Inconsistency of Bone Mineral Density Between Femoral Head and Proximal Femur After Femoral Neck Fracture Surgery Indicates Great Possibility of Femoral Head Necrosis.

On clinical observation, it was found that the bone mineral density (BMD) of the femoral head and proximal femur was not consistent in some patients with femoral neck fracture after surgery. The current study was performed to explore whether this phenomenon was associated with femoral head necrosis after surgery for femoral neck fracture. Bone mineral density inconsistency is when the difference of the sum of pixel values on both sides of the fracture line has exceeded 30%. Statistical analysis was performed on the clinical characteristics of 271 patients who had received the operation for femoral neck fracture. Chi-square test, Spearman rank correlation, independent sample t test, Kaplan-Meier method, and log-rank test, as well as univariate Cox regression and multivariate Cox regression, were used to analyze the potential relationship among related factors. It was revealed that the incidence of inconsistency in BMD between the femoral head and proximal femur was significantly increased in patients with femoral head necrosis after surgery for femoral neck fracture, and that the consistency was considerably high between BMD inconsistency and femoral head necrosis. The inconsistent BMD occurred 11.1 months earlier than the necrosis of the femoral head. Cox multivariate regression analysis indicated that the inconsistency in BMD between the femoral head and proximal femur after surgery for femoral neck fracture was an independent prognostic factor affecting femoral head necrosis. The inconsistent changes in BMD between the femoral head and proximal femur after surgery for femoral neck fracture indicate a great possibility of femoral head necrosis. [Orthopedics. 2021;44(2):e223-e228.].

Comparative proteomes change and possible role in different pathways of microRNA-21a-5p in a mouse model of spinal cord injury.

Our previous study found that microRNA-21a-5p (miR-21a-5p) knockdown could improve the recovery of motor function after spinal cord injury in a mouse model, but the precise molecular mechanism remains poorly understood. In this study, a modified Allen's weight drop was used to establish a mouse model of spinal cord injury. A proteomics approach was used to understand the role of differential protein expression with miR-21a-5p knockdown, using a mouse model of spinal cord injury without gene knockout as a negative control group. We found that after introducing miR-21a-5p knockdown, proteins that played an essential role in the regulation of inflammatory processes, cell protection against oxidative stress, cell redox homeostasis, and cell maintenance were upregulated compared with the negative control group. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis identified enriched pathways in both groups, such as the oxidative phosphorylation pathway, which is relevant to Parkinson's disease, Huntington's disease, Alzheimer's disease, and cardiac muscle contraction. We also found that miR-21a-5p could be a potential biomarker for amyotrophic lateral sclerosis, as miR-21a-5p becomes deregulated in this pathway. These results indicate successful detection of some important proteins that play potential roles in spinal cord injury. Elucidating the relationship between these proteins and the recovery of spinal cord injury will provide a reference for future research of spinal cord injury biomarkers. All experimental procedures and protocols were approved by the Experimental Animal Ethics Committee of Shandong University of China on March 5, 2014.

ß-Aescin shows potent antiproliferative activity in osteosarcoma cells by inducing autophagy, ROS generation and mitochondrial membrane potential loss.

PURPOSE: Osteosarcoma is one of the frequent bone tumor affecting mainly children and is associated with considerable mortality. The limited availability of anticancer drugs and less efficacious treatment options have led to poor survival rates of patients with osteosarcoma. Therefore, there is need to look for more viable treatment options and against this backdrop, natural products may prove handy. Therefore the aim of the present study was to evaluate the anticancer activity of a natural product of plant origin, ß-aescin, against U2OS human osteosarcoma cells. METHODS: U205 human osteosarcoma cell line was used in this study. Antiproliferative activity was determined by MTT assay. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were evaluated by flow cytometry. Autophagy was detected by monodansylcadaverine (MDC) staining and immunofluorescence. Protein expression was examined by western blotting. RESULTS: The results indicated that ß-aescin showed significant anticancer activity against U2OS human osteosarcoma cells and exhibited an IC50 of 40 µM. ß-aescin treatment caused significant increase in ROS and decrease in the MMP. The anticancer effect of ß-aescin was found to be due mainly to autophagic cell death as evidenced from MDC staining and immunofluorescence. Moreover, ß-aescin caused significant increase in the expression levels of LC3- II protein in U2OS osteosarcoma cells in a time and dosedependent manner. CONCLUSION: Taken together we propose that ß-aescin may prove a lead molecule in the management of osteosarcoma and deserves further research efforts.

Regulatory roles of microRNA-21 in fibrosis through interaction with diverse pathways (Review).

MicroRNA-21 (miR-21) is a small, non-coding RNA which can regulate gene expression at the post­transcriptional level. While the fibrogenic process is vital in tissue repair, proliferation and transition of fibrogenic cells combined with an imbalance of secretion and degradation of the extracellular matrix results in excessive tissue remodeling and fibrosis. Recent studies have indicated that miR­21 is overexpressed during fibrosis and can regulate the fibrogenic process in a variety of organs and tissues via diverse pathways. The present review summarized the significant roles of miR-21 in fibrosis and discussed the underlying key pathways.

Progranulin knockout accelerates intervertebral disc degeneration in aging mice.

Intervertebral disc (IVD) degeneration is a common degenerative disease, yet much is unknown about the mechanisms during its pathogenesis. Herein we investigated whether progranulin (PGRN), a chondroprotective growth factor, is associated with IVD degeneration. PGRN was detectable in both human and murine IVD. The levels of PGRN were upregulated in murine IVD tissue during aging process. Loss of PGRN resulted in an early onset of degenerative changes in the IVD tissue and altered expressions of the degeneration-associated molecules in the mouse IVD tissue. Moreover, PGRN knockout mice exhibited accelerated IVD matrix degeneration, abnormal bone formation and exaggerated bone resorption in vertebra with aging. The acceleration of IVD degeneration observed in PGRN null mice was probably due to the enhanced activation of NF-κB signaling and ß-catenin signaling. Taken together, PGRN may play a critical role in homeostasis of IVD, and may serve as a potential molecular target for prevention and treatment of disc degenerative diseases.

Efficacy and safety of linezolid in treating gram-positive bacterial infection in the elderly: a retrospective study.

Linezolid is commonly used for the treatment of drug-resistant Gram-positive bacterial infection. This study aimed to evaluate the efficacy and safety of linezolid in treating Gram-positive bacterial infection in the elderly from January 2010 to December 2012. Total 40 elderly patients (>60 years old) with Gram-positive bacterial infection were treated with linezolid and their demographic and clinical data were collected and analyzed. Among the 40 patients, 31 patients (77.5 %) were cured. Linezolid caused little adverse effects on liver and renal function. The main adverse effect was thrombocytopenia and its incidence was significantly associated with baseline platelet count and the duration of treatment (P < 0.05). Logistic regression analysis showed that the baseline platelet count <200 × 10(6)/mL, but not the age, the sex, the length of hospital stay, baseline levels of hemoglobin, alanine aminotransferase, or creatinine clearance rate was significantly associated with linezolid-induced thrombocytopenia. In conclusion, linezolid is effective to cure Gram-positive bacterial infection in the elderly and causes little adverse effects on liver and renal function. Timely monitoring of baseline platelet count may be helpful to guide the use of linezolid to avoid the occurrence of thrombocytopenia.

Circulating blood monocytes traffic to and participate in the periprosthetic tissue inflammation.

OBJECTIVE: To examine the trafficking of human circulating blood monocytes and their influence on the inflammation of periprosthetic tissues using a novel mouse-human chimera model. METHODS: Periprosthetic tissue and bone chips from patients with aseptic prosthetic loosening were implanted into the muscles of immune-deficient SCID mice depleted of host macrophages by periodic intraperitoneal injection of anti-asialo GM1 rabbit sera (ASGM1). Autologous patient peripheral blood monocytes (PBMCs) were labeled with PKH2 fluorescent dye and injected intraperitoneally into the implanted animals. Mice were sacrificed 14 days after PBMC transfusion for molecular and histological analyses. RESULTS: Patient periprosthetic tissues were well tolerated in SCID mice and preserved a high level of viability. Cell trafficking studies revealed the accumulation of fluorescent PBMC within the xenografts, with total cell counts in the xenografts significantly increased following the systemic PBMC infusion. PBMC infusion also promoted the expression of IL-1, IL-6, TNFalpha, and RANK within the periprosthetic tissue. CONCLUSION: Systemic PBMC migrated to the implanted periprosthetic tissues and contributed to the local inflammation. The data provide evidence that circulating blood monocytes may play a role in pathologic process during aseptic loosening of total joint replacement.

Quantitative anatomic basis of antegrade lag screw placement in posterior column of acetabulum.

BACKGROUND: Lag screw fixation has been recommended for treatment of acetabular and pelvic fracture for several years. The aim of the present study was to determine the projection of the axis of the posterior column on the inner table of the iliac wing in the supra-acetabular region. METHODS: Thirty adult dried bony hemipelves specimens and other five intact adult dried pelvic specimens were included in this study. The projection point of the axis of the posterior column of the acetabulum was determined on the inner table of the iliac wing of the hemipelves specimens. The perpendicular distance from the optimal entry point to the linea terminalis of pelvis was measured and recorded as the lateral distance. The same measurement along the linea terminalis from the optimal entry point to the junction between the anterior border of iliosacral articulation and the linea terminalis of pelvis was made and recorded as the posterior distance. The depth of the anchor path and the corresponding average retroversion angulation and extraversion angulation were also measured. According to the results acquired from this study, a series of 6.5 mm lag screws were inserted into the posterior column of each side of the other five intact specimens, respectively, to evaluate the position of the screws. The data were expressed as mean +/- SD and analyzed by using the descriptive methods with SPSS 10.0. RESULTS: The average length of lag screw was 104.8 +/- 4.2 mm. The average lateral distance was 16.8 +/- 2.1 mm. The average posterior distance was 23.5 +/- 3.4 mm. The corresponding average retroversion angulation and extraversion angulation were 57 degrees 36' +/- 4 degrees 28' and 119 degrees 18' +/- 2 degrees 32', respectively. The insertion of the single 6.5 mm lag screw of adequate length was possible in the posterior column along its anchor path and no accidental extraosseous or intraarticular screw placement had occurred. CONCLUSIONS: The present study describes a safe anchor path of antegrade lag screw fixation in the posterior column. Insertion of the lag screws of adequate length is possible in the posterior column along its functional axis.

Destructive pathological changes in the rat spinal cord due to chronic mechanical compression. Laboratory investigation.

OBJECT: Chronic mechanical compression of the spinal cord, which is commonly caused by degeneration of the spine, impairs motor and sensory functions insidiously and progressively. Yet the exact mechanisms of chronic spinal cord compression (SCC) remain to be elucidated. To study the pathophysiology of this condition, the authors developed a simple animal experimental model that reproduced the clinical course of mechanical compression of the spinal cord. METHODS: A custom-designed compression device was implanted on the exposed spinal cord of female Wistar rats between the T-7 and T-9 vertebrae. A root canal screw attached to a plastic plate was tightened 1 complete turn (1 pitch) every 7 days for 6 weeks. The placement of the compression device and the degree of compression were validated every week using radiography. Furthermore, a motor sensory deficit index was also calculated every week. After 3, 6, 9, or 12 weeks, the compressed T7-9 spinal cords were harvested and examined histologically. RESULTS: Lateral projection of the thoracic spine showed a progressively increasing rate of mean spinal cord narrowing in the compression group. Motor and sensory deficiencies were observed from Week 3 onward; paralysis was observed in 2 rats at Week 12. Motor deficiency appeared earlier than sensory deficiency. Obvious pathological changes were observed starting at Week 6. The number of neurons in the gray matter of rats with chronic compression of the spinal cord decreased progressively in the 6- and 9-week compression groups. In the white matter, myelin destruction and loss of axons and glia were noted. The number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive neurons increased in the ventral-to-dorsal direction. The number of TUNEL-positive cells increased from Week 6 onward and peaked at Week 9. CONCLUSIONS: This practical model accurately reproduces characteristic features of clinical chronic SCC, including progressive motor and sensory disturbances after a latency and insidious neuronal loss.