ObjectiveTo investigate the effects of Huanglian Jiedutang （HLJDT） on cognitive function in mice with ischemic stroke （IS） and to elucidate whether its neuroprotective effects are mediated by inhibition of the nuclear factor-κB （NF-κB） signaling pathway and subsequent suppression of NF-κB-regulated neuronal apoptosis. MethodsAn IS model was established using middle cerebral artery occlusion （MCAO）. Sixty C57BL/6J mice were randomly assigned to five groups （n =12 per group）， i.e.， sham operation， model， HLJDT low-dose （3.9 g·kg^-1·d^-1）， HLJDT high-dose （7.8 g·kg^-1·d^-1）， and Ginkgo biloba extract （GBE， 31.2 mg·kg^-1·d^-1）. Post-operatively， neurological deficit scores （Longa score）， cerebral infarct volume assessed by 2，3，5-triphenyltetrazolium chloride （TTC） staining， and brain water content were evaluated. Learning and memory were assessed using new object recognition （NOR） and fear conditioning （FC） tests. Hippocampal pathology was examined via hematoxylin and eosin （HE） staining. Immunofluorescence detected expression of glial fibrillary acidic protein （GFAP， astrocyte marker）， cellular oncogene Fos （c-Fos， neuronal activation marker）， and glutamate decarboxylase 65 （GAD65）. Western blot measured nuclear factor-κB inhibitor protein α （IκBα）， phosphorylated IκBα （p-IκBα）， NF-κB p65， phosphorylated NF-κB p65 （p-NF-κB p65）， ionic calcium binding adapter molecule 1 （Iba-1）， tumor necrosis factor （TNF）-α， interleukin （IL）-1β， and apoptosis-related proteins， such as cleaved cysteinyl aspartate-specific protease 3 （Caspase-3）， B-cell lymphoma 2 （Bcl-2）， and Bcl-2-associated X protein （Bax）. Real-time quantitative PCR （Real-time PCR） was used to assess mRNA levels of Iba-1， TNF-α， IL-1β， NF-κB p65， cleaved Caspase-3， Bax， and Bcl-2. ResultsCompared with the sham group， the model group exhibited significantly increased neurological deficit scores， brain water content， and cerebral infarct volume （P<0.01）. Hippocampal CA1 neurons were disorganized， showing nuclear pyknosis and karyolysis. NOR exploration time and FC freezing time were significantly reduced （P<0.01）. GFAP and c-Fos expression were increased， while GAD65 expression was decreased （P<0.01）. Cleaved Caspase-3 and Bax were upregulated， Bcl-2 was downregulated， and the Bax/Bcl-2 ratio was elevated （P<0.01）. Expression levels of p-IκBα， p-NF-κB p65， IL-1β， TNF-α， and Iba-1 were significantly increased （P<0.01）. Compared with the model group， HLJDT high-dose， low-dose， and GBE groups showed significant improvements in all parameters （P<0.01）. Among them， the HLJDT high-dose group showed the most pronounced neuronal structural recovery and superior performance in NOR and FC tests （P<0.01）. In this group， GFAP and c-Fos decreased， GAD65 increased （P<0.01）， apoptosis-related protein expression was reversed， and NF-κB signaling and related inflammatory factor expression were suppressed （P<0.01）. ConclusionHLJDT ameliorates cognitive dysfunction in mice after IS， potentially by inhibiting the NF-κB signaling pathway， thereby reducing neuroinflammation and hippocampal neuronal apoptosis.

Plant-derived exosome-like nanovesicles (PELNs), characterized by a natural lipid bilayer membrane, have rapidly emerged as a prominent research frontier in medicine owing to their unique biological properties and robust therapeutic potential. This review comprehensively examines the biological profiles, mechanistic functions, and recent engineering advancements of PELNs. In terms of composition, PELNs are uniquely enriched in plant-specific glycolipids, phosphatidylserine, secondary metabolites, and highly stable 2'-O-methylated miRNAs. This distinct molecular makeup endows them with exceptional biocompatibility, negligible immunogenicity, and the capacity for cross-species molecular communication. Mechanistically, PELNs demonstrate profound anti-inflammatory efficacy by suppressing the NF-κB and NLRP3 inflammasome pathways. They also serve as potent immune modulators, driving macrophage M1/M2 polarization and regulating T cell activity. Additionally, PELNs exhibit promising antitumor capabilities, targeting malignancies via reactive oxygen species (ROS) induction, TRAIL pathway activation, and tumor microenvironment remodeling. Crucially, the plant miRNAs encapsulated within PELNs remain highly stable in the gastrointestinal tract, allowing them to selectively alter gene expression in specific gut microbiota communities. This interaction deeply influences host immunity and metabolism, highlighting the vital role in cross-species regulation. Advancements in bioengineering have further expanded the clinical utility of PELNs. Targeted delivery efficiency can be significantly amplified via surface functionalization (e.g., folate and RGD sequences) and state-of-the-art drug loading technologies such as sonication and electroporation. Consequently, engineered PELNs surpass traditional synthetic nanocarriers in penetrating natural physiological barriers, particularly for oral and transdermal drug administration. Despite these advantages, clinical translation is currently hindered by the lack of standardized isolation protocols, challenges in scalable manufacturing, and the need for robust quality control frameworks. Looking forward, the integration of multi-omics approaches and AI-driven “molecular fingerprinting”—coupled with the design of synthetic biomimetic vesicles—will be instrumental in overcoming these bottlenecks, ultimately establishing PELNs as a next-generation platform for precision medicine and targeted nanotherapeutic delivery.

Objective: This study aimed to explore the correlation between balance function and core muscle activation in patients with adolescent idiopathic scoliosis (AIS), compared to healthy individuals. Methods: A total of 24 AIS patients and 25 healthy controls were recruited. The limits of stability (LOS) test were conducted to assess balance function, while surface electromyography was used to measure the activity of core muscles, including the internal oblique, external oblique, and multifidus. Diaphragm thickness was measured using ultrasound during different postural tasks. Center of pressure (COP) displacement and trunk inclination distance were also recorded during the LOS test. Results: AIS patients showed significantly greater activation of superficial core muscles, such as the internal and external oblique muscles, compared to the control group (p < 0.05). Diaphragm activation was lower in AIS patients during balance tasks (p < 0.01). Although no significant difference was observed in COP displacement between the groups, trunk inclination was significantly greater in the AIS group during certain tasks (p < 0.05). Conclusion These findings suggest distinct postural control patterns in AIS patients, highlighting the importance of targeted interventions to improve balance and core muscle function in this population.

Background: s/Aims: Sarcomatoid hepatocellular carcinoma (HCC) is a rare histological subtype of HCC characterized by extremely poor prognosis; however, its molecular characterization has not been elucidated. Methods: In this study, we conducted an integrated multiomics study of whole-exome sequencing, RNA-seq, spatial transcriptome, and immunohistochemical analyses of 28 paired sarcomatoid tumor components and conventional HCC components from 10 patients with sarcomatoid HCC, in order to identify frequently altered genes, infer the tumor subclonal architectures, track the genomic evolution, and delineate the transcriptional characteristics of sarcomatoid HCCs. Results: Our results showed that the sarcomatoid HCCs had poor prognosis. The sarcomatoid tumor components and the conventional HCC components were derived from common ancestors, mostly accessing similar mutational processes. Clonal phylogenies demonstrated branched tumor evolution during sarcomatoid HCC development and progression. TP53 mutation commonly occurred at tumor initiation, whereas ARID2 mutation often occurred later. Transcriptome analyses revealed the epithelial–mesenchymal transition (EMT) and hypoxic phenotype in sarcomatoid tumor components, which were confirmed by immunohistochemical staining. Moreover, we identified ARID2 mutations in 70% (7/10) of patients with sarcomatoid HCC but only 1–5% of patients with non-sarcomatoid HCC. Biofunctional investigations revealed that inactivating mutation of ARID2 contributes to HCC growth and metastasis and induces EMT in a hypoxic microenvironment. Conclusions We offer a comprehensive description of the molecular basis for sarcomatoid HCC, and identify genomic alteration (ARID2 mutation) together with the tumor microenvironment (hypoxic microenvironment), that may contribute to the formation of the sarcomatoid tumor component through EMT, leading to sarcomatoid HCC development and progression.

Ferroptosis is a programmed cell death depends on iron and lipid peroxidation,which has been recognized as the key pathogenic factor for the occurrence of various diseases in recent years,especially playing a significant role in neurodegenerative diseases.Ferroptosis triggers lipid peroxidation and oxidative stress in neuronal cells,leading to neuronal damage and death,thereby accelerating disease progression.Hydrogen sulfide,as an endogenous gaseous signaling molecule,exhibits multiple protective effects,including anti-inflammatory,antioxidant,and anti-ferroptosis properties.Hydrogen sulfide can effectively inhibit the occurrence of ferroptosis through various mechanisms,such as regulating iron metabolism,inhibiting lipid peroxidation,and enhancing the activity of antioxidant enzymes,thereby slowing down the progression of neurodegenerative diseases.This article reviews the related research progress on hydrogen sulfide and ferroptosis and ferroptosis-mediated neurodegenerative diseases,and analyzes the underlying mechanisms,aims to provide new insights and theoretical foundations for the treatment of neurodegenerative diseases.

Objective To explore the diagnostic value of multi-slice spiral CT in pulmonary nodules of different properties.Methods The clinical data of 150 patients with pulmonary nodules who were treated at Tongren People's Hospital from October 2022 to October 2023 were collected for a retrospective study.All patients underwent multi-slice spiral CT examinations,and the benign and malignant grouping was conducted based on the results of lung biopsy.The CT imaging characteristics and CT perfusion parameters of patients with benign pulmonary nodulesand malignant pulmonary nodules were compared,and the diagnostic value of multi-slice spiral CT for benign and malignant pulmonary nodules was evaluated.Results The results of lung biopsy showed that among the 150 patients with pulmonary nodules,there were 62 patients with malignant pulmonary nodules(malignant nodule group)and 88 patients with benign pulmonary nodules(benign nodule group).The proportion of calcification patients in the malignant nodule group was significantly lower than that in the benign nodule group,while the proportions of patients with vacuolar sign,lobulation sign,spinous protrusion,and spiculation sign were significantly higher than those in the benign nodule group,and the differences were statistically significant(P<0.05).There was no statistically significant difference in the mean transit time(MTT)between the malignant nodule group and the benign nodule group(P>0.05).The blood flow(BF),blood volume(BV),and permeability surface(PS)of patients in the malignant nodule group were significantly higher than those in the benign nodule group,and the differences were statistically significant(P<0.05).Taking the lung biopsy results of patients with pulmonary nodules as the gold standard,the diagnostic accuracy of multi-slice spiral CT for malignant nodules was 94.00%,the diagnostic sensitivity was 95.16%,the diagnostic specificity was 93.18%,the positive predictive value was 90.77%,and the negative predictive value was 96.47%.Conclusion There are significant differences in CT imaging features and perfusion parameters among patients with pulmonary nodules of different properties.Multi-slice spiral CT can effectively distinguish benign and malignant pulmonary nodules and has good diagnostic efficiency.

Aim To investigate the effect of dihydro-myricetin(DMY)on Ang Ⅱ-induced cardiac hypertro-phy in mice and the underlying mechanisms.Methods Fifty mice were randomly divided into control group,Ang Ⅱ group,Ang Ⅱ+catopril 12.0 mg·kg-1·d-1 group,AngⅡ+DMY 100 mg·kg-1·d-1 group,and Ang Ⅱ+DMY 200 mg·kg-1·d-1 group,with 10 mice in each group.The control mice were given saline by gavage,the drug intervention group was given DMY,and the positive drug group was given captopril;the mice in all groups except the control group were in-jected subcutaneously with Ang Ⅱ 1.0mg·kg-1·d-1.After four weeks,heart weight/body weight(HW/BW)and left ventricular weight/body weight(LVW/BW)ratios were calculated.The mRNA ex-pression of the fetal genes atrial natriuretic factor(ANF),brain natriuretic peptide(BNP),β-myosin heavy chain(β-MHC),adenosine triphosphate 5β-subunit(ATP 5β)and uncoupling protein 2(UCP2)were monitored,and the morphological changes of car-diac tissue were observed.Secondly,the creatine ki-nase isoenzyme(CK-MB),lactate dehydrogenase(LDH),free fatty acids(FFA)and lactic acid in ser-um were investigated.Lastly,the expression of AMP-activated proteinkinase(AMPK),peroxisome prolifer-ator-activated receptor alpha(PPAR-α)and T-cell nu-clear factor cytoplasmic 4(NFATc4)protein expres-sion were also detected.The Ang Ⅱ-induced H9C2 cardiomyocyte hypertrophy model was established and treated with the AMPK inhibitor compound C.The mRNA of ANF,BNP,β-MHC and the protein expres-sion of AMPK/PPAR-α were analyzed.Results DMY intervention significantly reduced HW/BW and LVW/BW in mice,fetal genes ANF,BNP,β-MHC and UCP2 mRNA expression decreased,whereas ATP 5 β mRNA increased,and the degree of hypertrophy of cardiomyocytes was alleviated.In addition,the serum levels of CK-MB,LDH,FFA and lactic acid were re-duced in DMY treated groups.Finally,DMY upregu-lated the protein expression of P-AMPK,AMPK and PPAR-α,and downregulated protein expression of NFATc4.In the Ang Ⅱ-induced cardiomyocyte hyper-trophy model,DMY pretreatment reduced the mRNA expression of fetal genes(ANF,BNP,β-MHC).However,when AMPK was inhibited by compound C,the expression of these fetal genes rebounded,accom-panied by decreased protein levels of AMPK and PPAR-α.Conclusions DMY can improve Ang Ⅱ-in-duced myocardial hypertrophy in mice by ameliorating disorders of glycolipid metabolism and increasing ener-gy supply to cardiomyocytes,and its mechanism is re-lated to the activation of the AMPK/PPAR-α pathway and the inhibition of NFATc4 expression.

Objective To explore the impact of suture configuration and fixation type on the biome-chanical strength of rotator cuff repair,using a factorial design study.Methods Sixteen fresh-frozen porcine shoulder samples were randomized into an anchorless double-row suture bridge transosseous su-tures(DS)group,an anchored double-row suture bridge transosseous-equivalent(DE)group,an an-chorless X-BOX construct transosseous sutures(XS)group,and an anchored X-BOX construct transos-seous-equivalent(XE)group,each of four,according to suture configuration(double-row suture bridge,traditional X-BOX construct)and fixation type(suture anchors,transosseous sutures).Then,their fatigue resistance(first-cycle excursion,gap length difference ratio,and the percentage of ex-posed footprints)and the failure strength(the maximum failure load and the re-tear type)were mea-sured using a biomechanical material testing machine.Results Different suture configurations affected failure strength(F=39.559,P<0.001),with the double-row suture bridge groups(693.07±58.35 N,746.76±138.57 N)showing significantly higher failure strength,compared to the traditional X-BOX groups(462.90±18.91 N,421.43±90.76 N).However,the fixation type did not significantly im-pact failure strength(F=1.161,P=0.302).Moreover,the suture configuration influenced the gap differ-ence ratio(F=7.781,P=0.016),but had no significant correlation with other fatigue resistance indica-tors(P>0.05).Meanwhile,failure strength and fatigue resistance were not correlated with fixation type,and the interaction between suture and fixation type(P>0.05).The incidence of failure types for the four suture configurations was as follows:Type I tendon tear:XS>XE>DS=DE;type II tendon tear:DS>XE>XS=DE;fixing material-related failure:DE>DS=XE=XS.Conclusion The failure strength and gap formation ratio in rotator cuff repair under fatigue loading are influenced by suture configuration,whereas no significant association has been observed with respect to fixation method,whether using transosseous sutures or suture anchors.

Objective:To investigate the related factors of cognitive impairment in middle-aged and old-aged patients with type 2 diabetes mellitus(T2DM).Methods:A total of 970 patients with T2DM(585 middle-aged group and 385 old-aged group)were selected from residents of a large community in Beijing from September to December 2018.The Mini-Mental State Examination(MMSE)was used to assess the cognitive func-tion.Multivariate logistic regression was used to analyze the related factors.Results:The detection rates of cognitive impairment were 12.0％and 13.5％in middle-aged and old-aged patients with T2DM,respectively.Among mid-dle-aged patients with T2DM,work(OR=0.22,95％CI:0.03-0.77)and education at the junior college or un-dergraduate level and above(OR=0.18,95％CI:0.04-0.55)were protective factors for cognitive impair-ment.Myocardial infarction(OR=4.13,95％CI:1.26-13.63)was a risk factor for cognitive impairment.Among old-aged patients with T2DM,drinking tea 1-2 times a week(OR=0.11,95％CI:0.01-0.58)and education at the junior college or undergraduate level and above(OR=0.19,95％CI:0.05-0.54)were protective factors for cognitive impairment.Stroke(OR=3.64,95％CI:1.55-8.39)and good sleep self-assessment(OR=2.75,95％CI:1.13-7.35)were risk factors for cognitive impairment.Conclusion:Cognitive impairment in middle-aged pa-tients with T2DM is related to work,education level and myocardial infarction,and cognitive impairment in old-aged patients with T2DM is related to lifestyle,education level and stroke.

Objective To investigate the ameliorative effects and mechanisms of six types of tea(green tea,cyan tea,red tea,white tea,black tea and yellow tea)on metabolic disorders in obesity mice induced by high-fat diet(HFD).Methods Four-week-old male C57BL/6J mice were randomly divided into 8 groups with 7 mice per group.An HFD-induced obese mouse model was established,and the mice in control group maintained on standard diet followed by intragastric administration of different teas for 5 weeks.The body weight,liver weight ratio,fasting blood glucose,and lipid profile of the mice were measured to assess glucose and lipid metabolism.Serum inflammatory factors including IL-6,tumor necrosis factor-alpha(TNF-α)and oxidative stress markers[malondialdehyde(MDA)and superoxide dismutase(SOD)were measured.Additionally,liver histopathology and the expression of key glycolipid metabolism-related genes,adenosine monophosphate-activated protein kinase(AMPK)and carnitine palmitoyltransferase 1(CPT-1),were analyzed to explore underlying mechanisms.Results Cyan tea significantly suppressed weight gain,demonstrating superior weight control.White tea markedly reduced fasting blood glucose levels and decreased the area under the curve of oral glucose tolerance test(OGTT)and insulin tolerance test(ITT),indicating synergistic improvements in glucose metabolism and insulin sensitivity.Yellow tea exhibited exceptional anti-inflammatory and antioxidant effects,reducing hepatic IL-6 and MDA while enhancing SOD activity.Green tea activated the lipid oxidation pathway by upregulating AMPK/CPT-1 expression.All kinds of tea significantly attenuated hepatic lipid droplet accumulation.Conclusion All six types of tea alleviated metabolic disorders by reducing hepatic fat content in obesity mice.However,different types of tea exert their unique effects on improving metabolic disorders through differential mechanisms such as glucose metabolism regulation,lipid oxidation,and anti-inflammatory and antioxidant actions.