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

Objective:To evaluate the relationship between hippocampal receptor-interacting protein kinase-1 (RIPK1) and nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasomes in postoperative neurocognitive dysfunction of aged rats with chronic knee arthritis pain.Methods:Sixty-four healthy male Sprague-Dawley rats, aged 18 months, weighing 500-550 g, were divided into 4 groups ( n=16 each) using a random number table method: chronic knee arthritis pain group (group P), chronic knee arthritis pain+ operation group (group PS), RIPK1 inhibitor necrostatin-1+ chronic knee arthritis pain+ operation group (group NPS), and DMSO+ chronic knee arthritis pain+ operation group (group DPS). The knee arthritis model was prepared by intra-articular injection of monosodium iodoacetate (MIA) 1 mg into the left knee joint, and 12 weeks later exploratory laparotomy was performed under sevoflurane anesthesia. Necrostatin-1 6.25 mg/kg and the equal volume of DMSO were intraperitoneally injected at 1 h before operation in NPS group and DPS group, respectively. Thermal pain threshold was measured at 1 week before MIA injection and 6 and 12 weeks after MIA injection. Morris water maze test was used to evaluate the cognitive function at 7 days after surgery. Hippocampal tissues were obtained for microscopic examination of the pathological changes (after HE staining) and for determination of the expression of RIPK1, phosphorylated RIPK1 (p-RIPK1), NLRP3, activated cysteine-aspartic protease caspase-1 (cl-caspase-1), apoptosis-associated speck-like protein containing a CARD (ASC) (by Western blot) and contents of interleukin-1beta (IL-1β) and IL-18 (by enzyme-linked immunosorbent assay). Results:Thermal pain threshold was significantly decreased at 6 and 12 weeks after MIA injection as compared with that before injection ( P<0.05), and there was no significant difference in thermal pain threshold among the four groups ( P>0.05). Compared with P group, the escape latency was significantly prolonged, the time of staying at the original platform quadrant was shortened, the number of crossing the original platform was reduced, the expression of RIPK1, p-RIPK1, NLRP3, cl-caspase-1 and ASC was up-regulated, and the contents of IL-1β and IL-18 were increased ( P<0.05), and pathological changes of hippocampal neurons were marked in PS group, DPS group and NPS group. Compared with PS group and DPS group, the escape latency was significantly shortened, the time of staying at the original platform quadrant was prolonged, the number of crossing the original platform was increased, the expression of RIPK1, p-RIPK1, NLRP3, cl-caspase-1 and ASC was down-regulated, the contents of IL-1β and IL-18 were decreased ( P<0.05), and pathological changes of hippocampal neurons were significantly attenuated in NPS group. Conclusions:Postoperative hippocampal RIPK1 function is enhanced in aged rats with chronic knee arthritis pain, which then activates NLRP3 inflammasomes, triggering neuroinflammation, and this process may be involved in the mechanism of postoperative neurocognitive dysfunction.

Background The effects of meteorological factors and air pollutants on ischemic heart disease (IHD) hospitalizations in Urumqi have not been fully understood. Objective To investigate the effects of meteorological conditions (temperature, relative humidity) and common air pollutants [fine particulate matter (PM_2.5), inhalable particulate matter (PM₁₀), ozone (O₃), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), and carbon monoxide (CO)] on the daily hospitalization volume of IHD, and to provide a scientific basis for the development of targeted prevention and management strategies. Methods Basic information of 90622 IHD hospitalized patients in Urumqi City was collected from January 1, 2014 to December 31, 2022, and daily air pollutant concentration data and meteorological data were collected during the same period. The meteorological data included daily mean temperature, daily maximum temperature, daily minimum temperature, and daily mean relative humidity, and the common air pollutants included PM_2.5, PM₁₀, daily maximum 8-h average concentration of O₃ (O₃_8 h), SO₂, NO₂, and CO. Descriptive statistical analyses (mean, standard deviation, and quartiles) were performed on the collected data. A distribution lag nonlinear model (DLNM) based on time-stratified case-crossover design was established to estimate the lagged effects (RR) as well as the cumulative lagged effects (RR_cum) of daily mean temperature, relative humidity, and different air pollutants on the number of IHD admissions, stratified by gender and age (<60 and ≥60 years). Subsequently, a generalized additive model (GAM) was used to explore the effects of cold waves (≤ P₅ of the daily minimum temperature and lasting ≥3 d) versus heat waves (≥ P₉₅ of the daily maximum temperature and lasting ≥3 d) on IHD hospitalizations and the potential interactions between temperature and the more influential air pollutants [particulate matter (PM) and O₃_8 h] on IHD hospitalizations. Results The maximum number of IHD hospitalizations in a single day in Urumqi from January 1, 2014 to December 31, 2022 was 100, and the average daily number of hospitalized IHD patients was 27. Daily mean temperature, relative humidity, and air pollutants had different nonlinear relationships and hysteresis with IHD hospitalizations. Extremely low temperatures (<P₁: −18 °C) showed the greatest risk to admission for the total IHD population at a cumulative lag of 31 d (lag0-31) (RR_cum=2.092, 95%CI: 1.261,3.471). Female [lag0-31, RR_cum and 95%CI: 3.416 (2.296,5.082)] and people ≥60 years old [lag0-31, RR_cum and 95%CI: 2.356 (1.681,3.303)] were more sensitive to extremely low temperatures. The risk of IHD hospitalization was greatest on lag20 for cold waves (RR=1.242, 95%CI: 1.053, 1.465), and no lagged effect of heat waves on the number of IHD hospitalizations was found. There was a positive interaction (SI >1, P<0.001) between temperature, PM, and O₃_8 h on the risk of IHD hospitalization, especially for low temperature-high PM and O₃_8 h. Conclusion Both low temperature and high pollutant concentrations associate with an increase in IHD hospitalizations with lagged effects in Urumqi from 2014 to 2022, while cold waves associate with a higher risk of IHD admissions. Females and people aged 60 years and older are at high risk.

Objective To summarize the experience of integrative palliative care at Peking Union Medi-cal College Hospital and provide a reference for promoting the integrative palliative care model.Methods Twenty cases receiving integrative palliative care at Peking Union Medical College Hospital were collected.The clinical characteristics,reasons for initiating integrative palliative care,the process of integrative palliative care,and feedback from these cases were summarized.Results Insomnia(11 cases,55％)and pain(9 cases,45％)were the most common symptoms requiring control in the 20 cases.The integrative palliative care team assisted in medical decision-making for 17 cases(85％),prepared end-of-life for 9 cases(45％),assisted in the transfer for 3 cases(15％),and provided comfort care for all the 20 cases(100％).Conclusions The integrative palliative care model can help alleviate suffering in end-of-life patients and provide support to patients'families and the original medical teams.This model is worth further promotion within class A tertiary hospitals.

Objective To investigate the effect of salidroside(SAL)on the proliferation and migration of human vascular endothelial cell line EA.hy926.Methods The cells were divided into control group and test groups of 1,10 and 100 nmol/L SAL,10 nmol/L SAL+2 μg/mL avastin(vascular endothelial growth factor(VEGF)blocker)group,10 nmol/L SAL+2 μg/mL IgG(blocker negative control)group,10 nmol/L SAL+8 μg/mL avastin group,10 nmol/L SAL+8 μg/mL IgG group,10 μmol/L YC-1[hypoxia inducible factor-1α(HIF-1α)blocker]group and 10 μmol/L YC-1+10 nmol/L SAL group.The proliferation and migration of EA.hy926 cells were detected by MTS assay and Transwell cell migration experiments.RT-qPCR and Western blot were used to measure the gene and protein level of HIF-1α and VEGF.The luciferase report gene experiment was used to find the effect of SAL on HIF-1α transcription activity of EA.hy926 cells.The guanylate cyclase activator(YC-1)was used as a HIF-1α blocker to verify potential effect of SAL on the expression of VEGF through HIF-1α.Results SAL significantly promoted proliferation of EA.hy926 cells(P＜0.05)and the proliferation promoting effect of SAL(10 nmol/L)was significantly reduced by the VEGF blocker bevacizumab avastin(2 μg/mL)(P＜0.05).SAL significantly promoted migration of EA.hy926 cells(P＜0.05),and this effect was significantly inhibited by avastin(8 μg/mL)(P＜0.05).SAL increased the expression of HIF-1α and VEGF gene and protein,and promoted the transcription of HIF-1α(P＜0.05).The level of HIF-1α and VEGF protein decreased by YC-1,a HIF-1α bloc-ker(P＜0.05).Conclusions HIF-1α/VEGF pathway is potentially involved in SAL promoted proliferation and migration of EA.hy926 cells.

Objective To construct the machine learning models based on the radiomic features of non-contrast and enhanced CT and to evaluate the predictive value in the risk stratification of gastrointestinal stromal tumor(GIST).Methods A total of 182 patients with pathologically confirmed GIST were randomly divided into a training set and a validation set at a ratio of 7∶3.The volume of interest(VOI)was outlined in the non-contrast phase,arterial phase and venous phase,and its radiomic features were extracted.The most valuable radiomic features were selected using the least absolute shrinkage and selection operator(LASSO)algorithm.The logistic regression(LR)classifier was used to construct the prediction models based on single-phase or multi-phase images.The predictive efficacy of the different models was compared by using receiver operating characteristic(ROC)curves.Results Four,three,and four radiomic features were selected in the non-contrast phase,arterial phase and venous phase,and 4 models were constructed in total.Among the single-phase models,the venous phase had better predictive efficacy,with the area under the curve(AUC)of 0.932[95％confidence interval(CI)0.873-0.969]and 0.924(95％CI 0.819-0.979)in the training and validation sets.The predictive efficacy of the combined model was improved,with the AUC of 0.946(95％CI 0.891-0.978)and 0.938(95％CI 0.838-0.986).Conclusion The venous phase model can predict the risk stratification of GIST accurately,and the prediction efficacy can be improved by combining the non-contrast and arterial phases.

Objective:To evaluate the role of transient receptor potential melastatin2 (TRPM2) in sevoflurane anesthesia-induced necroptosis in hippocampal neurons of aged rats.Methods:Sixty SPF-grade healthy male Sprague-Dawley rats, aged 22 months, weighing 550-600 g, were divided into 3 groups ( n=20 each) using a random number table method: control group (group C), sevoflurane anesthesia group (group M) and sevoflurane anesthesia+ TRPM2 inhibitor group (group M+ A). M and M+ A groups inhaled 2% sevoflurane for 5 h. In group M+ A, TRPM2 inhibitor ACA 20 mg/kg was intraperitoneally injected at 1 h before sevoflurane inhalation, and the equal volume of dimethyl sulfoxide was intraperitoneally injected in group C and group M. Morris water maze test was performed at 1 day after sevoflurane anesthesia. The escape latency, times of crossing the original platform and time spent in the original platform quadrant were collected. The expression of TRPM2 and necroptosis-related proteins (mixed lineage kinase domain-like protein [MLKL], receptor-interacting protein kinase-1 [RIPK1], phosphorylated MLKL [p-MLKL], and phosphorylated RIPK1 [p-RIPK1]) was detected by Western blot. The cytosolic Ca 2+ concentration in and necroptosis rate of hippocampal neurons were determined by flow cytometry. Results:Compared with group C, the escape latency was significantly prolonged, the times of crossing the original platform were decreased and the time spent in the original platform quadrant was shortened, the expression of TRPM2, MLKL, RIPK1, p-MLKL and p-RIPK1 was up-regulated, and the cytosolic Ca 2+ concentrations in hippocampal neurons and necroptosis rate of hippocampal neurons were increased in group M and group M+ A ( P<0.05). Compared with group M, the escape latency was significantly shortened, the times of crossing the original platform were increased, and the time spent in the original platform quadrant was prolonged, the expression of TRPM2, MLKL, RIPK1, p-MLKL and p-RIPK1 was down-regulated, and the cytosolic Ca 2+ concentrations in hippocampal neurons and necroptosis rate of hippocampal neurons were decreased in group M+ A ( P<0.05). Conclusions:Hippocampal TRPM2 is involved in the process of sevoflurane anesthesia-induced necroptosis in hippocampal neurons of aged rats.

Objective:To evaluate the effect of necrostatin-1 (Nec-1)pre-treatment on postoperative cognitive function in aged rats with chronic pain due to knee arthritis.Methods:One hundred and twenty healthy male Sprague-Dawley rats, aged 22 months, weighing 550-600 g, were divided into 4 groups ( n=30 each) using a random number table method: chronic pain due to knee arthritis group(group P), chronic pain due to knee arthritis + operation group (group PS), dimethyl sulfoxide (DMSO) + chronic pain due to knee arthritis + operation group (DMSO+ PS group), and necrostatin-1 + chronic pain due to knee arthritis + operation group (Nec-1+ PS group). The inflammation-induced knee arthritis model was developed by injecting monosodium iodoacetate (MIA) into the left joint cavity.The exploratory laparotomy under sevoflurane anesthesia was performed at 12 weeks after intra-articular MIA injection. In Nec-1+ PS group and DMSO+ PS group, necrosstatin-1 6.25 mg/kg and the equal dose of DMSO were intraperitoneally injected at 1 h before surgery, respectively. At 7 days after surgery, the Morris water maze test was used to evaluate the cognitive function, the activation of microglial cells in the dentate gyrus of hippocampus was observed by immunofluorescent staining, and the activation rate of microglia cells was calculated, the necrosis rate of neurons was determined by flow cytometry, the expression of receptor-interacting protein kinase 1 (RIPK1)and phosphorylated mixed lineage kinase domain-like protein (p-MLKL) was determined by Western blot, and the contents of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 were determined by enzyme-linked immunosorbent assay. Results:Compared with P group, the escape latency was significantly prolonged, the time of staying at the original platform quadrant was shortened, and the number of crossing the original platform was reduced, the activation rate of microglia cells in the hippocampal dentate gyrus and necrosis rate of hippocampal neurons were increased, the expression of RIPK1 and p-MLKL was up-regulated, and the contents of pro-inflammatory factors TNF-α, IL-1β and IL-6 in hippocampus were increased in PS, DMSO+ PS and Nec-1+ PS groups ( P<0.05). Compared with PS group and DMSO+ PS group, the escape latency was significantly shortened, the time of staying at the original platform quadrant was prolonged, and the number of crossing the original platform was increased, the activation rate of microglia cells in the hippocampal dentate gyrus and necrosis rate of hippocampal neurons were decreased, the expression of RIPK1 and p-MLKL was down-regulated, and the contents of pro-inflammatory factors TNF-α, IL-1β and IL-6 in hippocampus were decreased in Nec-1+ PS group ( P<0.05). Conclusions:Necrostatin-1 pre-treatment can improve postoperative cognitive function in aged rats with chronic pain due to knee arthritis, and the mechanism may be related to inhibition of necrosis in hippocampal neurons and reduction of neuroinflammation.

Parkinson's disease （PD） is a progressive chronic neurodegenerative disorder with a complex pathogenesis involving oxidative stress， neuroinflammation， mitochondrial dysfunction， and other factors. Currently， the clinical treatment of PD mainly includes levodopa， dopamine receptor agonists， monoamine oxidase B inhibitors， catechol-O-methyltransferase inhibitors， and anticholinergic drugs， but there is a lack of disease-modif g therapies that can definitively improve disease progression. According to the understanding of traditional Chinese medicine （TCM）， PD is characterized by asthenia in origin and sthenia in superficiality. It is primarily caused by liver-kidney Yin deficiency， Qi-blood insufficiency， and closely related to wind， fire， phlegm， and blood stasis. Numerous clinical practices have shown that TCM has significant clinical value in the prevention and treatment of PD， the management of motor and non-motor symptoms， and the neuroprotection of dopaminergic neurons. The underlying mechanisms of TCM include antioxidative stress， anti-neuroinflammation， and regulation of mitochondrial dysfunction. This article categorized and summarized the pathogenesis of PD， systematically elucidated the pharmacological actions and molecular mechanisms of TCM monomer extracts and compounds in the prevention and treatment of PD， and provided the latest clinical research progress， aiming to provide references for the development and clinical use of TCM for PD.

As the National Health Commission changes the management of novel corona virus infection, the situation and preventive policies for controlling the epidemic have also entered a new stage in China. Perioperative care strategies for orthopedic trauma such as designated isolation and nucleic acid test screening have also been adjusted in the new stage. Based on the perioperative work experiences in the new stage of epidemic from the frontline anti-epidemic staff of orthopedics in domestic hospitals and combined with the literature and relevant evidence-based medical data in perioperative care of orthopedic trauma patients under the current anti-epidemic policies at home and abroad, Chinese Orthopedic Association and Chinese Society of Traumatology organized relevant experts to formulate the Guideline for clinical perioperative care of orthopedic trauma patients in the new stage of novel corona virus infection ( version 2023). The guideline summarized 16 recommendations from the aspects of preoperative diagnosis and treatment, infection prevention, emergency operation and postoperative management to systematically standardize the perioperative clinical pathways, diagnosis and treatment processes of orthopedic trauma in the new stage of novel corona virus infection, so as to provide a guidance and reference for hospitals at all levels to carry out relevant work in current epidemic control policies.