Severe congenital neutropenia and liver abscess: Surgical treatment breaks the vicious cycle.

Here, we present a case with genetically confirmed SCN. The main symptom of the child was recurring fever. The combination of antibiotics combined with G-CSF injection was proved to be insufficient, and the patient developed "solid" liver abscess. After undergoing surgical anatomical hepatic lobectomy, the child's infection symptoms showed improvement. The postoperative culture of the purulent material from the liver infection lesion revealed an infection with Staphylococcus aureus. Our case raises the possibility of pathogen sources and routes of infection, clinical characteristics, and effective treatment for SCN patients with concomitant liver abscess.

Dopamine Functionalized Polyethylene Glycol for Improving Stability of Gold Nanoparticles against Reactive Oxygen Species in Serum.

PEGylation is the most effective antifouling method for the surface modification of gold nanoparticles (AuNPs). However, thiol-terminated polyethylene glycol (PEG) ligands tethered on the AuNPs are instable in serum and can detach from the AuNP surface, resulting in a significant reduce of their antifouling properties. Herein, it is reported that reactive oxygen species (ROS) is a major factor causing the detachment of PEG ligands from AuNP surfaces. By covalently backfilling dopamine-functionalized PEG on the AuNPs, the stability of PEG ligands on AuNP surface and the antifouling ability of AuNPs can be effectively improved. Tuning the balance between ROS and dopamine-functionalized PEG can be used as a new strategy to control the self-assembly of AuNPs and serum proteins.

PHLDA3 promotes lung adenocarcinoma cell proliferation and invasion via activation of the Wnt signaling pathway.

The PHLDA3 gene encodes a small 127 amino acid protein with a pleckstrin homology (PH)-only domain. The expression and significance of PHLDA3 in lung cancer remain unclear. Here, we investigated the role of PHLDA3 in tumor proliferation and invasion in lung adenocarcinoma. Immunohistochemistry and immunoblotting analyses were used to assess PHLDA3 expression in lung cancer tissues, and its correlation with clinicopathological factors in lung cancer. Plasmids encoding PHLDA3 and small interfering RNA against PHLDA3 were used to regulate the expression of PHLDA3 in lung cancer cells. Furthermore, the effects of PHLDA3 on lung cancer cell proliferation and invasion were investigated using the MTS, colony formation, Matrigel invasion, and wound healing assays. Co-immunoprecipitation analysis and inhibitors of both the Wnt signaling pathway and GSK3ß were used to explore the regulatory mechanisms underlying the role of PHLDA3 in lung cancer cells. PHLDA3 was found to be overexpressed in lung cancer tissues, and its expression was correlated with poor outcomes in lung adenocarcinoma patients. PHLDA3 expression promoted the proliferation, invasion, and migration of lung cancer cells. Overexpression of PHLDA3 activated the Wnt signaling pathway and facilitated epithelial-mesenchymal transition. Inhibition of Wnt signaling pathway activity, using XAV-939, reversed the effects of PHLDA3 overexpression in lung cancer cells; moreover, PHLDA3 could bind to GSK3ß. Inhibition of GSK3ß activity, using CHIR-99021, restored the proliferative and invasive abilities of PHLDA3 knockdown cells. Our findings demonstrate that PHLDA3 is highly expressed in lung adenocarcinomas and is correlated with poor outcomes. Furthermore, it promotes the proliferation and invasion of lung cancer cells by activating the Wnt signaling pathway.

DEK is highly expressed in breast cancer and is associated with malignant phenotype and progression.

DEK proto-oncogene (DEK) has been demonstrated as an oncogene and is associated with the development of many types of tumor; however, the expression and role of DEK in breast cancer remain unknown. The present study aimed to determine the role of DEK in the progression of breast cancer. The expression of DEK in 110 breast cancer tissues and 50 adjacent normal breast tissues was examined using immunohistochemistry. Furthermore, DEK expression was upregulated by DEK transfection or downregulated by DEK shRNA interference in MCF7 cells. Proliferative and invasive abilities were examined in MCF7 cells using MTT assay, colony-formation assay and transwell invasion assays. The results demonstrated that DEK expression level was significantly increased in breast cancer tissues compared with normal breast tissues. Furthermore, high DEK expression was associated with high histological grade, lymph node metastasis, advanced Tumor-Node-Metastasis stage and high Ki-67 index; however, DEK expression was not associated with the expression level of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. High DEK expression indicated poor prognosis in patients with breast cancer. DEK overexpression upregulated the protein expression of ß-catenin and Wnt and increased the proliferative and invasive abilities of breast cancer cells. DEK downregulation had the opposite effect. Taken together, the results from the present study demonstrated that high expression of DEK was common in patients with breast cancer and was associated with progression of the disease and poor prognosis, and that DEK overexpression promoted the proliferative and invasive abilities of breast cancer cells.

TRIP13 promotes the proliferation and invasion of lung cancer cells via the Wnt signaling pathway and epithelial-mesenchymal transition.

Thyroid hormone receptor interactor 13 (TRIP13) is an ATPase that has been found to be overexpressed in many tumors. The aim of this study was to investigate the role of TRIP13 and its mechanism of action in lung cancer. The expression of TRIP13 was examined in lung cancer tissues and corresponding normal lung tissues by western blotting. TRIP13 was overexpressed or knocked down by transient transfection or siRNA interference in lung cancer cells, respectively. The expression of key proteins associated with the Wnt signaling pathway and epithelial-mesenchymal transition (EMT) was assessed. The interaction between TRIP13 and low-density lipoprotein receptor-related protein 6 (LRP6) was examined by co-immunoprecipitation and laser confocal immunofluorescence. Moreover, this study determined the proliferative and invasive ability of cells through colony formation, cell proliferation, and Matrigel invasion assays. The expression of TRIP13 was higher in lung cancer tissues than in normal lung tissues (p = 0.002), and this correlated with poor patient prognosis (p < 0.001). In addition, overexpression of TRIP13 enhanced the levels of active ß-catenin and target proteins of the Wnt signaling pathways (p < 0.05). This study found that TRIP13 can co-localize and bind with LRP6. Furthermore, overexpression of TRIP13 caused the upregulation of N-cadherin, Snail, and vimentin, and the downregulation of E-cadherin (p < 0.05). The aforementioned results were reversed after knocking down the expression of TRIP13 (p < 0.05). TRIP13 is highly expressed in lung cancers, indicating poor prognosis. overexpression of TRIP13 promotes the proliferative and invasive ability of lung cancer cells via the activation of Wnt signaling pathway and EMT.

FAM83A Promotes Lung Cancer Progression by Regulating the Wnt and Hippo Signaling Pathways and Indicates Poor Prognosis.

FAM83A (family with sequence similarity 83, member A) has been found to be highly expressed in cancers. The purpose of this study was to clarify the role and mechanism of FAM83A in lung cancers. The expression of FAM83A in lung cancer cells was enhanced by gene transfection or knocked down by small interfering RNA interference. The key proteins of the Wnt signaling pathway, the Hippo signaling pathway, and epithelial-mesenchymal transition (EMT) were examined using Western blot. The proliferation and invasion of lung cancer cells were examined using cell proliferation, colony formation, and invasion assays. The expression of FAM83A in lung cancer tissues was significantly increased and was correlated with advanced tumor-node-metastasis (TNM) stage and poor prognosis. Overexpression of FAM83A enhanced the proliferation, colony formation, and invasion of lung cancer cells. Meanwhile, FAM83A overexpression increased the expression of active ß-catenin and Wnt target genes and the activity of EMT. Furthermore, in FAM83A-overexpressed cells, the activity of Hippo pathway was downregulated, whereas the expression of yes-associated protein (YAP) and its downstream targets cyclin E and CTGF were upregulated. The inhibitor of the Wnt signaling pathway, XAV-939, reversed the promoting effect of FAM83A on YAP, cyclin E, and CTGF. On knocking down the expression of FAM83A, we obtained the opposite results. However, the inhibitor of GSK3ß, CHIR-99021, restored the expression of YAP, cyclin E, and CTGF after FAM83A was knocked down. FAM83A is highly expressed in lung cancers and correlated with advanced TNM stage and poor prognosis. FAM83A promotes the proliferation and invasion of lung cancer cells by regulating the Wnt and Hippo signaling pathways and EMT process.

DEK promotes the proliferation and invasion of lung cancers and indicates poor prognosis in lung adenocarcinomas.

DEK has been revealed to be overexpressed in many cancers and associated with cancer progression. The aim of the present study was to elucidate the role of DEK with a specific focus on its underlying mechanism in lung cancers. DEK expression in lung cancers and normal lung tissues and the correlations between DEK expression and clinicopathological parameters of lung cancers were investigated using the data from The Cancer Genome Atlas (TCGA). DEK expression was upregulated by DEK transfection or downregulated by DEK shRNA interference in A549 and H1299 cells. The effects of DEK on the Wnt signaling pathway and epithelial­mesenchymal transition (EMT) were examined using western blotting. Proliferative and invasive abilities were observed in A549 and H1299 cells treated with DEK using an MTT assay, colony formation assay, and Transwell migration and invasion assays. The expression of DEK was higher in lung cancer tissues than that in normal lung tissues. DEK expression was positively correlated with the expression of epidermal growth factor receptor (EGFR) and KRAS in lung adenocarcinomas. High expression of DEK indicated poor prognosis in lung adenocarcinomas (P=0.018). Enhanced expression of DEK upregulated the levels of active­ß­catenin and Wnt target genes, such as cyclin D1, c­Myc and MMP7 and increased the proliferative and invasive abilities of lung cancer cells. Enhanced expression of DEK in A549 and H1299 cells also increased the levels of EGFR, KRAS, vimentin, Snail, and N­cadherin, and decreased the level of E­cadherin. The opposite results were obtained with knockdown of DEK expression. DEK was highly expressed in lung cancers and indicated poor prognosis in lung adenocarcinomas. DEK expression activated the Wnt signaling pathway and EMT process and promoted the proliferation and invasion of lung cancers.

Overexpression of KRT17 promotes proliferation and invasion of non-small cell lung cancer and indicates poor prognosis.

PURPOSE: Keratin 17 (KRT17) is a 48 KDa type I intermediate filament, which is mainly expressed in epithelial basal cells. KRT17 has been shown to be overexpressed in many malignant tumors and play an important role in the occurrence and development of tumors. Therefore, this study explored the role and underlying mechanism of KRT17 in non-small cell lung cancers (NSCLC). METHODS: KRT17 expression and its correlations with clinicopathological factors were examined in lung cancer tissues by immunohistochemistry. The prognosis value of KRT17 in NSCLCs was retrieved from The Cancer Genome Atlas (TCGA) online databases. The expression level of KRT17 was increased or decreased by KRT17 gene transfection or small RNA interference in lung cancer cells, respectively. Further, proliferation and invasiveness of lung cancer cells were determined by cell proliferation and invasion assays, respectively. Finally, expression levels of proteins related to Wnt signaling pathways and epithelial mesenchymal transition (EMT) were detected by Western blot. RESULTS: The expression level of KRT17 in NSCLCs was significantly higher than normal lung tissues. High expression of KRT17 predicted poor prognosis of patients with NSCLCs, especially lung adenocarcinomas, and was correlated with poor differentiation and lymphatic metastasis. Overexpression of KRT17 enhanced, while KRT17 knockdown inhibited, the proliferation and invasiveness of lung cancer cells. Overexpression of KRT17 up-regulated ß-catenin activity and levels of Wnt target genes, such as cyclin D1, c-Myc, and MMP7. Moreover, KRT17 promoted EMT by up-regulating Vimentin, MMP-9, and Snail expression and down-regulating E-cadherin expression. CONCLUSION: Overexpression of KRT17 is common in NSCLCs and indicates poor prognosis. Overexpression of KRT17 enhances the proliferation and invasiveness of NSCLC cells by activating the Wnt signaling pathway and EMT process. KRT17 is a potential indicator of NSCLC progression and poor survival.

Association of C8orf4 expression with its methylation status, aberrant ß-catenin expression, and the development of cervical squamous cell carcinoma.

Chromosome 8 open reading frame 4 (C8orf4) is an activator of Wnt signaling pathway, and participates in the tumorigenesis and progression of many tumors. The expression levels of C8orf4 and ß-catenin were assessed via immunohistochemical staining in 100 cervical squamous cell carcinoma (CSCC) tissues, 50 high-grade squamous intraepithelial lesions (HSILs), 50 low-grade squamous intraepithelial lesions (LSILs), and 50 normal cervical tissues. Bisulfite sequencing polymerase chain reaction analysis was used to examine the methylation status of the C8orf4 locus in CSCC and normal cervical tissues. The expression rates of C8orf4 and ß-catenin were significantly higher in CSCCs or HSILs than in LSILs or normal cervical tissues (P < .05). C8orf4 expression was positively correlated with the poor differentiation of CSCCs (P = .009), and with aberrant expression of ß-catenin in CSCCs (P = .002) and squamous intraepithelial lesions (P < .001). The methylation rate of C8orf4 in CSCCs was significantly lower than that in normal cervical tissues (P = .001). The Cancer Genome Atlas genomics data also confirmed that the mRNA expression of C8orf4 was positively associated with the copy number alteration of C8orf4 (correlation coefficient = 0.213, P < .001), and negatively correlated with the methylation level of C8orf4 (correlation coefficient = -0.408, P < .001). In conclusion, the expressions of C8orf4 and ß-catenin were synergistically increased in CSCCs and HSILs and higher than those in LSILs and normal cervical tissues. The methylation level of C8orf4 is decreased in CSCCs and is responsible for the increased expression of C8orf4.

Primary malignant mesothelioma of the diaphragm with liver invasion: A case report and review of literature.

RATIONALE: Malignant mesothelioma is a malignant tumor with poor prognosis, which usually originates in the pleura, peritoneum, and pericardial cavity. Mesotheliomas that originate from the diaphragm are very rare. Here, we report a case of primary malignant mesothelioma of the diaphragm with liver invasion. PATIENT CONCERNS: A 66-year-old woman was admitted to our hospital because of a "liver space-occupying lesion," without any special clinical symptoms. Imaging examinations suggested a cystic-solid mixed lesion in the right lobe of the liver. DIAGNOSIS: The tumor was diagnosed as epithelioid mesothelioma of the diaphragm with liver invasion. INTERVENTION: The patient underwent abdominal surgery in our hospital to remove the diaphragmatic mass, liver mass, and part of the diaphragm. OUTCOMES: The postoperative course was uneventful. LESSONS: Primary diaphragmatic malignant mesothelioma is very rare and may involve liver or lung tissue and be mistaken for liver or lung tumor. Accurate diagnosis depends on careful pathological examination. Immunohistochemical staining is very useful to distinguish this tumor from other liver or diaphragmatic tumors.

PRDM16 functions as a suppressor of lung adenocarcinoma metastasis.

BACKGROUND: The transcription factor PR domain containing 16 (PRDM16) is known to play a significant role in the determination and function of brown and beige fat. However, the role of PRDM16 in tumor biology has not been well addressed. Here we investigated the impact of PRDM16 on tumor growth and metastasis in lung cancer. METHODS: UALCAN database, immunoblotting and immunohistochemistry analysis were used to assess PRDM16 expression in lung cancer patients. Kaplan-Meier plotter database was used to analyze the overall survival of patients with lung cancer stratified by PRDM16 expression. PRDM16 overexpression and knockdown experiments were conducted to assess the effects of PRDM16 on growth and metastasis in vitro and in vivo, and its molecular mechanism was investigated in lung adenocarcinoma cells by chromatin immunoprecipitation-sequencing (ChIP-Seq), real time-quantitative PCR (RT-qPCR), luciferase assay, xenograft models and rescue experiments. RESULTS: PRDM16 was downregulated in lung adenocarcinomas, and its expression level correlated with key pathological characteristics and prognoses of lung adenocarcinoma patients. Overexpressing PRDM16 inhibited the epithelial-to-mesenchymal transition (EMT) of cancer cells both in vivo and in vitro by repressing the transcription of Mucin-4 (MUC4), one of the regulators of EMT in lung adenocarcinomas. Furthermore, deleting the PR domain from PRDM16 increased the transcriptional repression of MUC4 by exhibiting significant differences in histone modifications on its promoter. CONCLUSIONS: Our findings demonstrate a critical interplay between transcriptional and epigenetic modifications during lung adenocarcinoma progression involving EMT of cancer cells and suggest that PRDM16 is a metastasis suppressor and potential therapeutic target for lung adenocarcinomas.

An evidence-based etiology study of synovial cyst of knee cruciate ligament: a real or pseudo-cyst.

PURPOSE: Synovial cyst of knee cruciate ligament (SCKCL) is a rare condition but can cause severe knee pain. The understanding of its etiology is relatively poor. This current study aimed to elucidate the pathogenesis of SCKCL based on a series of histo- and cytopathological examination. METHODS: Ten SCKCL patients who underwent arthroscopy were enrolled, among five patients claimed past knee injury. Hematoxylin & eosin staining was conducted to the cyst wall tissue sections and Papanicolaou staining to the cyst fluid smear. Prussian blue staining was employed to both the wall section and fluid smear. Immumohistochemical staining for mesothelial cells (MC), epithelial cells (CK), vascular endothelial cells (CD31), monocytes (CD68), and hematogenous stem cells (CD117) were taken to elucidate the possible involvement of various cell types in the development of SCKCL. RESULTS: No erythrocyte was discovered in the fluid; however, Prussian blue stained hemosiderin particles were found in the cyst wall and fluid, suggesting past hemorrhage in all patients. Abundant lymphocytes and plasmocytes were observed in the cyst wall and fluid. In addition, the cyst lining was infiltrated with abundant CD68(+) monocytes while only few MC(+) mesothelial cells were sporadically observed in four samples. The cyst submucosa was also diffused with abundant CD68(+) monocytes and proliferated capillaries stained with CD31. CD117-positve hematogenous stem cells were sporadically observed in eight specimens. CONCLUSION: Our findings provided evidence that SCKCL is not a mature synovial cyst but rather an inflammatory pseudo-cyst. It may have resulted from past minor hemorrhage and intra-ligament chronic inflammation.

Overexpression of Nemo-like Kinase Promotes the Proliferation and Invasion of Lung Cancer Cells and Indicates Poor Prognosis.

BACKGROUND: Nemo-like kinase (NLK) is an evolutionarily conserved MAP kinaserelated kinase involved in the pathogenesis of several human cancers. OBJECTIVE: The aim of this study was to investigate the expression and role of NLK in lung cancers, and its underlying mechanisms. METHODS: We examined the expression of NLK in lung cancer tissues through western blot analysis. We enhanced or knocked down NLK expression by gene transfection or RNA interference, respectively, in lung cancer cells, and examined expression alterations of key proteins in the Wnt signaling pathway and in epithelial-mesenchymal transition (EMT). We also examined the roles of NLK in the proliferation and invasiveness of lung cancer cells by cell proliferation, colony formation, and Matrigel invasion assays. RESULTS: NLK expression was found to be significantly higher in lung cancer tissue samples than in corresponding healthy lung tissue samples. Overexpression of NLK correlated with poor prognosis of patients with lung cancer. Overexpression of NLK upregulated ß-catenin, TCF4, and Wnt target genes such as cyclin D1, c-Myc, and MMP7. N-cadherin and TWIST, the key proteins in EMT, were upregulated, while E-cadherin expression was reduced. Additionally, proliferation, colony formation, and invasion turned out to be enhanced in NLK-overexpressing cells. After NLK knockdown in lung cancer cells, we obtained the opposite results. CONCLUSION: NLK is overexpressed in lung cancers and indicates poor prognosis. Overexpression of NLK activates the Wnt signaling pathway and EMT and promotes the proliferation and invasiveness of lung cancer cells.

Mussel-inspired nano-silver loaded layered double hydroxides embedded into a biodegradable polymer matrix for enhanced mechanical and gas barrier properties.

In this paper, a facile, green and mussel-inspired method is presented to prepare silver loaded layered double hydroxides (Ag-LDHs@PDA and Ag-LDHs@TA-Fe(iii)) using a pre-synthesis polydopamine (PDA)/tannic acid (TA)-Fe(iii) layer as a nanoscale guide and PDA/TA itself as a reducing reagent to form uniform silver nanoparticles (AgNPs) on the surface of modified LDHs. Meanwhile, another kind of LDH, Ag-LDHs(PVP), was prepared via the direct reduction of the precursor [Ag(NH3)2]+ with polyvinyl pyrrolidone (PVP). And three kinds of Ag-LDHs/poly(ε-caprolactone) (PCL) nanocomposite were prepared by blending Ag-LDHs and pure PCL via a solution casting method to obtain homogeneous films. It is shown that the obtained AgNPs are distributed on the LDH surfaces uniformly. And the high loading and medium size of the AgNPs present in Ag-LDHs(PVP) give it the best antibacterial properties. However, compared with Ag-LDHs(PVP), the better dispersibilities of Ag-LDHs@PDA and Ag-LDHs@TA-Fe(iii) contribute to the greater aspect ratios of Ag-LDHs in the matrices, resulting in an increase in the number of tortuous paths for gas diffusion. Meanwhile, Ag-LDHs@PDA and Ag-LDHs@TA-Fe(iii) have stronger interactions with the PCL matrix, which is favorable for the existence of less interface defects in the matrix, resulting in an improvement in the mechanical and gas barrier properties. Therefore, mussel-inspired antibacterial Ag-LDHs/PCL nanocomposites show preferable mechanical and gas barrier properties.

Odd-skipped related 1 inhibits lung cancer proliferation and invasion by reducing Wnt signaling through the suppression of SOX9 and ß-catenin.

The odd-skipped related 1 (OSR1) gene encodes a zinc-finger transcription factor. The expression and significance of OSR1 in human tumors remains unclear. We found that OSR1 was downregulated in lung cancers, and its expression was correlated with poor differentiation. Overexpression of OSR1 by OSR1 gene transfection into H1299 cells (H1299-OSR1) inhibited the proliferation and invasion of lung cancer cells. Knockdown of OSR1 with small interfering (si)RNA against OSR1 in A549 cells (A549-siOSR1) enhanced the proliferation and invasion of lung cancer cells. Western blot analysis showed that the expression level of GSK3ß increased, while that of p-GSK3ß, nuclear ß-catenin, cyclin D1, c-Myc and matrix metallopeptidase 7 significantly decreased in the H1299-OSR1 cells, and this pattern was reversed in the A549-siOSR1 cells compared to that in the control cells. Furthermore, upregulation of sex-determining region Y-box 9 (SOX9) by SOX9 gene transfection increased the expression of ß-catenin, which was inhibited by OSR1. The mRNA and protein expression levels of SOX9 and ß-catenin were reduced in H1299-OSR1 cells and increased in A549-siOSR1 cells. In conclusion, the expression of OSR1 was more reduced in lung cancer tissues than in normal lung tissues, and was correlated with poor differentiation. OSR1 downregulated the activity of the Wnt signaling pathway by suppressing the expression of SOX9 and ß-catenin.

Diversity of ionizing radiation-resistant bacteria obtained from the Taklimakan Desert.

So far, little is known about the diversity of the radiation-resistant microbes of the hyperarid Taklimakan Desert. In this study, ionizing radiation (IR)-resistant bacteria from two sites in Xinjiang were investigated. After exposing the arid (water content of 0.8 ± 0.3%) and non-arid (water content of 21.3 ± 0.9%) sediment samples to IR of 3000 Gy using a (60)Co source, a total of 52 γ-radiation-resistant bacteria were isolated from the desert sample. The 16S rRNA genes of all isolates were sequenced. The phylogenetic tree places these isolates into five groups: Cytophaga-Flavobacterium-Bacteroides, Proteobacteria, Deinococcus-Thermus, Firmicutes, and Actinobacteria. Interestingly, this is the first report of radiation-resistant bacteria belonging to the genera Knoellia, Lysobacter, Nocardioides, Paracoccus, Pontibacter, Rufibacter and Microvirga. The 16s rRNA genes of four isolates showed low sequence similarities to those of the published species. Phenotypic analysis showed that all bacteria in this study are able to produce catalase, suggesting that these bacteria possess reactive oxygen species (ROS)-scavenging enzymes. These radiation-resistant bacteria also displayed diverse metabolic properties. Moreover, their radiation resistances were found to differ. The diversity of the radiation-resistant bacteria in the desert provides further ecological support for the hypothesis that the ionizing-radiation resistance phenotype is a consequence of the evolution of ROS-scavenging systems that protect cells against oxidative damage caused by desiccation.

The geometry of the bone structure associated with total hip arthroplasty.

Close adaptation of the prosthesis to the bone is the key to achieving optimal stability and fixation for total hip arthroplasty (THA). However, there have been no adequate studies of bone morphology, especially in different races. The aim of this study was to analyze the geometry of the acetabulum and proximal femur of people from South China, based on three-dimensional reconstruction, and to detect differences between different population subsets. CT scans were performed on 80 healthy volunteers (160 hips) from South China, comprising 40 males (80 hips) and 40 females (80 hips). The images were imported into Mimics 10.01 to perform 3D reconstruction. THA-associated anatomical parameters were measured and compared with other published data. In comparison with published data, it seemed that people from South China have smaller acetabular abduction angle, larger acetabular supro-inferior diameter, larger neck-shaft angle, smaller offset, thinner femoral shaft and more proximal isthmus, which needed to be further confirmed. There were significant differences between the genders in most parameters. As significant differences in canal flare index (CFI) and distal canal flare index (DCFI) were found between genders, it was concluded the most significant differences lay in the isthmus of the femur. Among the femora, according to Noble's classification we identified more normal types and fewer stovepipe and champagne-flute types than expected from the literature, indicating that uncemented prostheses would be suitable for most people from South China. Our findings reveal that simply choosing the smallest of a series of prostheses would not necessarily provide a good fit, due to the different trends from the proximal to the distal part of the femur. Significant variation exists in THA-associated anatomy between genders and population subsets. It is therefore imperative that each patient receives individual consideration rather than assuming all patients have the same anatomy, especially for different races.

Measurement and comparison of tibial posterior slope angle in different methods based on three-dimensional reconstruction.

BACKGROUND: The tibial posterior slope (PTS) is an important parameter for sagittal alignment which is associated with postoperative range of motion. However, the variations of different population subsets and different referential axes are still uncertain. METHODS: In this study, 80 healthy people from South China were recruited and measured on three-dimensional reconstruction of CT, with application of three referential axes, the proximal tibial long axis, the anterior and posterior cortices. RESULTS: The averages and standard deviations of medial PTS (MPTS) in the three methods were 8.43±3.06, 11.45±2.82 and 6.31±3.24, separately. The results of lateral PTS (LPTS) were 7.56±2.51, 10.17±2.42 and 5.22±2.59. There was no significant difference between the male and the female, and the two sides of one body. The results of the three axes varied but correlated with each other significantly. Through comparison it was found that, MPTS/LPTS of people from South China were different from the published data of other countries. CONCLUSIONS: Although PTS change markedly according to the reference axis, they show significant correlations with each other, and may be used safely. There are differences associated with races, but not gender nor the two sides of the body. CLINICAL RELEVANCE: The results of the study provided references for the reconstruction of the knee PTS, if the differences of reference axes, races and genders were considered.

The efficacy and safety of infliximab used in patients with ankylosing spondylitis after unilateral total hip arthroplasty.

A retrospective study was performed in patients with ankylosing spondylitis (AS) from south China, to investigate the efficacy and safety of infliximab after total hip arthroplasty (THA). Thirty-two AS patients were divided into two groups. The treatmen group recieved infliximab at four weeks after unilateral THA (11 patients) and were compare to a control group (21 patients). Patients in the control group were treated with traditional medications. Clinical assessment, laboratory examinations, and x-rays were performed pre- and postoperatively. The BASDAI score decreased more in the infliximab group at six and 12 months after THA, as did the CRP and ESR. The contralateral hips without arthroplasty of patients in the infliximab group improved significantly compared to the control group, in terms of Harris score (HHS), range of motion (ROM) and VAS. However, the hips with an arthroplasty in the control group had a better prognosis than those without arthroplasty of the infliximab group. Hips with arthroplasty in the infliximab group achieved better improvement of HHS than hips without arthroplasty in the control group, but not for ROM and pain relief. No radiological evidence of prosthetic loosening was found in either group. There was no significant difference of the incidence of adverse events between the two groups. Compared with THA, AS patients using infliximab only did not obtain as good an outcome. Infliximab was shown to be safe and could be effective to improve hip function and systemic symptoms.

Etanercept in the treatment of ankylosing spondylitis: a meta-analysis of randomized, double-blind, placebo-controlled clinical trials, and the comparison of the Caucasian and Chinese population.

BACKGROUND AND PURPOSE: Ankylosing spondylitis (AS) is a kind of rheumatic disease, leading to pain, fatigue, stiffness, and functional impairment, which seriously affects the quality of life. Etanercept, a fully human recombinant protein, has been applied for the treatment of AS. However, there has not been a systematic analysis for its efficacy and safety. METHODS: This meta-analysis of fourteen randomized, double-blind, placebo-controlled clinical trials with 1,570 participants was performed to investigate the efficacy and safety of etanercept, by means of calculating the overall relative risk, and to compare the different responses between the Caucasian population and the Chinese population. RESULTS: Generally, there was sufficient evidence to prove that etanercept has its advantages in both disease activity controlling and symptoms relieving, especially for axial joints compared with peripheric joints, without higher incidence of serious adverse events. INTERPRETATION: Our preliminary analysis provided that the Caucasian population has better response to etanercept treatment, with more treatment-emergent adverse events. Further specially designed clinical trials need to be performed to investigate the different responses between axial and peripheric joints, also between different races.