Coexistence of Ferromagnetism and Ferroelectricity in Cu-Intercalated Bilayer CrI3.

Design of two-dimensional (2D) multiferroic materials with two or more ferroic orders in one structure is highly desired in view of the development of next-generation electronic devices. Unfortunately, experimental or theoretical discovery of 2D intrinsic multiferroic materials is rare. Using first-principles calculation methods, we report the realization of multiferroics that couple ferromagnetism and ferroelectricity by intercalating Cu atoms in bilayer CrI3, Cux@bi-CrI3 (x = 0.03, 0.06, and 0.25). Our results show that the intercalation of Cu atoms leads to the inversion symmetry breaking of bilayer CrI3 and produces intercalation density-dependent out-of-plane electric polarization, around 18.84-90.31 pC·cm-2. Moreover, the switch barriers of Cux@bi-CrI3 in both polarization states are small, ranging from 0.31 to 0.69 eV. Furthermore, the magnetoelectric coupling properties of Cux@bi-CrI3 can be modulated via varying the metal ion intercalation density, and half-metal to semiconductor transition can be occurred by decreasing the intercalation density of metal ions. Our work paves a practical path for 2D magnetoelectron coupling devices.

GNG12 as A Novel Molecular Marker for the Diagnosis and Treatment of Glioma.

Purpose: GNG12 influences a variety of tumors; however, its relationship with glioma remains unclear. The aim of this study was to comprehensively investigate the relationship between GNG12 and the clinical characteristics and prognosis of glioma patients and reveal the mechanisms causing the malignant process of GNG12. Materials and Methods: We obtained information on clinical samples from multiple databases. The expression level of GNG12 was validated using a RT-qPCR and IHC. KM curves were used to assess the correlation between the GNG12 expression and OS of glioma patients. An ROC curve was drawn to assess the predictive performance of GNG12. Univariate and multivariate Cox analyses were performed to analyze the factors affecting the prognosis of patients with glioma. GSEA and TIMER databases were used to estimate the relationship between GNG12 expression, possible molecular mechanisms, and immune cell infiltration. CMap analysis was used to screen candidate drugs for glioma. Subsequent in vitro experiments were used to validate the proliferation and migration of glioma cells and to explore the potential mechanisms by which GNG12 causes poor prognosis in gliomas. Results: GNG12 was overexpressed in glioma patients and GNG12 expression level correlated closely with clinical features, including age and histological type, etc. Subsequently, the K-M survival analysis indicated that the expression level of GNG12 was relevant to the prognosis of glioma, and the ROC curve implied that GNG12 can predict glioma stability. Univariate and multivariate analyses showed that GNG12 represents a risk factor for glioma occurrence. GNG12 expression is closely associated with some immune cells. Additionally, several in vitro experiments demonstrated that down-regulation of GNG12 expression can inhibits the proliferation and migration capacity of glioma cells. Ultimately, the results for the GSEA and WB experiments revealed that GNG12 may promote the malignant progression of gliomas by regulating the cell adhesion molecule cell signaling pathway. Conclusion: In this study, we identified GNG12 as a novel oncogene elevated in gliomas. Reducing GNG12 expression inhibits the proliferation and migration of glioma cells. In summary, GNG12 can be used as a novel biomarker for the early diagnosis of human gliomas and as a potential therapeutic target.

Identification of PYGL as a key prognostic gene of glioma by integrated bioinformatics analysis.

Aim: PYGL has been reported to have carcinogenic effects in a variety of tumors. This study is the first to reveal the relationship between PYGL and the prognosis of glioma. Materials & methods: Analyzing the Chinese Glioma Genome Atlas database, the authors revealed the expression status and prognostic value of PYGL in gliomas and used quantitative real-time PCR to verify PYGL expression again. Subsequently, they used Gene Set Enrichment Analysis to explore the biological pathways that PYGL may participate in. The authors also used the tumor immune estimation resource database to explore the relationship between PYGL and tumor immune cells. Results: PYGL is involved in the malignant progression of glioma. Conclusions: PYGL can be used as a new biomarker and molecular target for evaluating the prognosis and immunotherapy of glioma.

ITGB3BP is a potential biomarker associated with poor prognosis of glioma.

Despite the growing recognition of ITGB3BP as an essential feature of various cancers, the relationship between ITGB3BP and glioma remains unclear. The main aim of this study was to determine the prognostic and diagnostic value of ITGB3BP in glioma. RNA-Seq and microarray data from 2222 glioma patients were included, and we found that the expression level of ITGB3BP in glioma tissues was significantly higher than that in normal brain tissues. Moreover, ITGB3BP can be considered an independent risk factor for poor prognosis and has great predictive value for the prognosis of glioma. Gene Set Enrichment Analysis results showed that ITGB3BP contributes to the poor prognosis of glioma by activating tumour-related signalling pathways. Some small-molecule drugs were identified, such as hexestrol, which may specifically inhibit ITGB3BP and be useful in the treatment of glioma. The TIMER database analysis results revealed a correlation between the expression of ITGB3BP and the infiltration of various immune cells in glioma. Our findings provide the first evidence that the up-regulation of ITGB3BP correlates with poor prognosis in human glioma. Thus, ITGB3BP is a potential new biomarker that can be used for the clinical diagnosis and treatment of glioma.

Overexpression of GINS4 is associated with poor prognosis and survival in glioma patients.

BACKGROUND: GINS4, an indispensable component of the GINS complex, is vital for a variety of cancer. However, no known empirical research has focused on exploring relationships between GINS4 and glioma. Thus, this study aims to understand and explain the role of GINS4 in glioma. METHOD: First, we used the data in the CGGA, TCGA, GEO, GEPIA, and HPA databases to explore the expression level of GINS4 in glioma, the correlation between GINS4 expression and the clinical features of glioma, its impact on the survival of glioma patients, and verified the analysis results through RT-qPCR, IHC, and meta-analysis. Subsequently, GSEA enrichment analysis is used to find the potential molecular mechanism of GINS4 to promote the malignant process of glioma and the anti-glioma drugs that may target GINS4 screened by CMap analysis. Moreover, we further explored the influence of the GINS4 expression on the immune microenvironment of glioma patients through the TIMER database. RESULTS: Our results suggested that GINS4 was elevated in glioma, and the overexpression of GINS4 was connected with a vast number of clinical features. The next, GINS4 as an independent prognostic factor, which can result in an unfavorable prognosis of glioma. Once more, GINS4 may be participating in the oncogenesis of glioma through JAK-STAT signaling pathways, etc. 6-thioguanine, Doxazosin, and Emetine had potential value in the clinical application of drugs targeting GINS4. Finally, the expression exhibited a close relationship with some immune cells, especially Dendritic cells. CONCLUSION: GINS4 is an independent prognostic factor that led to a poor prognosis of glioma. The present study revealed the probable underlying molecular mechanisms of GINS4 in glioma and provided a potential target for improving the prognosis of glioma.

Significantly high expression of NUP37 leads to poor prognosis of glioma patients by promoting the proliferation of glioma cells.

BACKGROUND: The carcinogenic effect of NUP37 has been reported recently in a variety of tumors, but its research in the field of glioma has not been paid attention. The main purpose of this study is to reveal the relationship between NUP37 and prognosis or clinical characteristics of glioma patients. METHODS: First, as a retrospective study, this study included thousands of tissue samples based on a variety of public databases and clinicopathological tissues. Second, a series of bioinformatics analysis methods were used to analyze the NUP37 and glioma samples from multiple databases such as the CGGA, TCGA, GEO, HPA, and GEPIA. Third, to analyze the relationship between the expression level of NUP37 in tumor tissues and cells and a variety of clinical prognostic molecular characteristics, whether it can be an independent risk factor leading to poor prognosis in glioma and whether it has clinical diagnostic value; GSEA was used to analyze the cancer-related signaling pathways that may be activated by high expression of NUP37. Fifth, CMap was used to analyze small molecule drugs that may inhibit NUP37 expression. Finally, the meta-analysis of thousands of tissue samples from seven datasets and cell proliferation and migration experiments confirmed that NUP37 has a malignant effect on glioma. RESULTS: NUP37 is highly expressed in glioma patient tissues and glioma cells, significantly correlates with reduced overall survival, and may serve as an independent prognostic factor with some diagnostic value. Silencing NUP37 suppresses malignant biological behaviors of glioma cells. 4 small molecule drugs that had potential targeting inhibitory effects on NUP37 overexpression. CONCLUSIONS: This study demonstrates for the first time a malignant role of NUP37 in glioma and provides a vision to unravel the complex pathological mechanisms of glioma and a potentially valuable biomarker for implementing individualized diagnosis and treatment of glioma.

Role of RHOC in evaluating an adverse prognosis in patients with glioma and its potential prognostic value.

In recent years, major discoveries have indicated that Ras homology family member C (RHOC) is involved in the occurrence and pathological progression of a number of malignant tumours; nevertheless, the role served by RHOC in glioma remains unclear. The present study aimed to gain further insight into the biological function and expression of RHOC in human glioma based on the Chinese Glioma Genome Atlas (CGGA). The current study analysed ~1,000 glioma samples from the CGGA. First, RHOC expression was analysed according to the clinical features associated with the prognosis of glioma, such as clinical stage, histological type and age. Second, the Kaplan-Meier method was used, revealing that the survival rate of patients with glioma with high RHOC expression was significantly lower than that of patients with low RHOC expression. Receiver operating characteristic curve analysis indicated that RHOC had moderate diagnostic value for patients with glioma. Gene set enrichment analysis indirectly indicated that RHOC mainly participated in the pathological mechanism of glioma through p53, extracellular matrix receptor interaction and focal adhesion. Finally, the aforementioned results were further verified using The Cancer Genome Atlas data and reverse transcription-quantitative PCR technology. To the best of our knowledge, the present study was the first comprehensive in-depth analysis of RHOC, revealing the potential value of RHOC as a novel oncogene in glioma. The current study provided a novel potential biomarker for the diagnosis and prognosis of glioma, and re-examined the pathological mechanism of glioma from a new perspective.

GNG5 is a novel oncogene associated with cell migration, proliferation, and poor prognosis in glioma.

BACKGROUND: Although many biomarkers have been reported for detecting glioma, the prognosis for the disease remains poor, and therefore, new biomarkers need to be identified. GNG5, which is part of the G-protein family, has been associated with different malignant tumors, though the role of GNG5 in glioma has not been studied. Therefore, we aimed to identify the relationship between GNG5 and glioma prognosis and identify a new biomarker for the diagnosis and treatment of gliomas. METHODS: We used data on more than a thousand gliomas from multiple databases and clinical data to determine the expression of GNG5 in glioma. Based on clinical data and CGGA database, we identified the correlation between GNG5 and multiple molecular and clinical features and prognosis using various analytical methods. Co-expression analysis and GSEA were performed to detect GNG5-related genes in glioma and possible signaling pathways involved. ESTIMATE, ssGSEA, and TIMER were used to detect the relationship between GNG5 and the immune microenvironment. Functional experiments were performed to explore the function of GNG5 in glioma cells. RESULTS: GNG5 is highly expressed in gliomas, and its expression level is positively correlated with pathological grade, histological type, age, and tumor recurrence and negatively correlated with isocitrate dehydrogenase mutation, 1p/19 co-deletion, and chemotherapy. Moreover, GNG5 as an independent risk factor was negatively correlated with the overall survival time. GSEA revealed the potential signaling pathways involved in GNG5 function in gliomas, including cell adhesion molecules signaling pathway. The ssGSEA, ESTIMATE, and TIMER based analysis indicated a correlation between GNG5 expression and various immune cells in glioma. In vivo and in vitro experiments showed that GNG5 could participate in glioma cell proliferation and migration. CONCLUSIONS: Based on the large data platform and the use of different databases to corroborate results obtained using various datasets, as well as in vitro and in vivo experiments, our study reveals for the first time that GNG5, as an oncogene, is overexpressed in gliomas and can inhibit the proliferation and migration of glioma cells and lead to poor prognosis of patients. Thus, GNG5 is a potential novel biomarker for the clinical diagnosis and treatment of gliomas.

Overexpressed XRCC2 as an independent risk factor for poor prognosis in glioma patients.

BACKGROUND: XRCC2, a homologous recombination-related gene, has been reported to be associated with a variety of cancers. However, its role in glioma has not been reported. This study aimed to find out the role of XRCC2 in glioma and reveal in which glioma-specific biological processes is XRCC2 involved based on thousands of glioma samples, thereby, providing a new perspective in the treatment and prognostic evaluation of glioma. METHODS: The expression characteristics of XRCC2 in thousands of glioma samples from CGGA and TCGA databases were comprehensively analyzed. Wilcox or Kruskal test was used to analyze the expression pattern of XRCC2 in gliomas with different clinical and molecular features. The effect of XRCC2 on the prognosis of glioma patients was explored by Kaplan-Meier and Cox regression. Gene set enrichment analysis (GSEA) revealed the possible cellular mechanisms involved in XRCC2 in glioma. Connectivity map (CMap) was used to screen small molecule drugs targeting XRCC2 and the expression levels of XRCC2 were verified in glioma cells and tissues by RT-qPCR and immunohistochemical staining. RESULTS: We found the overexpression of XRCC2 in glioma. Moreover, the overexpressed XRCC2 was associated with a variety of clinical features related to prognosis. Cox and meta-analyses showed that XRCC2 is an independent risk factor for the poor prognosis of glioma. Furthermore, the results of GSEA indicated that overexpressed XRCC2 could promote malignant progression through involved signaling pathways, such as in the cell cycle. Finally, doxazosin, quinostatin, canavanine, and chrysin were identified to exert anti-glioma effects by targeting XRCC2. CONCLUSIONS: This study analyzed the expression pattern of XRCC2 in gliomas and its relationship with prognosis using multiple datasets. This is the first study to show that XRCC2, a novel oncogene, is significantly overexpressed in glioma and can lead to poor prognosis in glioma patients. XRCC2 could serve as a new biomarker for glioma diagnosis, treatment, and prognosis evaluation, thus bringing new insight into the management of glioma.

Effects of Ultrasound-Guided Bilateral Cervical Plexus Block Combined with General Anesthesia in Patients Undergoing Total Parathyroidectomy and Partial Gland Autotransplantation Surgery.

BACKGROUND: The aim of this study is to evaluate the effect of ultrasound-guided bilateral cervical plexus block on general anesthesia, postoperative analgesia, and surgical outcomes in patients undergoing total parathyroidectomy with autotransplantation. PATIENTS AND METHODS: Forty-eight ASA III-IV patients with hyperparathyroidism secondary to renal failure were included: 24 patients received ultrasound-guided bilateral superficial and deep cervical plexus block combined with general anesthesia (group A), and 24 patients received general anesthesia alone (group B). Postoperative patient-controlled intravenous analgesia was provided with sufentanil 2 µg/kg. The primary outcome is the postoperative pain scores. Secondary outcomes include intraoperative remifentanil dosage, changes in hemodynamics, extubation time, and sufentanil consumption. Surgical outcomes regarding calcium, phosphorus and parathormone values were also noted. RESULTS: The patients in group A required less remifentanil than group B (2.56±0.92mg vs 3.38±0.84mg, P=0.002) and lower VAS scores at 1, 3, 10, 24, and 48h postoperatively (P < 0.001). While the systolic blood pressure in group A patients was significantly greater than that in group B at T3 (immediately after extubation, [138.33±11.36 vs 129.08±17.06 mmHg; P=0.032]), heart rates in group A were lower than in group B at 1 min before induction (T1 [89.46 ± 9.14 vs 96.71±14.19, P=0.042]) and 1 min after intubation (T2 [70.08 ± 5.35 vs 79.25 ± 11.81, P=0.002]). The extubation time in group A was shorter than that in group B (P < 0.001). There was no difference in calcium, phosphorus and parathormone values, nor in sufentanil consumption between the groups. CONCLUSION: Ultrasound-guided bilateral superficial and deep cervical plexus block combined with general anesthesia for TPTA is an effective strategy to improve anesthesia management and achieve better postoperative analgesia, and has no impact on surgical outcomes.

Biomechanical analysis of a novel clavicular hook plate for the treatment of acromioclavicular joint dislocation: A finite element analysis.

BACKGROUND: Clavicular hook plates are frequently used in clinical orthopedics to treat acromioclavicular joint dislocation. However, patients often exhibit acromial osteolysis and peri-implant fracture after hook plate fixation. To solve the above problems, we developed a novel double-hook clavicular plate and used finite element analysis (FEA) to investigate its biomechanical properties. METHODS: A finite element (FE) model was constructed and validated. Then, a double-hook clavicular plate, a single-hook clavicular plate, and an anatomical double-hook clavicular plate was implanted into the acromioclavicular joint and fixed with screws in groups 1, 2 and 3, respectively. Finally, a load was applied, and some indicators were recorded and analyzed. RESULTS: For both the proximal clavicular rotation angle and the distal clavicular displacement, the range of motion in groups 1 and 3 was more than 90% lower than that in group 2. The maximum von Mises stress of the clavicle in groups 1 and 3 was more than 45% lower than that in group 2. The maximum stress of the acromion in group 2 was significantly higher than that in groups 1 and 3, and that in group 3 was less than that in group 1, for both cortical and cancellous bone. CONCLUSIONS: The double-hook clavicular plate could immediately reconstruct the stability of the acromioclavicular joint, effectively reducing the stress of the bone around the clavicle and screws. Additionally, the double-hook clavicular plate could reduce the peak stress of the acromion and produce a more uniform stress distribution.

Abnormal expression of HOXD11 promotes the malignant behavior of glioma cells and leads to poor prognosis of glioma patients.

BACKGROUND: Homeobox D11 (HOXD11) plays an important role in a variety of cancers, but its precise role in gliomas remains unclear. This study aimed to explore the relationship between HOXD11 and gliomas by combining bioinformatics methods with basic experimental validation. MATERIALS AND METHODS: Obtain gene expression information and clinical information of glioma and non-tumor brain tissue samples from multiple public databases such as TCGA (666 glioma samples), CGGA (749 glioma samples), GEPIA(163 glioblastoma samples and 207 normal control samples), GEO (GSE4290 and GSE15824). Nine cases of glioma tissue and five cases of normal control brain tissue were collected from the clinical department of Henan Provincial People's Hospital for further verification. A series of bioinformatic analysis methods were used to confirm the relationship between HOXD11 expression and overall survival and clinical molecular characteristics of patients with glioma. RT-qPCR was used to verify the change of expression level of HOXD11 in glioma cells and tissues. MTT assay, colony formation assay, wound-healing assay, immunofluorescence staining, flow cytometry and western blotting were used to detect the effect of HOXD11 on the biological behavior of glioma cell line U251. RESULTS: The high expression of HOXD11 was significantly related to age, World Health Organization (WHO) grade, chemotherapy status, histological type, and even 1p19q codeletion data and isocitrate dehydrogenase (IDH) mutation. HOXD11, as an independent risk factor, reduces the overall survival of glioma patients and has diagnostic value for the prognosis of glioma. Gene Set Enrichment Analysis (GSEA) showed that HOXD11 was significantly enriched in cell signaling pathway such as cell cycle, DNA replication and so on. Finally, we confirmed that the knockout of HOXD11 can inhibit the proliferation and invasion of U251 glioma cells, and change the biological behavior of tumor cells by preventing the progression of cell cycle. CONCLUSIONS: HOXD11 may be used as a candidate biomarker for the clinical application of targeted drug and prognostic assessment treatment of glioma. In addition, This study will help to explore the pathological mechanism of glioma.

Biomechanical properties of a novel nonfusion artificial vertebral body for anterior lumbar vertebra resection and internal fixation.

The aim of the study was to evaluate the biomechanical properties of a novel nonfused artificial vertebral body in treating lumbar diseases and to compare with those of the fusion artificial vertebral body. An intact finite element model of the L1-L5 lumbar spine was constructed and validated. Then, the finite element models of the fusion group and nonfusion group were constructed by replacing the L3 vertebral body and adjacent intervertebral discs with prostheses. For all finite element models, an axial preload of 500 N and another 10 N m imposed on the superior surface of L1. The range of motion and stress peaks in the adjacent discs, endplates, and facet joints were compared among the three groups. The ranges of motion of the L1-2 and L4-5 discs in flexion, extension, left lateral bending, right lateral bending, left rotation and right rotation were greater in the fusion group than those in the intact group and nonfusion group. The fusion group induced the greatest stress peaks in the adjacent discs and adjacent facet joints compared to the intact group and nonfusion group. The nonfused artificial vertebral body could better retain mobility of the surgical site after implantation (3.6°-8.7°), avoid increased mobility and stress of the adjacent discs and facet joints.

ELK3: A New Molecular Marker for the Diagnosis and Prognosis of Glioma.

ETS transcription factor ELK3 (ELK3), a novel oncogene, affects pathological processes and progression of many cancers in human tissues. However, it remains unclear whether ELK3, as a key gene, affects the pathological process of gliomas and the prognosis of patients with gliomas. This study aimed to comprehensively and systematically reveal the correlation between ELK3 and the malignant progression of gliomas by analyzing clinical sample information stored in multiple databases. We revealed the putative mechanism of ELK3 involvement in malignant gliomas progression and identified a new and efficient biomarker for glioma diagnosis and targeted therapy. Based on the sample data from multiple databases and real-time quantitative polymerase chain reaction (RT-qPCR), the abnormally high expression of ELK3 in gliomas was confirmed. Kaplan-Meier and Cox regression analyses demonstrated that a high ELK3 expression was markedly associated with low patient survival and served as an independent biomarker of gliomas. Wilcox and Kruskal-Wallis tests revealed that expression of ELK3 was positively correlated with several clinical characteristics of patients with gliomas, such as age, WHO classification, and recurrence. Moreover, Cell Counting Kit-8 (CCK-8), immunofluorescence, and wound healing assays confirmed that ELK3 overexpression markedly promoted the proliferation and migration of glioma cells. Finally, gene set enrichment analysis (GSEA) and western blotting confirmed that overexpression of ELK3 regulated the JAK-STAT signaling pathway and upregulate the expression of signal transducer and activator of transcription 3 (STAT3) and phosphorylated STAT3 (P-STAT3) to promote the malignant transition of gliomas. Therefore, ELK3 may serve as an efficient biomarker for the diagnosis and prognosis of gliomas and it can also be used as a therapeutic target to improve the poor prognosis of patients with gliomas.

Biomechanical Comparison of a New Memory Compression Alloy Plate versus Traditional Titanium Plate for Anterior Cervical Discectomy and Fusion: A Finite Element Analysis.

OBJECTIVE: To compare the biomechanical properties of a new memory compression alloy plate and traditional titanium plate after anterior cervical discectomy and fusion (ACDF). METHODS: A finite element model of the C3-7 segments was developed and validated. The C5-6 disc was removed, and an intervertebral cage made of peek material was implanted. Then, a new memory compression alloy plate composed of Ti-Ni memory alloy and a traditional titanium plate were integrated at the C5-6 segment. All models were subjected to a load of 73.6 N to simulate the head weight and 1 Nm of flexion-extension, lateral bending, and axial rotation. The range of segmental motion (ROM) and stress on the prostheses, adjacent discs, and endplates were analyzed. RESULTS: Compared with intact status, ACDF with the new prothesis and traditional titanium plate reduced the ROM of C5-6 in six directions by 95.2%-100% and increased that of adjacent discs (C4-5 and C6-7) by 4.8%-112.5%. Adjacent disc stress peaks were higher for the traditional titanium plate (0.7-4.2 MPa) than for the new prosthesis (0.6-4.1 MPa). Endplate stress peaks were the highest in ACDF with the new prosthesis (15.6-53.3 MPa), followed by ACDF with traditional titanium plate (5.0-29.4 MPa). Stress peaks were significantly lower for the new prothesis (12.8-52.3 MPa) than for the traditional titanium plate (397.0-666.1 MPa). CONCLUSIONS: The new prosthesis improved the immediate stability of the surgical site and had an elastic modulus that was smaller than that of traditional titanium plate, making it conducive to reducing stress shielding and the impact on the adjacent intervertebral disc.

The effectiveness of intra-articular vs subacromial corticosteroid injection for frozen shoulder: Study protocol for a randomized controlled trial.

BACKGROUND: Intra-articular (IA) corticosteroid injection is a commonly used therapy for frozen shoulder (FS), but controversy still exists regarding the injection site with the best outcome. This randomized controlled trial is designed to determine whether corticosteroid injection into the subacromial space was not inferior to IA injection in patients with FS. METHODS: This study will be a single-center, randomized, and double-blinded trial. Sixty patients who meet inclusion criteria will be randomized in a ratio of 1:1 to either subacromial injection or IA injection group. The outcome evaluations will be conducted at 4 time points (baseline, 4, 8, and 12 weeks after the injection) by an independent physical therapist. The primary outcome measure is visual analog scale for pain, whereas the secondary outcomes include Constant score, and shoulder passive range of motion including abduction, forward elevation, external rotation at the side, and internal rotation at the side. DISCUSSION: This study has limited inclusion and exclusion criteria and a well-controlled intervention. This clinical trial is expected to provide evidence of proper site of corticosteroid injection for the treatment of FS. TRIAL REGISTRATION: This study protocol was registered in Research Registry (researchregistry5368).

Harmonically mode-locked Yb:CALGO laser pumped by a single-mode 1.2 W laser diode.

We present a SESAM mode locked Yb:CALGO laser with a harmonic repetition rate to the 300th order pumped by a single-mode fiber coupled laser diode. By fine tuning the internal angle between the laser beam and the normal axis through the gain medium, at pump power of 1.2 W, an average output power of 132 mW is achieved with a pulse duration of 777.6 fs and a repetition rate of 22.4 GHz. The amplification effect over several tens of roundtrips induced Fabry-Perot filtering of the anti-reflection (AR) coated gain medium is analyzed. The modulation depth increases and the FWHM of a passband Δυcrystal decreases with increasing roundtrip numbers in the laser crystal. The intra-cavity pulse shaping mechanism with a comb filter caused by the amplified etalon effect of the AR coated laser crystal leads to the overall mode spacing equal to the free spectral range of the gain medium other than the laser cavity and results in the high repetition rate running.

Generation of double-scale pulses in a LD-pumped Yb:phosphate solid-state laser.

We have demonstrated a generation of double-scale in a laser diode (LD)-pumped Yb:phosphate solid-state laser. The double-scale pulse with a spectrum bandwidth of 4.6 nm is obtained at a central wavelength of 1030 nm with maximum output power of 377 mW and 80 MHz repetition rate. The autocorrelation function of the double-scale pulse contained a 510 fs short peak and 12.51 ps long pedestal. To our best knowledge, this is the first demonstration of a double-scale pulse mode-locked solid-state laser.

Pump polarization insensitive and efficient laser-diode pumped Yb:KYW ultrafast oscillator.

We theoretically and experimentally report and evaluate a novel split laser-diode (LD) double-end pumped Yb:KYW ultrafast oscillator aimed at improving the performance of an ultrafast laser. Compared to a conventional unpolarized single-LD end-pumped ultrafast laser system, we improve the laser performance such as absorption efficiency, slope efficiency, cw mode-locking threshold, and output power by this new structure LD-pumped Yb:KYW ultrafast laser. Experiments were carried out with a 1 W output fiber-coupled LD. Experimental results show that the absorption increases from 38.7% to 48.4%, laser slope efficiency increases from 18.3% to 24.2%, cw mode-locking threshold decreases 12.7% from 630 to 550 mW in cw mode-locking threshold, and maximum output-power increases 28.5% from 158.4 to 221.5 mW when we switch the pump scheme from an unpolarized single-end pumping structure to a split LD double-end pumping structure.

Locking compression plate as an external fixator in the treatment of closed distal tibial fractures.

BACKGROUND: Tibial fractures often follow high-energy trauma, and although soft tissue can remain intact, poor blood supply can lead to skin necrosis, infections and potential amputation. We used closed reduction and locking compression plates as external fixators for treating closed distal tibial fractures with soft tissue compromise. The method aims to avoid those potential complications. METHODS: A retrospective series of 23 closed distal tibial fractures were treated using locking compression plates as external fixators. Protecting the blood supply was an essential intra-operative consideration, and postoperative physical therapy and partial weight bearing were encouraged early. Patients were followed at regular intervals and evaluated radiographically and clinically. RESULTS: The average time to radiological bony union was 29.4 weeks (range, 14-52 weeks). No infections were seen. Fractures in 22 cases (95.65 %) united, and most fractures healed in an acceptable position. All patients had good functional results and were fully weight bearing with a well-healed tibia at the final follow-up. CONCLUSIONS: Locking compression plates can be used as external fixators and provide a high rate of union, comfortable clinical course and excellent ankle-joint motion. Although indications are limited, this method is a suitable surgical approach for treating closed distal tibial fractures with soft tissue compromise.