A machine learning-based prediction model for in-hospital mortality among critically ill patients with hip fracture: An internal and external validated study.

INTRODUCTION: Few studies have investigated the in-hospital mortality among critically ill patients with hip fracture. This study aimed to develop and validate a model to estimate the risk of in-hospital mortality among critically ill patients with hip fracture. METHODS: For this study, data from the Medical Information Mart for Intensive Care III (MIMIC-III) Database and electronic Intensive Care Unit (eICU) Collaborative Research Database were evaluated. Enrolled patients (n=391) in the MIMIC-III database were divided into a training (2/3, n=260) and a validation (1/3, n=131) group at random. Using machine learning algorithms such as random forest, gradient boosting machine, decision tree, and eXGBoosting machine approach, the training group was utilized to train and optimize models. The validation group was used to internally validate models and the optimal model could be obtained in terms of discrimination (area under the receiver operating characteristic curve, AUROC) and calibration (calibration curve). External validation was done in the eICU Collaborative Research Database (n=165). To encourage practical use of the model, a web-based calculator was developed according to the eXGBoosting machine approach. RESULTS: The in-hospital death rate was 13.81% (54/391) in the MIMIC-III database and 10.91% (18/165) in the eICU Collaborative Research Database. Age, gender, anemia, mechanical ventilation, cardiac arrest, and chronic airway obstruction were the six model parameters which were identified using the Least Absolute Shrinkage and Selection Operator (LASSO) method combined with 10-fold cross-validation. The model established using the eXGBoosting machine approach showed the highest area under curve (AUC) value (0.797, 95% CI: 0.696-0.898) and the best calibrating ability, with a calibration slope of 0.999 and intercept of -0.019. External validation also revealed favorable discrimination (AUC: 0.715, 95% CI: 0.566-0.864; accuracy: 0.788) and calibration (calibration slope: 0.805) in the eICU Collaborative Research Database. The web-based calculator could be available at https://doctorwangsj-webcalculator-main-yw69yd.streamlitapp.com/. CONCLUSION: The model has the potential to be a pragmatic risk prediction tool that is able to identify hip fracture patients who are at a high risk of in-hospital mortality in ICU settings, guide patient risk counseling, and simplify prognosis bench-marking by controlling for baseline risk.

Analysis of risk factors related to the re-fracture of adjacent vertebral body after PKP.

BACKGROUND: This study aims to investigate the risk factors of vertebral re-fracture after percutaneous kyphoplasty (PKP) for osteoporosis vertebral compression fracture (OVCF), and to provide reference for clinical prevention. MATERIAL AND METHODS: A retrospective analysis was performed on 228 OVCF patients admitted on November 6, 2013, solstice, December 14, 2018, which met the inclusion criteria. There were 35 males and 193 females, with a male-to-female ratio of 3:20, and an age of 61-89 years. All patients were treated with PKP surgery with complete clinical data, and the rate of re-fracture was calculated according to whether re-fracture occurred after surgery, divided into the re-fracture group (24 cases) and the non-refracture group (204 cases). May be associated with subsequent fracture factors (gender, age, number of surgical segment vertebral body, whether with degenerative scoliosis, whether to fight osteoporosis) into a single-factor research, then the single-factor analysis was statistically significant risk factors for multiple logistic regression analysis, further defined after PKP holds the vertebral body fracture independent risk factors. Survival analysis was performed using the time of vertebral re-fracture after PKP as the end time of follow-up, the occurrence of re-fracture after PKP as the endpoint event, and the presence or absence of degenerative lateral curvature as a variable factor. RESULTS: All 228 vertebroplasty patients were followed up for a period of 1.8 to 63.6 months. The mean follow-up time was (28.8 ± 15.6) months, and the re-fracture rate was 10.5%. There were statistically significant differences between the re-fracture group and the non-refracture group in age, number of operative vertebral bodies, whether there was a combination of degenerative scoliosis and whether there was anti-osteoporosis treatment (P < 0.05). The results of univariate logistic regression analysis after excluding the mutual influence of various factors showed that the number of vertebral bodies and the group with lateral curvature might be the risk factors for PKP re-fracture after surgery. The above possible risk factors were included in multiple logistic regression analysis to show whether there were independent risk factors for scoliosis and vertebral re-fracture. Survival analysis showed that the mean survival time was 42.1 months, the P value was 0.00, and the mean 95% confidence interval was (34.4-49.7 months), indicating that the combination of degenerative lateral bending might be related to the occurrence of re-fracture. CONCLUSIONS: Combined scoliosis is an independent risk factor for re-fracture after OVCF laminoplasty and a possible risk factor for re-fracture after surgery.

[Analysis of related risk factors for the refracture of adjacent vertebral body after percutaneous kyphoplasty].

OBJECTIVE: To investigate the risk factors of vertebral refracture after percutaneous kyphoplasty (PKP) for osteoprotic vertebral compression fractures (OVCFs), and to provide reference for clinical prevention. METHODS: A retrospective analysis of 228 OVCFs patients who met the inclusion criteria admitted from November 6, 2013 to December 14, 2018. There were 35 males and 193 females, with a male-to-female ratio of 3∶20, and aged 58 to 91 years with an average of (69.70±7.03) years. All patients were treated with PKP and had complete clinical data. According to whether refracture occurred after operation, they were divided into refracture group (24 cases) and non refracture group (204 cases). Factors that may be related to refracture (including gender, age, surgical segment, number of vertebral bodies in the surgical segment, whether combined with degenerative scoliosis, whether anti-osteoporosis treatment) were included in the univariate analyses, and the single factor analysis of statistically significant risk factors was carried out with multiple Logistic regression analysis to further clarify the independent risk factors for vertebral body refracture after PKP. Survival analysis was performed using the time of vertebral refracture after PKP as the end time of follow up, the occurrence of refracture after PKP as the endpoint event, and the presence or absence of degenerative lateral curvature as a variable factor. RESULTS: All 228 patients were followed up for 1.8 to 63.6 months with an average of (28.8±15.6) months, and the refracture rate was 10.5%(24/228). There were statistically significant differences between two groups in age, number of operative vertebral bodies, whether combinedwith degenerative scoliosis and whether anti osteoporosis treatment (P<0.05). Univariate Logistic regression analysis showed that the number of vertebral bodies in the surgical segment and whether combined with degenerative scoliosis may be risk factors for refracture after PKP. Multiple Logistic regression analysis of the above possible risk factors showed that combined scoliosis was an independent risk factor for vertebral refracture of the vertebral body. Survival analysis showed that the mean survival time was 42.1 months, the P value was 0.00, and the mean 95% confidence interval was 34.4-49.7 months, indicating that the combination of degenerative lateral bending might be related to the occurrence of refracture. CONCLUSION: Combined scoliosis is an independent risk factor for refracture after OVCFs vertebroplasty, and it is also a possible high-risk factor for refracture after surgery.

RRY Inhibits Amyloid-ß1-42 Peptide Aggregation and Neurotoxicity.

BACKGROUND: Current understanding of amyloid-ß protein (Aß) aggregation and toxicity provides an extensive list of drugs for treating Alzheimer's disease (AD); however, one of the most promising strategies for its treatment has been tri-peptides. OBJECTIVE: The aim of this study is to examine those tri-peptides, such as Arg-Arg-Try (RRY), which have the potential of Aß1-42 aggregating inhibition and Aß clearance. METHODS: In the present study, in silico, in vitro, and in vivo studies were integrated for screening tri-peptides binding to Aß, then evaluating its inhibition of aggregation of Aß, and finally its rescuing cognitive deficit. RESULTS: In the in silico simulations, molecular docking and molecular dynamics determined that seven top-ranking tri-peptides could bind to Aß1-42 and form stable complexes. Circular dichroism, ThT assay, and transmission electron microscope indicated the seven tri-peptides might inhibit the aggregation of Aß1-42 in vitro. In the in vivo studies, Morris water maze, ELISA, and Diolistic staining were used, and data showed that RRY was capable of rescuing the Aß1-42-induced cognitive deficit, reducing the Aß1-42 load and increasing the dendritic spines in the transgenic mouse model. CONCLUSION: Such converging outcomes from three consecutive studies lead us to conclude that RRY is a preferred inhibitor of Aß1-42 aggregation and treatment for Aß-induced cognitive deficit.

Vertebral collapse and polymethylmethacrylate breakage after vertebroplasty: A case report.

RATIONALE: Vertebral augmentation has become the main treatment for osteoporotic vertebral fractures (VFs). In this article, we report a very rare case of vertebral collapse and polymethylmethacrylate (PMMA) breakage after vertebroplasty. We describe the clinical characteristics and revision surgery performed to remove the broken PMMA cement, maintain stability, and corrects the kyphotic deformity, and we analyze the possible causes. PATIENT CONCERNS: A 72-year-old man who suffered back pain underwent first lumbar vertebra (L1) percutaneous vertebroplasty (PVP) due to osteoporosis and a vertebral fracture in May 2013. Postoperatively, the patient's back pain was markedly alleviated. Unfortunately, his lumbar back pain recurred in November 2015. DIAGNOSES: Plain radiographs showed collapse of the L1 vertebral body, breakage of the PMMA cement, and severe kyphosis at the thoracolumbar junction. INTERVENTIONS: The posterior pedicle was internally fixed and an anterior artificial vertebral body implant was placed to maintain stability and correct the kyphotic deformity in a 2-step surgical procedure. OUTCOMES: The back pain was alleviated and the patient returned to daily life for more than two years. LESSONS: This case demonstrates that PVP is not a simple minimally invasive surgery, and significant postsurgical care is necessary. The true cause of this rare phenomenon remains unclear, but the long-term use of steroids, new injuries, and poorly corrected kyphosis after PVP may play a role. Surgeons must be aware of the kinds of complications that may occur, including rare complications such as vertebral lysis.

Smyd1b is required for skeletal and cardiac muscle function in zebrafish.

Smyd1b is a member of the Smyd family that is specifically expressed in skeletal and cardiac muscles. Smyd1b plays a key role in thick filament assembly during myofibrillogenesis in skeletal muscles of zebrafish embryos. To better characterize Smyd1b function and its mechanism of action in myofibrillogenesis, we analyzed the effects of smyd1b knockdown on myofibrillogenesis in skeletal and cardiac muscles of zebrafish embryos. The results show that knockdown of smyd1b causes significant disruption of myofibril organization in both skeletal and cardiac muscles of zebrafish embryos. Microarray and quantitative reverse transcription-PCR analyses show that knockdown of smyd1b up-regulates heat shock protein 90 (hsp90) and unc45b gene expression. Biochemical analysis reveals that Smyd1b can be coimmunoprecipitated with heat shock protein 90 α-1 and Unc45b, two myosin chaperones expressed in muscle cells. Consistent with its potential function in myosin folding and assembly, knockdown of smyd1b significantly reduces myosin protein accumulation without affecting mRNA expression. This likely results from increased myosin degradation involving unc45b overexpression. Together these data support the idea that Smyd1b may work together with myosin chaperones to control myosin folding, degradation, and assembly into sarcomeres during myofibrillogenesis.