CHRONIC CRITICAL ILLNESS-INDUCED MUSCLE ATROPHY: INSIGHTS FROM A TRAUMA MOUSE MODEL AND POTENTIAL MECHANISM MEDIATED VIA SERUM AMYLOID A.

ABSTRACT: Background: Chronic critical illness (CCI), which was characterized by persistent inflammation, immunosuppression, and catabolism syndrome (PICS), often leads to muscle atrophy. Serum amyloid A (SAA), a protein upregulated in critical illness myopathy, may play a crucial role in these processes. However, the effects of SAA on muscle atrophy in PICS require further investigation. This study aims to develop a mouse model of PICS combined with bone trauma to investigate the mechanisms underlying muscle weakness, with a focus on SAA. Methods: Mice were used to examine the effects of PICS after bone trauma on immune response, muscle atrophy, and bone healing. The mice were divided into two groups: a bone trauma group and a bone trauma with cecal ligation and puncture group. Tibia fracture surgery was performed on all mice, and PICS was induced through cecal ligation and puncture surgery in the PICS group. Various assessments were conducted, including weight change analysis, cytokine analysis, hematological analysis, grip strength analysis, histochemical staining, and immunofluorescence staining for SAA. In vitro experiments using C2C12 cells (myoblasts) were also conducted to investigate the role of SAA in muscle atrophy. The effects of inhibiting receptor for advanced glycation endproducts (RAGE) or JAK2 on SAA-induced muscle atrophy were examined. Bioinformatic analysis was conducted using a dataset from the GEO database to identify differentially expressed genes and construct a coexpression network. Results: Bioinformatic analysis confirmed that SAA was significantly upregulated in muscle tissue of patients with intensive care unit-induced muscle atrophy. The PICS animal models exhibited significant weight loss, spleen enlargement, elevated levels of proinflammatory cytokines, and altered hematological profiles. Evaluation of muscle atrophy in the animal models demonstrated decreased muscle mass, grip strength loss, decreased diameter of muscle fibers, and significantly increased expression of SAA. In vitro experiment demonstrated that SAA decreased myotube formation, reduced myotube diameter, and increased the expression of muscle atrophy-related genes. Furthermore, SAA expression was associated with activation of the FOXO signaling pathway, and inhibition of RAGE or JAK2/STAT3-FOXO signaling partially reversed SAA-induced muscle atrophy. Conclusions: This study successfully develops a mouse model that mimics PICS in CCI patients with bone trauma. Serum amyloid A plays a crucial role in muscle atrophy through the JAK2/STAT3-FOXO signaling pathway, and targeting RAGE or JAK2 may hold therapeutic potential in mitigating SAA-induced muscle atrophy.

Development and validation of an artificial intelligence mobile application for predicting 30-day mortality in critically ill patients with orthopaedic trauma.

BACKGROUND: Given the intricate and grave nature of trauma-related injuries in ICU settings, it is imperative to develop and deploy reliable predictive tools that can aid in the early identification of high-risk patients who are at risk of early death. The objective of this study is to create and validate an artificial intelligence (AI) model that can accurately predict early mortality among critical fracture patients. METHODS: A total of 2662 critically ill patients with orthopaedic trauma were included from the MIMIC III database. Early mortality was defined as death within 30 days in this study. The patients were randomly divided into a model training cohort and a model validation cohort. Various algorithms, including logistic regression (LR), extreme gradient boosting machine (eXGBM), decision tree (DT), support vector machine (SVM), random forest (RF), and neural network (NN), were employed. Evaluation metrics, including discrimination and calibration, were used to develop a comprehensive scoring system ranging from 0 to 60, with higher scores indicating better prediction performance. Furthermore, external validation was carried out using 131 patients. The optimal model was deployed as an internet-based AI tool. RESULTS: Among all models, the eXGBM demonstrated the highest area under the curve (AUC) value (0.974, 95%CI: 0.959-0.983), followed by the RF model (0.951, 95%CI: 0.935-0.967) and the NN model (0.922, 95%CI: 0.905-0.941). Additionally, the eXGBM model outperformed other models in terms of accuracy (0.915), precision (0.906), recall (0.926), F1 score (0.916), Brier score (0.062), log loss (0.210), and discrimination slope (0.767). Based on the scoring system, the eXGBM model achieved the highest score (53), followed by RF (42) and NN (39). The LR, DT, and SVM models obtained scores of 28, 18, and 32, respectively. Decision curve analysis further confirmed the superior clinical net benefits of the eXGBM model. External validation of the model achieved an AUC value of 0.913 (95%CI: 0.878-0.948). Consequently, the model was deployed on the Internet at https://30-daymortalityincriticallyillpatients-fnfsynbpbp6rgineaspuim.streamlit.app/, allowing users to input patient features and obtain predicted risks of early mortality among critical fracture patients. Furthermore, the AI model successfully stratified patients into low or high risk of early mortality based on a predefined threshold and provided recommendations for appropriate therapeutic interventions. CONCLUSION: This study successfully develops and validates an AI model, with the eXGBM algorithm demonstrating the highest predictive performance for early mortality in critical fracture patients. By deploying the model as a web-based AI application, healthcare professionals can easily access the tool, enabling them to predict 30-day mortality and aiding in the identification and management of high-risk patients among those critically ill with orthopedic trauma.

Knockdown of angiopoietin-like 4 suppresses sepsis-induced acute lung injury by blocking the NF-κB pathway activation and hindering macrophage M1 polarization and pyroptosis.

OBJECTIVE: Sepsis-induced acute lung injury (ALI) is a life-threatening disease. Macrophage pyroptosis has been reported to exert function in ALI. We aimed to investigate the mechanisms of ANGPTL4-mediated cell pyroptosis in sepsis-induced ALI, thus providing new insights into the pathogenesis and prevention and treatment measures of sepsis-induced ALI. METHODS: In vivo animal models and in vitro cell models were established by cecal ligation and puncture (CLP) method and lipopolysaccharide-induced macrophages RAW264.7. ANGPTL4 was silenced in CLP mice or macrophages, followed by the determination of ANGPTL4 expression in bronchoalveolar lavage fluid (BALF) or macrophages. Lung histopathology was observed by H&E staining, with pathological injury scores evaluated and lung wet and dry weight ratio recorded. M1/M2 macrophage marker levels (iNOS/CD86/Arg1), inflammatory factor (TNF-α/IL-6/IL-1ß/iNOS) expression in BALF, cell death and pyroptosis, NLRP3 inflammasome, cell pyroptosis-related protein (NLRP3/Cleaved-caspase-1/caspase-1/GSDMD-N) levels, NF-κB pathway activation were assessed by RT-qPCR/ELISA/flow cytometry/Western blot, respectively. RESULTS: ANGPTL4 was highly expressed in mice with sepsis-induced ALI, and ANGPTL4 silencing ameliorated sepsis-induced ALI in mice. In vivo, ANGPTL4 silencing repressed M1 macrophage polarization and macrophage pyroptosis in mice with sepsis-induced ALI. In vitro, ANGPTL4 knockout impeded LPS-induced activation and pyroptosis of M1 macrophages and hindered LPS-induced activation of the NF-κB pathway in macrophages. CONCLUSION: Knockdown of ANGPTL4 blocks the NF-κB pathway activation, hinders macrophage M1 polarization and pyroptosis, thereby suppressing sepsis-induced ALI.

Acute lung injury caused by sepsis: how does it happen?

Sepsis is a systemic inflammatory disease caused by severe infections that involves multiple systemic organs, among which the lung is the most susceptible, leaving patients highly vulnerable to acute lung injury (ALI). Refractory hypoxemia and respiratory distress are classic clinical symptoms of ALI caused by sepsis, which has a mortality rate of 40%. Despite the extensive research on the mechanisms of ALI caused by sepsis, the exact pathological process is not fully understood. This article reviews the research advances in the pathogenesis of ALI caused by sepsis by focusing on the treatment regimens adopted in clinical practice for the corresponding molecular mechanisms. This review can not only contribute to theories on the pathogenesis of ALI caused by sepsis, but also recommend new treatment strategies for related injuries.

Target Protein for Xklp2 Functions as Coactivator of Androgen Receptor and Promotes the Proliferation of Prostate Carcinoma Cells.

The activation of the androgen receptor (AR) pathway is crucial in the progression of human prostate cancer. Results of the present study indicated that the target protein xenopus kinesin-like protein (TPX2) enhanced the transcription activation of AR and promoted the proliferation of LNCaP (ligand-dependent prostate carcinoma) cells. The protein-protein interaction between AR and TPX2 was investigated using coimmunoprecipitation assays. Results of the present study further demonstrated that TPX2 enhanced the transcription factor activation of AR and enhanced the expression levels of the downstream gene prostate-specific antigen (PSA). TPX2 did this by promoting the accumulation of AR in the nucleus and also promoting the recruitment of AR to the androgen response element, located in the promoter region of the PSA gene. Overexpression of TPX2 enhanced both the in vitro and in vivo proliferation of LNCaP cells. By revealing a novel role of TPX2 in the AR signaling pathway, the present study indicated that TPX2 may be an activator of AR and thus exhibits potential as a novel target for prostate carcinoma treatment.

miR-27-3p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to the Antitumor Agent Olaparib by Targeting PSEN-1, the Catalytic Subunit of Γ-Secretase.

Olaparib has been used in the treatment of triple-negative breast cancer (TNBC) with BRCA mutations. In the present study, we demonstrated the effect of miR-27-3p on the γ-secretase pathway by regulating the sensitivity of TNBC cells to olaparib. miR-27-3p, a microRNA with the potential to target PSEN-1, the catalytic subunit of γ-secretase mediating the second step of the cleavage of the Notch protein, was identified by the online tool miRDB and found to inhibit the expression of PSEN-1 by directly targeting the 3'-untranslated region (3'-UTR) of PSEN-1. The overexpression of miR-27-3p inhibited the activation of the Notch pathway via the inhibition of the cleavage of the Notch protein, mediated by γ-secretase, and, in turn, enhanced the sensitivity of TNBC cells to the antitumor agent olaparib. Transfection with PSEN-1 containing mutated targeting sites for miR-27-3p or the expression vector of the Notch protein intracellular domain (NICD) almost completely blocked the effect of miR-27-3p on the Notch pathway or the sensitivity of TNBC cells to olaparib, respectively. Therefore, our results suggest that the miR-27-3p/γ-secretase axis participates in the regulation of TNBC and that the overexpression of miR-27-3p represents a potential approach to enhancing the sensitivity of TNBC to olaparib.

Gender-related differences in concomitant articular injuries after acute lateral patellar dislocation.

OBJECTIVES: To explore the gender differences in the concomitant articular injuries after acute lateral patellar dislocation (LPD). METHODS: Magnetic resonance images were prospectively analyzed in 166 patients after an acute LPD. Concomitant articular injuries included bone contusion, medial patellofemoral ligament (MPFL) injury, articular cartilage lesion, and vastus medialis obliquus (VMO) lesion. Statistical analyses were performed between the patient's gender and the incidence of concomitant articular injuries in adolescent and adult subgroups. RESULTS: The incidence of partial and complete MPFL tear in adolescent males and females were (45%, 50%) and (63.2%, 29.8%), respectively. Compared with adolescent females, adolescent males showed higher incidence of complete MPFL tear (P = 0.049). The incidence of articular cartilage lesion of patella in adolescent males and females were 40% and 21.1%, respectively. Compared with adolescent females, adolescent males showed higher incidence of articular cartilage lesion of the patella (P = 0.043). No correlations were identified in other injuries in the adolescent group. The incidence of partial and complete MPFL tear in adult males and females were (34.4%, 65.6%) and (56.8%, 37.8%), respectively. Compared with adult females, adult males showed higher incidence of complete MPFL tear (P = 0.036). The incidence of articular cartilage lesion of patella in adult males and females were 56.3% and 32.4%, respectively. Compared with adult females, adult males showed higher incidence of articular cartilage lesion of patella (P = 0.047). The incidence of VMO injury in adult males and females were 59.4% and 35.1%, respectively. Compared with adult females, adult males showed higher incidence of VMO injury (P = 0.044). No correlations were identified in other injuries in the adult group. CONCLUSIONS: Compared with females, males predispose to complete MPFL tear and articular cartilage lesion of patella after acute LPD. Compared with female adults, male adults predispose to VMO injury.

Hsa-miR-4271 downregulates the expression of constitutive androstane receptor and enhances in vivo the sensitivity of non-small cell lung cancer to gefitinib.

The efficacy of molecular targeting agents is dependent on the metabolism or nuclear receptor-mediated clearance of chemotherapy resistance-related factors such as cytochrome P450 (CYP) or ATP binding cassette subfamily B member 1 (ABCB1). In this study, we revealed the roles of the microRNA-4271/CAR (constitutive androstane receptor) axis in the regulation of the resistance to molecular anticancer targeting agents in non-small cell lung cancer (NSCLC) cells including two main categories of NSCLC: lung adenocarcinoma (AC) and large cell lung cancer (LCC). The expression of miR-4271 was negatively correlated with CAR expression in NSCLC tissues. MiR-4271 targeted CAR and inhibited the activation of the CAR signaling pathway. Overexpression of CAR in NSCLC enhanced the resistance of NSCLC cells to molecular targeting agents and miR-4271-infected NSCLC cells enhanced their sensitivity to molecular targeting agents such as Gefitinib. The mechanism-data showed that overexpression of miR-4271 decelerated the mechanism or the clearance of molecular targeting agents by targeting the 3'UTR (3' un-translation region). These results suggest that miR-4271 may contribute to the development of more effective strategies for the treatment of advanced NSCLC.

miR-596 suppresses the expression of Survivin and enhances the sensitivity of osteosarcoma cells to the molecular targeting agent anlotinib.

BACKGROUND: Osteosarcoma (OSA), the most common primary bone malignancy, is characterized by a wide spectrum of complicated pathologies and frequent distal metastasis and causes death in adolescents and young adults worldwide. Antitumor drug treatment strategies include various cytotoxic chemotherapy drugs, while molecular targeted therapy for OSA is currently less used. The present work revealed the role played by the miR-596/Survivin axis in affecting the sensitivity of OSA cells to anlotinib, a novel molecular targeting agent. METHODS: By virtual screening, we found that miR-596 might target Survivin by using an online tool (miRDB). RNA levels of miR-596 and Survivin in clinical specimens were examined with qPCR. The effect of miR-596 on anlotinib's antitumor effect was examined with MTT experiments, the subcutaneous tumor model, or the intramuscular tumor model. RESULTS: Overexpression of miR-596 via lentiviral particles repressed the protein level of Survivin in U2OS cells. Transfection of miR-596 enhanced the antitumor effect of anlotinib on U2OS cells or five cell lines derived from OSA patients. CONCLUSION: miR-596 targets Survivin and enhances the antitumor effect of anlotinib on OSA cells.

[Paraquat poisoning mechanism and its clinical treatment progress].

Paraquat (PQ) as a kind of sterile and herbicides, has effects of contact-kill and systemic action, which can be absorbed quickly by green plants and make them wither and die. Therefore, it is widely used in the agricultural production and occupies a large part in our country's pesticide market. PQ poisoning has become one of the most common pesticide poisoning in our country. PQ can be passivated when combining with soil, but it has great toxicity for human. There are still no specific antidotes for PQ poisoning at home and abroad, and the death rate of PQ oral poisoning is up to 95%. Clinically comprehensive treatment is adopted, including gastric lavage, intentional diarrhea, diuresis and blood perfusion. However, the therapeutic effect is not good and the case fatality rate keeps high. It has become one of the hot issues for emergency medicine study to search PQ's special efficiency measures. This paper briefly reviews PQ's poisoning mechanism and its clinical treatment progress to provide new exploration direction and treatment ideas for basic research and clinical treatment of PQ.

[Evaluation of adsorption effect of activated charcoal on oral paraquat poisoning: an experimental study on large animal].

OBJECTIVE: To study the adsorption effect of activated charcoal suspension on paraquat (PQ) in gastrointestinal tract of beagles exposed to PQ. METHODS: Twenty healthy male beagles were randomly divided into experimental group and control group, with 6 beagles in each group. 20% PQ solution (a dose of 30 mg/kg) was prescribed through stomach for beagles in both groups. After exposure to PQ for 30 minutes, the beagles in experimental group were given activated charcoal suspension (1.0 g/kg of type I activated charcoal powder mixed with 100 mL of normal saline) by gavage, while the control group was only given equal volume of normal saline. After exposure to PQ for 10 minutes, 30 minutes, and 1, 2, 4, 8, 12, 24, and 48 hours, blood was collected from hepatic portal veins and peripheral veins to detect the PQ concentration change in the plasma. The toxicokinetics software DAS 2.1.1 was applied to analyze PQ concentration and compare the change in toxicokinetics parameters between the both groups. The change in vital signs including heart rate (HR), respiratory rate (RR) and pulse oxygen saturation (SpO2) was dynamically monitored 10 minutes before exposure, 4 hours and each day from the 1st to the 7th day after exposure. RESULTS: After exposure to PQ, the poison concentration in the plasma of hepatic portal veins and peripheral veins in the control group rose quickly and reached peak 4 hours later. It fell quickly at first, and fell slowly 8 hours later. But in the experimental group, the increase rate to the peak was significantly slow. Besides, PQ peak fell more obviously than that in the control group and it was about 50% of the control group (µg/L: 123.50±11.67 vs. 255.18±12.29 in blood from hepatic portal veins, 122.35±11.72 vs. 250.86±11.15 in blood from peripheral veins). After 8 hours it fell much more quickly than that of the control group. After exposure to PQ for 48 hours, PQ concentration in the plasma was still lower than that of the control group (µg/L: 0.53±0.18 vs. 15.98±5.58 in blood from hepatic portal veins, 0.31±0.01 vs. 15.03±4.82 in blood from peripheral veins, both P < 0.01). With the toxicokinetics analysis, compared with the control group, the maximum concentration (Cmax) and area under the curve (AUC) of PQ in the plasma of hepatic portal veins and peripheral veins in the experimental group were significantly decreased [Cmax (µg/L): 125.07±9.49 vs. 255.18±12.29 in blood from hepatic portal veins, 123.38±9.52 vs. 250.86±11.15 in blood from peripheral veins; AUC (mg×L-1×h-1): 1.6±0.2 vs. 3.3±0.4 in blood from hepatic portal veins, 1.5±0.2 vs. 3.2±0.3 in blood from peripheral veins], time to the peak (Tmax) of PQ was slowed (hours: 5.3±1.9 vs. 4.0±0.0 in blood from hepatic portal veins, 4.7±1.5 vs. 4.0±0.0 in blood from peripheral veins), and PQ plasma half-life (t1/2) and mean retention time (MRT) were significantly shortened [t1/2 (hours): 3.8±1.2 vs. 15.4±3.7 in blood from hepatic portal veins, 3.5±1.0 vs. 15.5±2.7 in blood from peripheral veins; MRT (hours): 8.0±1.5 vs. 13.4±1.2 in blood from hepatic portal veins, 7.6±1.3 vs. 13.3±1.2 in blood from peripheral veins; all P < 0.01]. After exposure to PQ, HR and RR in both the experimental group and the control group increased and reached to the peak about the 4th day and then the increase rate began to slow down gradually; SpO2 slowed down gradually and reached to the valley about the 4th day and then it began to recover, but the change range of vital signs in the experimental group was smaller than that of the control group, and the parameters were significantly better than those of control group [4-day HR (bpm): 134.50±3.04 vs. 142.00±6.43, 4-day RR (times/min): 31.00±0.58 vs. 34.33±0.94, 4-day SpO2: 0.900±0.006 vs. 0.873±0.005, all P < 0.05]. CONCLUSIONS: Activated charcoal administrated at 30 minutes after PQ poisoning can slow down the increase rate of PQ concentration in the plasma, decrease the peak concentration and has less influence on vital signs in beagles.

Injury patterns of medial patellofemoral ligament and correlation analysis with articular cartilage lesions of the lateral femoral condyle after acute lateral patellar dislocation in adults: An MRI evaluation.

OBJECTIVES: The purpose of this study was to investigate the injury characteristics of medial patellofemoral ligament (MPFL), and to analyse the correlations between the injury patterns of MPFL and articular cartilage lesions of the lateral femoral condyle in adults with acute lateral patellar dislocation (LPD). METHODS: Magnetic resonance (MR) images were prospectively obtained in 121 consecutive adults with acute LPD. Images were acquired using standardised protocols and these were independently evaluated by two radiologists. RESULTS: Forty-eight cases of partial MPFL tear and 71 cases of complete MPFL tear were identified. Injuries occurred at an isolated femoral attachment (FEM) in 48 cases, an isolated patellar insertion (PAT) in 36 cases and an isolated mid-substance (MID) in five cases. More than one site of injury to the MPFL (COM) was identified in 30 cases. The prevalence rate of chondral and osteochondral lesions of the lateral femoral condyle were 4.2% (2/48) and 6.3% (3/48) in the FEM subgroup, 19.4% (7/36) and 22.2% (8/36) in the PAT subgroup and 6.7% (2/30) and 13.3% (4/30) in the COM subgroup, respectively. The PAT subgroup showed significantly higher prevalence rate of chondral and osteochondral lesions in the lateral femoral condyle when compared with the FEM subgroup. The prevalence rate of chondral and osteochondral lesions of the lateral femoral condyle were 8.5% (6/71) and 19.7% (14/71) in the complete MPFL tear subgroup and 10.4% (5/48) and 4.2% (2/58) in the partial MPFL tear subgroup, respectively. The subgroup of the complete MPFL tear showed significantly higher prevalence rate of osteochondral lesions in the lateral femoral condyle when compared with the subgroup of the partial MPFL tear. CONCLUSIONS: Firstly, the MPFL is most easily injured at the FEM, and secondly at the PAT in adults after acute LPD. The complete MPFL tear is more often concomitant with osteochondral lesions of the lateral femoral condyle than the partial MPFL tear. The isolated patellar-sided MPFL tear is more easily concomitant with chondral lesions and osteochondral lesions of the lateral femoral condyle than the isolated femoral-sided MPFL tear.

Injury patterns of medial patellofemoral ligament and correlation analysis with articular cartilage lesions of the lateral femoral condyle after acute lateral patellar dislocation in children and adolescents: An MRI evaluation.

OBJECTIVES: The purpose of this study was to investigate the injury characteristics of medial patellofemoral ligament (MPFL), and to analyse the correlations between the injury patterns of MPFL and articular cartilage lesions of the lateral femoral condyle in children and adolescents with acute lateral patellar dislocation (LPD). METHODS: Magnetic resonance (MR) images were prospectively obtained in 127 consecutive children and adolescents with acute LPD. Images were acquired using standardised protocols and these were independently evaluated by two radiologists. RESULTS: Fifty-four cases of partial MPFL tear and 69 cases of complete MPFL tear were identified. Injuries occurred at an isolated patellar insertion (PAT) in 47 cases, an isolated femoral attachment (FEM) in 41 cases and an isolated mid-substance (MID) in four cases. More than one site of injury to the MPFL (COM) was identified in 31 cases. The prevalence rate of chondral and osteochondral lesions of the lateral femoral condyle were 23.4% (11/47) and 29.8% (14/47) in the PAT subgroup, 7.3% (3/41) and 9.8% (4/41) in the FEM subgroup and 25.8% (8/31) and 32.3% (10/31) in the COM subgroup, respectively. The PAT and COM subgroups showed significantly higher prevalence rate of chondral and osteochondral lesions in the lateral femoral condyle when compared with the FEM subgroup. The prevalence rate of chondral and osteochondral lesions of the lateral femoral condyle were 17.4% (12/69) and 30.4% (21/69) in the complete MPFL tear subgroup and 20.4% (11/54) and 13% (7/54) in the partial MPFL tear subgroup, respectively. The subgroup of the complete MPFL tear showed significantly higher prevalence rate of osteochondral lesions in the lateral femoral condyle when compared with the subgroup of the partial MPFL tear. CONCLUSIONS: Firstly, the MPFL is most easily injured at the PAT, and secondly at the FEM in children and adolescents after acute LPD. The complete MPFL tear is more often concomitant with osteochondral lesions of the lateral femoral condyle than the partial MPFL tear. The isolated patellar-sided MPFL tear and the combined MPFL tear are more easily concomitant with chondral lesions and osteochondral lesions of the lateral femoral condyle than the isolated femoral-sided MPFL tear.

Evaluation of medial patellofemoral ligament tears after acute lateral patellar dislocation: comparison of high-frequency ultrasound and MR.

OBJECTIVES: The purpose of this study was to compare the diagnostic performance of high-frequency ultrasound with MR in the evaluation of medial patellofemoral ligament (MPFL) lesions after acute lateral patellar dislocation (LPD). METHODS: High-frequency ultrasound and MR images were prospectively obtained in 97 consecutive patients with acute LPD. Images were acquired using standardised protocols and were independently evaluated by two radiologists. The MPFL was assessed at three sites (patellar insertion, femoral attachment, and mid-substance) for signs of injury. RESULTS: Of a total of 291 sites in 97 MPFLs, 127 showed proven MPFL tear at surgery, including 51 sites of complete tear and 76 sites of partial tear. In a site-based analysis, the sensitivity, specificity, and accuracy of high-frequency ultrasound was 90.8%, 96.3%, and 94.6%, respectively, for partial MPFL tear and 86.3%, 96.3%, and 94%, respectively, for complete tear. For MR, the sensitivity, specificity, and accuracy was 81.6%, 95.7%, and 91.3%, respectively, for partial MPFL tear and 80.4%, 95.7%, and 92.1%, respectively, for complete tear. There was no statistical difference between high-frequency ultrasound and MR in the assessment of partial (P = 0.1, 0.777, 0.155) or complete (P = 0.425, 0.777, 0.449) MPFL lesions. Interobserver agreement was very good for high-frequency ultrasound and good for MR. CONCLUSIONS: Data suggest that high-frequency ultrasound and MR have similar diagnostic performance in the evaluation of MPFL lesions after acute LPD. KEY POINTS: • High-frequency ultrasound and MR were able to detect MPFL lesions after acute lateral patellar dislocation. • High-frequency ultrasound and MR showed similarly high accuracy in diagnosing MPFL lesions. • Interobserver agreement was very good for high-frequency ultrasound and good for MR.

Enzymatic preparation of 20(S, R)-protopanaxadiol by transformation of 20(S, R)-Rg3 from black ginseng.

20(S)-protopanaxadiol (PPD(S)) and 20(R)-protopanaxadiol (PPD(R)), the main metabolites of ginsenosides Rg3(S) and Rg3(R) in black ginseng, are potential candidates for anti-cancer therapy due to their pharmacological activities such as anti-tumor properties. In the present study, we report the preparation of PPD(S, R) by a combination of steaming and biotransformation treatments from ginseng. Aspergillus niger was isolated from soil and showed a strong ability to transform Rg3(S, R) into PPD(S, R) with 100% conversion. Furthermore, the enzymatic reactions were analyzed by reversed-phase HPLC, showing the biotransformation pathways: Rg3(S)-->Rh2(S)-->PPD(S) and Rg3(R)-->Rh2(R)-->PPD(R), respectively. In addition, 12 ginsenosides including 3 pairs of epimers, namely Rg3(S), Rg3(R), Rh2(S), Rh2(R), PPD(S) and PPD(R), were simultaneously determined by reversed-phase HPLC. Our study may be highly applicable for the preparation of PPD(S) and PPD(R) for medicinal purposes and also for commercial use.

Optimization of ginsenosides hydrolyzing beta-glucosidase production from Aspergillus niger using response surface methodology.

To optimize ginsenosides hydrolyzing beta-glucosidase production from Aspergillus niger, response surface methodology was carried out in two stages. The Plackett-Burman design was achieved to screen the important variables that influence beta-glucosidase production. Among 10 variables (wheat bran, soybean powder, CaCl(2), ginsenosides, KH(2)PO(4), MgSO(4), polyethylene glycol (PEG), medium volume, inoculum size, and stirring speed), it was found that wheat bran, KH(2)PO(4), and stirring speed had significant effect on beta-glucosidase activity due to very low p-values (p<0.05). Subsequently, wheat bran, KH(2)PO(4), and stirring speed were further optimized using central composite design. The optimal beta-glucosidase production was predicted to be 4650.14 U/ml with the combination of factors (wheat bran, 34.51 g/l; KH(2)PO(4), 1.78 g/l; stirring speed, 161.60 rpm/min). Finally, under optimal fermentation conditions, ginsenoside Rb(1) was converted to Rd and F(2) by A. niger within 10 min. Little compound K was detected at 30 min, and finally F(2) was completely transformed to compound K within 8 h. The putative conversion pathway of Rb(1) by A. niger was Rb(1), Rd, F(2), and compound K.

Researching on resonance characteristics influenced by the structure parameters of 1-3-2 piezocomposites plate.

The 1-3-2 composite is made of 1-3 composite and ceramic base. Its effective properties are calculated based on the linear piezoelectric theory and uniform field theory. The influence of piezoelectric phase volume fraction and composite aspect (thickness/width) on resonance characteristic of square 1-3-2 piezoelectric composite plate has been researched. In addition, some 1-3-2 composite samples were fabricated by dice-fill technology. The resonance frequency of samples was investigated. The results show that the experiment agrees well with the calculation. The pure thickness resonance mode of 1-3-2 composite will be gained when the volume fraction of ceramic bottom is less than 30%; that of ceramic rods is in the range of 30 approximately 80% and the ratio of thickness to width is less than 0.35.