This paper summarizes clinical experience in treating acne based on the staged therapeutic principles of "eruption in warm diseases". It is considered that acne results from wind-heat retained in the lungs， invading the ying level and obstructing the blood collaterals， and is primarily a disorder involving both the wei and ying systems. In clinical practice， the treatment emphasizes the use of acrid-cool and sweet-cold methods. The core prescription is namely Yinqiaosan Qu Douchi Jia Xishengdi Danpi Daqingye Bei Xuanshen Fang （from Epidemic Warm Diseases ［《温病条辨》］）， and is adjusted according to the stage of disease. In the non-inflammatory stage， when the pathogen initially attacks the wei level， treatment focuses on acrid-cool herbs to release the exterior， with supplementary bitter-sweet ingredients such as Yejuhua （Chrysanthemum Indicum）. In the inflammatory stage， with pronounced heat toxin in the qi level affecting the ying and blood， and local stagnation of qi and blood， the approach is to clear heat and resolve toxin， using blood-cooling and stasis-resolving herbs early to prevent progression. Herbs such as Pugongying （Taraxacum Mongolicum）， Zihuadiding （Viola Yedoensis）， Tiankuizi （Semiaquilegia Adoxoides）， Chonglou （Paris Polyphylla）， Machixian （Portulaca Oleracea）， Zaojiaoci （Gleditsia Sinensis）， Chuanshanjia （Manis Pentadactyla） may be added. In the post-inflammatory erythema stage， when yin of the ying level is depleted and internal deficiency-heat arises， sweet-cold herbs are recommended to nourish the stomach and generate fluids， with the possible addition of Yiwei Decoction （益胃汤）.

OBJECTIVE: To observe the effects of electroacupuncture at the pterygopalatine region on nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)-mediated pyroptosis and inflammatory factors in rats with allergic rhinitis (AR). METHODS: Twenty-four SD rats were randomly divided into a blank group, a model group, an acupuncture group and an electroacupuncture group, 6 rats in each group. Except for the blank group, OVA-induced AR model was established in the remaining groups. In the electroacupuncture group, the rats were treated with electroacupuncture at the bilateral pterygopalatine region, with disperse-dense wave, in frequency of 2 Hz/100 Hz and current of 0.5-1 mA, 15 min each time, once every other day, for 3 times. In the acupuncture group, the rats were treated with acupuncture at bilateral pterygopalatine region simply, without electrical stimulation. The rhinitis symptom score was observed, the pathomorphology of the nasal mucosa was observed by HE staining; the serum levels of OVA-specific immunoglobulin E (OVA-sIgE), interleukin (IL)-4, IL-6 and IL-1β were detected by ELISA; the mRNA expression of NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), cysteinyl aspartate specific proteinase-1 (caspase-1) and IL-18 in the nasal mucosa was detected by real-time PCR; the protein expression of NLRP3, ASC, caspase-1 and IL-18 in the nasal mucosa was detected by Western blot. RESULTS: Compared with the blank group, in the model group, the rhinitis symptom score was increased (P<0.01), the serum levels of OVA-sIgE, IL-4, IL-6 and IL-1β were increased (P<0.05), the nasal mucosa showed pathomorphology of inflammatory infiltration; the mRNA and protein expression of NLRP3, ASC, caspase-1 and IL-18 in the nasal mucosa was increased (P<0.05). Compared with the model group, in the electroacupuncture group, the rhinitis symptom score was reduced (P<0.01), the pathology of the nasal mucosa was improved; the serum levels of OVA-sIgE, IL-4, IL-6 and IL-1β were decreased (P<0.05); the mRNA and protein expression of NLRP3, ASC, caspase-1 and IL-18 in the nasal mucosa was decreased (P<0.05). CONCLUSION Electroacupuncture at the pterygopalatine region can exerting the anti-inflammatory effect by inhibiting NLRP3-mediated pyroptosis and inflammatory factor imbalance, thus alleviate rhinitis symptoms in AR rats.
Animals ; Electroacupuncture ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology* ; Rats ; Rats, Sprague-Dawley ; Rhinitis, Allergic/physiopathology* ; Pyroptosis ; Male ; Acupuncture Points ; Humans ; Female ; Interleukin-1beta/genetics* ; Interleukin-18/immunology* ; Interleukin-6/genetics* ; Caspase 1/immunology*

Megakaryocytes and hepatocytes are unique cells in mammals that undergo polyploidization through endomitosis in terminal differentiation. Many polyploidization regulators and underlying mechanisms have been reported, most of which are tightly coupled with development, organogenesis, and cell differentiation. However, the nature of endomitosis, which involves successful entry into and exit from mitosis without complete cytokinesis, has not yet been fully elucidated. We highlight that endomitosis is a new cell fate in the cell cycle, and tetraploidy is a critical stage at the bifurcation of cell fate decision. This review summarizes the recent research progress in this area and provides novel insights into how cells manipulate mitosis toward endomitosis. Endomitotic cells can evade the tetraploidy restrictions and proceed to multiple rounds of the cell cycle. This knowledge not only deepens our understanding of endomitosis as a fundamental biological process but also offers new perspectives on the physiological and pathophysiological implications of polyploidization.
Hepatocytes/physiology* ; Megakaryocytes/physiology* ; Humans ; Polyploidy ; Animals ; Cell Cycle/physiology* ; Cell Differentiation ; Mitosis/physiology*

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Objective:This study identifies independent predictive indicators to distinguish autoimmune gastritis from Helicobacter pylori ( H. pylori)-induced atrophic gastritis and validates their diagnostic performance to compare laboratory indicators of autoimmune gastritis and H. pylori-induced atrophic gastritis. Methods:A retrospective comparison of laboratory examination indicators was conducted for chronic atrophic gastritis patients with involvement of the gastric fundus and corpus, who were followed up at the Department of Gastroenterology, Xijing Hospital, from January 2014 to September 2024. Receiver operating characteristic (ROC) curves were utilized to determine the optimal cutoff points and corresponding diagnostic thresholds. In addition, multivariate logistic regression analysis was conducted to identify independent predictive indicators for autoimmune gastritis, with further assessment in a validation cohort.Results:A total of 139 patients with autoimmune gastritis and 209 patients with H. pylori-induced atrophic gastritis were included. Pepsinogen (PG) Ⅰ levels and the PG Ⅰ/PG Ⅱ ratio in patients with autoimmune gastritis were significantly lower than in those with H. pylori-induced atrophic gastritis [11.0 (4.8, 22.5) vs. 41.8 (32.2, 59.9) μg/L, U=722.00, P<0.001; 1.24 (0.75, 3.54) vs. 5.76 (4.31, 7.12), U=817.00, P<0.001], while gastrin levels were significantly higher [375 (84, 738) vs. 49 (35, 81) ng/L, U=378.00, P<0.001]. PG Ⅰ was identified as an independent predictive variable, with an area under the ROC curve of 0.847 (95% CI 0.791-0.904), sensitivity of 77.6%, specificity of 91.8%, positive predictive value of 80.5%, and negative predictive value of 90.5%. Conclusions:Significant differences in laboratory indicators were observed between autoimmune gastritis and H. pylori-induced atrophic gastritis in chronic atrophic gastritis involving gastric fundus and corpus. Besides, PG Ⅰ demonstrated good diagnostic performance in identifying autoimmune gastritis and can effectively differentiate between different types of atrophic gastritis.

Objective To analyze the characteristics of oral and maxillofacial injuries from military training and provide references for related prevention and treatment.Methods A retrospective analysis was conducted of the medical records of 111 patients with oral and maxillofacial military training injuries treated between 2014 and 2023.Results From 2014 to 2023,the number of hospitalized patients with maxillofacial military training injuries in the hospital trended upward.The top 3 training injuries in the spectrum of diseases were maxillofacial fractures(45.08％),maxillofacial space infections(28.83％),and temporomandibular joint injuries(18.92％).The average number of hospitalizations for all maxillofacial military training injuries was 1.33(1-4),and the median length of hospital stay was 8(5,12)days.The median hospitalization cost was 14 793.23(5236.18,24 255.25)yuan,and the improvement rate was 95.50％.Conclusion The number of patients hospitalized due to oral and maxillofacial military training injuries in this hospital is increasing year by year,and the injuries are mostly jaw fractures.Precautions should be taken to prevent maxillofacial training injuries.

ObjectiveTo investigate the effect of laminin subunit α3 （LAMA3） on the epithelial-mesenchymal transition （EMT）， invasion， and metastasis abilities of pancreatic cancer （PC）. MethodsA comprehensive analysis was performed for tumor- and EMT-related databases to identify the EMT genes associated with PC， especially LAMA3. The methods of qRT-PCR and Western blot were used to measure the expression level of LAMA3 in PC tissue and cell lines； immunofluorescence assay was used to determine the localization of LAMA3 in PANC-1 cells； Transwell assay was used to investigate the effect of LAMA3 on the invasion and migration abilities of PC cells. The t-test was used for comparison of continuous data between groups. ResultsThe analysis of the TCGA database identified 3 EMT-related oncogenes for PC， i.e.， LAMA3， AREG， and SDC1. The LASSO-Cox regression model showed that LAMA3 had the most significant impact on the prognosis of PC （risk score=0.256 1×LAMA3+0.043 1×SDC1+0.071 4×AREG）. The Cox model and nomogram showed that the high expression of LAMA3 was an independent risk factor for the poor prognosis of PC （hazard ratio=1.32， 95% confidence interval： 1.07‍ ‍—‍ 1.62， P<0.01）. Experimental results showed that there was a significant increase in the expression of LAMA3 in pancreatic cancer tissue compared with the normal pancreatic tissue. Compared with the HPDE cell line， there were varying degrees of increase in the expression of LAMA3 in pancreatic cancer AsPC-1， BxPC-3， PANC-1， MIA PaCa-2， and SW1990 cell lines， with the highest expression level in PANC-1 cells. The enrichment analysis showed that LAMA3 was associated with the biological processes and signaling pathways such as EMT， collagen metabolism， extracellular matrix degradation， the TGF-β pathway， and the PI3K pathway. After the knockdown of LAMA3， there were significant reductions in the expression levels of N-Cadherin， Vimentin， and Snail， while there was a significant increase in the expression level of E-Cadherin. Transwell assay showed that there were significant reductions in the invasion and migration abilities of PANC-1 cells after the knockdown of LAMA3. ConclusionLAMA3 is highly expressed in PC and can promote the EMT， invasion， and migration of PC cells， and therefore， LAMA3 may be used as a novel diagnostic marker and a new therapeutic target for PC.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Objective:To evaluate the improvement in the outcome of intracapsular condylar fractures(ICFs)treatment with pre-cise soft tissue reduction in combination with open reduction and internal fixation(PSTR-ORIF)by comparson with traditional open reduction and internal fixation(T-ORIF).Methods:40 patients with ICFs were treated by T-ORIF and PSTR-ORIF(n=20)re-spectively.Preoperative and 6-month postoperative whole-mouth panoramic tomography,CT and MRI imaging data were analyzed,the repositioning of the soft and hard tissues of temporomandibular joints(TMJs),the Helkimo index,clinical symptoms and subjec-tive symptoms were compared between the 2 groups.Results:In PSTR-ORIF(26 sides)and T-ORIF(27 sides)groups,the rate of complete anatomical restoration of fractured segments at 6 months after surgery was 96.15％and 81.48％,and the overall effective rate of ICF articular disc restoration was 96.15％and 74.07％respectively,the height of the ascending mandibular branch was bet-ter restored in patients with B-type fracture after surgery(P＜0.05).At 6 months postoperatively,patients in the PSTR-ORIF group showed significant improvement in mouth opening,mandibular anterior extension distance,and lateral movement compared with the T-ORIF group(P＜0.05).The Helkimo index showed that the PSTR-ORIF group got a significant improvement in the complaint symptom index score and the clinical symptom index score compared with the T-ORIF group(P＜0.05).Conclusion:PSTR-ORIF is more effective than T-ORIF in the treatment of ICFs for the healing of condylar fractures,restore postoperative TMJ mobility and reduce the postoperative joint discomfort through good repositioning of soft tissues.