BACKGROUND:During joint replacement, different materials of prosthesis can be used. Different prosthesis can produce different effects and the stress distribution of bone interface. OBJECTIVE:To explore the effects of different materials on the stress distribution and biomechanics of the bone interface of artificial hip joint. METHODS:The CT scan of the hip was carried out. The image data were saved in DICOM format and processed by MIMICS software. The 3D finite element model of the femur was obtained by ANSYS. A three dimensional finite element model of the femur was made with the material properties of the femur. Three kinds of different replacement prosthesis materials (Co Cr Mo aloy, titanium aloy and composite materials) were selected, and the specific requirements of the actual joint replacement were selected, and different types of prosthesis were designed in CAE software. In the STL format, the prosthesis model was imported into MIMICS, and the femur and prosthesis were assembled. The stress status of different prosthesis was analyzed, and the stress shielding rates of exterior and interior sides of middle and lower parts of the femur, right to and 30 mm below lesser trochanter and right to lesser trochanter of the proximal femur were calculated. RESULTS AND CONCLUSION:Through three-dimensional finite element analysis, a direct and accurate model of the femur and the three-dimensional model of the prosthesis were established. According to the actual situation, material assignment of the femoral three-dimensional finite element model was conducted to obtain the corresponding model. Thus, the properties of different materials of the femur were shown visualy. The femoral stress of cobalt chromium molybdenum aloy, titanium aloy, and composite material was simulated after replacement. Results found that the stress shielding rate can decrease in the middle and lower parts of the femur. After replacement, the femoral stress is higher than that of the intact femur. The experimental results show that the stress shielding of the joint was performed after joint replacement with Co Cr Mo aloy, titanium aloy and composite materials. Among them, the composite material is more close to the actual physiological environment of the human body, and it can better reduce the stress shielding effect, and is beneficial to the stress from the prosthesis to the femur.

Objective The effect of combined treatment of statins and calcium channel blockers(CCB) in elderly patients with isolated systolic hypertension(ISH) are not well understood.The purpose of the present study was to assess the additive effect of benidipine-atorvastatin combination therapy in old patients with ISH.Methods Ninety patients with ISH were randomized to receive: placebo(n=15),benidipine treatment(4-8 mg/d,n=25),atorvastatin(20 mg/d,n=25) and benidipine plus atorvastatin treatment(4-8 mg/d+20 mg/d,n=25) for 5 months.Serum concentrations of IL-6,IL-8,hsCRP,flow-mediated dilatation of the brachial artery,urine microalbumin,left ventricular mass index(LVMI),carotid intima-media thickness(CIMT),BP and plasma lipids profiles were examined before and after treatment.Results After 5-months of treatment,the combination treatment significantly reduced IL-6(IL-6 reduction magnitude,combination group: 6.5+6.3 ng/L vs benidipine group: 3.1?3.2 ng/L vs atorvastatin group: 3.3?2.3 ng/L,P

Objective To find out the correlation of C -reactive protein (CRP)and acute cerebral infarc-tion,and to provide research data for acute cerebral infarction.Methods 43 cases with acute cerebral infarction were set as the observation group,and 40 healthy people were set as the control group.The CRP level of the observation group and the control group,and CRP level of different infarction volume and neurological function defect degree were compared.The influence factors of CRP level were analyzed with single factor analysis and Logistic regression.Results The CRP level of the observation group was (14.19 ±2.60)mg/L,which was significantly higher than that of the control group (t =7.453,P <0.05).With the increase of infarction volume,CRP levels increased (t =3.451,8.534, 5.930,all P <0.05).With the increase of nerve function defect degree,CRP level elevated (t =3.845,9.077, 6.730,all P <0.05).CRP level and systolic blood pressure,fasting glucose,total cholesterol,fibrinogen were positively correlated (r =0.479,0.603,0.508,0.603,all P <0.05 ).Cerebral infarction,systolic blood pressure,fasting glucose,total cholesterol and fibrinogen were the influence factors of CRP level.Conclusion There is correlation between C -reactive protein and acute cerebral infarction;detecting CRP level can assist in diagnosis of cerebral infarction.It was favorable to prevent and control the occurrence and progress of acute cerebral infarction.

Objective To explore the correlation between TOP2A gene expression and TCM constitutional types of patients with triple-negative breast cancer.Methods The questionnaire for constitution of Chinese medicine was used to identify the TCM constitutional types of 71 patients with triple-negative breast cancer and TOP2A gene alterations were quantified by real-time PCR. 2-ΔΔCt was used to analyze the expressions of each group. SPSS17.0 was employed to analyze the correlation between TOP2A gene amplification and TCM constitutional types.Results Totally 71 patients were divided into general type (0 case), Qi deficiency type (18 cases), Yang deficiency type (10 cases), Yin deficiency type (12 cases), Qi stagnancy type (7 cases), blood stasis type (10 cases), phlegm wet calculus type (8 cases), damp-heat type (6 cases), and special type (0 case). All of them were biased constitutional types, of which Qi deficiency constitution (25.35%), Yin deficiency constitution (16.90%), blood stasis constitution (14.08%) took the majority. TOP2A gene amplification was negative correlated with each constitutional type (P<0.05).Conclusion Biased constitutional types were the main types of TCM constitutional type of patients with triple-negative breast cancer. The main three biased constitutional types of triple-negative breast cancer were Qi deficiency constitution, Yin deficiency constitution and blood stasis constitution. TOP2A gene expression in patients with triple-negative breast cancer was normal or less expressed, which predicted low chemotherapy sensitivity and poor prognosis.

Objective:To investigate the role of Nogo-B in mitochondrial reactive oxygen species(m-ROS)production and vascular remodeling in vascular smooth muscle cells(VSMCs), and to further clarify the molecular mechanism for Nogo-B in m-ROS production via regulating ATP synthase expression.Methods:A mouse model of vascular remodeling was established.The expression of Nogo-B in mouse smooth muscle cells was detected.Forty mice were divided into the AAV-NC+ control, AAV-NC+ angiotensin Ⅱ(AngⅡ), AAV-Nogo-B+ control and AAV-Nogo-B+ AngⅡ groups(n=10 for each group). VSMCs cultured in vitro were divided into the control group and the Nogo-B overexpression group(Ad-Nogo-B). The expression of Nogo-B in VSMCs in vitro stimulated with AngⅡ was detected.Through experiments conducted in vivo, Nogo-B was overexpressed in VSMCs, then VSMCs were stimulated with AngⅡ, and m-ROS production, tissue fibrosis and mitochondrial function were examined.The regulatory effects of Nogo-B on m-ROS production were explored.Molecular mechanisms for NoGO-B in vascular remodeling via regulating ATP synthase/m-ROS production were examined. Results:Compared with the control group, the expression of Nogo-B was decreased in VSMCs treated with AngⅡ(0.36±0.13 vs.1.00±0.13, t=8.44, P<0.05). The production of m-ROS, fibrosis and mitochondrial dysfunction were increased in VSMCs during vascular remodeling( P<0.05), while overexpression of Nogo-B significantly reduced m-ROS production, fibrosis and mitochondrial dysfunction( P<0.05). ATP synthase expression in VSMCs was positively regulated by Nogo-B.ATP synthase expression was higher in the AAV-Nogo-B+ AngⅡ group than in the AAV-NC+ AngⅡ group(0.86±0.14 vs.0.49±0.17, t=-3.97, P<0.05). The production of m-ROS was reduced by Nogo-B and was lower in the AAV-Nogo-B+ AngⅡ group than in the AAV-NC+ AngⅡ group(1.28±0.34 vs.3.26±0.57, t=7.18, P<0.05). Meanwhile, the ability of Nogo-B to mitigate the deleterious effects of oxidative stress in VSMCs could be offset by oligomycin. Conclusions:Nogo-B participates in vascular remodeling by regulating ATP synthase-mediated m-ROS production.

Objective:To investigate the mechanisms underlying the effect of levocarnitine on myocardial cell fibrosis, proliferation, apoptosis and migration.Methods:Between June and December 2022, an overexpression vector for tissue inhibitor-1 of metalloproteinase(TIMP-1)and siRNA TIMP-1 were used to transfect rat H9c2 cardiomyocytes(from the cell bank of the Chinese Academy of Sciences), and transfection efficiency was measured using fluorescence reverse transcription quantitative PCR(RT-qPCR). After treating H9c2 cells with angiotensin Ⅱ(AngⅡ), the expression of the MMP3 and TIMP-1 genes in the cells was detected by RT-qPCR.A CCK8 kit was used to assess the effect of levocarnitine intervention on the proliferation of myofibroblasts after overexpression or knockdown of TIMP-1.The effects of levocarnitine on apoptosis and migration of myofibroblasts were detected by flow cytometry and Transwell assays.Results:The RT-qPCR results showed that the expression level of the MMP3 gene(1.38±0.05)in cardiomyocytes treated with AngⅡ for 24 hours exhibited an upward trend( P<0.01), while the expression level of the TIMP-1 gene(0.71±0.03)showed a downward trend( P<0.01). In addition, H9c2 cells with TIMP-1 overexpression(905.98±24.17)and knockdown(0.18±0.01)%, respectively, were successfully constructed.Based on CCK-8 detection results, knockdown of TIMP-1(86.56±7.98)% was able to promote the proliferation of H9c2 cells induced by levocarnitine( P<0.01). Apoptosis experiments showed that inhibition of TIMP-1 expression(23.22±2.69)significantly reduced the apoptosis level of H9c2 cells induced by levocarnitine( P<0.01). Migration experiments showed that inhibition of TIMP-1 expression(217.67±23.44)significantly promoted the migration ability of H9c2 cells induced by levocarnitine( P<0.01). Conclusions:After intervention to reduce TIMP-1 expression, levocarnitine can promote proliferation, inhibit apoptosis and promote migration of myofibroblasts and may therefore ameliorate myocardial fibrosis.

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