ObjectiveThe malaria parasites remodel the host erythrocyte structure by exporting parasite proteins that interact with the membrane skeleton proteins of red blood cells (RBCs), facilitating their intracellular survival and pathogenicity. Skeleton-binding protein 1 (SBP1) is a conserved exported protein across Plasmodium species. In Plasmodium falciparum, SBP1 has been reported to interact with erythrocyte membrane skeleton proteins 4.1R and spectrin, while its contribution to erythrocyte remodeling and parasite virulence in Plasmodium berghei (Pb) remains unclear. This study aims to determine whether PbSBP1 associates with the host cytoskeletal protein 4.1R and to investigate its role in the remodeling of host RBCs and the pathogenicity of Plasmodium berghei. MethodsIn Plasmodium berghei, the relationship between PbSBP1 and the erythrocyte cytoskeletal protein 4.1R was examined using co-immunoprecipitation. A Pbsbp1 gene knockout mutant of Plasmodium berghei (Pbsbp1∆) was generated based on the principle of double crossover homologous recombination. The deformability of erythrocytes infected with Pbsbp1∆ parasites was assessed using microfluidic methods. Microchannels with an array of cylindrical pillars were used to detect modifications in infected RBC deformability. The infected RBCs were squashed between the rows and recovered between the columns and the transit velocity (μm/s) of infected RBCs travelling through the microchannel was recorded. The component of the erythrocyte membrane skeleton junctional complex, tropomodulin (TMOD), was fluorescently labeled, and the cytoskeletal network of infected erythrocytes was imaged using super-resolution stochastic optical reconstruction microscopy (STORM) to analyze ultrastructural changes in the cytoskeleton of wild-type (WT) and Pbsbp1∆-infected erythrocytes. Actin-based junctional complexes were displayed as individual clusters by the labeled TMOD in the STORM images, and the cluster densities and distances between adjacent clusters of infected RBCs were calculated. Additionally, rodent malaria models (BALB/c mice) and experimental cerebral malaria models (C57BL/6 mice) were employed to monitor the growth of Pbsbp1∆ and WT parasites during the intraerythrocytic stage and their capacity to induce cerebral malaria in mice. ResultsPbSBP1 may participate in the remodeling of infected erythrocytes through direct or indirect interaction with the erythrocyte cytoskeletal protein 4.1R. Microfluidic assays revealed that the deformability of erythrocytes infected with Pbsbp1∆ parasites was significantly enhanced compared to those infected with WT parasites. STORM imaging further demonstrated that the ultrastructure of the erythrocyte cytoskeleton in Pbsbp1∆-infected cells was altered relative to that in WT-infected erythrocytes. The distances between nearest neighbors of clusters had a tendency to increase while the cluster densities were decreased in Pbsbp1∆-infected RBCs compared to WT-infected RBCs. Subsequent phenotypic analysis indicated that the growth rate of Pbsbp1∆ parasites during the intraerythrocytic stage was significantly slower than that of WT parasites, and their ability to induce cerebral malaria in mice was also attenuated. These findings suggest that PbSBP1 is involved in the remodeling of the erythrocyte membrane skeleton, likely through its direct or indirect interaction with protein 4.1R, thereby regulating the deformability of infected erythrocytes and influencing the pathogenicity of the blood-stage parasites. ConclusionThis study establishes a role for PbSBP1 in host erythrocyte remodeling and parasite virulence, providing new research strategies for the prevention and treatment of malaria.

Attention deficit and hyperactive disorder （ADHD） is the most common neurodevelopmental disorder of childhood. It seriously impairs academic achievement， social interaction， and vocational development， and increases the risk of accidental injury and substance abuse. In some cases， the symptoms may also exert an indirect disruptive effect on public order. Its aetiology involves interactions among genetic， perinatal environmental， and psychosocial factors that cannot be fully disentangled by single clinical studies. Therefore， a systematic evaluation of existing animal models is essential for revealing pathophysiology and developing novel therapies. Using the keywords "attention deficit and hyperactive disorder"， "models， animal"， "validity"， and their English equivalents， we systematically searched PubMed， Web of Science， CNKI， and Wanfang for publications from 2000 to 2025 （retrieving 328 publications） and added further references by citation tracking. Eighty-six rodent ADHD models that provided detailed construction protocols， behavioural assessments， neurobiological mechanisms， or pharmacological data were included and classified into spontaneous genetic， genetically engineered， and environmentally induced paradigms. Their face， construct， and predictive validity were compared. Among spontaneous genetic models， spontaneously hypertensive rats reproduce hyperactivity， impulsivity， and stimulant responses well， yet hypertension and sex differences limit specificity. Acallosal mouse strains link corpus callosum absence to ADHD-like behaviours， but neurotransmitter studies remain scarce. Genetically engineered rodents—including dopamine transporter， neurokinin-1 receptor and mediator complex subunit 23 knockout or conditional gene knockout lines—precisely dissect dopaminergic， noradrenergic， synaptic， or epigenetic pathways， yet generally lack full phenotypic coverage， social-deficit modelling， and comorbidity representation， and are accompanied by adverse effects such as growth retardation or ocular defects. Environmentally induced models employ lead， polychlorinated biphenyls， alcohol， nicotine exposures， 6-hydroxydopamine lesions， neonatal hypoxia， early social isolation， or maternal stress to recapitulate core symptoms. However， dose-schedule standardisation is lacking. Behavioural reversibility diverges from clinical persistence， and non-specific phenotypes such as anxiety or depression are common. Overall， no single paradigm simultaneously achieves high validity across all three dimensions. Currently， ADHD models have progressed from single-factor simulations to multidimensional evaluation， yet significant gaps remain in genetic-background standardisation， sex differences， cross-species translation， and syndrome-differentiation modelling under traditional Chinese medicine. Future directions should integrate genetic， environmental， and epigenetic interactions， establish life-span validation systems， and incorporate computational neuroscience alongside integrative Chinese-Western strategies to enhance clinical relevance and translational utility， thereby providing robust evidence-based support for mechanistic elucidation， drug screening and precision intervention in ADHD.

The brain-gut interaction theory is a multidimensional integrative concept based on the brain-gut axis， involving neural， endocrine， and immune regulatory networks as well as the gut microbiota. Zang-fu organs （脏腑） theory in traditional Chinese medicine （TCM） shows a high degree of consistency with the brain-gut interaction theory， and the core functions such as the spleen and stomach governing the ascending of the clear and descending of the turbid， the liver governing the free flow of qi， and the heart governing mental and emotional activities are closely associated with the multi-level regulatory mechanisms of the brain-gut axis. TCM therapy can modulate brain-gut interactions through multiple pathways in the treatment of spleen and stomach diseases， including the regulation of gastrointestinal hormone secretion， neurotransmitter levels， the hypothalamic-pituitary-adrenal （HPA） axis， immune homeostasis and inflammatory responses， as well as the gut microecology. However， current basic research on the brain-gut interaction theory in TCM for spleen and stomach diseases still faces several challenges， such as difficulties in integrating TCM spleen-stomach theory with modern pathophysiology， lack of innovation in research concepts， and limitations in research methodologies. It is therefore proposed that multidisciplinary collaboration， multi-omics technologies， and targeted research approaches should be adopted to provide more comprehensive methods for basic research on TCM spleen and stomach diseases， thereby promoting the in-depth development of brain-gut interaction theory.

Objective:To study the alternation of plasma ghrelin in patients with acute pancreatitis (AP) and to evaluate the efficacy of gastric slow wave analysis in predicting the severity of AP.Methods:Clinical data and blood samples of 129 patients with AP and 16 individuals for normal physical examination in the Department of Gastroenterology, Jiangnan University Affiliated Central Hospital (Wuxi No.2 People's Hospital) from September 2018 to August 2024 were prospectively collected. Individuals with normal physical examinations were included in the normal control group, including 9 males and 7 females, aged (50.9±14.2) years. The finally enrolled 125 patients with AP included 82 males and 43 females, aged (49.5±15.6) years, which were grouped according to disease severity. Mild AP (MAP) was included in the MAP group ( n=84), while moderate to severe and severe acute AP were included in the non-MAP group ( n=41). The surface gastrogram of all AP patients was detected on the 2nd and 4th day after admission. The slow waves of gastric electricity were recorded, and gastric growth hormone-releasing hormone, C-reactive protein (CRP), etc. were detected simultaneously. Univariate and multivariate logistic regression analyses were conducted to analyze the influencing factors of AP severity (MAP or non-MAP). Receiver operating characteristic (ROC) curve was used to evaluate the indicators in predicting the severity of AP. Results:The levels of gastric growth hormone-releasing hormone in both the non-MAP group and MAP group on the 2nd and 4th day after admission were lower than those in normal control group (all P<0.05). The percentages of normal gastric electrical slow waves in the first and fourth leads, the mean percentages of normal gastric electrical slow waves in the four leads, and the main frequency on the 2nd day of admission in the non-MAP group were lower than those in the normal control group, and the main power and C-reactive protein were higher than those in the MAP group, the differences were statistically significant (all P<0.05). Multivariate logistic regression analysis showed the percentage of normal gastric electrical slow wave in the first lead on the 2nd day of admission ( OR=0.914, 95% CI: 0.869-0.961, P=0.001) and CRP ( OR=1.008, 95% CI: 1.002-1.013, P=0.012) were the influencing factors of the severity of AP. The area under the ROC curve of the percentage of normal gastric electrical slow wave in the first lead on the 2nd day of admission in predicting the severity of AP was 0.705, with a sensitivity of 97.6% and a specificity of 35.7%. Conclusion:The plasma gastric growth hormone-releasing hormone in patients with AP decreases in the early stage. The low percentage of normal slow waves in the first lead of gastric electrocardiogram on the 2nd day of admission is a risk factor for the severity of AP and can be used for the early prediction of the severity.

AIM To study the chemical constituents from Fomes officinalis(Vill.ex Fr.)Ames and their anti-inflammatory activities.METHODS The 95％ethanol extract from F.officinalis was isolated and purified by silica gel,Sephadex LH-20,HW-40C,MCI and semi-preparative HPLC,then the structures of obtained compounds were identified by physicochemical properties and spectral data.Their anti-inflammatory activities in vitro were evaluated by RAW264.7 model.RESULTS Twenty compounds were isolated and identified as asperginine A(1),laricinolic acid(2),methoxylaricinolic acid(3),fomeffic acid(4),19-acetoxy-13S-hydroxylabda-8(17),14-diene(5),bisbenzopyran(6),lariciresinol acetate(7),fomitopsin G(8),fomitopsin H(9),demalonyl fomitopsin H(10),fomlactone A(11),fomlactone B(12),fomefficinol A(13),fomefficinol B(14),laetiporins A(15),laetiporins B(16),dehydrosulphurenic acid(17),dehydroeburicoic acid(18),3-keto-dehydrosulfurenic acid(19),eburicoic acid(20).The IC50 values of compounds 7,13,20 were(4.00±1.02),(3.29±0.62),(3.22±0.94)μmol/L,respectively.CONCLUSION Compound 1 is a new compound,3,6,15,16 are isolated from this plant for the first time.Compounds 7,13,20 have strong anti-inflammatory activities.

Objective To evaluate the effect of Kaixin San(KXS)combined with fluoxetine on hippocampal neural stem cells in mice with chronic stress stress and depression.Methods A mouse model of depression was constructed using the method of chronic unpredictable stress stress,and the highest dose of KXS water extract and fluoxetine for clinical application was given for 28 days,and behavioral tests were carried out.Nissl staining was used to detect the pathological status of hippocampal tissues in mice.The expression of TUNEL and Nestin in mouse hippocampus was determined by immunofluorescence.Western blotting was used to detect the expressions of apoptotic proteins cleaved caspase-3 and caspase-3,pyroptosis proteins GSDMD and cleaved caspase-1,as well as the expression of neural stem cell marker Nestin in the hippocampus,and the expression of Wnt/β-catenin signaling pathway-related proteins in the hippocampus.Results The combination of KXS extract and fluoxetine can significantly improve the depression-like behavior of model mice,and the effect is better than fluoxetine alone.The combination inhibited the activation of apoptosis and pyroptosis signaling pathways in the hippocampus when used alone with high-dose fluoxetine,significantly upregulated the expression of Nestin,and regulated the expression of Wnt/β-catenin signaling pathway protein.Conclusion The combination of KXS and high-dose fluoxetine can improve apoptosis and pyroptosis in the hippocampus of stress stress and depression model mice,and upregulate the expression of neural stem cell marker Nestin by regulating the Wnt/β-catenin signaling pathway,which may be a key link to improve the antidepressant effect of the combination drug.

Objective:To investigate the radioactivity levels and variation trends of 90Sr in drinking water and food around the Qinshan Nuclear Power Plant in operation. Methods:From 2012 to 2022, the source, factory, and tap water was collected within 30 km around the Qinshan Nuclear Power Plant during the wet and dry seasons (i.e., May and October, respectively) each year to determine the 90Sr concentration in water. According to the dietary habits of local residents, four kinds of food, including rice, cabbage, mullet, and crucian carp, were collected to determine and analyze the 90Sr radioactivity concentration in food using the bis-(2-ethylhexyl) phosphoric acid extraction chromatographic method. Results:From 2012 to 2022, the 90Sr radioactivity concentrations in the source, factory, and tap water around the Qinshan Nuclear Power Plant ranged from 3.73 to 11.89 mBq/L, 2.95 to 9.83 mBq/L, and 3.12 to 8.70 mBq/L, respectively, showing nonsignificant fluctuations over the years. The 90Sr radioactivity concentrations in rice, cabbage, mullet, and crucian carp ranged from 0.02 to 0.46 Bq/kg (dry weight), 0.26 to 1.07 Bq/kg (fresh weight), 0.38 to 1.05 Bq/kg (fresh weight), and 0.08 to 1.32 Bq/kg (fresh weight), respectively, all below the national standard limits. Conclusions:From 2012 to 2022, the 90Sr radioactivity levels in drinking water and food around the Qinshan Nuclear Power Plant were at the background level and remained stable.

Aim To investigate the effect of long-chain non-coding RNA(lncRNA)GS1-124K5.4 targeting regulation of PRDX6 on proliferation,migration and in-vasion of lung squamous carcinoma(LUSC)cells and the underlying mechanism.Methods The expression level of lncRNA GS1-124K5.4 in lung cancer tissues and adjacent tissues of 60 patients with LUSC were de-termined by fluorescence in situ hybridization.The ex-pression level of lncRNA GS1-124K5.4 in human nor-mal lung cells and LUSC cells were determined by qRT-PCR.Two kinds of LUSC cells(NCI-H 1703,SK-MES-1)with highest expression level of lncRNA GS1-124K5.4 were selected for subsequent experi-ments.The distribution of lncRNA GS1-124K5.4 in cells was studied by fluorescence in situ hybridization and prokaryotic separation.The effect of knockdown of lncRNA GS1-124K5.4 on proliferation of NCI-H1703 and SK-MES-1 cells was studied by CCK-8 experiment and cell clone formation experiment;the effect of knockdown of lncRNA GS1-124K5.4 on migration of NCI-H1703 and SK-MES-1 cells was studied by cell scratch experiment and Transwell cell migration experi-ment;and the effect of knockdown of lncRNA GS1-124K5.4 on invasion of NCI-H1703 and SK-MES-1 cells was studied by Transwell invasion experiment.The protein to be bound by lncRNA GS1-124K5.4 was detected by RNA pull-down combined with mass spec-trometry and immune-precipitation.The effect of knockdown of lncRNA GS1-124K5.4 targeting PRDX6 on proliferation,migration and invasion of NCI-H1703 and SK-MES-1 cells was studied.Results(1)The fluorescence intensity of lncRNA GS1-124K5.4 in lung squamous cell carcinoma increased compared with that in adjacent tissues(P＜0.05),and the expression of lncRNA GS1-124K5.4 was related with lymph node metastasis and clinical stage(P＜0.05).(2)The ex-pression level of lncRNA GS1-124K5.4 in NCI-H1703,NCI-H520 and SK-MES-1 cells significantly increased(P＜0.05).(3)The result of fluorescence in situ hybridization experiment and nucleoplasm sepa-ration experiment showed that lncRNA GS1-124K5.4 was mainly distributed in cell nucleus.(4)The prolif-eration,migration and invasion ability of NCI-H1703 and SK-MES-1 cells with knockdown of lncRNA GS1-124K5.4 significantly decreased(P＜0.05).(5)PRDX6 protein to be bound to LncRNA GS1-124K5.4 was determined by RNA pull-down combined with mass spectrometry and immunoprecipitation.(6)The prolif-eration,migration and invasion ability of NCI-H1703 and SK-MES-1 cells with overexpression of lncRNA GS1-124K5.4 significantly increased(P＜0.05);the proliferation,migration and invasion ability of NCI-H1703 and SK-MES-1 cells with knockdown of PRDX6 significantly decreased(P＜0.05);the proliferation,migration and invasion ability of NCI-H1703 and SK-MES-1 cells with overexpression of lncRNAGS1-124K5.4 and knockdown of PRDX6 showed no signifi-cant change(P＞0.05).Conclusions LncRNA GS1-124K5.4 is highly expressed in lung squamous cell carcinoma,and it may promote the proliferation,migration and invasion of lung squamous carcinoma cells by targeting the expression of PRDX6 protein.

Objective:To explore the correlation between thyroid hormone levels and the 90-day prognosis in patients with severe pulmonary tuberculosis, with a particular focus on the impact of age.Methods:This retrospective cohort study included 156 patients(43 females, 113 males; ages ranging from 21 to 93 years)diagnosed with severe pulmonary tuberculosis between January 2022 and December 2023.Patients were categorized into deceased( n=46)and survived( n=110)groups based on their 90-day survival status.Further subcategorization into elderly and non-elderly subgroups was conducted.Thyroid hormone levels and other relevant laboratory markers were measured and analyzed. Results:Total triiodothyronine(TT3) [(0.92±0.36)nmol/L] and free triiodothyronine(FT3) [(2.19±0.87)pmol/L] in deceased group were lower than in survival group [TT3(1.09±0.38)nmol/L], FT3 [(2.79±0.99)pmol/L], both P<0.05.T3 levels positively correlated with 90-day survival (TT3: r=-0.202, P=0.011; FT3: r=-0.276, P<0.001).In elderly patients, this correlation was weakened (TT3: r=-0.071, P=0.526; FT3: r=-0.206, P=0.059), but remained significant in non-elderly patients (TT3: r=-0.360, P=0.002; FT3: r=-0.345, P=0.003).FT3 was a better prognostic indicator than TT3. Conclusions:Low serum T3 levels are indicative of a poor prognosis in severe pulmonary tuberculosis; however, their predictive value diminishes in elderly patients.

Aim To predict and verify the potential mechanism of the compatibility of"ginseng-astragalus-pueraria"in protecting islet morphology and improving insulin resistance by using network pharmacology.Methods The active ingredients and targets of the horn medicine were obtained from three platforms:TC-MSP,TCMIP,and BATMAN.The targets of type 2 dia-betes mellitus(T2DM)were obtained from three plat-forms:TTD,OMIM,and disgeNET.The PPI network was constructed by using the STRING database and Cy-toscape 3.9.1;GO and KEGG analysis were per-formed;POCASA 1.1 was used to predict protein binding sites,and AutoDock Vina1.1.2 was used for docking and experimental verification.Results"Gin-seng-astragalus-pueraria"screened out 2 021 targets,of which 152 were closely related to T2DM,and 10 key genes and the AGE-RAGE signaling pathway were i-dentified.Molecular docking showed that quercetin had good binding to RAGE,INS,and PI3K.Experi-ments showed that the horn drug increased insulin binding rate and secretion index and reduced serum in-sulin level and insulin resistance index.These data benefited from"ginseng-astragalus-pueraria"reducing the expression of AGE-RAGE,activating PI3K-Akt,in-hibiting NF-κB,and reducing the expression of IL-6,IL-1β and TNF-α.Conclusion The study suggests that"ginseng-astragalus-pueraria"regulates the AGE-RAGE/PI3K-Akt/NF-κB signaling pathway,repairs damaged islet morphology,and improves insulin resist-ance.