Classification and immunotherapy assessment of lung adenocarcinoma based on coagulation-related genes.

Introduction: This study on lung adenocarcinoma (LUAD), a common lung cancer subtype with high mortality. Aims: This study focuses on how tumor cell interactions affect immunotherapy responsiveness. Methods: Using public databases, we used non-negative matrix factorization clustering method, ssGSEA, CIBERSORT algorithm, immunophenotype score, survival analysis, protein-protein interaction network method to analyze gene expression data and coagulation-related genes. Results: We divided LUAD patients into three coagulation-related subgroups with varying immune characteristics and survival rates. A cluster of three patients, having the highest immune infiltration and survival rate, also showed the most potential for immunotherapy. We identified five key genes influencing patient survival using a protein-protein interaction network. Conclusion: This research offers valuable insights for forecasting prognosis and immunotherapy responsiveness in LUAD patients, helping to inform clinical treatment strategies.

LINC00707 inhibits myocardial fibrosis and immune disorder in rheumatic heart disease by regulating miR-145-5p/S1PR1.

LINC00707 is a lncRNA that can regulate a variety of diseases. This study mainly investigated that the expression of LINC00707 in rheumatic heart disease (RHD) and LINC00707 regulates S1PR1 by targeting miR-145-5p to inhibit myocardial fibrosis and immune disorder in RHD. A rat model of RHD induced by inactivated group A ß-hemolytic streptococcus (GSA) was established. Sixty female Lewis rats (8 weeks of age) were randomly divided into six groups, including control (Con), RHD, RHD+NC, RHD+LINC00707, RHD+miR-145-5p and RHD+LINC00707+miR-145-5p. The mRNA expression was detected by Quantitative Real-time polymerase chain reaction (qRT-PCR). Protein expression of S1PR1 was detected by western blot. The levels of myocardial damage markers (CK-MB, cTnl) and inflammatory immune markers (IL-6, IL-17 and IL-21) were measured by enzyme linked immunosorbent assay (ELISA). The Collagen III/I(COLIII/I) ratio, mRNA expression of COLIIIα1 and FSP1 of rat heart valve tissue in the RHD group was observably higher by comparison with the CON group. The expression of LINC00707 was observably lower in the RHD group. LINC00707 inhibited myocardial fibrosis and immune disorder in RHD. MiR-145-5p was the target gene of LINC00707 via Targetscan prediction. Luciferase reporter experiment confirmed that miR-145-5p was directly regulated by LINC00707. The expression of miR-145-5p in the RHD group was observably higher by comparison with the CON group and LINC00707 observably decreased the expression of miR-145-5p. miR-145-5p mimic reversed the inhibiting effect of LINC00707 on myocardial fibrosis and immune disorder. Furthermore, S1PR1 was confirmed to be downstream gene of miR-145-5p and low expressed in the RHD model. LINC00707 could inhibit myocardial fibrosis and immune disorder in RHD by regulating miR-145-5p/S1PR1.

[Clinical research of Bite-bumper combined with fixed appliance in treatment of lingual tipping deep bite].

OBJECTIVE: To study the mechanism and applicability of Bite-bumper combined with fixed appliance in treatment of lingual tipping deep bite. METHODS: 14 children aged 12-16 years old with lingual tipping deep bite participated in the experiment. Bite-bumper combined with fixed appliance was used to correct the deep bite. Clinic effect was observed. Lateral cephalograms were taken before treatment and after bite opening. The related hard tissues were estimated through the cephalograms. RESULTS: 1) The average duration for bite-opening with Bite-bumper and fixed appliance of 14 patients was 28 days. 2) After bite-opening, the changes in length direction of jaw (SNA, SNB, ANB) had no statistical variances. Anterior and posterior facial height (S-Go, ANS-Me) were increased. No significant changes were observed in the ratio of posterior facial height to anterior facial height (S-Go/N-Me), angle of mandibular plane (SN-MP) and Y axis. Labial incline in upper and lower incisors (U1-SN, L1-MP) and interincisa angle (U1-L1) were decreased. The posterior teeth (U6-PP, L6-MP) were extruded and the upper incisors (U1-PP) were intruded. The overbite was decreased. CONCLUSION: Bite-bumper combined with fixed appliance can be used effectively for deep bite correction and improve the short face of patients with lingual tripping deep overbite.