Objective: To conduct a scoping review on the types, construction methods and predictive performance of health literacy prediction models based on machine learning methods, so as to provide the reference for the improvement and application of such models. Methods: Publications on health literacy prediction models conducted using machine learning methods were retrieved from CNKI, Wanfang Data, VIP, PubMed and Web of Science from inception to May 1, 2024. The quality of literature was assessed using the Prediction Model Risk of Bias ASsessment Tool. Basic characteristics, modeling methods, data sources, missing value handling, predictors and predictive performance were reviewed. Results: A total of 524 publications were retrieved, and 22 publications between 2007 and 2024 were finally enrolled. Totally 48 health literacy prediction models were involved, and 25 had a high risk of bias (52.08%), with major issues focusing on missing value handling, predictor selection and model evaluation methods. Modeling methods included regression models, tree-based machine learning methods, support vector machines and neural network models. Predictors primarily encompassed factors at four aspects: individual, interpersonal, organizational and society/policy aspects, with age, educational level, economic status, health status and internet use appearing frequently. Internal validation was conducted in 14 publications, and external validation was conducted in 4 publications. Forty-two models reported the areas under the receiver operating characteristic curve, which ranged from 0.52 to 0.983, indicating good discrimination. Conclusion Health literacy prediction models based on machine learning methods perform well, but have deficiencies in risk of bias, data processing and validation.

Intraoperative cell salvage (IOCS) has been widely applied as an important blood conservation measure in surgical operations. However, there is currently a lack of clinical practice guidelines for the implementation of IOCS in patients with malignant tumors. This report aims to provide clinicians with recommendations on the use of IOCS in patients with malignant tumors based on the review and assessment of the existed evidence. Data were derived from databases such as PubMed, Embase, the Cochrane Library and Wanfang. The guideline development team formulated recommendations based on the quality of evidence, balance of benefits and harms, patient preferences, and health economic assessments. This study constructed seven major clinical questions. The main conclusions of this guideline are as follows: 1) Compared with no perioperative allogeneic blood transfusion (NPABT), perioperative allogeneic blood transfusion (PABT) leads to a more unfavorable prognosis in cancer patients (Recommended); 2) Compared with the transfusion of allogeneic blood or no transfusion, IOCS does not lead to a more unfavorable prognosis in cancer patients (Recommended); 3) The implementation of IOCS in cancer patients is economically feasible (Recommended); 4) Leukocyte depletion filters (LDF) should be used when implementing IOCS in cancer patients (Strongly Recommended); 5) Irradiation treatment of autologous blood to be reinfused can be used when implementing IOCS in cancer patients (Recommended); 6) A careful assessment of the condition of cancer patients (meeting indications and excluding contraindications) should be conducted before implementing IOCS (Strongly Recommended); 7) Informed consent from cancer patients should be obtained when implementing IOCS, with a thorough pre-assessment of the patient's condition and the likelihood of blood loss, adherence to standardized internally audited management procedures, meeting corresponding conditions, and obtaining corresponding qualifications (Recommended). In brief, current evidence indicates that IOCS can be implemented for some malignant tumor patients who need allogeneic blood transfusion after physician full evaluation, and LDF or irradiation should be used during the implementation process.

Abuse of amphetamine-based stimulants is a primary public health concern. Recent studies have underscored a troubling escalation in the inappropriate use of prescription amphetamine-based stimulants. However, the neurophysiological mechanisms underlying the impact of acute methamphetamine exposure (AME) on sleep homeostasis remain to be explored. This study employed non-human primates and electroencephalogram (EEG) sleep staging to evaluate the influence of AME on neural oscillations. The primary focus was on alterations in spindles, delta oscillations, and slow oscillations (SOs) and their interactions as conduits through which AME influences sleep stability. AME predominantly diminishes sleep-spindle waves in the non-rapid eye movement 2 (NREM2) stage, and impacts SOs and delta waves differentially. Furthermore, the competitive relationships between SO/delta waves nesting with sleep spindles were selectively strengthened by methamphetamine. Complexity analysis also revealed that the SO-nested spindles had lost their ability to maintain sleep depth and stability. In summary, this finding could be one of the intrinsic electrophysiological mechanisms by which AME disrupted sleep homeostasis.
Animals ; Methamphetamine ; Electroencephalography ; Male ; Sleep/drug effects* ; Central Nervous System Stimulants ; Delta Rhythm/drug effects* ; Sleep Stages/drug effects*

Objective:To explore the neuroprotective effect of α7 nicotinic acetylcholine receptor (α7nAChR) on rat models of Parkinson's disease (PD) and its underlying mechanism.Methods:Forty-eight 8-week-old SPF-grade SD rats were randomly divided into a normal control group, a PD model group, an α7nAChR empty vector group and an α7nAChR overexpression group, with 12 rats in each group. PD models in the latter 3 groups of rats were established by 6-hydroxydopamine (6-OHDA). Four weeks after modeling, rats in the latter 2 groups were injected with 2 μL α7nAChR overexpression lentivirus or empty vector lentivirus through stereotactic intracerebral injection, while rats in the normal control group did not receive any treatment. Two weeks after injection, the behavioral changes of these rats were detected by apomorphine-induced rotation test; the right substantia nigra pars compacta (SNc) was prepared and performed the following experiments: hematoxylin-eosin (HE) staining and Nissl staining were used to detect the neuron morphological changes, TUNEL was used to detect the neuron apoptosis, fluorescent double labeling was used to detect the expressions of tyrosine hydroxylase (TH) and α-synuclein (α-Syn), ELISA was used to detect the expressions of 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA), and Western blotting was used to detect the expressions of ferroptosis-related proteins (ferritin heavy chain 1 [FTH1], Sigma receptor 1 [S1R], glutathione peroxidase 4 [GPX4], long chain acyl-coa synthetase 4 [ACSL4], solute carrier family 7 member11 [SLC7A11]), and the expressions of proteins related to CAMKII/ERK pathway (phosphorylated calmodulin kinase Ⅱ [p-CAMK Ⅱ], phosphorylated extracellular signal regulated kinase [p-ERK], and phosphorylated Kirsten rat sarcoma viral oncogene homolog [p-KRAS]).Results:(1) Compared with the normal control group, the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly larger number of rotations ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly smaller number of rotations ( P<0.05). (2) HE staining and Nissl staining showed that the PD model group had decreased number of dopaminergic neurons and Nissl bodies, accompanied by neuronal distribution disorder, nuclear condensation or swelling; the α7nAChR-overexpression group had obviously improved appearance of dopaminergic neurons, with normal morphology and less cell degeneration. (3) TUNEL results showed that compared with the normal control group, the PD model group, α7nAChR empty vector group, and α7nAChR overexpression group had significantly higher apoptosis rate ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had statistically lower apoptosis rate ( P<0.05). (4) Double immunofluorescent staining results showed that compared with the normal control group (303.61±48.40, 13 985.80±1 956.06), the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly increased α-Syn expression (4 310.40±518.43, 3 846.60±524.47 and 1 033.55±59.98) and statistically decreased TH expression (760.97±57.26, 842.55±113.41 and 8 101.82±1 171.85) in the right SNc ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly decreased α-Syn expression and increased TH expression in the right SNc ( P<0.05). (5) ELISA results showed that the 4-HNE and MDA expressions in the right SNc of the PD model group, α7nAChR empty vector group and α7nAChR overexpression group were significantly higher than those in the normal control group ( P<0.05); the 4-HNE and MDA expressions in the α7nAChR overexpression group were significantly lower than those in the PD model group ( P<0.05). (6) Western blotting results showed that compared with the normal control group, the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly decreased FTH1, S1R, GPX4, and SLC7A11 protein expressions, and statistically increased ACSL4 protein expression in the right SNc ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly increased FTH1, S1R, GPX4, and SLC7A11 protein expressions and decreased ACSL4 protein expression in the right SNc ( P<0.05). Compared with the normal control group, the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly increased p-KRAS, p-CAMKII, and p-ERK protein expressions in the right SNc ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly decreased p-KRAS, p-CAMKII, and p-ERK protein expressions in the right SNc ( P<0.05). Conclusion:The α7nAChR may exert neuroprotective effect on PD rat models by regulating the CAMKII/ERK pathway and ferroptosis-related proteins.

Apical microsurgery is accurate and minimally invasive, produces few complications, and has a success rate of more than 90%. However, due to the lack of awareness and understanding of apical microsurgery by dental general practitioners and even endodontists, many clinical problems remain to be overcome. The consensus has gathered well-known domestic experts to hold a series of special discussions and reached the consensus. This document specifies the indications, contraindications, preoperative preparations, operational procedures, complication prevention measures, and efficacy evaluation of apical microsurgery and is applicable to dentists who perform apical microsurgery after systematic training.
Microsurgery/standards* ; Humans ; Apicoectomy ; Contraindications, Procedure ; Tooth Apex/diagnostic imaging* ; Postoperative Complications/prevention & control* ; Consensus ; Treatment Outcome

Instrument separation is a critical complication during root canal therapy, impacting treatment success and long-term tooth preservation. The etiology of instrument separation is multifactorial, involving the intricate anatomy of the root canal system, instrument-related factors, and instrumentation techniques. Instrument separation can hinder thorough cleaning, shaping, and obturation of the root canal, posing challenges to successful treatment outcomes. Although retrieval of separated instrument is often feasible, it carries risks including perforation, excessive removal of tooth structure and root fractures. Effective management of separated instruments requires a comprehensive understanding of the contributing factors, meticulous preoperative assessment, and precise evaluation of the retrieval difficulty. The application of appropriate retrieval techniques is essential to minimize complications and optimize clinical outcomes. The current manuscript provides a framework for understanding the causes, risk factors, and clinical management principles of instrument separation. By integrating effective strategies, endodontists can enhance decision-making, improve endodontic treatment success and ensure the preservation of natural dentition.
Humans ; Root Canal Therapy/adverse effects* ; Consensus ; Root Canal Preparation/adverse effects*

Objective To analyze the clinical and immunological characteristics of a rare case of CHARGE syndrome,we summarize the genotype and phenotype in the Chinese patient population,and explore the underlying immunopathogenic mechanisms.Methods Clinical data from a pediatric patient with CHARGE syndrome were collected and analyzed.A comprehensive analysis of the Chinese patient population was conducted.Gene analysis and immunological characterization were performed using flow cytometry,deep sequencing,and quantitative PCR.Results The proband was a premature female infant whose primary clinical manifestations included congenital heart disease,recurrent respiratory infections,respiratory failure,airway dysplasia,hearing impairment,and bilateral choroidal coloboma.Whole-exome sequencing revealed a de novo heterozygous nonsense mutation in the CHD7 gene,c.5122C＞T(p.Gln1708Ter),classified as pathogenic according to ACMG criteria.Immunological studies indicated impaired thymic output of T cells,significant alterations in the number and proportion of CD8+T cell subsets,increased apoptosis,and defective activation and production of key effector cytokines such as IFN-γ by CD8+T cells.However,no significant abnormalities were observed in peripheral lymphocyte proliferation.Conclusion CHARGE syndrome is a rare autosomal dominant genetic disorder primarily caused by mutations in the CHD7 gene.The main clinical features include ocular defects,cardiac disease,choanal atresia/cleft lip and palate,growth retardation,gonadal hypoplasia,and ear anomalies.This case study suggests that CHARGE syndrome is associated with abnormalities in the development,apoptosis,and effector functions of immune cells.

Objective To analyze the clinical and immunological characteristics of a rare case of CHARGE syndrome,we summarize the genotype and phenotype in the Chinese patient population,and explore the underlying immunopathogenic mechanisms.Methods Clinical data from a pediatric patient with CHARGE syndrome were collected and analyzed.A comprehensive analysis of the Chinese patient population was conducted.Gene analysis and immunological characterization were performed using flow cytometry,deep sequencing,and quantitative PCR.Results The proband was a premature female infant whose primary clinical manifestations included congenital heart disease,recurrent respiratory infections,respiratory failure,airway dysplasia,hearing impairment,and bilateral choroidal coloboma.Whole-exome sequencing revealed a de novo heterozygous nonsense mutation in the CHD7 gene,c.5122C＞T(p.Gln1708Ter),classified as pathogenic according to ACMG criteria.Immunological studies indicated impaired thymic output of T cells,significant alterations in the number and proportion of CD8+T cell subsets,increased apoptosis,and defective activation and production of key effector cytokines such as IFN-γ by CD8+T cells.However,no significant abnormalities were observed in peripheral lymphocyte proliferation.Conclusion CHARGE syndrome is a rare autosomal dominant genetic disorder primarily caused by mutations in the CHD7 gene.The main clinical features include ocular defects,cardiac disease,choanal atresia/cleft lip and palate,growth retardation,gonadal hypoplasia,and ear anomalies.This case study suggests that CHARGE syndrome is associated with abnormalities in the development,apoptosis,and effector functions of immune cells.

Objective:To explore the neuroprotective effect of α7 nicotinic acetylcholine receptor (α7nAChR) on rat models of Parkinson's disease (PD) and its underlying mechanism.Methods:Forty-eight 8-week-old SPF-grade SD rats were randomly divided into a normal control group, a PD model group, an α7nAChR empty vector group and an α7nAChR overexpression group, with 12 rats in each group. PD models in the latter 3 groups of rats were established by 6-hydroxydopamine (6-OHDA). Four weeks after modeling, rats in the latter 2 groups were injected with 2 μL α7nAChR overexpression lentivirus or empty vector lentivirus through stereotactic intracerebral injection, while rats in the normal control group did not receive any treatment. Two weeks after injection, the behavioral changes of these rats were detected by apomorphine-induced rotation test; the right substantia nigra pars compacta (SNc) was prepared and performed the following experiments: hematoxylin-eosin (HE) staining and Nissl staining were used to detect the neuron morphological changes, TUNEL was used to detect the neuron apoptosis, fluorescent double labeling was used to detect the expressions of tyrosine hydroxylase (TH) and α-synuclein (α-Syn), ELISA was used to detect the expressions of 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA), and Western blotting was used to detect the expressions of ferroptosis-related proteins (ferritin heavy chain 1 [FTH1], Sigma receptor 1 [S1R], glutathione peroxidase 4 [GPX4], long chain acyl-coa synthetase 4 [ACSL4], solute carrier family 7 member11 [SLC7A11]), and the expressions of proteins related to CAMKII/ERK pathway (phosphorylated calmodulin kinase Ⅱ [p-CAMK Ⅱ], phosphorylated extracellular signal regulated kinase [p-ERK], and phosphorylated Kirsten rat sarcoma viral oncogene homolog [p-KRAS]).Results:(1) Compared with the normal control group, the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly larger number of rotations ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly smaller number of rotations ( P<0.05). (2) HE staining and Nissl staining showed that the PD model group had decreased number of dopaminergic neurons and Nissl bodies, accompanied by neuronal distribution disorder, nuclear condensation or swelling; the α7nAChR-overexpression group had obviously improved appearance of dopaminergic neurons, with normal morphology and less cell degeneration. (3) TUNEL results showed that compared with the normal control group, the PD model group, α7nAChR empty vector group, and α7nAChR overexpression group had significantly higher apoptosis rate ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had statistically lower apoptosis rate ( P<0.05). (4) Double immunofluorescent staining results showed that compared with the normal control group (303.61±48.40, 13 985.80±1 956.06), the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly increased α-Syn expression (4 310.40±518.43, 3 846.60±524.47 and 1 033.55±59.98) and statistically decreased TH expression (760.97±57.26, 842.55±113.41 and 8 101.82±1 171.85) in the right SNc ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly decreased α-Syn expression and increased TH expression in the right SNc ( P<0.05). (5) ELISA results showed that the 4-HNE and MDA expressions in the right SNc of the PD model group, α7nAChR empty vector group and α7nAChR overexpression group were significantly higher than those in the normal control group ( P<0.05); the 4-HNE and MDA expressions in the α7nAChR overexpression group were significantly lower than those in the PD model group ( P<0.05). (6) Western blotting results showed that compared with the normal control group, the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly decreased FTH1, S1R, GPX4, and SLC7A11 protein expressions, and statistically increased ACSL4 protein expression in the right SNc ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly increased FTH1, S1R, GPX4, and SLC7A11 protein expressions and decreased ACSL4 protein expression in the right SNc ( P<0.05). Compared with the normal control group, the PD model group, α7nAChR empty vector group and α7nAChR overexpression group had significantly increased p-KRAS, p-CAMKII, and p-ERK protein expressions in the right SNc ( P<0.05); compared with the PD model group, the α7nAChR overexpression group had significantly decreased p-KRAS, p-CAMKII, and p-ERK protein expressions in the right SNc ( P<0.05). Conclusion:The α7nAChR may exert neuroprotective effect on PD rat models by regulating the CAMKII/ERK pathway and ferroptosis-related proteins.

Abstract Health literate schools (HeLit-Schools) play a significant role in fostering students health literacy. The paper elucidates the background and conceptual connotations of HeLit-Schools, and analyzes how HeLit-Schools effectively integrate and enhance the health literacy of schools in three aspects: philosophy and core drivers, strategy and method implementation, as well as evaluation mechanisms and standard setting. Furthermore, the paper explores the implications of foreign HeLit-Schools research and practice for China under the context of "Healthy China" construction, as well as the key strategies for Chinese schools in the implementation of HeLit-Schools, aiming to provide a new perspective and theoretical support for Chinese schools to practice the "Healthy China initiative" and strengthen school construction from the perspective of health literacy.