Myosteatosis is one of the common complications in patients with end-stage liver disease, which is significantly associated with poor outcomes after liver transplantation. Currently, diagnostic criteria of myosteatosis have not been established, and CT is the most commonly used for diagnosis. The pathogenesis of myosteatosis is multifactorial, and the pathophysiological mechanisms linking it to end-stage liver disease are not fully understood. An increasing number of scholars have recognized that the severity of myosteatosis is closely related to its clinical consequences, but there are no effective treatment options available. This article reviews the pathophysiological mechanisms and diagnostic methods of myosteatosis, and its impact on the prognosis of liver transplant recipients, and discusses current treatment strategies to provide references for the perioperative management of liver transplant recipients.

Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder caused by mutations in the NF1 gene located at 17q11.2. Plexiform neurofibromas (PN) are one of the common clinical manifestations of NF1, known as NF1-related plexiform neurofibromas (NF1-PN). Head and neck NF1-PN account for 42.9% of all cases. Tumors grow rapidly during childhood and adolescence, and they can exhibit widespread growth, causing severe head, face, and neck deformities, organ dysfunction, and even loss of function. NF1-PN have the potential to transform into malignant peripheral nerve sheath tumors (MPNSTs), known as NF1-associated MPNST (NF1-MPNST). Histopathology is the gold standard for diagnosing NF1-PN, magnetic resonance imaging (MRI) is the preferred imaging examination for NF1-PN, and PET/CT examination is a reliable method for early detection and diagnosis of NF1-MPNST. Genetic testing plays an important role in early diagnosis of tumors, monitoring tumor progression, genetic counseling, and molecular level treatment and management of the disease. This article proposes the goals and principles for treating NF1-PN in the head and neck region. The main treatment methods currently used are surgery and medication. Surgical treatment includes surgical resection, and tissue flap repair or allogeneic transplantation of composite tissue after surgical resection. The mitogen-activated protein kinase inhibitors (MEK) inhibitor Selumetinib is an effective medication used to treat NF1-PN patients aged 3 years and older with symptoms and who are unable to undergo surgery. A Phase Ⅱb trial of mirdametinib, a small-molecule inhibitor, has been completed in adults and children, and it is considered well tolerated in both groups. CRISPR/Cas9 technology is expected to become an effective means of NF1-PN gene therapy. The treatment method of NF1-MPNST is similar to that of soft tissue sarcoma. However, the safety of complete resection of extra-large tumors, protection of important tissues and organs during surgery, effective control of intraoperative bleeding, reconstruction of soft and hard tissue defects in the head and neck; prospective, multicenter, randomized, double-blind, controlled clinical trials of MEK inhibitors, as well as the use of CRISPR/Cas9 technique for gene therapy NF1-PN, are all current challenges. This article summarizes recent advances and ongoing challenges in the treatment of head and neck NF1-PN, aiming to provide a reference for clinicians and researchers.

BACKGROUND: To provide a comprehensive analysis of the landscape of artificial intelligence (AI) applications in cardiac arrest (CA). METHODS: Comprehensive searches were conducted in PubMed, the Cochrane Library, Web of Science, and EMBASE from database inception through 10 June 2025. Studies that applied AI in both in-hospital cardiac arrest (IHCA) and out-of-hospital cardiac arrest (OHCA) populations across the following domains were included: prediction of cardiac arrest occurrence, prognostication of CA outcomes, applications of large language models (LLMs), and evaluation of cardiopulmonary resuscitation (CPR) and other AI-driven interventions related to CA. RESULTS: The scoping review included 114 studies, encompassing data from 9,574,462 patients in total. AI was most commonly applied to the prediction of CA (overall, n=40; IHCA, n=30; OHCA, n=4; and both, n=6), CPR-related decision support during CA (n=16), and post-arrest prognosis and rehabilitation outcomes (overall, n=38; OHCA, n=21; IHCA, n=3; and both, n=14). Additional application areas included LLM-based applications (n=8), emergency call handling (n=4), wearable device-based detection (n=3), heart rhythm identification (n=2), education (n=2), and extracorporeal cardiopulmonary resuscitation (ECPR) candidate identification (n=1). Across all application scenarios, the highest area under the receiver operating characteristic curve (AUROC) value for pre-arrest CA prediction in IHCA patients was 0.998 using a multilayer perceptron (MLP) model, whereas the optimal AUROC for pre-arrest CA prediction in OHCA patients was 0.950 using extreme gradient boosting (XGBoost) or random forest (RF) models. For CPR-related decision support during CA, the highest AUROC achieved was 0.990 with a convolutional neural network (CNN) model. In prognostic prediction, the optimal AUROC for IHCA patients was 0.960 using XGBoost, while for OHCA patients it reached 0.976 using an MLP model. CONCLUSION: This review shows that AI is most commonly used for the prediction of CA and CPR-related support, as well as post-arrest and rehabilitation outcomes. Future research directions include drug discovery, post-resuscitation management, neurorehabilitation, and clinical trial innovation. Further studies should prioritize multicenter clinical trials to evaluate AI models in real-world settings and validate their effectiveness across diverse patient populations. Overall, AI has significant potential to improve clinical practice, and its role in CA application is increasingly important.

Oral squamous cell carcinoma (OSCC) is a common head and neck malignancy. Approximately 50% to 60% of patients with OSCC are diagnosed at a locally advanced stage (clinical staging III-IVa). Even with comprehensive and sequential treatment primarily based on surgery, the 5-year overall survival rate remains below 50%, and patients often suffer from postoperative functional impairments such as difficulties with speaking and swallowing. Programmed death receptor-1 (PD-1) inhibitors are increasingly used in the neoadjuvant treatment of locally advanced OSCC and have shown encouraging efficacy. However, clinical practice still faces key challenges, including the definition of indications, optimization of combination regimens, and standards for efficacy evaluation. Based on the latest research advances worldwide and the clinical experience of the expert group, this expert consensus systematically evaluates the application of PD-1 inhibitors in the neoadjuvant treatment of locally advanced OSCC, covering combination strategies, treatment cycles and surgical timing, efficacy assessment, use of biomarkers, management of special populations and immune related adverse events, principles for immunotherapy rechallenge, and function preservation strategies. After multiple rounds of panel discussion and through anonymous voting using the Delphi method, the following consensus statements have been formulated: 1) Neoadjuvant therapy with PD-1 inhibitors can be used preoperatively in patients with locally advanced OSCC. The preferred regimen is a PD-1 inhibitor combined with platinum based chemotherapy, administered for 2-3 cycles. 2) During the efficacy evaluation of neoadjuvant therapy, radiographic assessment should follow the dual criteria of Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 and immune RECIST (iRECIST). After surgery, systematic pathological evaluation of both the primary lesion and regional lymph nodes is required. For combination chemotherapy regimens, PD-L1 expression and combined positive score need not be used as mandatory inclusion or exclusion criteria. 3) For special populations such as the elderly (≥ 70 years), individuals with stable HIV viral load, and carriers of chronic HBV/HCV, PD-1 inhibitors may be used cautiously under the guidance of a multidisciplinary team (MDT), with close monitoring for adverse events. 4) For patients with a poor response to neoadjuvant therapy, continuation of the original treatment regimen is not recommended; the subsequent treatment plan should be adjusted promptly after MDT assessment. Organ transplant recipients and patients with active autoimmune diseases are not recommended to receive neoadjuvant PD-1 inhibitor therapy due to the high risk of immune related activation. Rechallenge is generally not advised for patients who have experienced high risk immune related adverse events such as immune mediated myocarditis, neurotoxicity, or pneumonitis. 5) For patients with a good pathological response, individualized de escalation surgery and function preservation strategies can be explored. This consensus aims to promote the standardized, safe, and precise application of neoadjuvant PD-1 inhibitor strategies in the management of locally advanced OSCC patients.

ObjectiveTo investigate the therapeutic efficacy of Danggui Shaoyaosan （DSS） on renal injury in db/db mice and its impact on endoplasmic reticulum stress （ERS） in renal tissues. MethodsThirty 8-week-old male db/db mice and six db/m mice were acclimated for one week， after which urinary microalbumin and blood glucose levels were monitored to establish a diabetic kidney disease （DKD） model. The model mice were randomly divided into a model group， an irbesartan group， and three DSS treatment groups with different doses （16.77， 33.54， and 67.08 g·kg^-1·d^-1）. A normal group was set as control. Each group was intragastrically administered with the corresponding drugs or saline for 8 weeks. After the intervention， general conditions were observed. Serum cystatin C （Cys-C）， 24-hour urinary total protein （24 h-UTP）， 24-hour urinary microalbumin （24 h-UMA）， urinary creatinine （Ucr）， and urea nitrogen （UUN） were measured. Transmission electron microscopy （TEM） was used to observe glomerular basement membrane （GBM） and ultrastructural changes of the endoplasmic reticulum （ER） in glomerular endothelial cells. Western blot， real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， and immunohistochemistry were used to analyze renal tissue structure and the expression of GRP78， CHOP， and related markers. ResultsCompared with the normal group， the mice in the model group showed curled posture， sluggish response， poor fur condition， increased levels of Cys-C， 24 h-UTP， 24 h-UMA， and UUN （P<0.05）， while Ucr decreased （P<0.05）. The GBM was significantly thickened， with podocyte and foot process fusion. The protein expressions of GRP78， CHOP， and ATF6 were significantly upregulated （P<0.05）， the mRNA levels of GRP78 and CHOP increased （P<0.05）， and immunohistochemistry showed an enhanced GRP78 signal （P<0.05）. After treatment， the mice exhibited improved behavior， normalized GBM and podocyte structure， improved ER morphology and markedly better biochemical indicators. Western blot， Real-time PCR， and immunohistochemistry indicated that the ERS-related markers were downregulated in the DSS treatment groups （P<0.05）， suggesting alleviated ERS and improved renal function. ConclusionDSS can effectively ameliorate renal pathological damage in db/db mice， possibly by regulating ERS in glomerular endothelial cells， although the underlying signaling mechanisms require further investigation.

ObjectiveTo investigate the mechanism of modified Si Junzitang and Shashen Maidong Tang ［Yiqi Yangyin Jiedu prescription （YQYYJD）］ in enhancing the sensitivity of cisplatin in epidermal growth factor receptor tyrosine kinase inhibitor （EGFR-TKI）-resistant lung adenocarcinoma cells based on aerobic glycolysis. MethodsThe effects of different concentrations of YQYYJD （0， 2， 3， 4， 5， 6， 7， 8 g·L^-1） and cisplatin （0， 3， 6， 9， 12， 15， 18， 21， 24， 27 mg·L^-1） on the proliferation and activity of PC9/GR cells were detected by the cell counting kit-8 （CCK-8） assay after 24 hours of intervention. The half-maximal inhibitory concentration （IC₅₀） for PC9/GR cells was calculated to determine the concentrations used in subsequent experiments. PC9/GR cells were divided into blank group （complete medium）， YQYYJD group （5 g·L^-1）， cisplatin group （12 mg·L^-1）， and combined group （YQYYJD 5 g·L^-1 + cisplatin 12 mg·L^-1）. After 24 hours of intervention， cell viability was measured using CCK-8 assay. Cell proliferation was assessed by colony formation assay， and cell migration was evaluated by scratch and Transwell assays. Glucose consumption， lactate production， and adenosine triphosphate （ATP） levels were measured by colorimetric assays. The expression levels of glycolysis-related proteins， including hexokinase 2 （HK2）， phosphofructokinase P （PFKP）， pyruvate kinase M2 （PKM2）， lactate dehydrogenase A （LDHA）， glucose transporter 1 （GLUT1）， and monocarboxylate transporter 4 （MCT4）， were determined by Western blot. ResultsBoth YQYYJD and cisplatin inhibited the viability of PC9/GR cells in a concentration-dependent manner. The IC₅₀ of PC9/GR cells for YQYYJD and cisplatin were 5.15 g·L^-1 and 12.91 mg·L^-1， respectively. In terms of cell proliferation， compared with the blank group， the cell survival rate and the number of colonies formed in the YQYYJD group， cisplatin group， and combined group were significantly decreased （P<0.01）. Compared with the YQYYJD and cisplatin groups， the combined group showed a further significant reduction in cell survival rate and colony formation （P<0.01）. In terms of cell migration， compared with the blank group， the cell migration rate and the number of cells passing through the Transwell membrane in the YQYYJD group， cisplatin group， and combined group were significantly decreased （P<0.01）. Compared with the YQYYJD and cisplatin groups， the combined group exhibited a further significant reduction in cell migration rate and the number of cells passing through the Transwell membrane （P<0.01）. In terms of glycolysis， compared with the blank group， glucose consumption， lactate production， and ATP levels in the YQYYJD group， cisplatin group， and combined group were significantly decreased （P<0.01）. Compared with the YQYYJD and cisplatin groups， the combined group showed a further significant reduction in glucose consumption， lactate production， and ATP levels （P<0.05）. Compared with the blank group， the protein expression levels of HK2， PFKP， PKM2， and LDHA in the YQYYJD， cisplatin， and combined groups were significantly decreased （P<0.01）. The combined group showed a further significant reduction in the expression levels of these proteins compared with the YQYYJD and cisplatin groups （P<0.01）. No significant differences were observed in the protein expression levels of GLUT1 and MCT4 among the groups. ConclusionYQYYJD can synergistically inhibit the proliferation and migration of PC9/GR cells and enhance their sensitivity to cisplatin. The mechanism may be related to the downregulation of the expression of glycolysis-related rate-limiting enzymes， including HK2， PFKP， PKM2， and LDHA， thereby inhibiting glycolysis.

Functional cure is currently the ideal treatment endpoint for chronic hepatitis B （CHB） in China and globally. HBsAg seroclearance and HBV DNA that cannot be detected in peripheral blood for more than 24 weeks marks the regression of hepatitis B virus （HBV） infection. However， there is still a lack of systematic description of the characteristics of intrahepatic HBV markers after HBsAg seroclearance. This article elaborates on the issues including the latest definition of functional cure， the characteristics of intrahepatic virological markers after HBsAg seroclearance， the significance of ultrasensitive serum HBsAg detection， and antiviral therapy for CHB patients with a low level of HBsAg， so as to improve the understanding of functional cure among clinicians.

Defects in the lip and perilabial regions can be caused by lip oncosurgery. Currently, there is a lack of clear classification and principles for repairing and reconstructing the lip and perilabial defects after lip tumor resection surgery. Lip defects are categorized into three types based on their extent by author: partial lip defects, full-thickness lip defects, and full-thickness lip defects with surrounding lip defects. The partial lip defects include four types: labial vermilion defects, labial cutaneous defects, labial mucosal defects, and through-and-through labial defects. There are four types of full-thickness lip defects, including less than half of labial defects, one half of labial defects, subtotal labial defects, and total labial defects. There are three types of full-thickness lip defects with surrounding lip defects, including through-and-through commissure and cheek defects, total labial and nasal defects, and total labial and chin defects. Different types of defects in the lip and perilabial region should be repaired during radical surgery for lip tumors. The methods of repair and reconstruction of lip and perilabial defects include primary closure, skin or mucosal grafting, local flaps, regional flaps, pedicle flaps, free flaps, and allogeneic dermal matrix (ADM). Multiple tissue flaps can also be combined for repair and reconstruction. Among them, the anteriorly based ventral tongue flap is an ideal tissue flap for repairing and reconstructing labial vermilion defects. The Abbe-Estlander flap is a very important technique for repairing and reconstructing lip defects. The combination of bilateral mental neurovascular V-Y island advancement flap and an anteriorly based ventral tongue flap for reconstruction of the total lower lip defect is a reliable and effective method. The Estlander flap, foldable supraclavicular fasciocutaneous island flap, or foldable facial-submental artery island flap can be used to repair the through-and-through labial commissure and cheek defects. Large perilabial defects such as total labial and chin defects or total labial and nasal defects require repair using pectoralis major muscle flaps, trapezius muscle flaps, free tissue flaps, or even a combination of multiple flaps. This article proposes the classification of lip and perilabial defects following oncosurgery and systematically elaborates on the functional repair and reconstruction of the defects, which has certain guiding and promotional application value for clinical practice.

Objective : To reveal the role of periodontal ligament stem cell-derived exosomes (PDLSC-Exos) in orthodontic bone remodeling, in order to provide new therapeutic strategies for orthodontic tooth movement (OTM). Methods : This study has been reviewed and approved by the Ethics Committee. Healthy periodontal ligament tissues from clinical orthodontic reduction extractions were collected, and periodontal ligament stem cells (PDLSCs) were isolated and cultured. When cultured to the third generation, their self-renewal ability and multidirectional differentiation potential were detected. PDLSC-Exos were isolated and purified by gradient centrifugation and identified by transmission electron microscopy, immunofluorescence, ZetaView, and nanoflow cytometry. The co-culture of 10 μg/mL PDLSC-Exos and PDLSCs (PDLSCs+Exos) induced osteogenic differentiation to evaluate the effect of osteogenesis. Bone marrow-mononuclear cells (BMMs), promoted by osteoclast differentiation [30 ng/mL macrophage colony stimulating factor (M-CSF) + 50 ng/mL receptor activator of nuclear factor-κ B ligand (RANKL)], and then were treated with 10 μg/mL PDLSC-Exos to assess the effect on osteoclasts. We established a rat model of OTM, and 50 μg/mL PDLSC-Exos was injected locally into the periodontal ligament before we established the model (OTM + Exos), every 2 days for 14 days. Alveolar bone remodeling was analyzed by micro-CT, and alveolar bone osteoclasts were analyzed by immunohistochemistry and immunofluorescence. Results: The isolated and purified PDLSCs met the basic characteristics of mesenchymal stem cells, and PDLSC-Exos had typical characteristics of extracellular vesicles. PDLSCs-Exos significantly promoted the osteogenic differentiation of PDLSCs, and promoted the osteoclast differentiation and bone resorption activity of BMMs (P < 0.05). The rate of alveolar bone remodeling in rats with local periodontal injection of PDLSC-Exos was significantly accelerated, and the tooth movement distance was significantly increased (P < 0.05); immunohistochemistry results showed that PDLSC-Exos promoted the differentiation of osteoclasts (P < 0.05). In addition, immunofluorescence showed that PDLSC-Exos co-localized with osteoclasts, indicating that PDLSC-Exos may promote osteoclast differentiation in vivo. Conclusion PDLSC-Exos accelerate the rate of orthodontic bone remodeling by promoting osteogenic differentiation of PDLSCs and osteoclast differentiation of BMMs, thereby accelerating OTM.

OBJECTIVE To assess the safety profile of sintilimab in combination with chemotherapy for the treatment of cholangiocarcinoma. METHODS The data of patients with cholangiocarcinoma from January 1st， 2021 to December 31st， 2022 were collected and divided into control group （29 cases） and observation group （18 cases） based on different medication regimens. Patients in the control group were treated with Gemcitabine hydrochloride for injection+Cisplatin for injection or Oxaliplatin for injection， the observation group was treated with Sintilimab injection based on the control group. Patients in each group underwent blood routine， liver and kidney function， biochemical and other examinations before and after each treatment cycle to observe the occurrence of adverse drug reactions. The correlation of adverse drug reactions with drugs was evaluated with Naranjo’s scale. RESULTS The correlation between blood toxicity and drug use was deemed “probable” in both groups； however， the observation group exhibited a significantly higher score， indicating a stronger correlation. In the control group， hepatotoxic reactions were classified as “suspicious” whereas in the observation group， they were categorized as “probable”. The correlation of gastrointestinal symptoms between the two groups was considered “possible”. Systemic symptoms， skin toxicity， musculoskeletal toxicity， endocrine toxicity and renal toxicity were all classified as having a “suspicious” correlation with drug use. The total incidence of blood toxicity in the observation group was significantly higher than control group （P＝0.014）. There was no statistically significant difference in the total incidences of hepatotoxic， gastrointestinal symptoms， systemic symptoms， skin toxicity， musculoskeletal toxicity， endocrine toxicity， renal toxicity， or the incidence of grade 3 or higher blood toxicity， hepatotoxic between the two groups （P＞0.05）. For the patients experiencing adverse drug reactions， the symptoms were alleviated following drug discontinuation or symptomatic supportive treatment. No fatalities occurred during the treatment period. CONCLUSIONS Sintilimab combined with chemotherapy may significantly increase the risk of blood toxicity in patients with cholangiocarcinoma， especially thrombocytopenia， but the adverse reactions are within a controllable range， and the overall safety is good.