Cemental tear is a rare and indetectable condition unless obvious clinical signs present with the involvement of surrounding periodontal and periapical tissues. Due to its clinical manifestations similar to common dental issues, such as vertical root fracture, primary endodontic diseases, and periodontal diseases, as well as the low awareness of cemental tear for clinicians, misdiagnosis often occurs. The critical principle for cemental tear treatment is to remove torn fragments, and overlooking fragments leads to futile therapy, which could deteriorate the conditions of the affected teeth. Therefore, accurate diagnosis and subsequent appropriate interventions are vital for managing cemental tear. Novel diagnostic tools, including cone-beam computed tomography (CBCT), microscopes, and enamel matrix derivatives, have improved early detection and management, enhancing tooth retention. The implementation of standardized diagnostic criteria and treatment protocols, combined with improved clinical awareness among dental professionals, serves to mitigate risks of diagnostic errors and suboptimal therapeutic interventions. This expert consensus reviewed the epidemiology, pathogenesis, potential predisposing factors, clinical manifestations, diagnosis, differential diagnosis, treatment, and prognosis of cemental tear, aiming to provide a clinical guideline and facilitate clinicians to have a better understanding of cemental tear.
Humans ; Dental Cementum/injuries* ; Consensus ; Diagnosis, Differential ; Cone-Beam Computed Tomography ; Tooth Fractures/therapy*

Objective:To evaluate the cost-effectiveness of interventional bronchoscopy with rigid bronchoscopy(scleroscope),laryngeal mask airway and endotracheal intubation access for the treatment of central airway stenosis.Methods:The data of patients with central airway stenosis who underwent interventional bronchoscopy under general anesthesia were collected,and divided into rigid bronchoscopy group,laryngeal mask group and tracheal intubation group.The average Cost-Effectiveness Ratio(CER)was calculated using total hospitalization cost and total surgery cost as the cost indices,and improvement of shortness of breath symptoms as the effect index.The stability of the evaluation result was analyzed by one-factor sensitivity analysis and probabilistic sensitivity analysis.Results:A total of 205 patients were included:rigid bronchoscopy group(66 patients),laryngeal mask group(64 patients)and tracheal intubation group(75 patients).The CERs were 8 851.29 for the rigid bronchoscopy group,10 942.62 for the laryngeal mask group,and 8 902.98 for the tracheal intubation group when using total hospitalization cost as the cost index.For total surgery cost,the CERs were 2 617.80,3 389.73,and 2 741.38,respectively.The order was rigid bronchoscopy＜tracheal intubation＜laryngeal mask.The main factors affecting the model results were the discount rate,non-surgical costs,and improvement of shortness of breath symptoms.Probabilistic sensitivity analysis shows that the results of the basic analysis are stable.Conclusion:Interventional bronchoscopy via rigid bronchoscope is the most economical method for treating central airway stenosis.

Objective:To evaluate the cost-effectiveness of interventional bronchoscopy with rigid bronchoscopy(scleroscope),laryngeal mask airway and endotracheal intubation access for the treatment of central airway stenosis.Methods:The data of patients with central airway stenosis who underwent interventional bronchoscopy under general anesthesia were collected,and divided into rigid bronchoscopy group,laryngeal mask group and tracheal intubation group.The average Cost-Effectiveness Ratio(CER)was calculated using total hospitalization cost and total surgery cost as the cost indices,and improvement of shortness of breath symptoms as the effect index.The stability of the evaluation result was analyzed by one-factor sensitivity analysis and probabilistic sensitivity analysis.Results:A total of 205 patients were included:rigid bronchoscopy group(66 patients),laryngeal mask group(64 patients)and tracheal intubation group(75 patients).The CERs were 8 851.29 for the rigid bronchoscopy group,10 942.62 for the laryngeal mask group,and 8 902.98 for the tracheal intubation group when using total hospitalization cost as the cost index.For total surgery cost,the CERs were 2 617.80,3 389.73,and 2 741.38,respectively.The order was rigid bronchoscopy＜tracheal intubation＜laryngeal mask.The main factors affecting the model results were the discount rate,non-surgical costs,and improvement of shortness of breath symptoms.Probabilistic sensitivity analysis shows that the results of the basic analysis are stable.Conclusion:Interventional bronchoscopy via rigid bronchoscope is the most economical method for treating central airway stenosis.

Amyotrophic Lateral Sclerosis (ALS) is a complex neurodegenerative disorder characterized by progressive axonopathy, jointly leading to the dying back of the motor neuron, disrupting both nerve signaling and motor control. In this review, we highlight the roles of axonopathy in ALS progression, driven by the interplay of multiple factors including defective trafficking machinery, protein aggregation, and mitochondrial dysfunction. Dysfunctional intracellular transport, caused by disruptions in microtubules, molecular motors, and adaptors, has been identified as a key contributor to disease progression. Aberrant protein aggregation involving TDP-43, FUS, SOD1, and dipeptide repeat proteins further amplifies neuronal toxicity. Mitochondrial defects lead to ATP depletion, oxidative stress, and Ca²⁺ imbalance, which are regarded as key factors underlying the loss of neuromuscular junctions and axonopathy. Mitigating these defects through interventions including neurotrophic treatments offers therapeutic potential. Collaborative research efforts aim to unravel ALS complexities, opening avenues for holistic interventions that target diverse pathological mechanisms.
Humans ; Amyotrophic Lateral Sclerosis/therapy* ; Animals ; Axons/metabolism* ; Mitochondria/metabolism* ; Motor Neurons/pathology*

A rapid quantitative immunochromatographic assay for procalcitonin(PCT)using metal-organic frameworks modified with gold and platinum nanoparticles(MAPs)as labels was established in this work.The detection probe was prepared by conjugating MAPs with anti-PCT monoclonal antibody via an electrostatic adsorption method.Anti-PCT polyclonal antibody and sheep anti-mouse IgG were sprayed onto the nitrocellulose(NC)membrane as the test line and quality control line,respectively,to construct immunochromatographic strip for PCT quantitative detection via signal-amplification-based sandwich immunoassay.The results showed that the MAP-based immunochromatographic test had high sensitivity,high specificity,and good stability.The dynamic range for detection of PCT was 0.61 pg/mL-320 ng/mL,the detection limit was 0.25 pg/mL,and the intra-day and inter-day precision(Relative standard deviation)were less than 15%.The results of real sample analysis showed that a quite low volume of sample was required for detection of PCT in whole blood,which was of great significance for the early diagnosis,monitoring and treatment,and prognosis of inflammation.

The objective of this study was to examine the effects of electroacupuncture on the expression of ATP-binding cassette transporter A1(ABCA1),ATP-binding cassette transporter G1(ABCG1),and class B type Ⅰ scavenger receptor(SR-B Ⅰ)genes and proteins in peritoneal macrophages of atherosclerotic rabbits.The study aimed to explore the mechanism underlying the treatment of atherosclerosis(AS)with electroacupuncture.Methods Twenty-six male New Zealand rabbits were randomly divided into the negative control group(n=7)and the modeling group(n=19)using a random number table method.The negative control group rabbits were fed a regular diet,while the modeling group was induced with a combination of high-fat feed and common carotid artery balloon injury surgery to create an AS model.After successful modeling,the rabbits in the modeling group were further divided into the model group,the electroacupuncture group,and the atorvastatin group,with 6 rabbits in each group.The rabbits in the electroacupuncture group received electroacupuncture at"'Neiguan'(PC6)","'Zusanli'(ST36)",and"'Guanyuan'(ST25)"acupoints,using a density wave,a current of 1 mA,and a frequency of 4 Hz/20 Hz,once a day.The needle was retained for 20 minutes each time,and a total of 4 courses of treatment were conducted,with 6 days per course.The rabbits in the atorvastatin group were administered atorvastatin calcium tablet suspension(1 mg/kg)orally once a day,for 6 days per course,with a total of 4 courses.After the interventions,HE staining was performed to observe the morphological changes in the common carotid artery tissue of the rabbits.Peritoneal macrophages were collected from the rabbits,and the mRNA expression levels of ABCA1,ABCG1,and SR-B Ⅰ were measured using real-time fluorescence PCR.The protein expression levels of ABCA1,ABCG1,and SR-B Ⅰ were detected using Western blotting.Results The negative control group exhibited smooth intima of common carotid artery in rabbits,while the model group displayed damaged intima of common carotid artery,thickened artery walls,and the formation of atherosclerotic plaques.The electroacupuncture group and atorvastatin group showed significant improvements in wall thickening and a reduction in plaque area.Compared with the negative control group,the mRNA and protein expressions of ABCA1,ABCG1,and SR-B Ⅰ in peritoneal macrophages of rabbits in the model group were reduced(P＜0.01).Compared with the model group,the electroacupuncture group and atorvastatin group exhibited increased mRNA and protein expressions of ABCA1,ABCG1,and SR-B Ⅰ in abdominal macrophages of rabbits(P＜0.01).Furthermore,the atorvastatin group demonstrated increased mRNA levels of ABCG1 and SR-B Ⅰ,as well as increased protein expressions of ABCA1,ABCG1,and SR-B Ⅰ in peritoneal macrophages of rabbits,in comparison to the electroacupuncture group(P＜0.01).Conclusion Electroacupuncture can enhance the expressions of ABCA1,ABCG1,and SR-B Ⅰ mRNA and protein in abdominal macrophages of AS rabbits,thereby promoting the process of cholesterol reverse transport.This may be one of the mechanisms underlying the effectiveness of acupuncture in the treatment of AS.

Background: and Purpose X-linked Charcot-Marie-Tooth disease type 1 (CMTX1) is characterized by peripheral neuropathy with or without episodic neurological dysfunction. We performed clinical, neuropathological, and genetic investigations of a series of patients with mutations of the gap-junction beta-1 gene (GJB1) to extend the phenotypic and genetic description of CMTX1. Methods: Detailed clinical evaluations, sural nerve biopsy, and genetic analysis were applied to patients with CMTX1. Results: We collected 27 patients with CMTX1 with GJB1 mutations from 14 unrelated families. The age at onset (AAO) was 20.9±12.2 years (mean±standard deviation; range, 2–45 years). Walking difficulties, weakness in the legs, and pes cavus were common initial symptoms. Compared with female patients, males tended to have a younger AAO (males vs. females=15.4±9.6 vs. 32.0±8.8 years, p=0.002), a longer disease course (16.8±16.1 vs. 5.5±3.8 years, p=0.034), and more-severe electrophysiological results. Besides peripheral neuropathy, six of the patients had special episodic central nervous system (CNS) evidence from symptoms, signs, and/or reversible white-matter lesions. Neuropathology revealed the loss of large myelinated fibers, increased number of regenerated axon clusters with abnormally thin myelin sheaths, and excessively folded myelin. Genetic analysis identified 14 GJB1 variants, 6 of which were novel. Conclusions These findings expand the phenotypic and genetic spectrum of CMTX1. Although CMTX1 was found to have high phenotypic and CNS involvement variabilities, detailed neurological examinations and nerve conduction studies will provide critical clues for accurate diagnoses. Further exploration of the underlying mechanisms of connexin 32 involvement in neuropathy or CNS dysfunction is warranted to develop promising therapies.

AIM To study the quassinoids and lignans from Brucea javanica (L.) Merr.and their anti-inflammatory activities.METHODS The extract was isolated and purified by silica gel,MCI,Sephadex LH-20 and HPLC,then the structures of obtained compounds were identified by physicochemical properties and spectral data.RESULTS Seven quassinoids were isolated and identified as bruceanic acid E (1),15-O-(3-hydroxy-3-methy1butanoyl)-brucealide (2),bruceine L (3),aglycone of yadanzioside D (4),javanicolide A (5),javanicolide C (6),bruceanic acid A (7).Four lignans were isolated and identified as cleomiscosin A (8),ceplignan (9),threo-guaiacylglycerol 8'-(4-hydroxymethyl-2-methoxyphenyl) ether (10),erythro-guaiacylglycerol 8'-(4-hydroxy-methyl-2-methoxyphenyl) ether (11).Compounds 3,8 could inhibit NO release in RAW264.7 cells.CONCLUSION Compounds 9-11 are isolated from Brucea genus for the first time.Compounds 3 and 8 have anti-inflammatory activities.

AIM To study the quassinoids and lignans from Brucea javanica (L.) Merr.and their anti-inflammatory activities.METHODS The extract was isolated and purified by silica gel,MCI,Sephadex LH-20 and HPLC,then the structures of obtained compounds were identified by physicochemical properties and spectral data.RESULTS Seven quassinoids were isolated and identified as bruceanic acid E (1),15-O-(3-hydroxy-3-methy1butanoyl)-brucealide (2),bruceine L (3),aglycone of yadanzioside D (4),javanicolide A (5),javanicolide C (6),bruceanic acid A (7).Four lignans were isolated and identified as cleomiscosin A (8),ceplignan (9),threo-guaiacylglycerol 8'-(4-hydroxymethyl-2-methoxyphenyl) ether (10),erythro-guaiacylglycerol 8'-(4-hydroxy-methyl-2-methoxyphenyl) ether (11).Compounds 3,8 could inhibit NO release in RAW264.7 cells.CONCLUSION Compounds 9-11 are isolated from Brucea genus for the first time.Compounds 3 and 8 have anti-inflammatory activities.

This study aimed to investigate the effect and molecular mechanism of sinomenine on proliferation, apoptosis, metastasis, and combination with inhibitors in human hepatocellular carcinoma HepG2 cells and SK-HEP-1 cells. The effect of sinomenine on the growth ability of HepG2 and SK-HEP-1 cells were investigated by CCK-8 assay, colony formation assay, and BeyoClick~(TM) EdU-488 staining. The effect of sinomenine on DNA damage was detected by immunofluorescence assay, and the effect of sinomenine on apoptosis of human hepatocellular carcinoma cells was clarified by Hoechst 33258 staining and CellEvent~(TM) Cystein-3/7Green ReadyProbes~(TM) reagent assay. Cell invasion assay and 3D tumor cell spheroid invasion assay were performed to investigate the effect of sinomenine on the invasion ability of human hepatocellular carcinoma cells in vitro. The effect of sinomenine on the regulation of protein expression related to the protein kinase B(Akt)/mammalian target of rapamycin(mTOR)/signal transducer and activator of transcription 3(STAT3) signaling pathway in HepG2 and SK-HEP-1 cells was examined by Western blot. Molecular docking was used to evaluate the strength of affinity of sinomenine to the target cysteinyl aspartate specific proteinase-3(caspase-3) and STAT3, and combined with CCK-8 assay to detect the changes in cell viability after combination with STAT3 inhibitor JSI-124 in combination with CCK-8 assay. The results showed that sinomenine could significantly reduce the cell viability of human hepatocellular carcinoma cells in a concentration-and time-dependent manner, significantly inhibit the clonogenic ability of human hepatocellular carcinoma cells, and weaken the invasive ability of human hepatocellular carcinoma cells in vitro. In addition, sinomenine could up-regulate the cleaved level of poly ADP-ribose polymerase(PARP), a marker of apoptosis, and down-regulate the protein levels of p-Akt, p-mTOR, and p-STAT3 in human hepatocellular carcinoma cells. Molecular docking results showed that sinomenine had good affinity with the targets caspase-3 and STAT3, and the sensitivity of sinomenine to hepatocellular carcinoma cells was diminished after STAT3 was inhibited. Therefore, sinomenine can inhibit the proliferation and invasion of human hepatocellular carcinoma cells and induce apoptosis, and the mechanism may be attributed to the activation of caspase-3 signaling and inhibition of the Akt/mTOR/STAT3 pathway. This study can provide a new reference for the in-depth research and clinical application of sinomenine and is of great significance to further promote the scientific development and utilization of sinomenine.
Humans ; Carcinoma, Hepatocellular/genetics* ; Proto-Oncogene Proteins c-akt/metabolism* ; Caspase 3/metabolism* ; Liver Neoplasms/genetics* ; Molecular Docking Simulation ; Sincalide/pharmacology* ; Cell Line, Tumor ; Cell Proliferation ; Hep G2 Cells ; TOR Serine-Threonine Kinases/metabolism* ; Apoptosis