which was then imported into Mimics software to obtain the three-dimensional geometric model. The finite element model of normal T11 - L2 segment was established by finite element software Abaqus and the validity of the model loading was verified. The finite element model of T11 vertebral compression fracture was established based on normal raw data. The clinical overextension reduction manipulation was simulated by different treatment methods and the changes in stress and displacement in different parts of injured vertebrae were analyzed. RESULTS: An effective finite element model of T11-L2 segment was established. The maximum stress, axial compression strength, axial compression stiffness, and transverse shear stiffness were significantly better in the percutaneous kyphoplasty and percutaneous vertebroplasty treatment group than in the conservative treatment group and open treatment group (P < 0.05). Additionally, there was no significant difference between the open treatment group and conservative treatment group, or between the PKP and PVP treatment group. CONCLUSION: Percutaneous vertebroplasty and percutaneous kyphoplasty not only met the requirements of normal functional kinematics of thoracolumbar spine, but also restored the stability of thoracolumbar spine. They had good biomechanical properties and remarkable application effects. The application of finite element analysis can help select a scientific, reasonable, and effective treatment scheme for the clinical diagnosis and treatment of osteoporotic thoracolumbar fractures.

Ring finger 220 promotes the stemness and progression of colon cancer cells via Ubiquitin specific peptidase 22-BMI1 axis.

Colorectal cancer (CRC) is ranked as the third most common malignancy worldwide. Therefore, it is urgent to screen novel and effective molecular drug targets for colorectal cancer therapeutics. In this study, the specific role and related mechanism underlying Ring finger (RNF) 220 in colon cancer were investigated. Firstly, RT-PCR assay was used to compare differences between expression levels of RNF220 in colorectal tumor and normal tissues. Western blot and RT-PCR assays were applied to examine the protein levels of RNF220 in normal colonic mucosa and colorectal cancer cells. We found that RNF220 was upregulated in colorectal cancer in patients and cell models. RNF220 promoted the proliferation and migration, invasion of colorectal cancer cells through BrdU incorporation, clone formation, transwell and wound healing assays. Spheroid formation and western blot assays illustrated that RNF220 promoted the stemness of colorectal cancer cells. Moreover, we found that RNF220 regulated BMI1 expression through USP22 by western blot. Finally, we discovered that RNF220 facilitated tumor growth in vivo through establishment of subcutaneous xenograft tumor mice model. In conclusion, RNF220 promoted the stemness and progression of colon cancer cells via the USP22-BMI1 axis.

[Association between endogenous hormones, hormone receptors and cervical cancer].

OBJECTIVE: To explore the relationship between the levels of estrogen (E2) and progestogen (P), expression of estrogen receptor (ER) and progesterone receptor (PR) and cervical cancer. METHODS: A case-control study with hospital and community controls was employed. The levels of serum estrogen and progesterone were detected by enzyme linked immunosorbent assay (ELISA) for 141 cervical cancer cases, 137 uterine myoma patients as controls and 129 health women as controls. ER and PR were measured by immunohistochemistry sABC in cervix tissues from patients with cervical cancer and uterus myoma as well. RESULTS: The levels of estrogen (47.49 ng/mL) and progesterone (2.34 pg/mL) in cases were significantly higher than those in both control groups. The association between estrogen and cervical cancer was significant both before and after menopause-adjusted, with over 89% of attributable risk percentage (ARP), and showed a dose-response relation. Using the lowest value of 2 pg/ml in follicular phase as cut off point for progesterone, there were no statistically significant difference between cases and controls, and neither in progesterone nor in premenopausal. The expressions of ER and PR in cases were lower than those in controls, even after being menopause-adjusted. CONCLUSION: The high level of endogenous estrogen and progestogen might increase the risk of cervical cancer. Compared with progestogen, estrogen showed a higher risk that was not influenced by menopause. In some sense, ER and PR may exert certain protective effect on progressing of cervical carcinogenesis.

[Analysis on synergistic action between estrogen, progesterone and human papillomaviruses in cervical cancer].

OBJECTIVE: To explore the effects of estrogen (E(2)) and progesterone (P) on cervical cancer and the synergistic action between estrogen, progesterone and human papillomaviruses (HPV). METHODS: Hoted-start polymerase chain reaction (HS-PCR) was used to detect HPVs, HPV16 and ELISA was used to assay E(2) and P on 141 cases with cervical cancer and on 129 healthy controls. RESULTS: Positive rates of HPVs and HPV16 were 75.2% and 46.8% respectively in cervical cancer group, significantly higher than that in controls. Levels of estrogen and progesterone in case group were significantly higher than that in controls and a dose-responded relationship between the levels of estrogen and cervical cancer was revealed. Estrogen and HPV showed an additive interaction in the development of cervical cancer. CONCLUSION: HPV16 infection played a principal role in the development of cervical cancer. The high levels of entogenous estrogen could increase the risk of cervical cancer and might serve as a cofactor in the development of HPV-induced cervical cancer.