Protrusive facial deformities, characterized by the forward displacement of the teeth and/or jaws beyond the normal range, affect a considerable portion of the population. The manifestations and morphological mechanisms of protrusive facial deformities are complex and diverse, requiring orthodontists to possess a high level of theoretical knowledge and practical experience in the relevant orthodontic field. To further optimize the correction of protrusive facial deformities, this consensus proposes that the morphological mechanisms and diagnosis of protrusive facial deformities should be analyzed and judged from multiple dimensions and factors to accurately formulate treatment plans. It emphasizes the use of orthodontic strategies, including jaw growth modification, tooth extraction or non-extraction for anterior teeth retraction, and maxillofacial vertical control. These strategies aim to reduce anterior teeth and lip protrusion, increase chin prominence, harmonize nasolabial and chin-lip relationships, and improve the facial profile of patients with protrusive facial deformities. For severe skeletal protrusive facial deformities, orthodontic-orthognathic combined treatment may be suggested. This consensus summarizes the theoretical knowledge and clinical experience of numerous renowned oral experts nationwide, offering reference strategies for the correction of protrusive facial deformities.
Humans ; Orthodontics, Corrective/methods* ; Consensus ; Malocclusion/therapy* ; Patient Care Planning ; Cephalometry

Enamel demineralization, the formation of white spot lesions, is a common issue in clinical orthodontic treatment. The appearance of white spot lesions not only affects the texture and health of dental hard tissues but also impacts the health and aesthetics of teeth after orthodontic treatment. The prevention, diagnosis, and treatment of white spot lesions that occur throughout the orthodontic treatment process involve multiple dental specialties. This expert consensus will focus on providing guiding opinions on the management and prevention of white spot lesions during orthodontic treatment, advocating for proactive prevention, early detection, timely treatment, scientific follow-up, and multidisciplinary management of white spot lesions throughout the orthodontic process, thereby maintaining the dental health of patients during orthodontic treatment.
Humans ; Consensus ; Dental Caries/etiology* ; Dental Enamel/pathology* ; Tooth Demineralization/etiology* ; Tooth Remineralization

Objective To study the clinical and pathological characteristics,as well as diagnosis,treatment methods and prognosis of adult patients with chronic active Epstein-Barr virus infection(CAEBVI).Methods Clinical and pathological data of 8 adult patients with CAEBVI admitted to a hospital in Gansu Province from January 2017 to December 2022 were collected retrospectively,clinical and histopathological characteristics,EBV-related test re-sults,as well as treatment and prognosis of patients were analyzed.Results Among 8 CAEBVI patients,3 were males and 5 were females,with the median age of 21.5 years.The median time from onset to diagnosis of CAEBVI was 7 months.The main manifestations were fever,pancytopenia(involving two or three peripheral blood lines),as well as lymph node enlargement,hepatomegaly and splenomegaly.The quantifications of plasma EBV nucleic acid(DNA)were all＞1.0 × 103.The sorting results of EBV infected cells showed that 3 cases were T lymphocytes in-fection,2 were NK cell infection,and 3 were co-infection of T lymphocytes and NK cells.Bone marrow cytological examination of 8 patients showed no atypical lymphocytes,while 6 patients showed hemophagocytic cells.Flow cy-tometey(FCM)typing results showed that no abnormal cell population was detected in all the 8 patients,and no myeloid,B lymphocyte,T lymphocyte and NK cell markers were expressed.The positive rate of T cell receptor(TCR)gene rearrangement was 37.5％(n=3).Histopathology showed that most cases(n=6,75.0％)expressed CD3,partial cases expressed CD4,CD8,CD56,TIA-1,and EBV encoded RNA(EBER),all were positive.The survival rate of patients after treatment was 50.0％(n=4),the follow-up time was 6-51 months,the 1-year sur-vival rate was 85.7％,and the median survival time was 24 months.Conclusion CAEBVI is characterized by varia-ble clinical manifestations that may lead to fatal complications.Early diagnosis and individualized treatment should be performed to reduce mortality of patients.

Pyroptosis is a form of lytic programmed cell death executed by a family of pore-forming proteins named gasdermin (GSDM). Pyroptosis plays crucial roles in host defense against pathogen infection and eliminating abnormal and harmful cells, while excessive pyroptosis causes inflammatory diseases including cytokine storm and septic shock. Mammalian GSDMs, except for pejvakin (PJVK), adopt an autoinhibited two-domain architecture, in which the N-terminal cytotoxic domain (GSDM-N) is restrained in an inactive state by the intramolecular interaction with the C-terminal inhibitory domain (GSDM-C). These two-domain proteins are activated by upstream protease cleavage within the interdomain linkers. The unleashed GSDM-N binds to acidic phospholipids in the cytoplasmic leaf of plasma membranes and undergoes dramatic conformational changes and oligomerization, then assembling into transmembrane pores for pyroptosis induction. GSDM pores lead to membrane rupture, cell swelling, and cytosol release, thereby mobilizing proinflammatory responses. GSDMs are evolutionarily conserved and have been discovered across all kingdoms of life, including bacteria, fungi, invertebrates such as cnidarians and mollusks, and all vertebrates. Proteolytic cleavage to liberate the pore-forming activity of GSDM-N appears to be a universal mechanism for most GSDMs activation, despite low sequence homology among the GSDMs from diverse species. However, recent studies discover that there exist noncanonical GSDMs lack of functional C-terminal inhibitory domains in some lower eukaryotic species. These noncanonical GSDMs are activated by unprecedent mechanisms independent of proteolytic cleavage. TrichoGSDM, present in the basal metazoan Trichoplax adhaerens, is a pore-forming domain-only protein and exists as a disulfides-linked autoinhibited dimer. Reduction of the disulfides by the conserved cytoplasmic antioxidant system, including glutathione (GSH) and thioredoxin (Trx), generates pore-forming active monomers capable of inducing lytic cell death. In filamentous fungus Neurospora crassa, polymorphic regulator of cell death-1 (rcd-1) encodes two GSDM-like proteins RCD-1-1 and RCD-1-2 in incompatible haplostrains, which trigger pyroptosis-like cell death in nonself discrimination (allorecognition) upon encountering during somatic cell fusion. RCD-1-1 and RCD-1-2 are both monomers and structurally similar to mammalian GSDM-N domains, lacking autoinhibitory fragments. They alone could bind acidic phospholipids, and associate with cell membrane in a resting state. Coexistence of RCD-1-1 and RCD-1-2 leads to formation of RCD-1-1/RCD-1-2 heterodimers through molecular mating, which further oligomerize into membrane-inserted pores, causing rapid lytic cell death. These findings reveal mechanistic diversities in GSDM activation and indicate versatile functions of GSDMs. Due to the highly proinflammatory nature of pyroptosis, the pore-forming activities of GSDMs have been illustrated to be precisely regulated at multiple levels. GSDMD transcription and expression is characterized to be induced by interferon regulatory factors 2 (IRF2). mRNA alternative splicing of GSDMB generates various isoforms, some of which exhibit potent pore-forming activity whereas the others bear none. Additionally, different types of post-translational modifications have been identified on GSDMs, playing distinct regulatory roles. For examples, itaconation of GSDMD, succinylation of GSDMD and GSDME, and phosphorylation of GSDMA, GSDMD and GSDME, negatively regulate GSDM pore formation, thereby inhibiting pyroptosis. Conversely, palmitoylation of GSDMD and GSDME, and ubiquitination of GSDMD promote the pore-forming activities and pyroptosis. Moreover, some proteases can cleave within the GSDM-N domains to block their pore-forming activities. On the other hand, bacterial pathogens evolve specific effectors to hijack host pyroptotic defense pathway through targeting upstream caspases, GSDMs or plasma membrane phospholipids. Given the crucial roles of GSDMD in immune defense and pathological inflammation, a few small-molecule inhibitors have been found to directly inhibit GSDMD activity. Since the identification of GSDMs as the executioners of pyroptosis, the GSDM family has attracted broad attention in immunology researches. Significant progress has been made to greatly advance our knowledge about how GSDMs action, and what are the immunological functions of pyroptosis. Investigations of GSDM-targeting therapies are emerging as a promising translational direction. In this paper, we review recent progress in the field of pyroptosis researches, with focus on various molecular mechanisms underlying GSDMs activation and regulation. The biological implication and future direction of pyroptosis research are also discussed.

Colorectal cancer(CRC)is highly heterogeneous,but traditional TNM staging cannot distinguish the heterogeneity of CRC well,which can no longer meet the treatment needs.Integrating the clinical features,molecular genetic changes in cancer tissue,transcriptome and proteome changes,as well as immune matrix characteristics,the consensus molecular subtype(CMS)of CRC is by far the best description of its heterogeneity.This paper first discusses the molecular genetic changes of three types of CRC cancer tissues(chromosomal instability,microsatellite instability,and CpG island methylation phenotype).Then it systematically elaborates on the clinical characteristics,treatment directions,and prognosis evaluation of CRC patients with different CMS subtypes,as well as their relationship with immunotherapy and changes in gut microbiota.With the continuous improvement of sequencing technology and the prospective precision medicine clinical trial exploration,the"multi-molecule multi-drug"treatment model based on CMS typing will become the core of future precision medicine and personalized medicine.

Lipopolysaccharides (LPS) are major outer membrane components of Gram-negative bacteria. Unlike most Gram-negative bacteria, Acinetobacter baumannii can still survive and acquire polymyxin resistance after complete loss of LPS. Previous studies of LPS-deficient Acinetobacter baumannii mostly focused on LPS-deficient strains induced by polymyxin, whose background was complex and unstable. To investigate LPS loss-mediated polymyxin resistant-Acinetobacter baumannii, this study constructed a stable and clear background LPS-deficient strain by knocking out lpxC gene in Acinetobacter baumannii ATCC 19606 with CIRSPR/Cas9, and then studied the phenotypic changes of the lpxC-deficient strain including morphology, growth rate, antibiotic susceptibility, virulence, membrane permeability, and membrane potential. Animal experiments were approved by the Animal Care and Welfare Committee Institute of Medicinal Biotechnology, CAMS and PUMC (approval number: IMB-20240119D₉). The results indicated that the lpxC gene of Acinetobacter baumannii ATCC 19606 was successfully knocked out. After losing the lpxC, the strain underwent the morphological change from rod-shaped to spherical. Furthermore, it leads to reduced growth rate, enhanced membrane permeability, decreased membrane potential, lower virulence, and increased antibiotic susceptibility to β-lactams, quinolones, aminoglycosides, macrolides, glycopeptides. The lpxC deletion results in significant changes in membrane homeostasis and adaptability of Acinetobacter baumannii. Understanding the phenotypic changes of colistin-resistant Acinetobacter baumannii mediated by LPS loss is useful for exploring the resistance mechanism of Acinetobacter baumannii and developing new therapeutic strategies.

China prospective multicenter birth cohort (Prospective Omics Health Atlas birth cohort, POHA birth cohort) study was officially launched in 2022. This study, in collaboration with 12 participating units, aims to establish a high-quality, multidimensional cohort comprising 20 000 naturally conceived families and assisted reproductive families. The study involves long-term follow-up of parents and offspring, with corresponding biological samples collected at key time points. Through multi-omics testing and analysis, the study aims to conduct multi-omics big data research across the entire maternal and infant life cycle. The goal is to identify new biomarkers for maternal and infant diseases and provide scientific evidence for risk prediction related to maternal diseases and neonatal health.

Objective:To explore the characteristics of brain dynamic activity in patients with schizophrenia by using functional magnetic resonance imaging(fMRI).Methods:Forty-three patients with schizophrenia and 31 normal controls were recruited and under fMRI scanning.The Positive and Negative Symptom Scale(PANS)was used to assess the severity of clinical symptoms.The DPABI software were used to compute dReHo and dFC.Granger causality analysis was used to calculate the effective connectivity between the significant brain regions of dReHo and the whole brain.Two sample t-test was performed to compare the difference of dReHo and dFC be-tween patients with schizophrenia and normal controls.Results:The dReHo of left postcentral gyrus(LPG)(P＜0.01,cluster-level FWE corrected)in patients with schizophrenia was decreased.The Dfc was increased between left postcentral and left middle frontal gyrus,left superior medial frontal gyrus,right calcarine,left medial cingulum gyrus,right supplementary motor area(P＜0.01,uncorrected).Compared with normal controls,patients with schiz-ophrenia showed decreased effective connectivity from LPG to right putamen.Conclusion:It suggests that the ab-normal functional activity of the postcentral gyrus mightcontribute to the neural physiopathology in patients with schizophrenia.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.