AIM:To investigate the expression levels of serum sirtuin 6(Sirt6)and nicotinamide adenine dinucleotide phosphate oxidase 2(NOX2)in patients with primary glaucoma and their correlation with the severity of the disease. METHODS:This study is a cross-sectional study. Patients diagnosed with primary glaucoma at the hospital from August 2022 to June 2025 were enrolled and divided into mild-to-moderate and severe groups based on the mean deviation of visual field defects, along with healthy individuals as a control group. Clinical data were collected, and serum levels of Sirt6 and NOX2 were measured using enzyme-linked immunosorbent assay(ELISA). Correlations between serum Sirt6 and NOX2 levels and clinical parameters were analyzed. Multivariate Logistic regression was used to identify factors influencing disease severity, and the diagnostic efficacy of serum Sirt6 and NOX2 levels was evaluated using receiver operating characteristic(ROC)curves. RESULTS:A total of 120 patients with primary glaucoma(58 males, 62 females, mean age 60.08±8.19 y)and 100 controls(46 males, 56 females, mean age 60.23±8.67 y)were enrolled in this study. There were no statistically significant differences in sex or age between the two groups(both P>0.05). The intraocular pressure and serum NOX2 expression level in the primary glaucoma group were significantly higher than those in the control group, while the Sirt6 level was significantly lower than in the control group(all P<0.001). The AUC values of serum Sirt6 and NOX2 in the diagnosis of primary glaucoma were 0.733 and 0.770, respectively, with optimal cutoff values of 2.35 and 4.25 ng/mL, respectively. The AUC of the combined diagnosis of the two was 0.901, and its efficacy was obviously better than that of a single indicator(Zcombination-Sirt6=5.317, Zcombination-NOX2=4.720, P<0.001).The severe group had lower serum Sirt6 expression levels(P<0.05), and higher NOX2 expression levels(P<0.05)than the mild-to-moderate group. Serum Sirt6 expression levels were prominently negatively correlated with mean intraocular pressure(r=-0.354, P<0.05); NOX2 expression levels were prominently positively correlated with mean intraocular pressure(r=0.240, P<0.05). Multivariate Logistic regression analysis showed that a decrease in serum Sirt6 expression levels(OR=0.229, 95%CI: 0.090-0.581), an increase in serum NOX2 expression levels(OR=2.649, 95%CI: 1.658-4.232), an increase in mean intraocular pressure(OR=1.278, 95%CI: 1.118-1.462)which were risk factors for the progression to severe glaucoma. The AUC values of serums Sirt6 and NOX2 expression levels in diagnosing severe primary glaucoma were 0.794 and 0.800, respectively, the AUC, sensitivity, and specificity of the combined diagnosis of the two were 0.916, 80.00%, and 89.33%, respectively, and the combined diagnostic efficacy was better than that of a single indicator(Zcombination-Sirt6=2.627, P=0.009, Zcombination-NOX2=2.762, P=0.006). CONCLUSION:The decreased serum Sirt6 and increased NOX2 expression levels in patients with primary glaucoma are significantly correlated with disease severity, and the combined detection demonstrates good diagnostic value for primary glaucoma and its severity.

Objective:To investigate the preventive and therapeutic effects and mechanisms of Dachaihu decoction(DCD)on dextran sodium sulfate(DSS)-induced ulcerative colitis(UC)and liver injury in mice,as well as the association between DCD benefits and gut microbiota modulation.Methods:Mice were treated with DCD(20.10 and 10.05 g/kg)for 2 weeks,with free access to drinking water containing 3%DSS in the second week to induce UC.Histopathological examination,RT-qPCR and 16S rRNA sequencing were used to investigate the effect of DCD on UC mice.Results:DCD pretreatment significantly alleviated weight loss,bloody diarrhea with mucus,histopathological abnormalities of the colon,and colon shortening in mice with DSS-induced UC.In addition,DCD pretreat-ment significantly upregulated the levels of Occludin,ZO-1,and MUC-2 in the colon and protected the intestinal barrier of mice.DCD pretreatment also alleviated inflammatory cell infiltration in the colon and the liver and significantly reduced the expression levels of the proinflammatory factors such as IL-1β,IL-6,TNF-α,iNOS,COX-2,and NLRP3,thereby exerting a protective effect against UC and liver injury.It should be noted that DCD corrected gut micro-biota imbalance in UC mice by enriching probiotic bacteria such as Lactobacillus and Bifidobacterium and reducing harmful bacteria such as Norank_f_Desulfovibrionaceae and Escherichia-Shigella.Conclusion:DCD can alleviate DSS-induced UC and exert a liver-protecting effect by protecting intestinal barrier,inhibiting inflam-mation,and regulating gut microbiota.

Amino acid metabolism plays a critical role in the progression and development of breast cancer. Cancer cells, including those in breast cancer, reprogram amino acid metabolism to meet the demands of rapid proliferation, survival, and immune evasion. This includes alterations in the uptake and utilization of amino acids, such as glutamine, serine, glycine, and arginine, which provide essential building blocks for biosynthesis, energy production, and redox homeostasis. Notably, the metabolic phenotypes of breast cancer cells vary across molecular subtypes and disease stages, emphasizing the need for patient stratification and personalized therapeutic strategies. Advances in multi-level diagnostics, including phenotyping and predictive tools, such as AI-based analysis and body fluid profiling, have highlighted the potential for tailoring treatments to individual metabolic profiles. Enzymes, such as glutaminase and serine hydroxymethyltransferase, often upregulated in breast cancer, represent promising therapeutic targets. Understanding the interplay between amino acid metabolism and breast cancer biology, alongside the integration of personalized medicine approaches, can uncover novel insights into tumor progression and guide the development of precision therapies. This review explores the metabolic pathways of amino acids in breast cancer, with a focus on their implications for personalized treatment strategies.
Humans ; Breast Neoplasms/therapy* ; Female ; Amino Acids/metabolism*

Lung transplantation is currently the only recognized effective treatment for end-stage lung disease and has improved the quality of life for patients. However, lung transplantation still faces many challenges, including rejection, infection, post-transplant acute kidney injury, post-transplant diabetes mellitus, ischemia-reperfusion injury and donor shortage, etc. Chinese lung transplantation scholars made a series of important progress in the field of clinical research in 2024, focusing on the study and solution of the above problems, and providing new ideas for lung transplantation surgery. This article systematically reviews the clinical research and technological innovation in the field of lung transplantation in 2024, summarizes the achievements of clinical research in the field of lung transplantation in China in 2024, and aims to providing new directions and strategies for future research.

Lung transplantation is the optimal treatment for end-stage lung diseases and can significantly improve prognosis of the patients. However, postoperative complications such as infection, rejection, ischemia-reperfusion injury, and other challenges (like shortage of donor lungs) , limit the practical application of lung transplantation in clinical practice. Chinese research teams have been making continuous efforts and have achieved breakthroughs in basic research on lung transplantation by integrating emerging technologies and cutting-edge achievements from interdisciplinary fields, which has strongly propelled the development of this field. This article will comprehensively review the academic progress made by Chinese research teams in the field of lung transplantation in 2024, with a focus on the achievements of Chinese teams in basic research on lung transplantation. It aims to provide innovative ideas and strategies for key issues in the basic field of lung transplantation and to help China's lung transplantation cause reach a higher level.

Schizophrenia is a chronic and debilitating mental disorder.Around 20%to 40%of patients do not respond well to normal antipsychotic medication,and are ultimately diagnosed with treatment-resistant schizophrenia(TRS),representing the most severe and challenging form of schizophrenia.Currently,clozapine is the standard treatment for TRS.Early identification and standardized treatment can be beneficial to patients with TRS by controlling acute-phase symptoms as soon as possible,reducing suicidal rate and improving their quality of life.Under the guidance of the Steering Committee,this consensus was formed after multiple discussions by 30 psychiatric experts and anonymous Delphi surveys including 17 consensus opinions on treatment-resistant schizophrenia,which cover risk factors and prevention,diagnosis and evaluation,standardized clozapine treatment and management of adverse reactions,treatment regimens for clozapine resistance and intolerance,and psychosocial intervention,etc.The consensus-making process also incorporated evidence-based medicine to help standardize and guide diagnosis and treatment for adults with TRS in China.

Objective To explore the mechanism by which Liqi Huoxue Dripping Pill(LQHXDP)inhibits cardiomyocyte apoptosis in rats with myocardial ischemia-reperfusion injury(MIRI).Methods Male Sprague-Dawley(n=96)rats were randomly assigned to a normal,sham-operated,model,LQHXDP,adenovirus negative control(Ad-shNC),adenovirus-mediated HIF-1α knockdown(Ad-shHIF-1α),LQHXDP+Ad-shNC,or LQHXDP+Ad-shHIF-1α group using a random number table.LQHXDP was administered daily via oral gavage at 175.0 mg/(kg·d)for 10 consecutive days.On day 7,recombinant adenovirus was injected into the left ventricular wall of rats in the corresponding groups at multiple points.On day 10,the MIRI model was established by ligating the left anterior descending coronary artery.The sham-operated group underwent thoracotomy and suture placement without coronary ligation.Samples were collected after reperfusion was completed.Serum creatine kinase isoenzymes(CK-MB),cardiac troponin I(cTnI),and heart-type fatty acid binding protein(H-FABP)levels were measured using enzyme-linked immunosorbent assay.2,3,5-Triphenyltetrazolium chloride staining was used to measure the volume ratio of myocardial infarction.HE staining was performed to observe the morphology of myocardial tissue.Terminal transferase uridyl nick end labeling assay was conducted to analyze the apoptosis rate of cardiomyocytes,and Western blotting was used to detect the expression of key proteins in the apoptosis(B-cell lymphoma-2[Bcl-2],Bcl-2 associated X protein[Bax],and cleaved cysteinyl aspartate specific proteinase 3[Cleaved-Caspase-3]and HIF-1α/Bcl-2-adenovirus E1B 19 kDa interacting protein 3(BNIP3)signaling pathway(HIF-1α,heme oxygenase-1[HO-1],and BNIP3).Results LQHXDP pretreatment significantly reduced serum CK-MB,cTnI,and H-FABP levels,as well as the myocardial infarction volume ratio in rats with MIRI.LQHXDP also improved myocardial tissue morphology,decreased cardiomyocyte apoptosis,upregulated Bcl-2 protein expression,and downregulated Bax,Cleaved-Caspase-3,HIF-1α,HO-1,and BNIP3 protein expressions(P<0.05).However,adenovirus-mediated shRNA HIF-1α impaired the effects of LQHXDP pretreatment in attenuating myocardial injury and inhibiting apoptosis in MIRI rats(P<0.05).Conclusion LQHXDP reduces cardiomyocyte apoptosis and protects rat myocardium from MIRI by regulating the HIF-1α/BNIP3 signaling pathway.

AIM:To study the protective effect of transient receptor potential vanilic acid subtype 1(TRPV1)agonist capsaicin(CAP)on traumatic blood loss shock rats,and to further explore its possible mechanism by network pharmacology.METHODS:Forty-five SD rats were divided into 5 groups by random number table method:normal group,shock group,lactated Ringer's solution(LR)group,CAP pretreatment(single administration before shock)group,CAP pre-final administration(twice administration before and after shock)group,with 9 rats in each group for survival observation.Then 32 SD rats were divided into 4 groups according to the results of survival experiment:normal group,shock group,LR group,CAP pre-final administration group,with 8 rats in each group for blood pressure,hemodynamics,arterial blood gas,vascular reactivi-ty and hepaticand renal blood flow.At the same time,the potential mechanism of CAP in the treat-ment of traumatic hemorrhagic shock was investi-gated by network pharmacology.Furthermore,ap-ply the dataset to validate and analyse the diagnos-tic value of the hub genes.RESULTS:Rats in shock group died within hours of the completion of the shock model,and the mean survival time was 1.25(0.42,6.21)h.LR resuscitation could improve the survival of rats to some extent.The survival rate and survival time of rats in the CAP pretreatment group were slightly increased as compared with the LR group,while twice administration of CAP be-fore and after shock(CAP pre-final administration)resulted in better outcomes than LR resuscitation alone.Further results indicated that CAP pre-final administration significantly reduced the blood lac-tic acid level,improved the vasoconstrictive and di-astolic reactivity,and increased the liver and kidney blood flow of shock rats as compared with LR group.The improvement of hemodynamics and blood gas indexes in CAP group was slightly higher than LR group,but there was no statistical signifi-cance.A total of 37 genes related to CAP anti-trau-matic hemorrhage shock were obtained by net-work pharmacology.KEGG enrichment analysis showed that the Ca ion signaling pathway and Ras signaling pathway were significantly enriched.Vali-dation of the dataset showed that the expression levels of CXCR4,NF-kB1,GFPA and NTF3 hub gene were significantly different in the normal and shock groups,and that CXCR4 has a high diagnostic value for traumatic haemorrhagic shock.CONCLUSIONS:CAP,the TRPV1 agonist,significantly improved vas-cular function,increased organ blood flow,and cor-rected the lactic acidosis in rats with traumatic hemorrhagic shock,thus markedly improved the survival outcomes.The mechanism may be related to Ca ion signal pathway and Ras signal pathway.CXCR4,NF-kB1,GFPA and NTF3 may be having an important role in it.

Objective To investigate the differences in cortical activation and functional connectivity during speech under different cognitive loads in young individuals.Methods Twenty-one participants(mean age 21.9±1.33 years)were instructed to read short sentences embedded with color words under both congruent(where the color words matched the font color)and incongruent(where the color words did not match the font color)condi-tions.The color words required reading the font color instead of the word itself.Functional near-infrared spectros-copy(fNIRS)was utilized to analyze differences in cortical activation(changes in HbO concentration)and functional connectivity(Pearson correlation of HbO between brain regions)in the dorsolateral prefrontal cortex(DLPFC)and supplementary motor area(SMA)bilaterally.Results The fNIRS results revealed significant increase in HbO con-centration changes in the RDLPFC(t=3.4,P=0.003),LDLPFC(t=2.58,P=0.019),RSMA(t=3.59,P=0.002),and LSMA(t=4.06,P=0.001)under the incongruent condition compared to the congruent condition.Additionally,there was a significant enhancement in the correlation between RDLPFC and LDLPFC(t=2.44,P=0.025).However,the differences in correlation between left and right SMA,as well as between SMA and DLPFC,were not statistically significant(P＞0.05).Conclusion These findings suggest that during speech under incongru-ent conditions,increased cognitive load leads to elevated cortical activation in the DLPFC and SMA,along with in-creased functional connectivity between the left and right DLPFC.

Schizophrenia is a chronic and debilitating mental disorder.Around 20%to 40%of patients do not respond well to normal antipsychotic medication,and are ultimately diagnosed with treatment-resistant schizophrenia(TRS),representing the most severe and challenging form of schizophrenia.Currently,clozapine is the standard treatment for TRS.Early identification and standardized treatment can be beneficial to patients with TRS by controlling acute-phase symptoms as soon as possible,reducing suicidal rate and improving their quality of life.Under the guidance of the Steering Committee,this consensus was formed after multiple discussions by 30 psychiatric experts and anonymous Delphi surveys including 17 consensus opinions on treatment-resistant schizophrenia,which cover risk factors and prevention,diagnosis and evaluation,standardized clozapine treatment and management of adverse reactions,treatment regimens for clozapine resistance and intolerance,and psychosocial intervention,etc.The consensus-making process also incorporated evidence-based medicine to help standardize and guide diagnosis and treatment for adults with TRS in China.