A root-knot nematode effector targets the Arabidopsis cysteine protease RD21A for degradation to suppress plant defense and promote parasitism.

Meloidogyne incognita is one of the most widely distributed plant-parasitic nematodes and causes severe economic losses annually. The parasite produces effector proteins that play essential roles in successful parasitism. Here, we identified one such effector named MiCE108, which is exclusively expressed within the nematode subventral esophageal gland cells and is upregulated in the early parasitic stage of M. incognita. A yeast signal sequence trap assay showed that MiCE108 contains a functional signal peptide for secretion. Virus-induced gene silencing of MiCE108 impaired the parasitism of M. incognita in Nicotiana benthamiana. The ectopic expression of MiCE108 in Arabidopsis suppressed the deposition of callose, the generation of reactive oxygen species, and the expression of marker genes for bacterial flagellin epitope flg22-triggered immunity, resulting in increased susceptibility to M. incognita, Botrytis cinerea, and Pseudomonas syringae pv. tomato (Pst) DC3000. The MiCE108 protein physically associates with the plant defense protease RD21A and promotes its degradation via the endosomal-dependent pathway, or 26S proteasome. Consistent with this, knockout of RD21A compromises the innate immunity of Arabidopsis and increases its susceptibility to a broad range of pathogens, including M. incognita, strongly indicating a role in defense against this nematode. Together, our data suggest that M. incognita deploys the effector MiCE108 to target Arabidopsis cysteine protease RD21A and affect its stability, thereby suppressing plant innate immunity and facilitating parasitism.

Integrative identification of hub genes in development of atrial fibrillation related stroke.

BACKGROUND: As the most common arrhythmia, atrial fibrillation (AF) is associated with a significantly increased risk of stroke, which causes high disability and mortality. To date, the underlying mechanism of stroke occurring after AF remains unclear. Herein, we studied hub genes and regulatory pathways involved in AF and secondary stroke and aimed to reveal biomarkers and therapeutic targets of AF-related stroke. METHODS: The GSE79768 and GSE58294 datasets were used to analyze AF- and stroke-related differentially expressed genes (DEGs) to obtain a DEG1 dataset. Weighted correlation network analysis (WGCNA) was used to identify modules associated with AF-related stroke in GSE66724 (DEG2). DEG1 and DEG2 were merged, and hub genes were identified based on protein-protein interaction networks. Gene Ontology terms were used to analyze the enriched pathways. The GSE129409 and GSE70887 were applied to construct a circRNA-miRNA-mRNA network in AF-related stroke. Hub genes were verified in patients using quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: We identified 3,132 DEGs in blood samples and 253 DEGs in left atrial specimens. Co-expressed hub genes of EIF4E3, ZNF595, ZNF700, MATR3, ACKR4, ANXA3, SEPSECS-AS1, and RNF166 were significantly associated with AF-related stroke. The hsa_circ_0018657/hsa-miR-198/EIF4E3 pathway was explored as the regulating axis in AF-related stroke. The qRT-PCR results were consistent with the bioinformatic analysis. CONCLUSIONS: Hub genes EIF4E3, ZNF595, ZNF700, MATR3, ACKR4, ANXA3, SEPSECS-AS1, and RNF166 have potential as novel biomarkers and therapeutic targets in AF-related stroke. The hsa_circ_0018657/hsa-miR-198/EIF4E3 axis could play an important role regulating the development of AF-related stroke.

The Mutation of BTG2 Gene Predicts a Poor Outcome in Primary Testicular Diffuse Large B-Cell Lymphoma.

Introduction: Primary testicular diffuse large B-cell lymphoma (PT-DLBCL) is a rare and aggressive form of mature B-cell lymphoma commonly found in elder males, but its genetic features are poorly understood. In this study, we had performed target-sequencing of 360 lymphoma-related genes on 76 PT-DLBCL patients with a median age of 65 (33-89). Our data provide a comprehensive understanding of the landscape of mutations in a small subset of PT-DLBCL. Methods: A total of 76 PT-DLBCL patients were sequenced, and their clinical data and follow-up data were collected. The relationship between mutated genes, clinical data and prognosis and survival of PT-DLBCL patients was retrospectively analyzed by statistical software. Results: We observed a median of 15 protein-altering variants per patient in our data and was identified recurrent oncogenic mutations of 360 lymphoma-related genes involved in PT-DLBCL, including PIM1 (74%), MYD88 (50%), KMT2D (38%), KMT2C (34%), BTG2 (34%), TBL1XR1 (34%) and ETV6 (24%). Compared with classic DLBCL, PT-DLBCL showed an increased mutation frequency of PIM1, MYD88, BTG2, while NOTCH1 appeared exclusive mutated with PIM1, MSH3 and ETV6. Cox risk model regression analysis showed that age ≥60 years, IPI 3-5 points, BTG2 gene mutation and extranodal organ invasion suggested poor prognosis. Finally, we constructed an OS predict model of PT-DLBCL patients using above factors with a high accuracy. Conclusion: In conclusion, our results revealed genomic characterization of PT-DLBCL, and the mutation of BTG2 was an independent factor predicting a poor prognosis.

The Prognostic Role of Cyclin D1 in Multiple Myeloma: A Systematic Review and Meta-Analysis.

Purpose: Cyclin D1 has been identified as a proto-oncogene associated with the uncontrolled proliferation of tumor cells. This systematic review and meta-analysis aims to estimate the prognostic significance of cyclin D1 in multiple myeloma (MM) patients. Method: We searched for qualified data in PubMed, Embase, and Web of Science up to February 2020. Data quality was assessed by the Newcastle-Ottawa scale (NOS). Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were used to evaluate the relationship between cyclin D1 expression and overall survival (OS), progression-free survival (PFS)/event-free survival (EFS) in patients with MM. Result: A total of 13 studies involving 961 patients were included. Overall, pooled analysis revealed significant heterogeneity between cyclin D1 expression and the prognosis of MM (OS, HR = 1.08, 95% CI: 0.71-1.64, I2 = 67.9%; PFS/EFS, HR = 0.97, 95% CI: 0.49-1.93, I2 = 85.8%). Subgroup analysis revealed that the prolongation of OS was relevant to increased expression of cyclin D1 in MM patients in the relapsed and refractory group (OS, HR = 0.46, 95% CI: 0.24-0.90). Another subgroup assessment of OS established that MM patients with CCND1 overexpression in the bortezomib group had longer survival time (HR = 0.30, 95% CI: 0.11-0.82), whereas, those overexpressing CCND1 in the conventional chemotherapy group had poor prognosis (HR = 2.19, 95% CI: 1.18-4.08). We also found that increased cyclin D1 expression correlated favorably with PFS in the autologous stem cell transplantation (ASCT) (HR = 0.45, 95% CI: 0.28-0.73) or reverse transcription-polymerase chain reaction (RT-PCR) group (HR = 0.41, 95% CI: 0.26-0.64). Conclusion: The result of this meta-analysis suggested that CCND1 overexpression might be a predictive biomarker for MM patients when treated with bortezomib, receiving ASCT, or in relapsed and refractory period.

Recombinant unpurified rETXH106P/ CTB-rETXY196E protects rabbits against Clostridium perfringens epsilon toxin.

Epsilon toxin (ETX), produced by Clostridium perfringens types B and D, has been touted as a potential biological weapon and is known to induce fatal enterotoxemia in a variety of livestock animals. For the efficient production of recombinant proteins with the objective of investigating the effects of different recombinant vaccines against ETX, a bicistronic design (BCD) expression system including the ETX coding sequence with mutation of amino acid 106 from Histidine to Proline (ETXH106P) in the first cistron, followed by Cholera Toxin B (CTB) linked with the ETX coding sequence with mutation of amino acid 196 from Tyrosine to Glutamic acid (ETXY196E) in the second cistron, was generated under the control of a single promoter. Rabbits were immunized twice with five inactivated recombinant Escherichia coli (E. coli) vaccines containing 100 µg/ml of the recombinant mutant rETXH106P/CTB-rETXY196E proteins mixed with different adjuvants. Apart from rETXH106P/CTB-rETXY196E-IMS1313-vaccinated rabbits, the neutralizing antibody titers of rETXH106P/CTB-rETXY196E-vaccinated rabbits were higher after the initial immunization than those administered the ETX toxoid or current commercial vaccines. rETXH106P/CTB-rETXY196E mixed with ISA201 induced the highest neutralizing antibody titer of 120 after the first immunization, suggesting that 0.1 ml of pooled sera could neutralize 120× mouse LD100 (100% lethal dose) of ETX. Following the second vaccination, rETXH106P/CTB-rETXY196E mixed with ISA201 or GR208 produced the highest neutralizing titer of 800. Rabbits from all vaccinated groups were completely protected from a 2× rabbit LD100 of ETX challenge. These results show that these novel recombinant proteins can induce a strong immune response and represent potential targets for the development of a commercial vaccine against the C. perfringens epsilon toxin.

Single versus dual elastic nails for closed reduction and antegrade intramedullary nailing of displaced fifth metacarpal neck fractures.

Closed reduction and internal fixation with antegrade intramedullary nails is a feasible and effective treatment for displaced fifth metacarpal neck fractures (FMNFs). The present study aimed to compare clinical and radiological outcomes in patients with displaced FMNFs after treatment with single or dual antegrade elastic intramedullary nails (AEIMNs). Thirty-three patients were treated with a single 2.0 mm AEIMN and 34 patients were treated with two 1.5 mm AEIMNs. Clinical and radiological outcomes included grip strength, active range of motion (ROM), active flexion and extension of the fifth metacarpophalangeal (MCP) joint, dorsal angulation loss, and metacarpal shortening of the fifth metacarpal at 12 months after treatment. No significant difference was observed between the two groups with respect to grip strength, ROM or flexion of the fifth MCP joint. The average values of dorsal angulation loss, metacarpal shortening, and extension of the fifth MCP joint of the dual nails group were better than those of the single nail group (dorsal angulation loss, 2.79 ± 1.93° vs. 4.05 ± 1.59°, P = 0.009; metacarpal shortening, 1.66 ± 0.80 mm vs. 2.12 ± 0.88 mm, P = 0.028; extension of the fifth MCP joint, 7.71 ± 4.43° vs. 4.82 ± 4.09°, P = 0.012). In conclusion, dual AEIMNs fixation provided better MCP extension and radiological outcomes than single AEIMN fixation.

A new low-profile anatomic locking plate for fixation of comminuted, displaced greater tuberosity fractures of the proximal humerus.

BACKGROUND: Although various implants exist for the fixation of isolated greater tuberosity fractures, few implants are specifically designed for such fractures. The purpose of this study was to investigate the clinical and radiologic outcomes of open reduction-internal fixation with a low-profile anatomic locking plate for comminuted greater tuberosity fractures of the proximal humerus. METHODS: From November 2012 to February 2018, 24 patients with displaced and comminuted isolated greater tuberosity fractures were treated with the new low-profile anatomic locking plate. To determine clinical outcomes, we evaluated active range of motion; the visual analog scale pain score; the Constant-Murley score; the Disabilities of the Arm, Shoulder and Hand score; radiographs; and complications. RESULTS: In all cases, a mean follow-up period of 29.3 months (range, 18-48 months) was completed. All patients achieved bone union with a mean healing time of 11.3 weeks (range, 8-16 weeks). The mean Constant-Murley score was 91.1 points (range, 69-100 points), with a rate of good to excellent results of 95.8%. The average Disabilities of the Arm, Shoulder and Hand score was 9.9 points (range, 2-25 points), and the mean visual analog scale pain score was 1.1 points (range, 0-4 points). Mean active forward flexion, abduction, external rotation, and internal rotation (level) were 157°, 152°, and 40°, and T11, respectively. Postoperatively, 1 patient had persistent shoulder stiffness, and 1 patient had recurrence of shoulder dislocation because of a falling injury during badminton. No serious complications such as subacromial impingement, malunion, nonunion, loss of reduction, or implant failure occurred. CONCLUSIONS: The new low-profile anatomic locking plate was useful for the treatment of comminuted isolated greater tuberosity fractures as it provided reliable stability and satisfactory radiographic and functional results. The described technique is a simple and effective method and provides a new reliable option for the treatment of isolated greater tuberosity fractures.

The role of cystatin C as a proteasome inhibitor in multiple myeloma.

Objectives: Bone destruction and renal impairment are two frequent complications of multiple myeloma (MM). Cystatin C, an extracellular cysteine proteinase inhibitor, is encoded by the housekeeping gene CST3 and associated with human tumors. The role of cystatin C in multiple myeloma has been revealed recently. The purpose of this study was to explore the role of cystatin C as a proteasome inhibitor in multiple myeloma. Methods : A comprehensive literature review was conducted through Pubmed to summarize the published evidence on cystatin C in multiple myeloma. English literature sources since 1999 were searched, using the terms cystatin C, multiple myeloma. Results: cystatin C is a sensitive indicator for the diagnosis of myeloma nephropathy and has a dual role in myeloma bone disease. Also, cystatin C reflects tumor burden and is strongly associated with prognosis in patients with multiple myeloma. Conclusion: Cystatin C have great diagnostic and prognostic value in multiple myeloma. It can provide a new treatment direction for MM by designing and searching for antagonists of cystatin C or cysteine protease agonists using cystatin C as a therapeutic target.

ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L.

This study aimed to investigate whether annexin A7 (ANXA7) could promote the cell cycle, proliferation and cell adhesion-mediated drug resistance (CAM-DR) of multiple myeloma (MM) cells by up-regulating cell division cycle 5-like (CDC5L). As a result, ANXA7 expression was increased in the serum of MM patients and the expression of ANXA7 and CDC5L was also increased in MM cell lines. ANXA7 overexpression promoted the proliferation and cycle of U266 and RPMI8226 cells. The expression of proliferation cell nuclear antigen (PCNA), KI67, cyclin dependent kinase 1 (CDK1) and cyclinB1 in transfected cells was consistent with the changes of proliferation and cell cycle. In co-culture system of BMSC cells and MM cells, expression of CD44, ICAM1 and VCAM1 in MM cells was increased, which was further increased by ANXA7 overexpression. Bortezomib could increase the apoptosis of U266 and RPMI8226 cells. In co-culture system of BMSC cells and MM cells, the promotion effects of bortezomib on apoptosis of MM cells was decreased, which was further suppressed by ANXA7 overexpression. The above effects exerted by ANXA7 overexpression could be reversed by ANXA7 interference. Moreover, ANXA7 was proved to be combined with CDC5L. CDC5L interference could inhibit the promotion effects of ANXA7 overexpression on proliferation and cell cycle and inhibition effects of ANXA7 overexpression on apoptosis of MM cells treated with bortezomib in co-culture system. In conclusion, ANXA7 could promote the cell cycle, proliferation and CAM-DR of MM cells by up-regulating CDC5L.

Hydroxygenkwanin Suppresses Non-Small Cell Lung Cancer Progression by Enhancing EGFR Degradation.

Epidermal growth factor receptor (EGFR) is frequently overexpressed and mutated in non-small cell lung cancer (NSCLC), which is the major type of lung cancer. The EGFR tyrosine kinase inhibitors (TKIs) are the approved treatment for patients harboring activating mutations in the EGFR kinase. However, most of the patients treated with EGFR-TKIs developed resistance. Therefore, the development of compounds exhibiting unique antitumor activities might help to improve the management of NSCLC patients. The total flavonoids from Daphne genkwa Sieb. et Zucc. have been shown to contain antitumor activity. Here, we have isolated a novel flavonoid hydroxygenkwanin (HGK) that displays selective cytotoxic effects on all of the NSCLC cells tested. In this study, we employed NSCLC cells harboring EGFR mutations and xenograft mouse model to examine the antitumor activity of HGK on TKI-resistant NSCLC cells. The results showed that HGK suppressed cancer cell viability both in vitro and in vivo. Whole-transcriptome analysis suggests that EGFR is a potential upstream regulator that is involved in the gene expression changes affected by HGK. In support of this analysis, we presented evidence that HGK reduced the level of EGFR and inhibited several EGFR-downstream signalings. These results suggest that the antitumor activity of HGK against TKI-resistant NSCLC cells acts by enhancing the degradation of EGFR.

The GSK­3ß/ß­catenin signaling pathway is involved in HMGB1­induced chondrocyte apoptosis and cartilage matrix degradation.

Knee osteoarthritis (KOA) is a common joint disease with a high incidence rate among middle­aged and elderly individuals. However, the precise underlying pathological mechanisms and effective treatment of this disease remain to be determined. To explore the effect of high mobility group box 1 (HMGB1) on chondrocyte apoptosis and catabolism, the ATDC5 cell line was cultured as an in vitro model for cartilage research. Cultured cells were treated with recombinant HMGB1 at different concentrations. Hoechst staining and flow cytometry demonstrated that HMGB1 administration significantly induced apoptosis of ATDC5 cells, which was the same as the effect of interleukin­1ß treatment. HMGB1 also induced cartilage matrix degradation, as shown by Alcian blue staining. Moreover, HMGB1 markedly upregulated the expression levels of matrix metallopeptidases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), while genetic silencing of HMGB1 significantly suppressed their expressions. The glycogen synthase kinase (GSK)­3ß/ß­catenin pathway was activated upon HMGB1 treatment. Pharmacological inhibitors or HMGB1 knockdown inactivated the GSK­3ß/ß­catenin pathway, inhibited the expression levels of downstream genes, including MMPs and ADAMTS, and attenuated the apoptosis of ATDC5 cells. Furthermore, the data demonstrated that HMGB1 promoted chondrocyte dysfunction via the regulation of estrogen sulfotransferase and Runt­related transcription factor 2. Thus, the findings of the present study demonstrated that HMGB1 induces chondrocyte cell apoptosis via activation of GSK­3ß/ß­catenin and the subsequent expression of multiple targeted genes.

Immunization of rabbits with recombinant Clostridium perfringens alpha toxins CPA-C and CTB-CPA-C in a bicistronic design expression system confers strong protection against challenge.

The Clostridium perfringens alpha toxin (CPA), encoded by the plc gene, is the causative pathogen of gas gangrene, which is a lethal infection. In this study, we used an E. coli system for the efficient production of recombinant proteins and developed a bicistronic design (BCD) expression construct consisting of two copies of the C-terminal (247-370) domain of the alpha toxin (CPA-C) in the first cistron, followed by Cholera Toxin B (CTB) linked with another two copies of CPA-C in the second cistron that is controlled by a single promoter. Rabbits were immunized twice with purified proteins (rCPA-C rCTB-CPA-C) produced in the BCD expression system, with an inactivated recombinant E. coli vaccine (RE), C. perfringens formaldehyde-inactivated alpha toxoid (FA-CPA) and C. perfringensl-lysine/formaldehyde alpha toxoid (LF-CPA) vaccines. Following the second vaccination, 0.1 mL of pooled sera of the RE-vaccinated rabbits could neutralize 12× mouse LD100 (100% lethal dose) of CPA, while that of the rCPA-C rCTB-CPA-C-vaccinated rabbits could neutralize 6× mouse LD100 of CPA. Antibody titers against CPA were also assessed by ELISA, reaching titers as high as 1:2048000 in the RE group; this was significantly higher compared to the C. perfringens alpha toxoid vaccinated groups (FA-CPA and LF-CPA). Rabbits from all vaccinated groups were completely protected from a 2× rabbit LD100 of CPA challenge. These results demonstrate that the recombinant proteins are able to induce a strong immune responses, indicating that they may be potentially utilized as targets for novel vaccines specifically against the C. perfringens alpha toxin.

Three-dimensional mitral valve structure in predicting moderate ischemic mitral regurgitation improvement after coronary artery bypass grafting.

OBJECTIVE: Focusing on 3-dimensional mitral valve structure, this study investigated predictors for moderate ischemic mitral regurgitation (IMR) improvement after off-pump coronary artery bypass grafting (OPCAB). METHODS: This study included 143 patients (age 67.6 ± 7.6 years, 32.9% female) with previous myocardial infarction and moderate IMR undergoing OPCAB. Preoperative 3-dimensional echocardiographic data were analyzed, focusing on mitral annular geometry and leaflet tethering model. Patients were grouped according to IMR at 1-year postoperative follow-up into improved (n = 65), with no or mild IMR, and failure (n = 70), with moderate or severe IMR, groups. Groups were compared to identify predictors of IMR improvement after OPCAB. RESULTS: Eight patients died within 1 year. At 1 postoperative year, improved group included 65 patients; failure group included 70. Improved group had less preoperative annular flattening (smaller nonplanar angle) and segmental leaflet tethering (smaller A3, P1, P2, and P3 tethering angles) than failure group. Nonplanar angle (P < .001) and P3 tethering angle (P < .001) were independent predictors of moderate IMR improvement after OPCAB. Receiver operator characteristic curves defined P3 tethering angle of 28.8° (sensitivity of 78.6%, specificity of 84.6%) and nonplanar angle of 158.1° (sensitivity, 64.3% and specificity of 86.2%) as the cutoff values. CONCLUSIONS: Preoperative moderate IMR can be improved by OPCAB in selected patients. Less annular flattening and P3 leaflet tethering may predict improvement of moderate IMR after OPCAB, suggesting that the annular nonplanar saddle shape and less leaflet tethering toward P3 segment are important for the prognosis of moderate IMR.

Influence of Medial Support Screws on the Maintenance of Fracture Reduction after Locked Plating of Proximal Humerus Fractures.

BACKGROUND: Technical aspects of the correct placement of medial support locking screws in the locking plate for proximal humerus fractures remain incompletely understood. This study was to evaluate the clinical relationship between the number of medial support screws and the maintenance of fracture reduction after locked plating of proximal humerus fractures. METHODS: We retrospectively evaluated 181 patients who had been surgically treated for proximal humeral fractures (PHFs) with a locking plate between September 2007 and June 2013. All cases were then subdivided into one of four groups as follows: 75 patients in the medial cortical support (MCS) group, 26 patients in the medial multiscrew support (MMSS) group, 29 patients in the medial single screw support (MSSS) group, and 51 patients in the no medial support (NMS) group. Clinical and radiographic evaluations included the Constant-Murley score (CM), visual analogue scale (VAS), complications, and revision surgeries. The neck-shaft angle (NSA) was measured in a true anteroposterior radiograph immediately postoperation and at final follow-up. One-way analysis of variance or Kruskal-Wallis test was used for statistical analysis of measurement data, and Chi-square test or Fisher's exact test was used for categorical data. RESULTS: The mean postoperative NSAs were 133.46° ± 6.01°, 132.39° ± 7.77°, 135.17° ± 10.15°, and 132.41° ± 7.16° in the MCS, MMSS, MSSS, and NMS groups, respectively, and no significant differences were found (F = 1.02, P = 0.387). In the final follow-up, the NSAs were 132.79° ± 6.02°, 130.19° ± 9.25°, 131.28° ± 12.85°, and 127.35° ± 8.50° in the MCS, MMSS, MSSS, and NMS groups, respectively (F = 4.40, P = 0.008). There were marked differences in the NSA at the final follow-up between the MCS and NMS groups (P = 0.004). The median (interquartile range [IQR]) NSA losses were 0.0° (0.0-1.0)°, 1.3° (0.0-3.1)°, 1.5° (1.0-5.2)°, and 4.0° (1.2-7.1)° in the MCS, MMSS, MSSS, and NMS groups, respectively (H = 60.66, P < 0.001). There were marked differences in NSA loss between the MCS and the other three groups (MCS vs. MMSS, Z = 3.16, P = 0.002; MCS vs. MSSS, Z = 4.78, P < 0.001; and MCS vs. NMS, Z = 7.34, P < 0.001). There was also significantly less NSA loss observed in the MMSS group compared to the NMS group (Z = -3.16, P = 0.002). However, there were no significant differences between the MMSS and MSSS groups (Z = -1.65, P = 0.225) or the MSSS and NMS groups (Z = -1.21, P = 0.099). The average CM scores were 81.35 ± 9.79, 78.04 ± 8.97, 72.76 ± 10.98, and 67.33 ± 12.31 points in the MCS, MMSS, MSSS, and NMS groups, respectively (F = 18.68, P < 0.001). The rates of excellent and good CM scores were 86.67%, 80.77%, 65.52%, and 43.14% in the MCS, MMSS, MSSS, and NMS groups, respectively (χ2 = 29.25, P < 0.001). The median (IQR) VAS scores were 1 (0-2), 1 (0-2), 2 (1-3), and 3 (1-5) points in the MCS, MMSS, MSSS, and NMS groups, respectively (H = 27.80, P < 0.001). Functional recovery was markedly better and VAS values were lower in the MCS and MMSS groups (for CM scores: MCS vs. MSSS, P < 0.001; MCS vs. NMS, P < 0.001; MMSS vs. MSSS, P = 0.031; and MMSS vs. NMS, P < 0.001 and for VAS values: MCS vs. MSSS, Z = 3.31, P = 0.001; MCS vs. NMS, Z = 4.64, P < 0.001; MMSS vs. MSSS, Z = -2.09, P = 0.037; and MMSS vs. NMS, Z = -3.16, P = 0.003). CONCLUSIONS: Medial support screws might help enhance mechanical stability and maintain fracture reduction when used to treat PHFs with medial metaphyseal comminution or malreduction.

Fabrication and Photoluminescence Study of Large-Area Ordered and Size-Controlled GeSi Multi-quantum-well Nanopillar Arrays.

Large-area ordered GeSi multi-quantum-well nanopillar array (MQW-NPA) samples with different nanopillar lateral sizes (270, 120, and 70 nm) are fabricated by a cost-effective and scalable dry-etching process in combination with nanosphere lithography technique. A significant enhancement in photoluminescence (PL) intensity has been observed in the GeSi MQW-NPA samples compared with the as-grown GeSi MQW one. Nanopillar samples with different lateral sizes show different enhancements in PL intensity. The enhancements are analyzed quantitatively and attributed to three factors. One is the antireflection of the nanopillar structures. Another is an enhanced extraction in nanopillar arrays at the emission wavelength. Thirdly, the GeSi quantum wells in close proximity to the substrates would have more contribution to the PL than before etching. Our results show that all the three factors should be taken into account in designing and fabricating surface microstructures of GeSi MQW materials in order to improve their optical properties.

Tissue levels of leukemia inhibitory factor vary by osteoarthritis grade.

The objective of this study was to observe the expression of leukemia inhibitory factor (LIF) in animals and in different clinical grades of patient osteoarthritic tissues. Thirty-five rabbits were used in a Colombo model of experimental osteoarthritis (OA). Five rabbits each were sacrificed on postoperative days 3, 7, 14, 28, 42, 56, and 84. Immunohistochemistry analysis for LIF expression and distribution in the cartilage and synovium of animals was performed at these times. Sixty-seven samples of human articular tissue were obtained from patients with different grades of OA according to symptoms and radiographic inspection. The mRNA expression of LIF was determined by reverse transcription polymerase chain reaction, and LIF protein was determined by enzyme-linked immunosorbent assay (ELISA). The results showed a slight expression of LIF in normal cartilage tissue but less in synovium tissue; however, the expression of LIF was marked in synovial lining cells and superficial and middle-layer cartilage in animal OA (P<.05). Leukemia inhibitory factor mRNA was expressed at the highest level in moderate degrading subchondral bone, and LIF was expressed at the highest level in seriously degrading articular cartilage tissue. These results were similar to those found with ELISA. This study suggests that LIF in OA articular tissues varies by clinical symptoms and grade. It plays an important role in the pathogenesis of OA.

Left atrial and right atrial deformation in patients with coronary artery disease: a velocity vector imaging-based study.

BACKGROUND: Impaired left ventricular (LV) function has been shown by strain rate (SR) imaging in patients with coronary artery disease (CAD). Our aim was to investigate global and regional, systolic and diastolic left atrial (LA) and right atrial (RA) longitudinal deformation in CAD using velocity vector imaging. METHODS: Echocardiographic and velocity vector imaging studies were performed in 20 patients with mild CAD, 40 patients with severe CAD and 25 controls. Maximal atrial volume, peak atrial longitudinal strain (ε(s)) and SR during LV systole (SRs), SR during early LV filling (SRe) and late LV filling (SRa) were measured. Longitudinal strain during atrial contraction (ε(a)) was obtained at the onset of P-wave on electrocardiography, and ε(a)/ε(s) was calculated. RESULTS: Longitudinal peak ε(s) and SRs of LA showed decreased trend among CAD patients. The global and lateral LA SRe were prominently lower, while RA ε(a), SRa and ε(a)/ε(s) were prominently higher in 2 CAD groups than control group (P value <0.05). As compared with controls and patients with other single-vessel disease, LA SRa and ε(a)/ε(s) ratio were significantly increased among patients with exclusively left anterior descending coronary artery (LAD) stenosis (SRa 1.14±0.38 s(-1), 1.10±0.41 s(-1), 1.45±0.46 s(-1), P value<0.05; ε(a)/ε(s) 0.44±0.11, 0.44±0.20, 0.57±0.12, P value<0.01). CONCLUSIONS: Apparently decreased SRe of LA and increased ε(a), SRa and ε(a)/ε(s) of RA were found in CAD patients with preserved LVEF and E/E' in gray zone. SRa and ε(a)/ε(s) of LA were found to significantly increase in those with LAD stenosis.

Genomic differences between Actinobacillus pleuropneumoniae serotypes 5b and 3 and their distribution and transcription among 15 serotypes.

The development of serotyping-based diagnostic methods and multivalent vaccines has been significantly hampered due to the limited information available on the genetic differences among the 15 currently known serotypes of Actinobacillus pleuropneumoniae. In this study, using the GenomeComp informatics software, differential genes were screened and identified between the complete genome sequences of the serotypes 5b (L20 strain, highly virulent) and 3 (JL03 strain, weakly virulent), 84 presented uniquely in strain L20, while 57 were only found in JL03 strain. Of these, 75 encode putative proteins and 66 encode hypothetical proteins, including phage-related proteins, Apx toxin, capsular polysaccharide biosynthesis proteins, ATP-binding cassette (ABC) transporters, Clp-like proteases, fimbrial protein (Flp), various glycosyltransferases, methylases, integrases, and other proteins related to virulence. To confirm and further characterize the differential genes, we carefully selected 34 proven or putative virulence genes which were extremely useful on researching into detection and vaccine of A. pleuropneumoniae, and investigated the distribution and transcription of these genes among the 15 serotypes through polymerase chain reaction, reverse transcriptase- polymerase chain reaction and sequencing, and different distribution and transcription patterns of the differential genes in each serotype were first found and described. These information of these differential genes among the 15 serotypes of A. pleuropneumoniae may greatly serve as an indicator for future research on the pathogenic mechanisms of different serotypes, serotyping-based diagnostic methods, and multivalent vaccines.

[Construction and characterization of a brucella suis S2 strain with a chloramphenicol resistance marker].

Vaccination has not been used widely because of the interference in the discrimination between infected and vaccinated animals in immune-screening procedures. In the present study, chloramphenicol resistance gene (Cm(r)) was cloned into the genomic DNA of brucella suis S2 strain by homologous recombination with knocking out the WbkC gene, and obtained the recombinant rS2-WbkC. Further study confirmed that rS2-WbkC was conversed into rough-phenotype form smooth-phenotype. The recombinant keeps the ability to chloramphenicol resistance after 25 passages in tryptic soy agar (TSA). Mice tests showed rS2-WbkC offered similar protection to S2 strain, but more safe than S2. Serum collected form rS2-WbkC immunized mice could be easily distinguished from antiserum produced by smooth-phenotype brucella abortus. In view of these result, rS2-WbkC is a promising candidate for vaccine strain.