What Factors Are Associated With Postoperative Ischiofemoral Impingement After Bernese Periacetabular Osteotomy in Developmental Dysplasia of the Hip?

BACKGROUND: Any abnormal structures that contribute to the narrowing of the ischiofemoral space could induce ischiofemoral impingement. Bernese periacetabular osteotomy (PAO) medializes the hip center and, therefore, decreases contact stress on the cartilage in developmental dysplasia of the hip (DDH). However, medialization of the hip center might also narrow the ischiofemoral space, which may increase the risk of postoperative ischiofemoral impingement in patients with acetabular dysplasia who are undergoing PAO. Furthermore, the dysplastic hip has less ischiofemoral space and less space for the quadratus femoris. A few studies have focused on the amount of medialization of the hip center, but the proportion of postoperative ischiofemoral impingement after PAO has not been investigated. QUESTIONS/PURPOSES: (1) What proportion of patients develop ischiofemoral impingement after undergoing unilateral PAO for DDH? (2) What radiographic factors are associated with postoperative ischiofemoral impingement in patients who underwent PAO for DDH? (3) How much hip center medialization is safe so as to avoid postoperative ischiofemoral impingement during PAO? METHODS: Between 2014 and 2016, we treated 265 adult patients who had symptomatic residual acetabular dysplasia (lateral center-edge angle less than 20°) using PAO. During that time, we generally offered PAO to patients with acetabular dysplasia when the patients had no advanced osteoarthritis (Tönnis grade < 2). Of those, we considered only patients who underwent primary PAO without femoral osteotomy as potentially eligible. Based on that, 65% (173 of 265) were eligible; a further 9% (24 of 265) were excluded due to leg length discrepancy, spine disorders, or joint replacement in the contralateral side, and another 6% (17 of 265) of patients were lost before the minimum study follow-up of 2 years or had incomplete datasets, leaving 50% (132 of 265) for analysis in this retrospective study at a mean of 2.70 ± 0.71 years. The diagnosis of ischiofemoral impingement was defined by symptoms, MRI, and diagnostic ischiofemoral injection. We ascertained the percentage of patients with this diagnosis to answer the first research question. To answer the second question, we divided the patients into two groups: PAO patients with ischiofemoral impingement and PAO patients without ischiofemoral impingement. The demographic data and preoperative imaging parameters of patients in both groups were compared. There were statistical differences in acetabular version, ischial angle, neck-shaft angle, the presence of positive coxa profunda sign, McKibbin index, ischiofemoral space, quadratus femoris space, anterior acetabular section angle, and the net amount of hip center medialization. To investigate potential factors associated with postoperative ischiofemoral impingement in patients who underwent PAO, these factors underwent binary logistic regression analysis. To answer the third question, the cutoff value of the net amount of hip center medialization was evaluated using receiver operator characteristic curve and the Youden index method. RESULTS: We found that 26% (35 of 132) of PAO dysplastic hips had postoperative ischiofemoral impingement. After controlling for confounding variables such as acetabular version, ischial angle, femoral neck version, McKibbin index, and ischiofemoral space, we found that an increasing neck-shaft angle (odds ratio 1.14 [95% confidence interval 1.01 to 1.29]; p = 0.03), a positive coxa profunda sign (OR 0.13 [95% CI 0.03 to 0.58]; p < 0.01), and an increasing net amount of hip center medialization (OR 2.76 [95% CI 1.70 to 4.47]; p < 0.01) were associated with postoperative ischiofemoral impingement in patients with DDH who underwent PAO (R 2 = 0.73). The cutoff values of neck-shaft angle was 138.4°. The cutoff values of the net amount of hip center medialization was 1.9 mm. CONCLUSIONS: Postoperative ischiofemoral impingement could occur in patients with acetabular dysplasia who have undergone PAO after hip center medialization. An increasing neck-shaft angle, a positive coxa profunda sign on preoperative imaging, and excessive medialization of the hip center are factors associated with ischiofemoral impingement development in these patients. Therefore, we suggest that physicians measure the ischiofemoral space on a preoperative CT when patients with DDH have an increasing neck-shaft angle (> 138.4°) or a positive coxa profunda sign on radiological imaging. During PAO, the amount of hip center medialization should be carefully controlled to keep these patients from developing postoperative ischiofemoral impingement. LEVEL OF EVIDENCE: Level III, therapeutic study.

LncRNA-CIR promotes articular cartilage degeneration in osteoarthritis by regulating autophagy.

Osteoarthritis (OA) is a common joint disease that is regarded as a local inflammatory response caused by joint instability and accompanied by the progressive degeneration of articular cartilage. However, the molecular mechanisms involved in the maintenance of articular cartilage remain a subject of debate and research. This study aims to analyze the roles of long noncoding RNA (lncRNA)CIR and autophagy in cartilages and determine their overall contribution to the degradation of extracellular matrix. Patients with OA possessed high levels of lncRNA-CIR and MMP3 and low level of COL2A1. The levels of autophagy-related proteins, including LC3BI/II and beclin-1, increased from 12 h to 48 h. The use of si-lncRNA-CIR reversed the trend compared with that in the OA group. The negative effect of lncRNA-CIR was assessed in vivo by establishing a model of surgically induced OA. Moreover, si-lncRNA-CIR-treated joints exhibited fewer OA changes than saline-treated joints. Results were confirmed by histopathological grading of the models by using the Osteoarthritis Research Society International Scoring System and the outcomes of immunohistochemistry for LC3B-II and MMP-3. Overall, lncRNA-CIR played a negative role in the OA process by activating autophagy.

Autophagy protects meniscal cells from glucocorticoids-induced apoptosis via inositol trisphosphate receptor signaling.

Intra-articular injection of glucocorticoids (GCs) has been widely used in the management of osteoarthritis and rheumatoid arthritis. Nevertheless, several studies showed that GCs had toxic effects on chondrocytes as well as synovial cells. Previously we reported the protective role of autophagy in the degeneration of meniscal tissues. However, the effects of GCs on autophagy in the meniscal cells have not been fully elucidated. To investigate whether GCs can regulate autophagy in human meniscal cells, the meniscal cells were cultured in vitro and exposed in the presence of dexamethasone. The levels of apoptosis and autophagy were investigated via flow cytometry as well as western blotting analysis. The changes of the aggrecanases were measured using real-time PCR. The role of autophagy in dexamethasone-induced apoptosis was investigated using pharmacological agents and RNA interference technique. An agonist of inositol 1,4,5-trisphosphate receptor (IP3R) was used to investigate the mechanism of dexamethasone-induced autophagy. The results showed that dexamethasone induced autophagy as well as apoptosis in normal human meniscal cells. Using RNA interference technique and pharmacological agents, our results showed that autophagy protected the meniscal cells from dexamethasone-induced apoptosis. Our results also indicated that dexamethasone increased the mRNA levels of aggrecanases. This catabolic effect of dexamethasone was enhanced by 3-MA, the autophagy inhibitor. Furthermore, our results showed that dexamethasone induced autophagy via suppressing the phosphorylation of IP3R. In summary, our results indicated that autophagy protected meniscal cells from GCs-induced apoptosis via inositol trisphosphate receptor signaling.

Efficacy of treatment in peri-pelvic Morel-Lavallee lesion: a systematic review of the literature.

BACKGROUND: Morel-Lavallee lesion (MLL) of the peri-pelvic region is less common and various treatments have been introduced to manage the lesion. No standard treatment is recommended. We performed a systematic review of literature to (1) identify the classification of peri-pelvic MLL; (2) review the treatments of the lesion and their complications; (3) define the optimal treatment of peri-pelvic MLL. METHODS: A systematic search was performed via PubMed, ISI Web of Knowledge, and Embase for English abstract articles from 1966 to 2012. We identified 21 articles detailing 153 patients with peri-pelvic MLL, most of which were level IV studies. The treatments and clinical results were reviewed. RESULTS: For peri-pelvic MLL patients, surgical intervention was better than conservative therapy. Sclerhodesis method is attended with good outcome in the symptomatic MLL patients without fractures. Patients with peri-pelvic fractures could be managed with local suction drainage or open debridement with dead space closure technique during fracture fixation. The delayed-diagnosis cases might be treated with mass resection when fibrosis capsule was obtained in magnetic resonance imaging. CONCLUSIONS: Peri-pelvic MLL can be treated with various surgical methods depending on the formation of fibrosis capsule and associated injuries. Dead space closure technique is emphasized in the treatment of MLL. Higher quality of literature is required to prove this result in future research.

[Generation and characterization of peripheral nerve animal model of pure motor/sensory nerve fibers].

OBJECTIVE: To generate peripheral nerve animal model of pure motor nerve fibers/pure sensory nerve fibers, and identify them. METHODS: The SPF SD rats were adopted in this study, and divided into 3 groups. In group A, we ablated L2-L4 ventral roots (VRs) to generate peripheral nerve animal model of pure sensory fibers. In group B, we ablated L2-L4 dorsal root ganglions (DRGs) to generate peripheral nerve animal model of pure motor fibers. Two time end-points were set as 2 weeks and 4 weeks. Neuron cells in lumbar spinal cords were detected by immunohistochemical staining with antibody of neuronal nuclei (NeuN). Motor neuron cells in lumbar spinal cords of pure motor fiber animal models and sensory neuron cells in lumbar spinal cords of pure sensory fiber animal models were counted respectively, and then compared to that of normal animals. Femoral nerves distal to the furcation were stained in osmium tetroxide, and then myelinated nerve fibers in the muscle branch and cutaneous branch of femoral nerve were counted respectively. RESULTS: The mean numbers of sensory neuron cells and motor neuron cells in normal lumbar spinal cords were 62.57 ± 1.02 and 29.73 ± 3.03 per 10 × 20 visual field respectively. For different end-points, the mean numbers of sensory neuron cells after ablating vental foots were 62.12 ± 1.77 (2 weeks), 62.15 ± 1.32 (4 weeks) per 10 × 20 visual field respectively; the mean numbers of motor neuron cells after ablating DRGs were 30.12 ± 0.44 (2 weeks), 30.00 ± 1.87 (4 weeks) per 10 × 20 visual field respectively. In group A, motor axons in muscle branch were degenerated as the sensory axons in muscle branch and cutaneous branch were not changed. The senory axons in femoral nerve for the two end-points were 1 558.17 ± 50.14 (2 weeks) and 1 544.00 ± 47.42 (4 weeks). In group B, sensory axons in muscle branch were degenerated as the motor axons were reserved. The motor axons in muscle branch for the two end-points were 387.67 ± 48.50 (2 weeks) and 393.50 ± 27.86 (4 weeks). There was no statistically significant difference in these mean numbers for the two end-points. The degenerating axons and myelin sheath had not been totally eliminated by the endpoint of 2 weeks. CONCLUSION: Peripheral nerve animal model of pure motor fibers can be generated by ablating L2-L4 DRGs; peripheral nerve animal model of pure sensory fibers can be generated by ablating L2-L4 ventral roots. The degenerating axons and myelin sheath have been totally eliminated by the end-point of 4 weeks. Ablating the ventral roots does not influence the survival of sensory neuron cells; and ablating the DRGs does not influence the survival of motor neuron cells.

[Effects of Bushen Jiedu Recipe and Jianpi Jiedu Recipe containing plasma on dendritic cells of chronic hepatitis B virus infection patients under different immune states].

OBJECTIVE: To compare the effects of Bushen Jiedu Recipe (BJR) and Jianpi Jiedu Recipe (JJR) containing plasma on dendritic cells (DCs) of chronic hepatitis B virus (HBV) infection patients under different immune states. METHODS: Recruited were 36 chronic HBV infection outpatients from First Affiliated Hospital of Hunan University of Traditional Chinese Medicine from April 2010 to January 2011. They were assigned to the immune tolerance group (18 cases) and the immune clearance group (18 cases).Another 10 healthy subjects were recruited as the healthy control group. Their anticoagulated peripheral venous blood was respectively collected. The peripheral blood mononuclear cells (PBMCs) were isolated and further extracted for incubating DCs. The DCs were intervened by BJR and JJR containing plasma. The morphology of DCs was identified. The expressions of CD1alpha, CD80, CD86, and HLA-DR were detected. The level of interferon-alpha (IFN-alpha) in the supernatant was observed by ELISA. RESULTS: The CD80 expression level was lower in the immune clear group than in the healthy control group before intervention (P < 0.05). The expression levels of CD80, CD86, and HLA-DR were lower in the immune tolerance group than in the healthy control group before intervention (P < 0.05).The IFN-alpha expression level was lower in the immune tolerance group and the immune clearance group than in the healthy control group before intervention (P < 0.05). The expression levels of CD80, HLA-DR, and IFN-alpha were lower in the immune tolerance group than in the immune clearance group before intervention (P < 0.05). Compared with the same group before intervention, the CD80 expression significantly increased in each treatment group (P < 0.05). After intervention the expression levels of CD80 and HLA-DR were higher in the immune tolerance group than in the immune clearance group in the same time phase, and the CD86 expression level was higher in the BJR group than in the immune clearance group in the same time phase, showing statistical difference (P < 0.05). CONCLUSIONS: The middle dose BJR and the small dose JJR both could promote the recovery of DCs in chronic HBV infection patients. Besides, BJR showed more prominent effects on the function of DCs in chronic HBV infection patients in the immune tolerance stage.

High mobility group box chromosomal protein 1 in acute-on-chronic liver failure patients and mice with ConA-induced acute liver injury.

High mobility group box chromosomal protein 1 (HMGB1) is an important proinflammatory molecule in many inflammatory disorders, but little is known about its role in acute-on-chronic liver failure (ACLF). Here, we investigated the relationship between the expression of HMGB1 and the disease onset and severity of ACLF patients and mice with acute liver injury/failure induced by concanavalin A (ConA). Peripheral blood mononuclear cells (PBMCs) and serum from ACLF patients were collected, and a mouse model of acute liver injury/failure was induced by ConA. HMGB1 mRNA expression in patient PBMCs or in murine livers and serum HMGB1 protein in ACLF patients and mice were assayed by RT-PCR and Western blotting, respectively. HMGB1 translocation in hepatocytes of ConA-treated mice was assessed by immunohistochemical staining. Up-regulated HMGB1 mRNA levels in PBMCs and accumulated protein in serum were both correlated with disease severity in ACLF patients. In the animal model, HMGB1 levels increased at 4 h and reached its peak value at 8-12 h after challenge with ConA, which suggests that HMGB1 is a relatively late proinflammatory cytokine compared with TNF-α. Translocation of HMGB1 from the nucleus to the cytoplasm in hepatocytes was correlated with the severity of liver injury in mice. While specific anti-HMGB1 antibodies and nicotine protected mice from acute liver injury/failure by reducing mortality and improving liver tissue injury, treatment with recombinant HMGB1 led to an increased mortality due to ConA challenge. Thus, the data from the present study suggest that HMGB1 plays a critical role in the systemic inflammation of ACLF and could be a potential therapeutic target in the treatment of ACLF.

Left-right determination factor is down-regulated in fibrotic renal tissue of human hydronephrosis.

OBJECTIVE: • To compare the expressions of common fibrosis-relevant genes in hydronephrosis-induced fibrotic renal tissues and normal human renal tissues, thereby providing insights into the cellular and molecular mechanisms of renal fibrosis resulting from hydronephrosis. PATIENTS AND METHODS: • A total of 12 extensively fibrotic renal tissue samples from patients with hydronephrosis (H-group) and six normal renal tissue samples from patients who underwent nephrectomy for renal cell carcinoma (N-group), along with their clinical data, were collected at Renmin Hospital of Wuhan University in China between October 2005 and August 2007. • These tissue samples were compared for their transforming growth factor-ß (TGF-ß)/bone morphogenetic protein (BMP) pathway-related gene profiles using a real-time polymerase chain reaction (PCR) microarray. • Subsequently, reverse transcriptase-PCR assays were used to validate the expression changes of left-right determination factor (LEFTY), a gene of interest, at the mRNA level. • The different expression of LEFTY at the protein level was confirmed by western blotting and immunohistochemistry assays. RESULTS: • The results showed that 49 genes were differently expressed in fibrotic renal tissues relative to normal control tissues. Among these genes, 25 were up-regulated and 24 were down-regulated. • LEFTY-B, one of the most markedly altered genes, was down-regulated 13.55-fold compared with N-group tissues. • RT-PCR showed that the LEFTY-A (6.05-fold down-regulated, P < 0.001) and LEFTY-B (12.5-fold down-regulated, P < 0.001) genes, two members of the LEFTY family in human tissues, were both significantly down-regulated in H-group tissues. • Similarly, down-regulations of LEFTY-A (0.25-fold vs N-group, P < 0.001) and LEFTY-B (0.20-fold vs N-group, P < 0.001) proteins were detected by western blotting (P < 0.001). • Immunohistochemical staining showed different distributions of LEFTY in the two tissue samples, and quantitative image analyses confirmed that LEFTY protein expression was lower in H-group tissues than in N-group tissues (P < 0.001). CONCLUSIONS: • The gene and protein expressions of LEFTY were found to be down-regulated in extensively fibrotic renal tissues induced by hydronephrosis. • LEFTY may represent an ideal candidate for a therapeutic target for renal fibrosis.

YueF overexpression inhibits cell proliferation partly through p21 upregulation in renal cell carcinoma.

YueF is a novel putative tumor suppressor gene that can inhibit proliferation and induce apoptosis in hepatoma cells, but its role in renal cell carcinoma (RCC) remains unclear. Here, we examined the expression of the YueF gene in RCC tissues and the effect of YueF on cell proliferation in RCC 786-0 cells. The results showed that YueF was expressed at high levels in normal kidney tissues and cell lines but was reduced or absent in RCC tissues and 786-0 cells. Lentivirus-mediated YueF overexpression in RCC 786-0 cells caused cell-cycle arrest in the G1 phase and dramatically reduced proliferation in culture. YueF overexpression resulted in increased protein levels of p53 and p21(WAF1/Cip1), whereas the protein levels of cyclin D1 and pRb were decreased. The proliferation defects caused by YueF overexpression could be partially rescued by the expression of p21 siRNA. These findings suggest a critical role for p21 in the YueF-induced growth inhibition of 786-0 cells and provide novel insights into the mechanism underlying the tumor-suppressive action of YueF.

[Time distribution characteristics of traffic injury in different age groups in Beijing from 2004 to 2008].

OBJECTIVE: To analyze the time distributions of traffic accidents happening in different age groups in Beijing from 2004 to 2008, and to provide information on the prevention and rescue. METHODS: The traffic injury cases recorded by Beijing Emergency Medical Center from 2004 to 2008 were analyzed, and the data were separated by age: the youth (0-17 years old), the adult (18-64 years old) and the senior adult (above 65 years old). The constituent ratios of hours and months were calculated to describe the states and time distributions of all the cases. RESULTS: The high peaks of accidents for the youth group occurred in the periods 7:00 to 8:00 (6.77%, 39) and 16:00 to 18:00 (10.38%, 60;10.73%, 62), and for the senior adult group appeared in the period 9:00 to 11:00 (11.19%, 151; 11.04%, 149). The adult group showed a stable trend during the period 8:00 to 24:00. The amount of traffic injury happening in these three groups had the same status monthly, which turned out that most traffic accidents happened in October for all the groups (12.11%, 70; 10.38%, 1 257; 12.30%, 166), and February had the smallest number (4.15%, 24; 5.28%, 640; 5.26%, 71). CONCLUSION: The time distributions of traffic injury within these three groups do not show the same situation daily but do monthly. The emergency treatment team and traffic control personnel should pay attention to this and have special protocol for different cases to increase the efficiency of the prehospital rescue.

[Characteristics analyses of road traffic injury in Beijing in 2009].

OBJECTIVE: To analyze the characteristics and laws of road traffic accidents in Beijing, and provide some accident-prevention measures. METHODS: The data from Beijing Emergency Medical Center were managed by computer,then the descriptive statistical analyses were made. RESULTS: (1) A total of 2 984 traffic accidents with relatively complete information were recorded in our research,in which 42 people were led to death and 2 942 injured. Most of the casualties were male. The ages of the injured segments were mainly between 18 to 59 years.(2) The number of the injured in accidents between the motor vehicles was the largest, which was 1 883; The deaths caused by accidents between the motor vehicles and pedestrians were the most, with the number of 26;Major vicious accidents were mainly caused by accidents between the motor vehicles and the number was 11.(3) In one day accidents mainly happened at 8:00-10:00 ,and 14:00-18:00.(4) The most common injuries were the head and face injuries, with the number of 921, followed by multi-site combined injuries with the number of 761, and lower limb injuries, with the number of 541.(5) Human factors were the main causes of accidents, followed by vehicle factors. CONCLUSION: The illegal driving and walking through the pedestrian lane were the main causes of car accidents. Strengthening traffic safety education of the public, especially of the floating population, rigorous training of drivers for traffic rules and regulations, enhancing the public awareness of road safety, and improving the road traffic management and control measures were the main measures to prevent and control traffic injuries.

[Study on the functions of peripheral dendritic cells in chronic hepatitis B virus infection patients of Gan-depression Pi-deficiency syndrome and Gan-Dan damp-heat syndrome under different immune states].

OBJECTIVE: To observe the functions of peripheral dendritic cells (DCs) in chronic hepatitis B virus (HBV) infection patients of Gan-depression Pi-deficiency syndrome (GPS) and Gan-Dan damp-heat syndrome (GDS) under different immune states, thus to study the features of the immune expressions of the two syndromes in chronic HBV infection, providing objective evidence for Chinese medicine syndrome typing. METHODS: The 40 chronic HBV patients were randomly assigned to two groups according to the immune state. Of them, there were 20 chronic HBV patients (under the condition of immune clearance; consisting of 10 patients of GPS and 10 of GDS) and 20 chronic HBV carriers (under the condition of immune tolerance; consisting of 10 patients of GPS and 10 of GDS). Besides, 10 healthy graduate volunteers of Hunan University of Traditional Chinese Medicine were recruited as the healthy control group. Their peripheral blood mononuclear cells (PBMCs) were cultured in vitro. The exterior morphological features and ultrastructure were observed by inverted microscope and electron microscope. The expressions of HLA-DR, CD80, CD86, and CDIa of the DCs surface were detected. The secretory levels of IL-12 in the supernate of DCs were detected by ELISA reagent kit. The proliferation capacities of allogeneic mixed lymphocyte were detected using MTT. The function features of DCs in the chronic HBV patients of two syndrome types under different immune states were compared, thus analyzing the difference of each index between the two syndrome types. RESULTS: Compared with the healthy control group, the expression rates of CD86, CD80, and HLA-DR decreased in the HBV carriers group (of the two syndrome types), showing statistical difference (P < 0.05). The expression rate of CD80 decreased in the HBV group (of the two syndrome types), showing statistical difference (P < 0.05). The expression rates of CD86 and HLA-DR were lower in the GPS group than in the GDS group. The expression rate of CD80 was lower in the GPS group than in the GDS group, showing statistical difference (P < 0.05). The proliferation capacities of IL-12 and T lymphocytes were lower in the HBV patients group than in the healthy control group (P < 0.05). The proliferation capacities of IL-12 and T lymphocytes were lower in the GPS group than in the GDS group, showing statistical difference (P < 0.05). CONCLUSIONS: The functions of peripheral DCs in chronic HBV infection of patients of the GPS and the GDS under different immune states were different. The phenotype and function tests of DCs provided objective evidence for Chinese syndrome typing of chronic hepatitis B, thus reflecting the features of immune expressions of the two syndrome types and the immunology connotation.

Outcomes After Management of Subspine and Femoroacetabular Impingement Using a Direct Anterior Mini-Open Approach.

BACKGROUND: Subspine impingement (SSI) has been commonly managed with arthroscopic decompression. However, arthroscopic decompression is a demanding technique, as under- or over-resection of the anterior inferior iliac spine (AIIS) could lead to inferior outcomes. An anterior mini-open approach has also been used in the management of femoroacetabular impingement (FAI), and it could provide adequate visualization of the anterior hip joint without a long learning curve. PURPOSE/HYPOTHESIS: The objective of the current study was to compare the outcomes of SSI patients with FAI who underwent arthroscopic subspine decompression and osteoplasty with a group undergoing subspine decompression and osteoplasty using a modified direct anterior mini-open approach. It was hypothesized that there would be no significant difference in outcomes between the groups. STUDY DESIGN: Cohort study; Level of evidence, 3. METHODS: We reviewed the records of SSI patients who underwent decompression surgery (arthroscopic or mini-open) at our institution from June 1, 2015 to December 31, 2016. Both groups underwent the same postoperative rehabilitation protocol. Preoperative and 2-year postoperative patient-reported outcomes were compared using the modified Harris Hip Score (mHHS), International Hip Outcome Tool-33 (iHOT-33), and Hip Outcome Score-Activities of Daily Living (HOS-ADL). Major and minor complications as well as reoperation rates were recorded. RESULTS: Included were 47 patients (49 hips) who underwent subspine decompression using an anterior mini-open approach and 35 patients (35 hips) who underwent arthroscopic subspine decompression. There were no differences in demographic and radiological parameters between the groups, and patients in both groups showed significant improvement in all outcome scores at follow-up. The pre- to postoperative improvement in outcome scores was also similar between groups (mini-open vs arthroscopy: mHHS, 26.30 vs 27.04 [P = .783]; iHOT-33, 35.76 vs 31.77 [P = .064]; HOS-ADL, 26.09 vs 22.77 [P = .146]). In the mini-open group, 10 of the 47 patients had temporary meralgia paresthetica, and fat liquefaction was found in 1 female patient. There were no reoperations in the mini-open group. CONCLUSION: Subspine decompression using the anterior mini-open approach had similar outcomes to arthroscopic decompression in the management of SSI. The lateral femoral cutaneous nerve should be protected carefully during use of the anterior mini-open approach.

Glucocorticoids induce apoptosis and matrix metalloproteinase-13 expression in chondrocytes through the NOX4/ROS/p38 MAPK pathway.

Based on the results from our previous study, dexamethasone (Dex) increases reactive oxygen species (ROS) levels and subsequently induces cell death and matrix catabolism in chondrocytes. Nevertheless, the mechanism underlying this phenomenon remains unclear. Nicotinamide adenine dinucleotide (phosphate) (NADPH) oxidase 4 (NOX4) is one of the major enzymes responsible for intracellular ROS production during the inflammatory process. The objective of the current study was to investigate the role of NOX4 in Dex-induced ROS over-production. Healthy chondrocytes were harvested from the cartilage debris from 6 female patients. NOX4 and p38 mitogen-activated protein kinase (MAPK) expression levels in these cells were evaluated in the presence of Dex. Changes in the number of apoptotic and viable Dex-treated chondrocytes were recorded after the cells were treated with NOX and p38 MAPK inhibitors. Changes in matrix metalloproteinase 13 (MMP-13) expression levels in Dex-treated chondrocytes were also investigated. The Dex treatment increased NOX4 expression via the glucocorticoid receptor (GR). Treatment of cells with apocynin, a NOX inhibitor, decreased intracellular ROS levels and inhibited p38 MAPK activation. Treatment of cells with a ROS scavenger also reduced p38 MAPK expression. Treatment of cells with a NOX inhibitor, ROS scavenger and p38 MAPK inhibitor rescued chondrocytes from Dex-induced apoptosis. Moreover, treatment of cells with these agents blocked MMP-13 expression in Dex-treated chondrocytes. NOX4 silencing also suppressed p38 MAPK and MMP-13 expression. Dex triggered apoptosis and MMP-13 expression through the NOX4/ROS/p38 MAPK signaling pathway. NOX4 may be a therapeutic target in the management of Dex-induced complications.

[Serum level of HMGB1 in patients with hepatitis B and its clinical significance].

OBJECTIVE: To investigate whether there is a possible role of pro-inflammatory cytokine high mobility group box protein 1 (HMGB1) causing liver failure in severe hepatitis B patients. METHODS: Serum HMGB1 levels of chronic hepatitis B (CHB) patients with different clinical conditions were measured and the correlations between HMGB1 and TBil or PTA were analyzed. (1) 54 chronic hepatitis B patients in different clinical conditions were enrolled in our study. Their serum TBil and PTA levels were detected by routine methods. (2) Their serum HMGB1 levels were also detected. 100 KD super-filtration columns were used to get rid of large proteins in the serum and 10 KD columns were used to condense the protein. Western blot was used to determine HMGB1 levels, and correlations between HMGB1 and TBil or PTA were analyzed. RESULTS: The detection rates of serum HMGB1 were 100% (23/23), 90% (9/10), and 55% (6/11) in 23 patients with hepatic failure, 10 patients with chronic severe hepatitis B, and 11 patients with chronic moderate hepatitis B respectively. The concentration of serum HMGB1 levels in these three groups was (83.4+/-21.3), (78.1+/-19.5) and (60.3+/-14.3) microg/L respectively. Serum HMGB1 was not detected in normal healthy controls and hardly detected in convalescent and mild hepatitis patients. There were positive correlations between HMGB1 and TBil and negative correlations between HMGB1 and PTA. CONCLUSION: HMGB1 levels in serum were closely associated with disease severity in chronic hepatitis B patients. HMGB1 may play a key role in the pathogenesis of chronic severe hepatitis B and liver failure.

Kidney stones may increase the risk of coronary heart disease and stroke: A PRISMA-Compliant meta-analysis.

BACKGROUND: We aimed to quantitatively assess the potential relationship between kidney stones and coronary heart disease or stroke. METHODS: A meta-analysis was conducted on eligibly studies published before 31 May 2016 in PubMed or Embase. The data were pooled, and the relationship was assessed by the random-effect model with inverse variance-weighted procedure. The results were expressed as relative risk (RR) with 95% confidence intervals (95%CI). RESULTS: Eight studies of 11 cohorts (n = 11) were included in our analysis with 3,658,360 participants and 157,037 cases. We found that a history of kidney stones was associated with increased risk of coronary heart disease (CHD) (RR = 1.24; 95%CI: 1.14-1.36; I = 79.0%, n = 11); similar effect on myocardial infarction, a serious condition of CHD, was observed (RR = 1.24; 95%CI: 1.10-1.40; I = 80.4%, n = 8). We also found that a history of kidney stones may increase the risk of stroke (RR = 1.21, 95%CI: 1.06-1.38; I = 54.7%, n = 4). In subgroup analysis, the risk of coronary heart disease was higher in men (RR = 1.23, 95%CI: 1.02-1.49) while the risk for stroke was higher in women (RR = 1.12; 95%CI: 1.03-1.21). No obvious publications bias was detected (Egger test: P = .47). CONCLUSION: Kidney stones are associated with increased risk of coronary heart disease and stroke, and the effect may differ by sex.

Effect of active Notch signaling system on the early repair of rat sciatic nerve injury.

It is all known that dedifferentiated Schwann cells (SCs) play an important role in neural regeneration, and Notch signaling has complex and extensive regulatory functions in dedifferentiated SCs. So studies have focused on how to improve peripheral nerve repair by regulating proliferation and dedifferentiation in SCs with Notch signaling meloculars.We have found SCs can be activated when adding Recombinant rat jagged1/FC chimera (an activator of the Notch signaling system) in vivo. Compared with that of the control groups, at 4 weeks post-surgery nerve regeneration and functional rehabilitation in the Recombinant rat jagged1/FC chimera group were advanced significantly, and the expression of neurotrophic factors in the regenerated nerves was elevated largely. These results indicated that SCs activated by Notch signaling could promote nerve repair effectively in the early regenerative stage, suggesting the possible clinical application for the treatment of peripheral nerve defects.

L-arginine-glycine amidinotransferase, betaine-homocysteine S-methyltransferase, and neuropolypeptide H3 are diminished in renal clear cell carcinoma of humans.

OBJECTIVE: To identify renal clear cell carcinoma-associated marker proteins. METHODS: Twelve patients with renal cell carcinoma (RCC) were collected and processed in the Department of Urology, Renmin Hospital, Wuhan University, China, between January 2008 and September 2009. Two-dimensional polyacrylamide gel electrophoresis and matrix assisted laser desorption ionisation time-of-flight mass spectrometry (MALDI-TOF-MS) were employed to investigate differentially expressed protein spots between RCC tissues and adjacent normal tissues, then reverse transcription polymerase chain reaction and western blot were employed to confirm the proteomic results. RESULTS: One protein spot was upregulated, 13 were downregulated, and 22 were absent in RCC tissues. Four of the absent proteins were L-arginine-glycine amidinotransferase (AGAT), Betaine-homocysteine S-methyltransferase (BHMT), Ketohexokinase (KHK), and Neuropolypeptide h3 (NPh3). The reverse transcriptase-polymerase chain reaction analysis demonstrated mRNA expression of AGAT, BHMT, and Nph3 was significantly decreased in 12 RCC tissues. In addition, Western blot analysis showed AGAT protein was absent in 11/12, BHMT in 9/12, and Nph3 in 5/12 RCC tissues. CONCLUSION: Absence of AGAT, BHMT, and Nph3 is common events in clear cell RCC; hence, it may be involved in the development of RCC; therefore, they have the potential to be tumor markers for diagnosis, treatment, and prognosis of RCC patients.

Interferon-γ improves renal interstitial fibrosis and decreases intrarenal vascular resistance of hydronephrosis in an animal model.

OBJECTIVES: To investigate the effect of interferon (IFN)-γ administration on renal interstitial fibrosis (RIF) and intrarenal vascular resistance of diseased kidneys in a reversible unilateral ureteral obstruction (RUUO) animal model. METHODS: Thirty-six male Sprague-Dawley rats were randomly divided into three groups: RUUO with intramuscular IFN-γ treatment (400 IU/d; RUUO + IFN), RUUO with vehicle treatment, and sham operation. RUUO was induced by clamping the left ureter using a small polyethylene tube. The obstruction was reversed seven days after the operation by removing the tube. Six animals in each group were killed at days 7 and 14. The intrarenal resistive index (RI) of diseased kidneys was measured by colored Doppler flow imaging. RIF was evaluated using Masson's trichrome staining. RESULTS: The obstruction was successfully reversed in all animals. At day 7, the RIF scores were 32.1 ± 3.1 and 40.3 ± 3.1 in the RUUO + IFN group and the RUUO group, respectively. The RI increased by 87% in the RUUO group and by 64% in the RUUO + IFN group compared with sham. At day 14, the RIF scores decreased to 24.6 ± 3.9 in the RUUO + IFN group, but increased to 50.8 ± 4.4 in the RUUO group. The increase of RI was reduced to 64% in the RUUO group and to 20% in the RUUO + IFN group. Ureteral obstruction induced few lesions in the contralateral kidneys, and IFN-γ administration had no significant effect on them, although it exerted an antifibrotic effect on the obstructed kidneys. CONCLUSIONS: IFN-γ administration restored or preserved renal histology and hemodynamics in an animal model of renal fibrosis after surgical reversal of hydronephrosis.