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*

Oral submucous fibrosis(OSF)is a chronic and inflammatory mucosal disease caused by betel quid chewing,which belongs to oral potentially malignant disorders.Abnormal fibroblast differentiation leading to disordered collagen metabolism is the core process underlying OSF development.The epithelium,which is the first line of defense against the external environment,can convert external signals into pathological signals and participate in the remodeling of the fibrotic microenvironment.However,the specific mechanisms by which the epithelium drives fibroblast differentiation remain unclear.In this study,we found that Arecoline-exposed epithelium communicated with the fibrotic microenvironment by secreting exosomes.MiR-17-5p was encapsulated in epithelial cell-derived exosomes and absorbed by fibroblasts,where it promoted cell secretion,contraction,migration and fibrogenic marker(α-SMA and collagen type I)expression.The underlying molecular mechanism involved miR-17-5p targeting Smad7 and suppressing the degradation of TGF-β receptor 1(TGFBR1)through the E3 ubiquitination ligase WWP1,thus facilitating downstream TGF-β pathway signaling.Treatment of fibroblasts with an inhibitor of miR-17-5p reversed the contraction and migration phenotypes induced by epithelial-derived exosomes.Exosomal miR-17-5p was confirmed to function as a key regulator of the phenotypic transformation of fibroblasts.In conclusion,we demonstrated that Arecoline triggers aberrant epithelium-fibroblast crosstalk and identified that epithelial cell-derived miR-17-5p mediates fibroblast differentiation through the classical TGF-β fibrotic pathway,which provided a new perspective and strategy for the diagnosis and treatment of OSF.

Oral submucous fibrosis(OSF)is a chronic and inflammatory mucosal disease caused by betel quid chewing,which belongs to oral potentially malignant disorders.Abnormal fibroblast differentiation leading to disordered collagen metabolism is the core process underlying OSF development.The epithelium,which is the first line of defense against the external environment,can convert external signals into pathological signals and participate in the remodeling of the fibrotic microenvironment.However,the specific mechanisms by which the epithelium drives fibroblast differentiation remain unclear.In this study,we found that Arecoline-exposed epithelium communicated with the fibrotic microenvironment by secreting exosomes.MiR-17-5p was encapsulated in epithelial cell-derived exosomes and absorbed by fibroblasts,where it promoted cell secretion,contraction,migration and fibrogenic marker(α-SMA and collagen type I)expression.The underlying molecular mechanism involved miR-17-5p targeting Smad7 and suppressing the degradation of TGF-β receptor 1(TGFBR1)through the E3 ubiquitination ligase WWP1,thus facilitating downstream TGF-β pathway signaling.Treatment of fibroblasts with an inhibitor of miR-17-5p reversed the contraction and migration phenotypes induced by epithelial-derived exosomes.Exosomal miR-17-5p was confirmed to function as a key regulator of the phenotypic transformation of fibroblasts.In conclusion,we demonstrated that Arecoline triggers aberrant epithelium-fibroblast crosstalk and identified that epithelial cell-derived miR-17-5p mediates fibroblast differentiation through the classical TGF-β fibrotic pathway,which provided a new perspective and strategy for the diagnosis and treatment of OSF.

Variations in the dynein axonemal heavy chain gene, dynein axonemal heavy chain 6 (DNAH6), lead to multiple morphological abnormalities of the flagella. Recent studies have reported that these deficiencies may result in sperm head deformation. However, whether DNAH6 is also involved in human acrosome biogenesis remains unknown. The purpose of this study was to investigate DNAH6 gene variants and their potential functions in the formation of defective sperm heads and flagella. Whole-exome sequencing was performed on a cohort of 375 patients with asthenoteratozoospermia from the First Affiliated Hospital of Anhui Medical University (Hefei, China). Hematoxylin and eosin staining, scanning electron microscopy, and transmission electron microscopy were performed to analyze the sperm morphology and ultrastructure. Immunofluorescence staining and Western blot analysis were conducted to examine the effects of genetic variants. We identified three novel deleterious variants in DNAH6 among three unrelated families. The absence of inner dynein arms and radial spokes was observed in the sperm of patients with DNAH6 variants. Additionally, deficiencies in the acrosome, abnormal chromatin compaction, and vacuole-containing sperm heads were observed in these patients with DNAH6 variants. The decreased levels of the component proteins in these defective structures were further confirmed in sperm from patients with DNAH6 variants using Western blot. After intracytoplasmic sperm injection (ICSI) treatment, the partner of one patient with a DNAH6 variant achieved successful pregnancy. Overall, novel variants in DNAH6 genes that contribute to defects in the sperm head and flagella were identified, and the findings indicated ICSI as an effective clinical treatment for such patients.

AIM:To observe the expression of microRNA-126-5p during myocardial injury and its role in myo-cardial cell injury induced by adriamycin(also called doxorubicin, DOX).METHODS: The BALB/c mouse model of DOX-induced acute and chronic myocardial injury was established via intraperitoneal injection of DOX.HE staining was applied to observe the morphological changes of myocardial tissues.Lactate dehydrogenase(LDH)in serum was detected and PowerLab system was used to detect the influence of DOX on the changes of ±dp/dtmax.The expression of microRNA-126-5p in injured myocardial tissues and the H 9c2 cells exposed to DOX was detected by real-time PCR.Gain-and loss-of-function experiments were conducted to detect the role of microRNA-126-5p in H9c2 cells treated with DOX on LDH release and caspase-3 activation.RESULTS:In acute and chronic DOX myocardial damage models in mice,HE staining showed disarranged myocardial fibers, dissolved myofibril and inflammatory cell infiltration.Higher serum LDH level and lower ±dp/dtmaxin DOX-treated mice than those in normal mice were found.Compared with the normal mice, the expression level of microRNA-126-5p was significant increased in the myocardium with DOX-induced injury.Similarly,the expression level of microRNA-126-5p was significant increased in the H9c2 cells treated with DOX.In addition, over-expression of microRNA-126-5p decreased cell viability and promoted apoptosis,while microRNA-126-5p ablation promoted the viability and inhibited the apoptosis of H9c2 cells.CONCLUSION:The microRNA-126-5p expression is up-regulated in myocar-dial injury induced by DOX,and microRNA-126-5p inhibits cell viability and promotes apoptosis induced by DOX.

Objective To explore the prospective monitoring and control methods for missing reporting of health-care-associated infection(HAI)cases,analyze its implementation efficacy,provide basis for formulating targeted strategy for monitoring missing report of HAI.Methods From January 2016 to June 2017,the quality control circle (QCC)method was used to prospectively monitor HAI cases in hospitalized patients,missing reporting of HAI was controlled.Results "Information system intelligence screening+mobile messaging alerts+ HAI supervision"trinity monitoring model for avoid missing reporting of HAI cases was established,after the first round of PDCA(plan, do,check,action)cycle,missing reporting rate of HAI decreased from 79.16% before QCC to 59.75% after QCC, difference was statistically significant (χ2＝208.821,P＝0.000).Compared with missing reporting rate of HAI af-ter the first round of PDCA,missing reporting rate of HAI after the second round of PDCA dropped to 26.18%, difference was statistically significant (χ2＝200.075,P＝0.002).Conclusion Active prospective prevention and control before missing reporting of HAI can effectively avoid missing reporting of HAI cases.

Objective: To compare the middle and long term clinical outcomes of one-stop hybrid coronary revascularization, coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) in treating the patients with multivessel coronary artery disease; to explore the optimal indication of one-stop hybrid technology. Methods: Our research included in 3 groups: Hybrid group, n=141 patients received one-stop hybrid coronary revascularization in our hospital from 2006-06 to 2010-16. Meanwhile, 5797 patients received CABG and 4254 received PCI, the major pre-operative risk factors were studied by Logistic regression analysis to calculate propensity score, adjacent matching was used to respectively select 141 subjects from CABG and PCI patients to make 1:1 match with Hybrid group as CABG group and PCI group. EuroSCORE and SYNTAX score were used to make risk stratification in all 3 groups. By EuroSCORE system: low risk ≤ 2, medium risk (3-5) and high risk ≥ 6; by SYNTAX score system: low risk ≤ 24, medium risk (25-29) and high risk ≥ 30. The incidence of major adverse cardiac/cerebral vascular events (MACCE) was compared among 3 groups at different risk stratifications. Results: The mean follow-up time was 4.5 years up to 2015-01. The overall incidence of MACCE was lower in Hybrid group (9.9％) than PCI group (27.7％), P<0.001; while it was similar between Hybrid group and CABG group (19.1％), P=0.150. By EuroSCORE stratification, the incidence of MACCE in low risk and medium risk patients were similar among 3 groups; while in high risk patients, the incidence was lower in Hybrid group than both CABG group (P=0.017) and PCI group (P<0.001). By SYNTAX score stratification, the incidence of MACCE in low risk and medium risk patients were similar among 3 groups; while in high risk patients, the incidence was lower in Hybrid group than PCI group (P<0.001), it was similar between Hybrid group and CABG group (P=0.355). Conclusion: One-stop hybrid technology had the better middle and long term outcomes for treating multivessel coronary artery disease patients with high risk stratification, which provided an alternative strategy in clinical practice.

Objectives: The purpose of this study was to compare the 30-day clinical outcome after simultaneous hybrid coronary revascularization (HCR) with off-pump coronary artery bypass grafting (OPCABG) in patients with multivessel coronary artery disease and evaluate the safety and efficiency of simultaneous hybrid coronary revascularization strategy. Methods: Simultaneous HCR was performed in 533 patients with multivessel coronary artery disease at Fuwai hospital from January 2009 to January 2017. These patients were 1:1 matched with patients underwent OPCABG using propensity score matching method. The primary endpoint was major adverse cardiac or cerebrovascular events (MACCE) over the 30-day follow-up post-surgery, and the second endpoints were in-hospital outcomes, including chest tube drainage, transfusion rate, mechanical ventilation time and length of stay in intensive care unit. Results: Chest tube drainage post-surgery (ml)(714 [523, 971] vs 965 [716, 1 220], P<0.001),Blood transfusion rate (19.7% vs 34.0%, P=0.024), mechanical ventilation time (hours) (12.6[9.3, 15.7] vs 16.0 [12.8, 18.7], P<0.001), and stay in intensive care unit (hours) (21.7[19.8, 42.4] vs 41.6[23.6, 70.0], P<0.001) were all significantly reduced in the simultaneous HCR group than in OPCABG group. Mortality, myocardial infarction, stroke, repeat revascularization rate and accumulated MACCE rate during the 30-day follow-up were similar between HCR group and OPCABG group .Conclusions: For selected patients with multivessel coronary artery disease, simultaneous HCR provided a safe and effective alternative revascularization strategy. Simultaneous HCR is associated with less blood loss, faster recovery, and fewer perioperative complications and achieved similar and favorable early outcomes as compared with OPCABG strategy.

OBJECTIVETo investigate the protective effect of ginsenoside Rg1 on oxygen-glucose deprivation (OGD) in PC-12 cells, and preliminarily discuss the potential molecular mechanism of mTOR/Akt/FoxO3 signaling pathway.

METHODThe OGD PC-12 cell model was established. The cell viability was measured by MTT assay. After the pretreatment with Rg1 with the concentration of 10, 20, 40 micromol x L(-1) for 24 h, the cell viability was observed. Lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) ac- tivity and malondialdehyde (MDA) level were detected by colorimetry assay. mTOR, p-Akt(ser473), p-Akt(tjr308), Akt, p-FoxO3, FoxO3 in cytoplasm and nucleus, and total FoxO3 protein expression were detected by Western blot assay.

RESULTOGD could significantly in- hibit cell proliferation in 4-24 h in a time-dependent manner. After pretreatment for 24 h, Rg1 (20, 40 micromol x L(-1)) could notably elevate the cell viability and SOD viability and reduce the LDH release and MDA content. Besides, Rg1 also inhibited OGD-induced mTOR and p-Akt(ser473) decreases. After treatment for 6 h, OGD could reduce FoxO3 phosphorylation and promote FoxO3 in cytoplasm. This data suggested that Rg1 could protect PC-12 cell injury through mTOR/p-Akt/FoxO3 signaling pathway.

CONCLUSIONGinsenoside Rg1 could attenuate OGD-induced PC-12 cell injury. Its action mechanism may be closely related to activation of mTOR/p-Akt/FoxO3 signaling pathway.

Animals ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Forkhead Box Protein O3 ; Forkhead Transcription Factors ; genetics ; metabolism ; Ginsenosides ; pharmacology ; Glucose ; metabolism ; Oxygen ; metabolism ; PC12 Cells ; Protective Agents ; pharmacology ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Rats ; Signal Transduction ; drug effects ; TOR Serine-Threonine Kinases ; genetics ; metabolism

For the problems that 3 first-class ternary hospitals which are not directly affiliated to medical universities are facing in cultivating high-educated staff's scientific abilities,analyze the importance to carry out scientific work in clinic and discuss how to improve their scientific abilities from hospitals,departments and high-educated staff themselves.