To explore the advantages of traditional Chinese medicine （TCM） and integrative TCM-Western medicine approaches in the treatment of diabetic microvascular complications （DMC）， refine key pathophysiological insights and treatment principles， and promote academic innovation and strategic research planning in the prevention and treatment of DMC. The 38th session of the Expert Salon on Diseases Responding Specifically to Traditional Chinese Medicine， hosted by the China Association of Chinese Medicine， was held in Beijing， 2024. Experts in TCM， Western medicine， and interdisciplinary fields convened to conduct a systematic discussion on the pathogenesis， diagnostic and treatment challenges， and mechanism research related to DMC， ultimately forming a consensus on key directions. Four major research recommendations were proposed. The first is addressing clinical bottlenecks in the prevention and control of DMC by optimizing TCM-based evidence evaluation systems. The second is refining TCM core pathogenesis across DMC stages and establishing corresponding "disease-pattern-time" framework. The third is innovating mechanism research strategies to facilitate a shift from holistic regulation to targeted intervention in TCM. The fourth is advancing interdisciplinary collaboration to enhance the role of TCM in new drug development， research prioritization， and guideline formulation. TCM and integrative approaches offer distinct advantages in managing DMC. With a focus on the diseases responding specifically to TCM， strengthening evidence-based support and mechanism interpretation and promoting the integration of clinical care and research innovation will provide strong momentum for the modernization of TCM and the advancement of national health strategies.

ObjectiveTo investigate the clinical and pathological features of intrahepatic intraductal papillary neoplasm of the bile duct （IPNB）， and to improve the understanding， diagnosis， and treatment of this disease. MethodsA retrospective analysis was performed for four patients who underwent surgical resection in Beijing Chaoyang Hospital， Capital Medical University， from January 2010 to December 2025 and were diagnosed with intrahepatic IPNB based on pathological examination. The clinical， imaging， and pathological features of these patients were summarized， and a literature review was performed for related articles in China and globally. ResultsAmong the four patients， there were three female patients and one male patient， with a median age of 65 years， and clinical manifestations included jaundice， abdominal pain or diarrhea， and asymptomatic findings on physical examination. The main imaging manifestation was bile duct dilatation or solid-cystic space-occupying lesion. Pathological typing revealed one case each of the gastric， intestinal， pancreatobiliary， and oncocytic types， and there was one patient with low-grade intraepithelial neoplasia and three patients with high-grade intraepithelial neoplasia， among whom one patient also had invasive carcinoma. ConclusionIntrahepatic IPNB is a rare precancerous lesion of the liver with diverse clinical， imaging， and pathological manifestations， and radical surgical resection remains the cornerstone of treatment.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Artificial intelligence (AI), particularly deep learning, has demonstrated remarkable performance in medical imaging across a variety of modalities, including X-ray, computed tomography (CT), magnetic resonance imaging (MRI), ultrasound, positron emission tomography (PET), and pathological imaging. However, most existing state-of-the-art AI techniques are task-specific and focus on a limited range of imaging modalities. Compared to these task-specific models, emerging foundation models represent a significant milestone in AI development. These models can learn generalized representations of medical images and apply them to downstream tasks through zero-shot or few-shot fine-tuning. Foundation models have the potential to address the comprehensive and multifactorial challenges encountered in clinical practice. This article reviews the clinical applications of both task-specific and foundation models, highlighting their differences, complementarities, and clinical relevance. We also examine their future research directions and potential challenges. Unlike the replacement relationship seen between deep learning and traditional machine learning, task-specific and foundation models are complementary, despite inherent differences. While foundation models primarily focus on segmentation and classification, task-specific models are integrated into nearly all medical image analyses. However, with further advancements, foundation models could be applied to other clinical scenarios. In conclusion, all indications suggest that task-specific and foundation models, especially the latter, have the potential to drive breakthroughs in medical imaging, from image processing to clinical workflows.
Humans ; Artificial Intelligence ; Deep Learning ; Diagnostic Imaging/methods* ; Magnetic Resonance Imaging ; Tomography, X-Ray Computed ; Positron-Emission Tomography

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background and Aims:The long non-coding RNA SOX2 overlapping transcript(SOX2-OT)is involved in the regulation of cancer cell cycle and proliferation.Bioinformatics analysis has revealed potential binding sites among miR-409-3p,SOX2-OT,and membrane binding protein annexin A2(ANXA2).This study aims to investigate the expression and functional role of the SOX2-OT/miR-409-3p/ANXA2 axis in gastric cancer cells.Methods:qRT-PCR was used to measure the expression levels of SOX2-OT,miR-409-3p,and ANXA2 mRNA in gastric cancer tissues and cell lines.Gastric cancer cells were transfected with SOX2-OT shRNA plasmid(sh-SOX2-OT),co-transfected with sh-SOX2-OT and miR-409-3p inhibitor,or co-transfected with sh-SOX2-OT and ANXA2 overexpression plasmid.The control groups included blank,shRNA-negative control,inhibitor-negative control,and overexpression plasmid-negative control.Expression levels of SOX2-OT,miR-409-3p,and ANXA2 mRNA,cell proliferation,migration/invasion,apoptosis,and protein expression of Ki-67,cleaved caspase-3,Bax,MMP-9,and ANXA2 were assessed.Dual-luciferase reporter assays were conducted to confirm the targeting relationships among miR-409-3p,SOX2-OT,and ANXA2.A xenograft tumor model in nude mice was used to evaluate the effect of SOX2-OT on gastric cancer tumor growth in vivo.Results:SOX2-OT and ANXA2 expression levels were significantly upregulated,while miR-409-3p was downregulated in gastric cancer tissues(vs.adjacent non-cancerous tissues)and gastric cancer cell lines(vs.normal gastric epithelial cells)(all P＜0.05).In gastric cancer cels,knockdown of SOX2-OT led to decreased expression of SOX2-OT and ANXA2 mRNA and increased expression of miR-409-3p(all P＜0.05),and this was accompanied by reduced proliferation and migration/invasion abilities,and increased apoptosis(all P＜0.05);protein levels of ANXA2,Ki-67,and MMP-9 were significantly decreased,whereas cleaved caspase-3 and Bax levels were significantly increased(all P＜0.05).These effects were reversed by co-transfection with the miR-409-3p inhibitor or ANXA2 overexpression plasmid(all P＜0.05).Dual-luciferase assays confirmed the direct targeting relationships among miR-409-3p,SOX2-OT,and ANXA2.In vivo,knockdown of SOX2-OT significantly inhibited tumor growth in nude mice,with reduced SOX2-OT and increased miR-409-3p expression,as well as decreased ANXA2 and Ki-67 protein positivity in xenograft tissues(all P＜0.05).Conclusion:SOX2-OT is upregulated in gastric cancer cells and may promote malignant behaviors by competitively binding miR-409-3p,thereby relieving its inhibition on ANXA2.The SOX2-OT/miR-409-3p/ANXA2 axis may represent a potential molecular target for gastric cancer therapy.

Background and Aims:The long non-coding RNA SOX2 overlapping transcript(SOX2-OT)is involved in the regulation of cancer cell cycle and proliferation.Bioinformatics analysis has revealed potential binding sites among miR-409-3p,SOX2-OT,and membrane binding protein annexin A2(ANXA2).This study aims to investigate the expression and functional role of the SOX2-OT/miR-409-3p/ANXA2 axis in gastric cancer cells.Methods:qRT-PCR was used to measure the expression levels of SOX2-OT,miR-409-3p,and ANXA2 mRNA in gastric cancer tissues and cell lines.Gastric cancer cells were transfected with SOX2-OT shRNA plasmid(sh-SOX2-OT),co-transfected with sh-SOX2-OT and miR-409-3p inhibitor,or co-transfected with sh-SOX2-OT and ANXA2 overexpression plasmid.The control groups included blank,shRNA-negative control,inhibitor-negative control,and overexpression plasmid-negative control.Expression levels of SOX2-OT,miR-409-3p,and ANXA2 mRNA,cell proliferation,migration/invasion,apoptosis,and protein expression of Ki-67,cleaved caspase-3,Bax,MMP-9,and ANXA2 were assessed.Dual-luciferase reporter assays were conducted to confirm the targeting relationships among miR-409-3p,SOX2-OT,and ANXA2.A xenograft tumor model in nude mice was used to evaluate the effect of SOX2-OT on gastric cancer tumor growth in vivo.Results:SOX2-OT and ANXA2 expression levels were significantly upregulated,while miR-409-3p was downregulated in gastric cancer tissues(vs.adjacent non-cancerous tissues)and gastric cancer cell lines(vs.normal gastric epithelial cells)(all P＜0.05).In gastric cancer cels,knockdown of SOX2-OT led to decreased expression of SOX2-OT and ANXA2 mRNA and increased expression of miR-409-3p(all P＜0.05),and this was accompanied by reduced proliferation and migration/invasion abilities,and increased apoptosis(all P＜0.05);protein levels of ANXA2,Ki-67,and MMP-9 were significantly decreased,whereas cleaved caspase-3 and Bax levels were significantly increased(all P＜0.05).These effects were reversed by co-transfection with the miR-409-3p inhibitor or ANXA2 overexpression plasmid(all P＜0.05).Dual-luciferase assays confirmed the direct targeting relationships among miR-409-3p,SOX2-OT,and ANXA2.In vivo,knockdown of SOX2-OT significantly inhibited tumor growth in nude mice,with reduced SOX2-OT and increased miR-409-3p expression,as well as decreased ANXA2 and Ki-67 protein positivity in xenograft tissues(all P＜0.05).Conclusion:SOX2-OT is upregulated in gastric cancer cells and may promote malignant behaviors by competitively binding miR-409-3p,thereby relieving its inhibition on ANXA2.The SOX2-OT/miR-409-3p/ANXA2 axis may represent a potential molecular target for gastric cancer therapy.

Acute idiopathic maculopathy(AIM)is an inflammatory lesion of unknown cause that primarily affects the macula. It follows a unique natural course, distinct from other maculopathy, often manifesting as a sudden loss of visual acuity followed by flu-like symptoms that gradually resolve as the disease subsides. A comprehensive understanding of the unique history, multimodal imaging, and a thorough systematic examination are crucial in determining the final diagnosis of AIM. The treatment and prognosis of AIM remain controversial. Meanwhile, it presents similar clinical manifestations and pathological changes to various chorioretinopathy, posing challenges for clinical differentiation. This article provides a review of its pathogenesis, clinical symptoms, multimodal imaging features, diagnosis and differential diagnosis, treatment and prognosis, in order to reduce misdiagnosis and mistreatment while enhancing comprehension of AIM.