This study reports the findings from using time-domain nuclear magnetic resonance (TD-NMR) to analyze the pore structures of cotton fibers. Cotton fibers, which swell and soften in water, present challenges for conventional pore measurement techniques. TD-NMR overcomes these by measuring the transverse relaxation time (T2) of water protons within the fibers, indicative of internal pore sizes. We established a T2-to-pore size conversion equation using mixed cellulose ester membranes. This enabled differentiation between strongly bound, loosely bound, and free water within the fibers, and detailed the water distribution. A method for measuring the pore size distribution of wet cotton fiber was developed using TD-NMR. We then examined how various pretreatments affect the fibers' internal pores by comparing their pore size distribution and porosity. Specifically, caustic mercerization primarily enlarges the porosity and size of larger pores, while liquid ammonia treatment increases porosity but reduces the size of smaller pores. This research confirms TD-NMR's utility in assessing cotton fabrics' wet processing performance.
Understanding the bonding nature between actinides and main-group elements remains a key challenge in actinide chemistry due to the involvement of f orbitals. Herein, we propose a unique "aromaticity-assisted multiconfiguration" (AAM) model to elucidate the bonding nature in actinide nitrides (An2N2, An = Ac, Th, Pa, U). Each planar four-membered An2N2 with equivalent An-N bonds possesses four delocalized π electrons and four delocalized σ electrons, forming a new family of double Möbius aromaticity that contributes to the molecular stability. The unprecedented aromaticity further supports actinide nitrides to exhibit multiconfigurational characters, where the unpaired electrons (2, 4 or 6 in naked Th2N2, Pa2N2 or U2N2, respectively) either are spin-free and localized on metal centres or form metal-ligand bonds. High-level multiconfigurational computations confirm an open-shell singlet ground state for actinide nitrides, with small energy gaps to high spin states. This is consistent with the antiferromagnetic nature observed experimentally in uranium nitrides. The novel AAM bonding model can be authenticated in both experimentally identified compounds containing a U2N2 motif and other theoretically modelled An2N2 clusters and is thus expected to be a general chemical bonding pattern between actinides and main-group elements.
Panax ginseng C. A. Meyer is a dual-purpose plant for medicine and food, its polysaccharide is considered as an immune enhancer. Four polysaccharides, WGP-20-F, WGP-40-F, WGP-60-F and WGP-80-F were obtained from ginseng via water extraction and gradient ethanol precipitation with different molecular weights (Mw) of 1.720 × 106, 1.434 × 106, 4.225 × 104 and 1.520 × 104 Da, respectively. WGP-20-F and WGP-40-F which with higher Mw and a triple-helix structure are glucans composed of 4-É-Glcp, do not show remarkable immunoregulatory effects. WGP-60-F and WGP-80-F are heteropolysaccharides mainly composed of 4-É-Glcp and also contain t-É-Araf, 5-É-Araf and 3,5-É-Araf. They are spherical branched conformations without a triple-helix structure and can effectively increase the index of immune organs, lymphocyte proliferation, activate macrophages to regulate the immune system in mice and further enhance immune functions by improving delayed-type hypersensitivity reaction and antibody response. These results indicated that WGP-60-F and WGP-80-F could be used as potential immune enhancers, and gradient ethanol precipitation can be applied for the preparation of ginseng bioactive polysaccharide.
OBJECTIVES: The long-term risk of developing glaucoma after vitrectomy remains uncertain. This retrospective population-based cohort study aimed to explore this risk following vitrectomy for macular pucker or hole. METHODS: Utilizing Taiwan's National Health Insurance Research Database (NHIRD), we included patients who were older than 18 years and had undergone vitrectomy surgery between 2011 and 2019. Exclusions were made for patients with prior diagnoses of glaucoma, congenital or secondary glaucoma, as well as those who had received previous vitreoretinal treatments or had undergone multiple vitrectomies. RESULTS: After an average follow-up period of 51 and 53 months respectively for the vitrectomized and non-vitrectomized group, our results showed a relative risk of 1.71 for glaucoma development in the vitrectomized group. Higher adjusted hazard ratios were also observed for open-angle glaucoma and normal tension glaucoma. Increased risks were associated with male sex, obstructive sleep apnoea, and migraine. In the subgroup analysis, phakic eyes at baseline and those who had undergone cataract surgery post-vitrectomy were associated with a lower risk of glaucoma development during follow-up. Among all glaucoma events, pseudophakic status at baseline had the shortest interval to glaucoma development following vitrectomy. CONCLUSIONS: These findings underscore the potential relationship between vitrectomy and glaucoma onset, emphasizing the need for vigilant monitoring and early detection of glaucoma in post-vitrectomy patients.
OBJECTIVE: To evaluate the heart response of Erdheim-Chester disease (ECD) through continuous follow-up within our large cohort, for which there is a lack of understanding. METHODS: We conducted a retrospective analysis of clinical data from patients with ECD with cardiac involvement diagnosed at our centre between January 2010 and August 2023. We assessed the heart response by integrating pericardial effusion and metabolic responses. RESULTS: A total of 40 patients were included, with a median age of 51.5 years (range: 29-66) and a BRAFV600E mutation rate of 56%. The most common imaging manifestations observed were pericardial effusion (73%), right atrium (70%) and right atrioventricular sulcus infiltration (58%). Among 21 evaluable patients, 18 (86%) achieved a heart response including 5 (24%) complete response (CR) and 13 (62%) partial response (PR). The CR rate of pericardial effusion response was 33%, while the PR rate was 56%. Regarding the cardiac mass response, 33% of patients showed PR. For cardiac metabolic response, 32% and 53% of patients achieved complete and partial metabolic response, respectively. There was a correlation between pericardial effusion response and cardiac metabolic response (r=0.73 (95% CI 0.12 to 0.83), p<0.001). The median follow-up was 50.2 months (range: 1.0-102.8 months). The estimated 5-year overall survival was 78.9%. The median progression-free survival was 59.4 months (95% CI 26.2 to 92.7 months). Patients who received BRAF inhibitors achieved better heart response (p=0.037) regardless of treatment lines. CONCLUSION: We pioneered the evaluation of heart response of ECD considering both pericardial effusion and cardiac metabolic response within our cohort, revealing a correlation between these two indicators. BRAF inhibitors may improve heart response, regardless of the treatment lines.
BACKGROUND/PURPOSE: Curative technologies improve patient's survival and/or quality of life but increase financial burdens. Effective prevention benefits all three. We summarize estimation methods and provide examples of how much money is spent per quality-adjusted life year (QALY) or life year (LY) on treating a catastrophic illness under a lifetime horizon and how many QALYs/LYs and lifetime medical costs (LMC) could be potentially saved by prevention. METHODS: We established cohorts by interlinkages of Taiwan's nation-wide databases including National Health Insurance. We developed methods to estimate lifetime survival functions, which were multiplied with the medical costs and/or quality of life and summed up to estimate LMC, quality-adjusted life expectancy (QALE) and lifetime average cost per QALY/LY for catastrophic illnesses. By comparing with the age-, sex-, and calendar year-matched referents simulated from vital statistics, we obtained the loss-of-QALE and loss-of-life expectancy (LE). RESULTS: The lifetime cost-effectiveness ratios of ventilator-dependent comatose patients, dialysis, spinal cord injury, major trauma, and cancers were US$ 96,800, 16,200-20,000, 5500-5,900, 3400-3,600, and 2900-11,900 per QALY or LY, respectively. The successful prevention of lung, liver, oral, esophagus, stomach, nasopharynx, or ovary cancer would potentially save US$ 28,000-97,000 and > 10 QALYs; whereas those for end-stage kidney disease, stroke, spinal injury, or major trauma would be US$ 55,000-300,000 and 10-14 QALYs. Loss-of-QALE and loss-of-LE were less confounded indicators for comparing the lifetime health benefits of different technologies estimated from real-world data. CONCLUSIONS: Integration of prevention with treatment for resources allocation seems feasible and would improve equity and efficiency.
The plastic deformation of TWIP steel is greatly inhibited during the expansion process. The stress-strain curves obtained through expansion experiments and observations of fracture morphology confirmed the low plastic behavior of TWIP steel during expansion deformation. Through an analysis of the mechanical expansion model, it was found that the expansion process has a lower stress coefficient and a faster strain rate than stretching, which inhibits the plasticity of TWIP steel during expansion deformation. Using metallographic microscopy, transmission electron microscopy, and EBSD to observe the twin morphology during expansion deformation and tensile deformation, it was found that expansion deformation has a higher twin density, which is manifested in a denser twin arrangement and a large number of twin deliveries in the microscopic morphology. During the expansion deformation process, dislocation slips are hindered by twins, the free path of the slips is reduced, and dislocations accumulate significantly. The accumulation area is the initial point of crack expansion. The results show that the significant dislocation accumulation caused by the delivery of a large number of twins under expansion deformation is the main reason for the decrease in the plasticity of TWIP steel.
What is already known about this topic?: Mucosal IgA plays a crucial role in host immunity against respiratory viruses. Recent studies suggest that it has the potential to mitigate the transmission of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant. However, a comprehensive population-based analysis examining mucosal IgA levels following the winter 2022 wave of the coronavirus disease 2019 (COVID-19) pandemic is yet to be conducted. What is added by this report?: In our study involving 3,421 participants, we documented IgA responses subsequent to SARS-CoV-2 infection. A significant proportion of individuals sustained increased levels of IgA for over six months. These levels were also observed in individuals with prior infections who underwent asymptomatic reinfections, indicating an active production of IgA antibodies. Further, individuals with multiple vaccinations or severe symptoms tended to display elevated IgA levels after recovery. What are the implications for public health practice?: IgA in the nasal mucosa is crucial for defense against SARS-CoV-2 infection. These insights can enhance our knowledge of immune responses following infection and have provided certain reference values for disease prevention and control strategies.
BACKGROUND: Chromobox Homolog 1 (CBX1) plays a crucial role in the pathogenesis of numerous diseases, including the evolution and advancement of diverse cancers. The role of CBX1 in pan-cancer and its mechanism in hepatocellular carcinoma (HCC), however, remains to be further investigated. METHODS: Bioinformatics approaches were harnessed to scrutinize CBX1's expression profile, its association with tumor staging, and its potential impact on patient outcomes across various cancers. Single-cell RNA sequencing data facilitated the investigation of CBX1 expression patterns at the individual cell level. The CBX1 expression levels in HCC and adjacent non-tumor tissues were quantified through Real-Time Polymerase Chain Reaction (RT-PCR), Western Blotting (WB), and Immunohistochemical analyses. A tissue microarray was employed to explore the relationship between CBX1 levels, patient prognosis, and clinicopathological characteristics in HCC. Various in vitro assays-including CCK-8, colony formation, Transwell invasion, and scratch tests-were conducted to assess the proliferative and motility properties of HCC cells upon modulation of CBX1 expression. Moreover, the functional impact of CBX1 on HCC was further discerned through xenograft studies in nude mice. RESULTS: CBX1 was found to be upregulated in most cancer forms, with heightened expression correlating with adverse patient prognoses. Within the context of HCC, elevated levels of CBX1 were consistently indicative of poorer clinical outcomes. Suppression of CBX1 through knockdown methodologies markedly diminished HCC cell proliferation, invasive capabilities, migratory activity, Epithelial-mesenchymal transition (EMT) processes, and resistance to Tyrosine kinase inhibitors (TKIs). Contrastingly, CBX1 augmentation facilitated the opposite effects. Subsequent investigative efforts revealed CBX1 to be a promoter of EMT and a contributor to increased TKI resistance within HCC cells, mediated via the IGF-1R/AKT/SNAIL signaling axis. The oncogenic activities of CBX1 proved to be attenuable either by AKT pathway inhibition or by targeted silencing of IGF-1R. CONCLUSIONS: The broad overexpression of CBX1 in pan-cancer and specifically in HCC positions it as a putative oncogenic entity. It is implicated in forwarding HCC progression and exacerbating TKI resistance through its interaction with the IGF-1R/AKT/SNAIL signaling cascade.
BACKGROUND: Hepatocellular carcinoma (HCC) is a primary liver tumor generally diagnosed based on radiographic findings. Metastatic disease is typically associated with increased tumor diameter, multifocality, and vascular invasion. We report a case of a patient who presented with extrahepatic HCC metastasis to a portocaval lymph node with occult hepatic primary on computed tomography (CT). We review the literature for cases of extrahepatic HCC presentation without known hepatic lesions and discuss strategies to differentiate between metastatic and ectopic HCC. CASE SUMMARY: A 67-year-old male with remotely treated hepatis C was referred for evaluation of an enlarging portocaval, mixed cystic-solid mass. Serial CT evaluations demonstrated steatosis, but no cirrhosis or liver lesions. Endoscopic ultrasound demonstrated a normal-appearing pancreas, biliary tree, and liver. Fine needle aspiration yielded atypical cells. The differential diagnosis included duodenal or pancreatic cyst, lymphoproliferative cyst, stromal or mesenchymal lesions, nodal involvement from gastrointestinal or hematologic malignancy, or duodenal gastro-intestinal stromal tumor. After review by a multidisciplinary tumor board, the patient underwent open surgical resection of a 5.2 cm × 5.5 cm retroperitoneal mass with pathology consistent with moderately-differentiated HCC. Magnetic resonance imaging (MRI) subsequently demonstrated a 1.2 cm segment VIII hepatic lesion with late arterial enhancement, fatty sparing, and intrinsic T1 hyperintensity. Alpha fetoprotein was 23.3 ng/mL. The patient was diagnosed with HCC with portocaval nodal involvement. Review: We surveyed the literature for HCC presenting as extrahepatic masses without history of concurrent or prior intrahepatic HCC. We identified 18 cases of extrahepatic HCC ultimately found to represent metastatic lesions, and 30 cases of extrahepatic HCC found to be primary, ectopic HCC. CONCLUSION: Hepatocellular carcinoma can seldomly present with extrahepatic metastasis in the setting of occult primary. In patients with risk factors for HCC and lesions suspicious for metastatic disease, MRI may be integral to identifying small hepatic lesions and differentiating from ectopic HCC. Tumor markers may also have utility in establishing the diagnosis.
Targeted therapy is effective in many tumor types including lung cancer, the leading cause of cancer mortality. Paradigm defining examples are targeted therapies directed against non-small cell lung cancer (NSCLC) subtypes with oncogenic alterations in EGFR, ALK and KRAS. The success of targeted therapy is limited by drug-tolerant persister cells (DTPs) which withstand and adapt to treatment and comprise the residual disease state that is typical during treatment with clinical targeted therapies. Here, we integrate studies in patient-derived and immunocompetent lung cancer models and clinical specimens obtained from patients on targeted therapy to uncover a focal adhesion kinase (FAK)-YAP signaling axis that promotes residual disease during oncogenic EGFR-, ALK-, and KRAS-targeted therapies. FAK-YAP signaling inhibition combined with the primary targeted therapy suppressed residual drug-tolerant cells and enhanced tumor responses. This study unveils a FAK-YAP signaling module that promotes residual disease in lung cancer and mechanism-based therapeutic strategies to improve tumor response.
Carcinoma, Non-Small-Cell Lung , Drug Resistance, Neoplasm , Lung Neoplasms , Signal Transduction , Transcription Factors , YAP-Signaling Proteins , Humans , Lung Neoplasms/drug therapy , Lung Neoplasms/genetics , Lung Neoplasms/metabolism , Signal Transduction/drug effects , Transcription Factors/metabolism , Transcription Factors/genetics , Carcinoma, Non-Small-Cell Lung/drug therapy , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/metabolism , Carcinoma, Non-Small-Cell Lung/pathology , YAP-Signaling Proteins/metabolism , Cell Line, Tumor , Animals , Drug Resistance, Neoplasm/genetics , Adaptor Proteins, Signal Transducing/metabolism , Adaptor Proteins, Signal Transducing/genetics , Neoplasm, Residual , Mice , Focal Adhesion Kinase 1/metabolism , Focal Adhesion Kinase 1/genetics , ErbB Receptors/metabolism , ErbB Receptors/genetics , Anaplastic Lymphoma Kinase/metabolism , Anaplastic Lymphoma Kinase/genetics , Anaplastic Lymphoma Kinase/antagonists & inhibitors , Proto-Oncogene Proteins p21(ras)/genetics , Proto-Oncogene Proteins p21(ras)/metabolism , Focal Adhesion Protein-Tyrosine Kinases/metabolism , Antineoplastic Agents/therapeutic use , Antineoplastic Agents/pharmacology , Xenograft Model Antitumor Assays
OBJECTIVES: This study aims to assess the specific PM2.5-bound metallic elements that contribute to asthma emergency department visits by using a case-crossover study design. METHODS: This study analyzed data from 11,410 asthma emergency department visits as case group and 22,820 non-asthma onset dates occurring one week and two weeks preceding the case day as controls from 2017 to 2020. PM2.5 monitoring data and 35 PM.2.5-bound metallic elements from six different regions in Taiwan were collected. Conditional logistic regression models were used to assess the relationship between asthma and PM2.5-bound metallic elements. RESULTS: Our investigation revealed a statistically significant risk of asthma emergency department visits associated with PM2.5 exposure at lag 0, 1, 2, and 3 during autumn. Additionally, PM2.5-bound hafnium (Hf), thallium (Tl), rubidium (Rb), and aluminum (Al) exhibited a consistently significant positive correlation with asthma emergency department visits at lags 1, 2, and 3. In stratified analyses by area, age, and sex, PM2.5-bound Hf showed a significant and consistent correlation. CONCLUSIONS: This study provides evidence of PM2.5-bound metallic elements effects in asthma exacerbations, particularly for Hf. It emphasizes the importance of understanding the origins of these metallic elements and pursuing emission reductions to mitigate regional health risks.
AIMS: To document the prevalence of skin problems associated with insulin pump use and identify contributing factors among children with type 1 diabetes mellitus in China. METHODS: In total, 461 children were recruited from an online community (i.e., a Wechat group) of pediatric patients with T1DM. A self-developed questionnaire was filled in by parents, collecting the information on social demographics, disease, and insulin pump therapy related characteristics and skin problems. We applied the Mann-Whitney U test, Chi square test and logistic regression analysis to identify the factors associated with skin problems. RESULTS: Of the 461 responders, 308 (66.8 %) children were reported to have skin problems. More specifically, 38.8 % had pigmentation changes, 22.3 % allergy/dermatitis, 20.2 % scaring, 11.5 % pain, 10.8 % infection, 10.6 % subcutaneous lipohypertrophy, and 6.1 % lipoatrophy. Logistic regression analysis showed that independent associated factors of skin problems were the caregiver's educational level as college or above, patient having skin allergies, and using the Brand 2 insulin pump (p values < 0.05). CONCLUSIONS: The present study documents the prevalence of skin problems and identifies associated factors, such as caregiver's education, patients skin allergies, and using a specific brand of pump. Health education should address these factors in addition to the traditionally emphasized factors.
In this work, an energy decomposition analysis (EDA) method with the strategy of density matrix, called DM-EDA, is proposed on the basis of single reference electronic structure calculations. Different from traditional EDA methods, instead of an intermediate state wave function, the EDA terms in DM-EDA are expressed in the forms of the density matrix. This method can be carried out with various kinds of density matrices. With the efficient implementation, DM-EDA not only greatly improves the computational efficiency but also provides quantitative knowledge of intermolecular interactions with a large number of monomers.
BACKGROUND: Two-dimensional ultrathin Ti3C2 (MXene) nanosheets have gained significant attention in various biomedical applications. Although previous studies have described the accumulation and associated damage of Ti3C2 nanosheets in the testes and placenta. However, it is currently unclear whether Ti3C2 nanosheets can be translocated to the ovaries and cause ovarian damage, thereby impairing ovarian functions. RESULTS: We established a mouse model with different doses (1.25, 2.5, and 5 mg/kg bw/d) of Ti3C2 nanosheets injected intravenously for three days. We demonstrated that Ti3C2 nanosheets can enter the ovaries and were internalized by granulosa cells, leading to a decrease in the number of primary, secondary and antral follicles. Furthermore, the decrease in follicles is closely associated with higher levels of FSH and LH, as well as increased level of E2 and P4, and decreased level of T in mouse ovary. In further studies, we found that exposure toTi3C2 nanosheets increased the levels of Beclin1, ATG5, and the ratio of LC3II/Ι, leading to autophagy activation. Additionally, the level of P62 increased, resulting in autophagic flux blockade. Ti3C2 nanosheets can activate autophagy through the PI3K/AKT/mTOR signaling pathway, with oxidative stress playing an important role in this process. Therefore, we chose the ovarian granulosa cell line (KGN cells) for in vitro validation of the impact of autophagy on the hormone secretion capability. The inhibition of autophagy initiation by 3-Methyladenine (3-MA) promoted smooth autophagic flow, thereby partially reduced the secretion of estradiol and progesterone by KGN cells; Whereas blocking autophagic flux by Rapamycin (RAPA) further exacerbated the secretion of estradiol and progesterone in cells. CONCLUSION: Ti3C2 nanosheet-induced increased secretion of hormones in the ovary is mediated through the activation of autophagy and impairment of autophagic flux, which disrupts normal follicular development. These results imply that autophagy dysfunction may be one of the underlying mechanisms of Ti3C2-induced damage to ovarian granulosa cells. Our findings further reveal the mechanism of female reproductive toxicity induced by Ti3C2 nanosheets.
Autophagy , Granulosa Cells , Nanostructures , Ovary , Titanium , Animals , Female , Autophagy/drug effects , Titanium/toxicity , Titanium/chemistry , Titanium/pharmacology , Mice , Ovary/drug effects , Ovary/metabolism , Nanostructures/chemistry , Granulosa Cells/drug effects , Granulosa Cells/metabolism , Signal Transduction/drug effects , TOR Serine-Threonine Kinases/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Ovarian Follicle/drug effects , Ovarian Follicle/metabolism , Oxidative Stress/drug effects , Proto-Oncogene Proteins c-akt/metabolism
Ovarian metastasis is one of the major causes of treatment failure in patients with gastric cancer (GC). However, the genomic characteristics of ovarian metastasis in GC remain poorly understood. In this study, we enroll 74 GC patients with ovarian metastasis, with 64 having matched primary and metastatic samples. Here, we show a characterization of the mutation landscape of this disease, alongside an investigation into the molecular heterogeneity and pathway mutation enrichments between synchronous and metachronous metastasis. We classify patients into distinct clonal evolution patterns based on the distribution of mutations in paired samples. Notably, the parallel evolution group exhibits the most favorable prognosis. Additionally, by analyzing the differential response to chemotherapy, we identify potential biomarkers, including SALL4, CCDC105, and CLDN18, for predicting the efficacy of paclitaxel treatment. Furthermore, we validate that CLDN18 fusion mutations improve tumor response to paclitaxel treatment in GC with ovarian metastasis in vitro and vivo.
Biomarkers, Tumor , Mutation , Ovarian Neoplasms , Paclitaxel , Stomach Neoplasms , Paclitaxel/therapeutic use , Humans , Stomach Neoplasms/genetics , Stomach Neoplasms/drug therapy , Stomach Neoplasms/pathology , Female , Ovarian Neoplasms/genetics , Ovarian Neoplasms/drug therapy , Ovarian Neoplasms/pathology , Biomarkers, Tumor/genetics , Claudins/genetics , Claudins/metabolism , Evolution, Molecular , Animals , Middle Aged , Prognosis , Cell Line, Tumor , Mice , Transcription Factors/genetics , Transcription Factors/metabolism , Aged , Antineoplastic Agents, Phytogenic/therapeutic use
Background: Osteoporosis is becoming more common worldwide, imposing a substantial burden on individuals and society. The onset of osteoporosis is subtle, early detection is challenging, and population-wide screening is infeasible. Thus, there is a need to develop a method to identify those at high risk for osteoporosis. Objective: This study aimed to develop a machine learning algorithm to effectively identify people with low bone density, using readily available demographic and blood biochemical data. Methods: Using NHANES 2017-2020 data, participants over 50 years old with complete femoral neck BMD data were selected. This cohort was randomly divided into training (70%) and test (30%) sets. Lasso regression selected variables for inclusion in six machine learning models built on the training data: logistic regression (LR), support vector machine (SVM), gradient boosting machine (GBM), naive Bayes (NB), artificial neural network (ANN) and random forest (RF). NHANES data from the 2013-2014 cycle was used as an external validation set input into the models to verify their generalizability. Model discrimination was assessed via AUC, accuracy, sensitivity, specificity, precision and F1 score. Calibration curves evaluated goodness-of-fit. Decision curves determined clinical utility. The SHAP framework analyzed variable importance. Results: A total of 3,545 participants were included in the internal validation set of this study, of whom 1870 had normal bone density and 1,675 had low bone density Lasso regression selected 19 variables. In the test set, AUC was 0.785 (LR), 0.780 (SVM), 0.775 (GBM), 0.729 (NB), 0.771 (ANN), and 0.768 (RF). The LR model has the best discrimination and a better calibration curve fit, the best clinical net benefit for the decision curve, and it also reflects good predictive power in the external validation dataset The top variables in the LR model were: age, BMI, gender, creatine phosphokinase, total cholesterol and alkaline phosphatase. Conclusion: The machine learning model demonstrated effective classification of low BMD using blood biomarkers. This could aid clinical decision making for osteoporosis prevention and management.
Bone Density , Machine Learning , Osteoporosis , Humans , Female , Middle Aged , Male , Osteoporosis/diagnosis , Aged , Algorithms , Nutrition Surveys , Logistic Models , Support Vector Machine
