The prevalence of Class III malocclusion varies among different countries and regions. The populations from Southeast Asian countries (Chinese and Malaysian) showed the highest prevalence rate of 15.8%, which can seriously affect oral function, facial appearance, and mental health. As anterior crossbite tends to worsen with growth, early orthodontic treatment can harness growth potential to normalize maxillofacial development or reduce skeletal malformation severity, thereby reducing the difficulty and shortening the treatment cycle of later-stage treatment. This is beneficial for the physical and mental growth of children. Therefore, early orthodontic treatment for Class III malocclusion is particularly important. Determining the optimal timing for early orthodontic treatment requires a comprehensive assessment of clinical manifestations, dental age, and skeletal age, and can lead to better results with less effort. Currently, standardized treatment guidelines for early orthodontic treatment of Class III malocclusion are lacking. This review provides a comprehensive summary of the etiology, clinical manifestations, classification, and early orthodontic techniques for Class III malocclusion, along with systematic discussions on selecting early treatment plans. The purpose of this expert consensus is to standardize clinical practices and improve the treatment outcomes of Class III malocclusion through early orthodontic treatment.
Humans ; Malocclusion, Angle Class III/classification* ; Orthodontics, Corrective/methods* ; Consensus ; Child

Objective: To analyze changes in Rh system antibodies among antibody-positive patients and evaluate the efficacy of Rh phenotype-matched electronic cross-matching (hereinafter referred to as Rh-ECM). Methods: A retrospective analysis was performed on antibody screening data of 48 254 patients in our hospital from December 2023 to March 2025. The antibody screening results were compared between the pre-application phase (n=46 346, control group) and post-application phase (n=48 254, experimental group) of Rh-ECM technology, focusing on the changes in the proportion of Rh system antibodies, with statistical analysis conducted using SPSS 26.0 software. Meanwhile, the initial and re-examination situations of Rh antibody in the antibody screening of approximately 20 000 person-times each before (June 2019 to June 2020, n=21 048) and after (July 2020 to April 2021, n=20 965) of Rh-ECM were evaluated to explore the influence of Rh-ECM on the detection rate of Rh antibody. Results: After Rh-ECM implementation, 345 positive cases (0.7%) (345/48 254) were detected among 48 254 patients, primarily consisting of mns system antibodies (128 cases, 37.1%) (128/345) and rh system antibodies (95 cases, 27.5%) (95/345). Before Rh-ECM implementation, 199 positive cases (0.4%) (199/46 346) were detected among 46 346 patients, with rh system antibodies accounting for 97 cases (48.7%) (97/199). The difference in the composition ratio of Rh antibodies between the two phases was statistically significant (P<0.001), and the relative risk ratio of Rh antibody detection after Rh-ECM implementation was 56.5% compared to before. Another set of data analysis showed that before Rh-ECM, there were 37 cases with initial positive results and 8 cases with re-examination positive results; after Rh-ECM, these numbers were 44 and 2 respectively There was a statistically significant difference in the re-examination positive rate of Rh antibodies between the two stages (P<0.05). Conclusion: The implementation of Rh-ECM technology significantly reduced the proportion of Rh system antibodies among patients with positive antibody screening results. This suggests that Rh-ECM can effectively reduce the detection rate of Rh antibodies, which may be related to the reduced risk of antibody production due to Rh-matched transfusion, thus improving transfusion safety. Therefore, Rh-ECM is worthy of broader promotion in clinical transfusion testing.

Objective:To evaluate the role of G-protein coupled receptor 37 (GPR37) in cognitive dysfunction in a mouse model of neuropathic pain.Methods:SPF-grade healthy male C57BL/6 mice and GPR37 knockout (GPR37-KO) mice, aged 3 months, with a body weight of approximately 20 g, were divided into 4 groups ( n=6 each) using a random number table method: control group (Con group), neuropathic pain group (NPP group), GPR37-KO+ control group (GPR37-KO Con group) and GPR37-KO+ neuropathic pain group (GPR37-KO NPP group). The mouse model of neuropathic pain was established by ligation of the sciatic nerve. The thermal paw withdrawal latency (TWL) and mechanical paw withdrawal threshold (MWT) were measured at 7 days after surgery. The open field test and Morris water maze test were performed at 28 days after surgery. The mice were subsequently sacrificed, and the medial prefrontal cortex (mPFC) was obtained for determination of the level of phosphorylated calcium/calmodulin-dependent protein kinase Ⅱ(p-CAMKⅡ) and expression of brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD-95). Results:Compared to Con group, no significant changes were found in the parameters in GPR37-KO Con group ( P>0.05), and TWL was significantly shortened, MWT was decreased, the time the animal spent in central area was prolonged and the platform-crossing times were increased in the open field test, and the escape latency was prolonged and platform-crossing times were decreased in the Morris water maze test, and the expression of p-CAMKⅡ, BDNF and PSD-95 in the mPFC was down-regulated in NPP group ( P<0.05). Compared with NPP group, TWL was significantly shortened, MWT was decreased, the time the animal spent in central area was prolonged and the platform-crossing times were increased in the open field test, and the escape latency was prolonged and platform-crossing times were decreased in the Morris water maze test, and the expression of p-CAMKⅡ, BDNF and PSD-95 in the mPFC was down-regulated in GPR37-KO NPP group ( P<0.05). Conclusions:GPR37 is involved in the development of cognitive dysfunction in mice with neuropathic pain, and the mechanism may be related to its modulation of synaptic plasticity.

Objective To study the molecular mechanism of Bel subtype caused by mutation p.R168W of glycosyltransferase B.Methods Serological test,SSP-PCR and direct sequence the Exon6 and Exon 7 of the ABO gene.Construct a 3D molecular model and predict the structural impact of GTB protein mutations.Results A antigen or B antigen can't be detected on the surface of the propositus' RBC,and only anti-A antibodies were detected in her serum.But serological test indicated her daughter's blood type was a normal B type.SSP-PCR test indicated propositus' ABO gene type is O1 B.By gene sequencing the Exon 6 and Exon 7 of the ABO gene,a ABO Bel allel(c.502C＞T,p.R168W)was discoverd in both the propositus and her daughter.Through the propositus' daughter coexisted Bel gene with normal B gene,her blood type was a normal B type.Conclusions ABO gene c.502C＞T mutations cause Bel phenotypes in patients by reducing the stability of GTB.