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 By conducting evidence evaluation research on literatures,this study aims to reveal the o-verall characteristics and research hotspots in the field of combat trauma-related infections,ultimately providing data support for the prevention and control of such infections.METHODS Relevant research in this field was sys-tematically collected from open-source databases to construct a dataset.The overall characteristics,research hotspots,prevention and control strategies,and future challenges of trauma-related infections were summarized and analyzed.RESULTS From 2004 to 2024,184 papers were published.The United States contributed the most publications,with Uniformed Services University of the Health Sciences being the most productive research insti-tution and Professor Clinton K.Murray as the author with the highest number of publications.The top five key-words with the highest frequency were combat related injury,infection,Acinetobacter baumannii,epidemiology and management.Among the publicly published literature data on war trauma-related infections,blast injuries ac-counted for the largest proportion,mainly multi-site injuries,with limb injuries being the most common.Bacteri-al infections were more common than fungal infections,with gram-negative bacteria being predominant and A.baumannii being the most common.Besides early wound management and the use of antibacterial drugs,in-creased attention should be paid to infection prevention and control in austere environments and the development of novel countermeasures.These advancements are critical to address projected changes in combat trauma,inclu-ding increasingly complex injuries and substantially elevated risks of infection and antimicrobial resistance.CONCLUSION This study systematically presents research hotspots,developmental trends,and prospects in com-bat trauma-related infections through evidence evaluation study,providing novel perspectives for researchers and facilitating further development in this field.

OBJECTIVE By conducting evidence evaluation research on literatures,this study aims to reveal the o-verall characteristics and research hotspots in the field of combat trauma-related infections,ultimately providing data support for the prevention and control of such infections.METHODS Relevant research in this field was sys-tematically collected from open-source databases to construct a dataset.The overall characteristics,research hotspots,prevention and control strategies,and future challenges of trauma-related infections were summarized and analyzed.RESULTS From 2004 to 2024,184 papers were published.The United States contributed the most publications,with Uniformed Services University of the Health Sciences being the most productive research insti-tution and Professor Clinton K.Murray as the author with the highest number of publications.The top five key-words with the highest frequency were combat related injury,infection,Acinetobacter baumannii,epidemiology and management.Among the publicly published literature data on war trauma-related infections,blast injuries ac-counted for the largest proportion,mainly multi-site injuries,with limb injuries being the most common.Bacteri-al infections were more common than fungal infections,with gram-negative bacteria being predominant and A.baumannii being the most common.Besides early wound management and the use of antibacterial drugs,in-creased attention should be paid to infection prevention and control in austere environments and the development of novel countermeasures.These advancements are critical to address projected changes in combat trauma,inclu-ding increasingly complex injuries and substantially elevated risks of infection and antimicrobial resistance.CONCLUSION This study systematically presents research hotspots,developmental trends,and prospects in com-bat trauma-related infections through evidence evaluation study,providing novel perspectives for researchers and facilitating further development in this field.

Based on the clinical thinking of combining diseases and patterns， we combined disease identification， pattern differentiation， and constitution identification， and put forward the theory of identifying and treating critical hypertension， which is "examining the symptoms first， identifying the constitutions as reference， and combining the diseases and patterns". Firstly， the starting point of identifying the disease is to examine the symptoms， and those with precise diagnosis and strong specificity will be diagnosed with the disease， while those with relatively broad diagnosis and fuzzy characteristics will be emphasised on identifying constitutions and differentiating patterns. Focusing on the impact of constitution identification on disease identification and pattern differentiation， constitution identification could be the basis when no symptoms to identify， and based on the theory of "constitution-disease correlation" and "constitution-pattern correlation" to improve the understanding of borderline hypertension from the group and individual level， which helps to identify and predict the development of the diseases and patterns； if the symptoms are complicated and difficult to identify， it is necessary to take syndrome as the outline， use the syndrome to unify the disease， and then refer to the constitution to legislate and prescribe medications. This paper summarizes the traditional Chinese medicine clinical differentiation and treatment strategy of borderline hypertension clear and easy to grasp， with a view to provide a feasible and efficient reference for prevention and treatment of borderline hypertension with traditional Chinese medicine.

Objective:To explore the predictive value of serum adiponectin (APN) in parenteral nutrition associated cholestasis (PNAC) in premature infants.Methods:A retrospective analysis was conducted on the clinical data of 85 premature infants treated with PN (parenteral nutrition) at the Yiyang Central Hospital from January to December 2021. According to whether PNAC occurred during hospitalization, the infants were divided into 34 PNAC group and 51 non PNAC group. A comparison was made between the PNAC group and the non PNAC group. The serum APN levels in children of different gestational ages in the PNAC group were analyzed, and the risk factors for PNAC in premature infants were analyzed. The predictive value of serum APN in premature PNAC was analyzed.Results:The serum APN levels in the PNAC group were lower than those in the non PNAC group at weeks 1, 3, and 5, and the difference was statistically significant (all P<0.01). The serum APN levels in children with gestational age<34 weeks in the PNAC group were lower than those in children with gestational age≥34 weeks at 1, 3, and 5 weeks, and the differences were statistically significant (all P<0.05). Multivariate logistic regression analysis showed that gestational age, birth weight, sepsis, fasting time, duration of PN, accumulation of fat emulsion, initial amount of amino acids, and accumulation of amino acids were all risk factors for PNAC in premature infants (all P<0.05). The area under the curve (AUC) of serum APN for predicting PNAC in premature infants was 0.814(95% CI: 0.722-0.906), with a sensitivity of 0.69, specificity of 0.88, and a cutoff value of 13.28 mg/L. Conclusions:Serum APN has a high predictive value for the occurrence of PNAC in premature infants, and should be closely monitored in clinical practice.

Objective:To investigate the clinical efficacy and prognosis of sacubatrovalsartan combined with dapagliflozin in patients with heart failure with reduced ejection fraction (HFrEF).Methods:Totally 206 consecutive patients with HFrEF in our hospital from March 2021 to September 2021 were enrolled and randomly(random number) divided into the control group ( n = 51), the sacubatrovalsartan group ( n = 52), the dapagliflozin group ( n=51) and the combined treatment group ( n= 52). The baseline clinical data of patients and laboratory examination results were collected. The changes of related results before and after treatment in each group were analyzed and compared. After discharge, the enrolled patients were followed up by outpatient or telephone for an average of 6 months to determine whether the patients had heart failure rehospitalization, ventricular arrhythmia, major adverse cardiovascular events (MACE), etc. Results:After anti-heart failure treatment, there were significant differences in NT-proBNP, left ventricular ejection fraction (LVEF) and soluble growth stimulating gene 2 protein (ST2) among the four groups. NT-proBNP and ST2 in the combined treatment group were significantly lower than those in the other groups, and LVEF was significantly higher. Compared with the control group, the rehospitalization due to heart failure and MACE events in the other three groups were significantly lower ( P < 0.05), and the combined treatment group had the lowest ( P < 0.05). The Kaplan-Meier survival curve showed that the survival probability of the other groups was significantly higher than that of the control group, and was the highest in the combined treatment group. Conclusions:The clinical efficacy and prognosis of HFrEF patients could be significantly improved after the treatment of sacubatrovalsartan combined with dapagliflozin.

BACKGROUND: This study aimed to evaluate the correlation between long non-coding RNA (lncRNA)-related single nucleotide polymorphisms (SNPs) and susceptibility to silicosis. METHODS: First, RNA-sequencing (RNA-seq) data were comprehensively analyzed in the peripheral blood lymphocytes of eight participants (four silicosis cases and four healthy controls) exposed to silica dust to identify differentially expressed lncRNAs (DE-lncRNAs). The functional SNPs in the identified DE-lncRNAs were then identified using several databases. Finally, the association between functional SNPs and susceptibility to silicosis was evaluated by a two-stage case-control study. The SNPs of 155 silicosis cases and 141 healthy silica-exposed controls were screened by genome-wide association study (GWAS), and the candidate SNPs of 194 silicosis cases and 235 healthy silica-exposed controls were validated by genotyping using the improved Mutiligase Detection Reaction (iMLDR) system. RESULTS: A total of 76 DE-lncRNAs were identified by RNA-seq data analysis (cut-offs: fold change > 2 or fold change < 0.5, P < 0.05), while 127 functional SNPs among those 76 DE-lncRNAs were identified through multiple public databases. Furthermore, five SNPs were found to be significantly correlated with the risk of silicosis by GWAS screening (P < 0.05), while the results of GWAS and iMLDR validation indicated that the variant A allele of rs1814521 was associated with a reduced risk of silicosis (OR = 0.76, 95% CI = 0.62-0.94, P = 0.011). CONCLUSION The presence of the SNP rs1814521 in the lncRNA ADGRG3 is associated with susceptibility to silicosis. Moreover, ADGRG3 was found to be lowly expressed in silicosis cases. The underlying biological mechanisms by which lncRNA ADGRG3 and rs1814521 regulate the development of silicosis need further study.
Case-Control Studies ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Polymorphism, Single Nucleotide ; RNA, Long Noncoding/genetics* ; Silicosis/genetics*

Objective:To investigate the influence of death receptor 3 ( Dr3) gene deficiency on the intestinal mucosal inflammation in different mice colitis models, and explore the relationship of Dr3 gene deficiency and intestinal mucosal permeability. Methods:Nine female Dr3 gene deficiency ( Dr3-/-) mice and 9 wild type (WT) mice were collected and set as Dr3-/--DSS group and WT-DSS group. The mice of 2 groups received 2.5% dextran sodium sulfate (DSS) for 5 days and sterile water for 2 days as a cycle and 4 cycles were manipulated to construct a chronic colitis model of mice. The male WT and Dr3-/- mice were collected as donor mice and initial T lymphocytes from two types of donor mice were sorted respectively by immunomagnetic separation and flow cytometry. A enteritis model of mice induced by T cells adoptive transfer was constructed on the recipient mice including Rag1-/- (WT transfer group) and Dr3-/-Rag1-/- ( Dr3-/- transfer group) mice by the peritoneal injection of T lymphocytes from WT and Dr3-/- mice respectively. The body mass, stool property and occult blood of mice were observed, and the disease activity index (DAI) was calculated. The degree of intestinal mucosal injury and inflammatory cell infiltration in mice were observed under microscope, and the histological score of enteritis was calculated. The intestinal mucosal permeability of mice was detected by fluorescein isothiocyanate (FITC) -dextran serum fluorescence method. The differences of DAI score, histological score and FITC-dextran content between the two groups were compared. Results:The DAI scores of mice in Dr3-/--DSS group were significantly higher than those in WT-DSS group on the 12th, 19th and 26th day after establishing the model (all P<0.05) . The rectal histological score of WT-DSS group 4 weeks after establishing the model was significantly higher than that of cecum and colon (10.130 ± 1.540 vs. 3.667 ± 0.236 and 7.222 ± 1.199, all P<0.05) , suggesting that the degree of rectal inflammation in WT-DSS group was the most serious. The histological score of colon in Dr3-/--DSS group was significantly higher than that of cecum and rectum (11.330 ± 1.167 vs. 7.556 ± 1.519 and 9.500 ± 0.824, all P<0.05) , suggesting that the degree of colonic inflammation in Dr3-/--DSS group was the most serious. The histological scores of cecum and colon in Dr3-/--DSS group were significantly higher than those of WT-DSS group (cecum: 7.556 ± 1.519 vs. 3.667 ± 0.236, P = 0.022; colon: 11.330 ± 1.167 vs. 7.222 ± 1.199, P = 0.026) , but there was no significant difference in rectal histological score between the two groups ( P>0.05) , suggesting that Dr3 gene deficiency aggravated the inflammation of cecum and colon. The rectal histological score of WT transfer group 6 weeks after establishing the model was significantly higher than that of duodenum, jejunum, terminal ileum, cecum and middle colon (all P<0.05) , suggesting that the degree of rectal inflammation in WT transfer group was the most serious. The histological score of cecum in Dr3-/- transfer group was significantly higher than that of duodenum, jejunum, terminal ileum, middle colon and rectum (all P<0.05) , suggesting that the degree of cecal inflammation in WT transfer group was the most serious. Compared with WT transfer group, the scores of small intestine including duodenum, jejunum and terminal ileum in Dr3-/- transfer group were significantly higher (17.667 ± 0.943 vs. 14.667 ± 1.167, P<0.05) , and the infiltration of inflammatory cells in small intestine was more obvious (duodenum: 4.000 ± 0.289 vs. 3.222 ± 0.401, P = 0.135; jejunum: 4.000 ± 0.236 vs. 3.111 ± 0.309, P<0.05; ileum: 4.889 ± 0.309 vs. 3.889 ± 0.261, P<0.05) . It was suggested that Dr3 gene deficiency aggravated intestinal inflammation. The content of FITC-dextran in eye venous blood of Dr3-/- mice was significantly higher than that of WT mice (656.0 ± 60.9 vs. 403.8 ± 54.8, P<0.05) , the content of FITC-dextran in Dr3-/--DSS group was significantly higher than that of WT-DSS group (1176.4 ± 109.5 vs. 545.7 ± 97.8, P<0.05) , the content of FITC-dextran in Dr3-/-transfer group was significantly higher than that of WT transfer group (1270.5 ± 112.2 vs. 711.0 ± 71.5, P<0.05) , and the content of FITC-dextran in Dr3-/-Rag1-/- mice was significantly higher than that of Rag1-/- mice (714.5 ± 62.9 vs. 501.8 ± 59.8, P<0.05) , suggesting that the intestinal mucosal permeability of Dr3 gene deficient mice was higher. Conclusion:Dr3 gene deficiency in mice increases intestinal mucosal permeability, destroys intestinal mucosal barrier function, and aggravates intestinal proximal inflammation in experimental colitis, suggesting that Dr3 gene may play the protective role in intestinal inflammation by regulating intestinal mucosal permeability.

Objective:To investigate the influence of death receptor 3 ( Dr3) gene deficiency on the intestinal mucosal inflammation in different mice colitis models, and explore the relationship of Dr3 gene deficiency and intestinal mucosal permeability. Methods:Nine female Dr3 gene deficiency ( Dr3-/-) mice and 9 wild type (WT) mice were collected and set as Dr3-/--DSS group and WT-DSS group. The mice of 2 groups received 2.5% dextran sodium sulfate (DSS) for 5 days and sterile water for 2 days as a cycle and 4 cycles were manipulated to construct a chronic colitis model of mice. The male WT and Dr3-/- mice were collected as donor mice and initial T lymphocytes from two types of donor mice were sorted respectively by immunomagnetic separation and flow cytometry. A enteritis model of mice induced by T cells adoptive transfer was constructed on the recipient mice including Rag1-/- (WT transfer group) and Dr3-/-Rag1-/- ( Dr3-/- transfer group) mice by the peritoneal injection of T lymphocytes from WT and Dr3-/- mice respectively. The body mass, stool property and occult blood of mice were observed, and the disease activity index (DAI) was calculated. The degree of intestinal mucosal injury and inflammatory cell infiltration in mice were observed under microscope, and the histological score of enteritis was calculated. The intestinal mucosal permeability of mice was detected by fluorescein isothiocyanate (FITC) -dextran serum fluorescence method. The differences of DAI score, histological score and FITC-dextran content between the two groups were compared. Results:The DAI scores of mice in Dr3-/--DSS group were significantly higher than those in WT-DSS group on the 12th, 19th and 26th day after establishing the model (all P<0.05) . The rectal histological score of WT-DSS group 4 weeks after establishing the model was significantly higher than that of cecum and colon (10.130 ± 1.540 vs. 3.667 ± 0.236 and 7.222 ± 1.199, all P<0.05) , suggesting that the degree of rectal inflammation in WT-DSS group was the most serious. The histological score of colon in Dr3-/--DSS group was significantly higher than that of cecum and rectum (11.330 ± 1.167 vs. 7.556 ± 1.519 and 9.500 ± 0.824, all P<0.05) , suggesting that the degree of colonic inflammation in Dr3-/--DSS group was the most serious. The histological scores of cecum and colon in Dr3-/--DSS group were significantly higher than those of WT-DSS group (cecum: 7.556 ± 1.519 vs. 3.667 ± 0.236, P = 0.022; colon: 11.330 ± 1.167 vs. 7.222 ± 1.199, P = 0.026) , but there was no significant difference in rectal histological score between the two groups ( P>0.05) , suggesting that Dr3 gene deficiency aggravated the inflammation of cecum and colon. The rectal histological score of WT transfer group 6 weeks after establishing the model was significantly higher than that of duodenum, jejunum, terminal ileum, cecum and middle colon (all P<0.05) , suggesting that the degree of rectal inflammation in WT transfer group was the most serious. The histological score of cecum in Dr3-/- transfer group was significantly higher than that of duodenum, jejunum, terminal ileum, middle colon and rectum (all P<0.05) , suggesting that the degree of cecal inflammation in WT transfer group was the most serious. Compared with WT transfer group, the scores of small intestine including duodenum, jejunum and terminal ileum in Dr3-/- transfer group were significantly higher (17.667 ± 0.943 vs. 14.667 ± 1.167, P<0.05) , and the infiltration of inflammatory cells in small intestine was more obvious (duodenum: 4.000 ± 0.289 vs. 3.222 ± 0.401, P = 0.135; jejunum: 4.000 ± 0.236 vs. 3.111 ± 0.309, P<0.05; ileum: 4.889 ± 0.309 vs. 3.889 ± 0.261, P<0.05) . It was suggested that Dr3 gene deficiency aggravated intestinal inflammation. The content of FITC-dextran in eye venous blood of Dr3-/- mice was significantly higher than that of WT mice (656.0 ± 60.9 vs. 403.8 ± 54.8, P<0.05) , the content of FITC-dextran in Dr3-/--DSS group was significantly higher than that of WT-DSS group (1176.4 ± 109.5 vs. 545.7 ± 97.8, P<0.05) , the content of FITC-dextran in Dr3-/-transfer group was significantly higher than that of WT transfer group (1270.5 ± 112.2 vs. 711.0 ± 71.5, P<0.05) , and the content of FITC-dextran in Dr3-/-Rag1-/- mice was significantly higher than that of Rag1-/- mice (714.5 ± 62.9 vs. 501.8 ± 59.8, P<0.05) , suggesting that the intestinal mucosal permeability of Dr3 gene deficient mice was higher. Conclusion:Dr3 gene deficiency in mice increases intestinal mucosal permeability, destroys intestinal mucosal barrier function, and aggravates intestinal proximal inflammation in experimental colitis, suggesting that Dr3 gene may play the protective role in intestinal inflammation by regulating intestinal mucosal permeability.

OBJECTIVE: To investigate the regulatory effect of metformin on regulatory T cells (Treg) in acidic environment. METHODS: CD4 CD25 Treg cells were obtained by magnetic bead sorting. Treg and conventional T cells (Tcon) cells were cultured for 24-72 h in pH 7.4 or pH 6.7 medium, and the cell proliferation, apoptosis and Foxp3 expression were detected by flow cytometry. Real-time PCR was used to detect the expression levels of the genes related with glucose metabolism. Thirty-two C57BL/6 male mouse models bearing subcutaneous prostate cancer xenograft derived from RM-1 cells were randomized into 4 equal groups for treatment with PBS, metformin, tumor vaccine, or both metformin and the vaccine. The treatment started on the 4th day following tumor cell injection, and metformin (100 mg/kg) or PBS was administered by intraperitoneal injection on a daily basis; the vaccine was intramuscularly injected every 4 days. The tumor size was continuously monitored, and the mice were euthanized on day 25 after tumor implantation to obtain tumor and blood samples. Flow cytometry was used to detect the changes in CD4, CD8, CD4Foxp3 cell subsets in the tumor tissue and peripheral blood. RESULTS: Treg cells showed significantly enhanced proliferation ( < 0.05) while the proliferation of Tcon cells was suppressed in acidic medium ( < 0.001). Treg cells cultured in acidic medium showed significantly increased expressions of OXPHOS-related genes pgc1a ( < 0.001) and cox5b ( < 0.01), which did not vary significantly in Tcon cells in acidic medium. Treg cells exhibited significantly decreased apoptosis in acidic medium ( < 0.01) with increased Foxp3 cells ( < 0.001) and intracellular alkaline levels ( < 0.01). Metformin obviously reversed the acid tolerance of Treg cells without producing significant effect on Tcon cells. In the animal experiment, both metformin ( < 0.05) and vaccine ( < 0.01) alone reduced the tumor volume, but their combined treatment more potently reduced the tumor volume ( < 0.001). Metformin alone did not obviously affect CD4 cells or CD8 cells but significantly decreased the percentage of CD4Foxp3 ( < 0.05); the vaccine alone significantly increased CD4 cells and CD8 cells ( < 0.001) and also the percentage of CD4Foxp3 cells ( < 0.05). The combined treatment, while reducing the percentage of CD4Foxp3cells to a level lower than that in the vaccine group ( < 0.01), produced the strongest effect to increase CD4 cells and CD8 cells ( < 0.01). CONCLUSIONS Metformin can inhibit the proliferation and function of regulatory T cells in an acidic environment and enhance the effect of tumor vaccine by reducing the proportion of Treg cells to achieve the anti-tumor effect.
Animals ; Cell Proliferation ; Forkhead Transcription Factors ; Male ; Metformin ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes, Regulatory