BACKGROUND:Percutaneous kyphoplasty is the main treatment for senile osteoporotic thoracolumbar fractures, but increasing number of patients who have not been treated with anti-osteoporosis therapy after operation develop secondary fractures due to decreased bone mineral density and changes of stress. OBJECTIVE:To investigate the feasibility of consecutive 2-year zoledronic acid treatment following percutaneous kyphoplasty for preventing secondary vertebral fracture. METHODS: 186 elderly patients with thoracolumbar compressive fractures were divided into experimental (n=84) and control (n=102) groups based on their willingness to receive zoledronic acid treatment or not after percutaneous kyphoplasty. The experimental group was treated with calcium and alfacalcidol fololwed by 2 years of zoledronic acid treatment, while only calcium and alfacalcidol treatment was done in the control group. The bone mineral density, pain and function were respectively assessed by dual energy X-ray absorptiometry, visual analogue scale and Oswestry disability index, and the number of refractures was calculated at baseline and at the 2nd year after the second injection of zoledronic acid. RESULTS AND CONCLUSION:The bone mineral density, visual analogue scale and Oswestry disability index scores at 2 years after treatment in both two groups were significantly superior to those at baseline (P < 0.05). The number of refractures in the experimental group (n=1) was significantly less than that in the control group (n=9) (P < 0.05). These results suggest that zoledronic acid can prevent secondary fractures after percutaneous kyphoplasty in the elderly with osteoporotic thoracolumbar fractures, improve long-term function and clinical effectiveness.

The effects of drugs on intracellular calcium concentration(［Ca2+］i) were investigated with fura-2 fluorescence technique to investigate ATP and thrombin-induced Ca2+ entry in bovine aortic endothelial cells(BAEC). It was found that application of ATP and thrombin gave rise to biphasic ［Ca2+］i elevation. ATP or thrombin only triggered a fraction of cyclopiazonic acid(CPA)-sensitive Ca2+ store, which was enough to activate Ca2+ entry. The Ca2+ release induced by thrombin resulted from the activation of phospholipase C(PLC), whereas the PLC-independent mechanism was involved in ATP-induced Ca2+ release. Nifedipine had no effect on ATP and thrombin- induced Ca2+ entry. SK&F 96365 and ginsenoside-2A inhibited both ATP and CPA-induced Ca2+ entry, however no effect of them on thrombin-induced Ca2+ entry was found. The inhibitory effects of SK&F 96365 and ginsenoside-2A on CPA-induced Ca2+ entry were less than that on ATP-induced Ca2+ entry. The Ca2+ influx sensitive to SK&F 96365 was not the same as that to ginsenoside-2A. These observations suggest that both ATP and thrombin evoke Ca2+ release and Ca2+ influx by activation of different receptor. However their mechanisms appear different.

BACKGROUND:In recent years,computer-assisted navigation has gradually attracted attention in the medical field.Some scholars have reported that the clinical effects of computer navigation in total knee arthroplasty vary.To explore the clinical effect of the new generation of Brainlab Knee 3 navigation system,this study is conducted. OBJECTIVE:To analyze the application effect of computer navigation system(Brainlab Knee 3)combined with gap balance technology in total knee arthroplasty. METHODS:A total of 71 patients received total knee arthroplasty at the Department of Joint Surgery of Dalian Second People's Hospital from November 2020 to May 2021.In the navigation group,35 patients underwent total knee arthroplasty by computer navigation combined with gap balance.In the traditional group,36 patients underwent osteotomy with traditional surgical instruments.The difference between medial and lateral joint spaces,knee range of motion,hospital for special surgery knee score,hip-knee-ankle angle,deviation values of coronal femoral component angle,coronal tibial component angle,and sagittal tibial component angle were compared between the two groups. RESULTS AND CONCLUSION:(1)In the navigation group,the differences of intraoperative medial and lateral joint gap at knee extension 0,1,and 2 mm were found in 19,14,and 2 cases,respectively.The gap difference was 0 mm in 18 cases,1 mm in 15 cases and 2 mm in 2 cases at 90° degree knee flexion.In the traditional group,the gap difference at knee extention was 0 mm in 10 cases,1 mm in 20 cases,and 2 mm in 6 cases.The gap difference at 90 degree knee flexion was 0 mm in 10 cases,1 mm in 15 cases and 2 mm in 8 cases.(2)The operation time in the navigation group was longer than that in the traditional group(P<0.05),and two patients in the navigation group developed lower limb intermuscular vein thrombosis after surgery,and none of the patients in the traditional group had complications.(3)The range of motion between the two groups increased significantly at 6 and 12 months after surgery,and the range of motion in the navigation group was higher than that in the traditional group(P<0.05).(4)At 12 months after surgery,the hospital for special surgery knee scores of both groups increased significantly,and the hospital for special surgery knee score in the navigation group was higher than that in the traditional group(P<0.05).(5)At 6 months after surgery,the deviation values of hip-knee-ankle angle,coronal femoral component angle,coronal tibial component angle,and sagittal tibial component angle of navigation group were significantly lower than those in the traditional group(P<0.05).(6)The results showed that computer navigation technique combined with gap balance in total knee arthroplasty had advantages in postoperative range of motion,lower limb alignment and the accuracy of tibial prosthesis component position,and joint function recovered well.

Objective:To observe the expression levels of Toll-like receptor 4 (TLR4) signaling pathway-related proteins and their phosphorylation in the liver tissues of rats with inorganic arsenic poisoning, and to explore the role of TLR4-mediated inflammatory signaling pathway in arsenic-induced liver fibrosis injury.Methods:Eighteen healthy weanling SD rats were divided into 3 groups according to their body weight (80 - 100 g) using a random number table (6 rats in each group, half males and half females). The control group was given 10 ml/kg of normal saline by gavage. The sodium arsenite (NaAsO 2) exposure group was given 10 mg/kg of NaAsO 2 by gavage. The TAK-242 intervention group was given 10 mg/kg of NaAsO 2 by gavage, and 0.5 mg/kg of TAK-242 was also administered intraperitoneally to inhibit TLR4 after 12 weeks. All rats were administered 6 days a week for 36 weeks. At the end of the treatment, the liver tissues and serum of the rats in each group were collected. HE and Masson staining were used to observe the pathological and fibrotic changes of the liver tissues. Automatic biochemical analyzer was used to detect serum liver function indexes of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP). Western blot was used to detect the expression changes of rat liver fibrosis protein α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), Vimentin and TLR4 signaling pathway-related proteins TLR4, nuclear factor κB (NF-κB)-p65 subunit (p65), NF-κB-p50 subunit (p50) and their phosphorylation p-p65 and p-p50 expression levels. Enzyme-linked immunosorbent assay (ELISA) was used to detect the secretion levels of inflammatory related factors interleukin (IL)-6, tumor necrosis factor-α (TNF-α) and IL-10. Results:HE and Masson staining results showed that compared with the control group, the NaAsO 2 exposure group showed significant inflammatory cell infiltration, hepatocyte necrosis and collagen fibrous deposition, while the TAK-242 intervention group showed improvement of the inflammatory cell infiltration and reduction of collagen fibrous deposition compared with the NaAsO 2 exposure group. The results of serum liver function indexes showed that ALT, AST and ALP in NaAsO 2 exposure group were increased compared with the control group, but the TAK-242 intervention group was significantly decreased compared with the NaAsO 2 exposure group ( P < 0.05). Western bolt results showed that in NaAsO 2 exposure group, the expression levels of fibrosis protein α-SMA, TGF-β1 and Vimentin (1.04 ± 0.19, 0.92 ± 0.14, 1.20 ± 0.21) and TLR4 signaling pathway-related proteins and their phosphorylation TLR4, p50, p-p50 and p-p65 (1.16 ± 0.21, 0.95 ± 0.16, 1.24 ± 0.23, 1.56 ± 0.25) were higher than the control group (0.44 ± 0.08, 0.42 ± 0.08, 0.72 ± 0.07, 0.69 ± 0.15, 0.71 ± 0.11, 0.46 ± 0.07, 0.54 ± 0.11, P < 0.05), and the TAK-242 intervention group (0.60 ± 0.13, 0.59 ± 0.16, 0.49 ± 0.11, 0.47 ± 0.08, 0.86 ± 0.09, 0.79 ± 0.14, 1.02 ± 0.17) were lower than the NaAsO 2 exposure group ( P < 0.05). There was no significant difference in the expression level of TLR4 signal pathway-related protein p65 among the three groups ( F = 14.29, P = 0.053). ELISA results showed that the secretion levels of IL-6 and TNF-α [(98.89 ± 4.58), (83.25 ± 4.57) ng/g] in rats liver tissues of the NaAsO 2 exposure group were higher than the control group [(27.30 ± 3.92), (27.77 ± 1.83) ng/g, P < 0.05], while the secretion level of IL-10 [(36.88 ± 3.86) ng/g] was lower than the control group [(77.96 ± 7.87) ng/g, P < 0.05]. In TAK-242 intervention group, IL-6 and TNF-α secretion levels [(44.32 ± 3.60), (36.51 ± 2.93) ng/g] were lower and IL-10 secretion level [(60.40 ± 4.94) ng/g] was higher compared with the NaAsO 2 exposure group ( P < 0.05). Conclusion:TLR4-mediated inflammatory signaling pathway-related proteins and their phosphorylation are highly expressed in the liver tissues of rats with inorganic arsenic poisoning, and inhibition of TLR4 signaling pathway could significantly reduce the degree of liver fibrosis injury caused by inorganic arsenic in rats.

TORCH, which is considered as a series of pathogens, including the Toxoplasma gondii, Rubella virus, Cytomegalovirus or Herpes simplex virus, often infects the pregnant women to induce the the fetus or newborn infection by transplacental infection or exposure to contaminated genital tract secretions at delivery. Increasing evidence have been confirmed that the infection of TORCH may cause the miscarriage, premature birth, malformed fetus, stillbirth, intrauterine growth retardation, neonatal multiple organ dysfunction and other adverse pregnancy outcomes. For most TORCH-infections cases may lacking the effective treatments during pregnancy, and it is important to achieve the effacing monitoring of TORCH infections before and during pregnancy. The laboratory testing of TORCH has the great significance. However, the consensus opinions still need to improve the the standardization of TORCH testing process and the correct interpretation. Based on the characteristics of the TORCH detection method, this article gives a consensus opinion on the standardized detection and clinical application of TORCH from the laboratory perspective according to the characteristics and types of infection of different pathogens.

Background Long-term exposure to sodium arsenite leads to its accumulation in the liver and liver injury as a result. Previous studies showed that mesenchymal cells play an important role in hepatic fibrosis, and epithelial-mesenchymal transformation (EMT) is considered to be a main source of mesenchymal cells. Objective To investigate the effects of sodium arsenite at different doses on liver fibrosis and EMT-related protein expressions in SD rats. Methods Twenty-four healthy weaned SD rats, half male and half female, were randomly divided into four groups according to body weight, with 6 rats in each group. The four groups were control group (gavage with 10.0 mL·kg⁻¹ physiological saline), 2.5 mg·kg⁻¹ sodium arsenite group, 5.0 mg·kg⁻¹ sodium arsenite group, and 10.0 mg·kg⁻¹ sodium arsenite group. All rats were gavaged 6 d per week for 36 weeks and weighed once a week, the serum and liver tissues of rats were collected and weighed, then the organ coefficient was calculated. Hematoxylin-eosin staining and Masson's trichrome staining were used to determine the pathological changes of hepatic fibrosis in rats. The serum secretion levels of hyaluronic acid (HA), laminin (LN), procollagen Ⅲ N-terminal propeptide (PⅢNP), and collagen Ⅳ (COL-Ⅳ) in rats were detected by enzyme-linked immunosorbent assay (ELISA). The protein expressions of HSCs activation-related proteins, such as α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1), as well as EMT-related markers, such as E-cadherin, N-cadherin, Vimentin, and Snail, were detected by Western blotting. Results Compared with the control group, the 10.0 mg·kg⁻¹ sodium arsenite group showed decreased body weight (P<0.05) and increased liver coefficient (P<0.05) of female and male rats. The pathological staining showed that, compared with the control group, a large number of inflammatory cells were observed in liver tissue of rats exposed to sodium arsenite, liver parenchymal cells were also liquefied, necrotic, and denatured, and the collagen positive staining area of liver tissue showed an upward trend along with the increase of arsenic exposure dose (P<0.05). The results of ELISA and Western blotting showed that the serum secretion levels of HA, LN, PⅢNP, and COL-Ⅳ in the 5.0 and 10.0 mg·kg⁻¹ sodium arsenite groups were higher than those in the control group and the 2.5 mg·kg⁻¹ sodium arsenite group (P<0.05). Compared with the control group, the expressions of α-SMA and TGF-β1 proteins in liver tissue were increased in each sodium arsenite exposure group (P<0.05), the expression levels of E-cadherin protein were decreased (P<0.05), and the expression levels of N-cadherin, Vimentin, and Snail were increased (P<0.05). Conclusion Sodium arsenite exposure can induce HSCs activation and liver fibrosis injury in SD rats, resulting in increased extracellular matrix secretion levels, accompanied by EMT in liver tissue, suggesting that EMT is closely related to the process of liver fibrosis caused by arsenic.

Background Arsenic is a well-known environmental toxicant. Hepatic fibrosis could occur dueto excessive or long-term exposure to arsenic, while associated molecular mechanisms remain undefined. Mitogen-inducible gene 6 (Mig-6) exhibits a protective effect on numerous diseases or cancers. However, the specific role of Mig-6 in the mechanisms of arsenite-induced hepatic fibrosis remains indistinct. Objective To investigate the specific role of Mig-6 in the activation of hepatic stellate cells (HSC) and the deposition of extracellular matrix (ECM) induced by sodium arsenite (NaAsO₂). Methods Human hepatic stellate cells (Lx-2) were treated with 0, 1.875, 3.75, 7.5, and 15 μmol·L⁻¹ of NaAsO₂ for 24 h, or with 7.5 μmol·L⁻¹ NaAsO₂ for 0, 12, 24, 48, and 72 h. Additionally, Lx-2 cells were transfected by pcDNA3.1(+)/Mig-6, then treated with 7.5 μmol·L⁻¹ NaAsO₂ for 24 h; a blank control group, a pcDNA3.1(+)-control group, a pcDNA3.1(+)/Mig-6 group, and an arsenic (7.5 μmol·L⁻¹ NaAsO₂) group were also set up. After transfection, the cells and culture supernatants were collected, and the protein levels of Mig-6, α-smooth muscle actin (α-SMA), and transforming growth factor-β1 (TGF-β1) in Lx-2 cells were identified by Western blotting analysis; moreover, the secretion levels of main ECM components in supernatants such as hyaluronic acid (HA), laminin (LN), collagens IV (COL-IV), and procollagen-III (PIIINP) were tested by ELISA. Results The Mig-6 expression decreased in the 3.75, 7.5, and 15 μmol·L⁻¹ NaAsO₂ groups (0.561±0.095, 0.695±0.048, and 0.401±0.030) compared to the control group (1.000±0.000) in Lx-2 cells (P<0.05). After administration with 7.5 μmol·L⁻¹ of NaAsO₂ for 24, 48, and 72 h, the Mig-6 expression (0.856±0.036, 0.515±0.077, 0.491±0.060) decreased compared with the 0 h group (1.000±0.000) (P<0.05). After over-expression of Mig-6, the results of Lx-2 activation related protein levels showed that compared to the control group, the α-SMA and TGF-β1 expression were up-regulated in the arsenic group (P<0.05); meanwhile, the α-SMA and TGF-β1 in the Mig-6 over-expression combined arsenic exposure group reduced compared to the arsenic (7.5 μmol·L⁻¹) group (P<0.05). The results of ELISA showed that compared with the control group, the HA, LN, PIIINP, COL-IV in the arsenic group were up-regulated (P<0.05); while compared to the arsenic group, the HA, LN, PIIINP, and COL-IV in the Mig-6 over-expression combined with arsenic exposure group were decreased (P<0.05). Conclusion Arsenic down-regulates Mig-6 expression in HSC, and over-expression of Mig-6 can reverse the activation of HSC and ECM deposition induced by arsenic exposure. It suggests that Mig-6 plays a protective role in arsenic-induced HSC activation and ECM deposition.