Antioxidant and anti-inflammatory function of Eupatorium adenophora Spreng leaves (EASL) on human intestinal Caco-2 cells treated with tert-butyl hydroperoxide.

Chronic non-communicable diseases (CNCDs) pose a significant public health challenge. Addressing this issue, there has been a notable breakthrough in the prevention and mitigation of NCDs through the use of antioxidants and anti-inflammatory agents. In this study, we aim to explore the effectiveness of Eupatorium adenophora Spreng leaves (EASL) as an antioxidant and anti-inflammatory agent, and its potential applications. To construct a cellular model of oxidative damage and inflammation, Caco-2 cells were treated with tert-butyl hydroperoxide (t-BHP). The biocompatibility of EASL-AE with Caco-2 cells was assessed using the MTT assay, while compatibility was further verified by measuring LDH release and the protective effect against oxidative damage was also assessed using the MTT assay. Additionally, we measured intracellular oxidative stress indicators such as ROS and 8-OHdG, as well as inflammatory pathway signalling protein NFκB and inflammatory factors TNF-α and IL-1ß using ELISA, to evaluate the antioxidant and anti-inflammatory capacity of EASL-AE. The scavenging capacity of EASL-AE against free radicals was determined through the DPPH Assay and ABTS Assay. Furthermore, we measured the total phenolic, total flavonoid, and total polysaccharide contents using common chemical methods. The chemical composition of EASL-AE was analyzed using the LC-MS/MS technique. Our findings demonstrate that EASL-AE is biocompatible with Caco-2 cells and non-toxic at experimental levels. Moreover, EASL-AE exhibits a significant protective effect on Caco-2 cells subjected to oxidative damage. The antioxidant effect of EASL-AE involves the scavenging of intracellular ROS, while its anti-inflammatory effect is achieved by down-regulation of the NFκB pathway. Which in turn reduces the release of inflammatory factors TNF-α and IL-1ß. Through LC-MS/MS analysis, we identified 222 compounds in EASL-AE, among which gentianic acid, procaine and L-tyrosine were the compounds with high antioxidant capacity and may be the effective constituent for EASL-AE with antioxidant activity. These results suggest that EASL-AE is a natural and high-quality antioxidant and anti-inflammatory biomaterial that warrants further investigation. It holds great potential for applications in healthcare and other related fields.

Sensor Head Temperature Distribution Reconstruction of High-Precision Gravitational Reference Sensors with Machine Learning.

Temperature fluctuations affect the performance of high-precision gravitational reference sensors. Due to the limited space and the complex interrelations among sensors, it is not feasible to directly measure the temperatures of sensor heads using temperature sensors. Hence, a high-accuracy interpolation method is essential for reconstructing the surface temperature of sensor heads. In this study, we utilized XGBoost-LSTM for sensor head temperature reconstruction, and we analyzed the performance of this method under two simulation scenarios: ground-based and on-orbit. The findings demonstrate that our method achieves a precision that is two orders of magnitude higher than that of conventional interpolation methods and one order of magnitude higher than that of a BP neural network. Additionally, it exhibits remarkable stability and robustness. The reconstruction accuracy of this method meets the requirements for the key payload temperature control precision specified by the Taiji Program, providing data support for subsequent tasks in thermal noise modeling and subtraction.

IgG is an aging factor that drives adipose tissue fibrosis and metabolic decline.

Aging is underpinned by pronounced metabolic decline; however, the drivers remain obscure. Here, we report that IgG accumulates during aging, particularly in white adipose tissue (WAT), to impair adipose tissue function and metabolic health. Caloric restriction (CR) decreases IgG accumulation in WAT, whereas replenishing IgG counteracts CR's metabolic benefits. IgG activates macrophages via Ras signaling and consequently induces fibrosis in WAT through the TGF-ß/SMAD pathway. Consistently, B cell null mice are protected from aging-associated WAT fibrosis, inflammation, and insulin resistance, unless exposed to IgG. Conditional ablation of the IgG recycling receptor, neonatal Fc receptor (FcRn), in macrophages prevents IgG accumulation in aging, resulting in prolonged healthspan and lifespan. Further, targeting FcRn by antisense oligonucleotide restores WAT integrity and metabolic health in aged mice. These findings pinpoint IgG as a hidden culprit in aging and enlighten a novel strategy to rejuvenate metabolic health.

Abhd2, a Candidate Gene Regulating Airway Remodeling in COPD via TGF-ß.

Purpose: The typical characteristic of COPD is airway remodeling, affected by environmental and genetic factors. However, genetic studies on COPD have been limited. Currently, the Abhd2 gene is found to play a critical role in maintaining alveolar architecture and stability. The research aims to investigate the predictive value of Abhd2 for airway remodeling in COPD and its effect on TGF-ß regulation. Methods: In humans, Abhd2 protein was obtained from peripheral blood monocytes. Peripheral blood TGF-ß, pulmonary surfactant proteins (SPs), metalloproteinases, inflammatory indicators (WBC, NEU, NLR, EOS, CRP, PCT, D-Dimer), chest CT (airway diameter and airway wall thickness), pulmonary function, and blood gas analysis were used to assess airway remodeling. In animals, Abhd2 deficient mice (Abhd2Gt/Gt) using gene trapping and C57BL6 mice were injected intraperitoneally with CSE to construct COPD models. HE staining, Masson staining and immunohistochemistry were used to observe the pathological changes of airway in mice, and RT-PCR, WB, ELISA and immunofluorescence were used to detect the expression of secreted proteins and EMT markers. Results: COPD patients with worse pulmonary function and higher airway remodeling-related inflammatory factors had lower Abhd2 protein expression. Moreover, indicators followed the same trend for COPD patients grouped by prognosis (Group A vs Group B). Serum TGF-ß was negatively correlated with Abhd2 protein expression, FEV1/FVC, FEV1, and FEV1% PRED. In mice, Abhd2 depletion promoted deposition of TGF-ß, leading to more pronounced emphysema, airway thickening, increased alveolar macrophage infiltration, decreased AECII number and SPs, and EMT phenomenon. Conclusion: Downregulation of Abhd2 can promote airway remodeling in COPD by modulating repair after injury and EMT via TGF-ß. This study suggests that Abhd2 may serve as a biomarker for assessing airway remodeling and guiding prognosis in COPD.

Genomic analysis and biomarker discovery of thymic cancer based on whole exome sequencing: A retrospective cohort study / 中国胸心血管外科临床杂志

@#Objective To examined gene mutations in thymic carcinoma (TC) patients and to explore prognostic correlates and potential targets for therapy. Methods We retrospectively included TC patients in Sichuan Cancer Hospital between January 2015 and Febuary 2021.Whole-exome sequencing was performed on tumor tissues from TC patients and their control peripheral blood samples, and the raw data were subjected to bioinformatics analysis and statistical analysis. Results We finally included 24 TC patients with 16 males and 8 females at a median age of 55 (42-74) years. The highest frequency of single nucleotide mutations in this cohort were in the TTN gene (42%), HSPG2 (29%), and OBSCN (29%). Higher frequency of copy number variations occurred in ZNF276 gene (54%, loss), BEND3 (50%, loss), DHODH (50%, loss), and VAC14 (50%, loss). Microsatellite instability (MSI) phenotype was found in 25% of the patients, and the mean tumor mutation burden (TMB) was 9.86. Conclusion This study is the first comprehensive analysis of the mutation profile of thymic carcinoma in China to date. The mutation frequencies of TTN, OBSCN, and ZNF276 genes were high. The biomarker analysis suggests that patients may benefit from immunotherapy and have a long effective survival.

Nuclear factor-KB signaling pathway and gender differences in alcoholic liver fibrosis / 解剖学报

Objective To investigate the relationship between nuclear factor(NF)-κB signaling pathway and gender differences in alcoholic liver fibrosis. Methods C57BL/6 N mice at 7-8 weeks of age were randomly divided into: male normal group, male model group, female normal group and female model group of 20 mice each. The normal group was fed with control liquid diet for 8 weeks, and the model group was fed with alcoholic liquid diet for 8 weeks combined with 31.5% ethanol gavage (5g/kg twice a week) to establish an alcoholic liver fibrosis model. The mice were executed at the end of 8 weekends, and the alanine aminotransferase (ALT), aspartate aminotransferase (AST) activity, estradiol (E

Recent progress of targeting Nrf2-ferroptosis to treat brain injury after ischemic stroke / 中国临床药理学与治疗学

Emerging evidences suggest that ferroptosis plays a vital role in the pathophysiological process of brain injury after Ischemic stroke. Accumulating evidence supports pharmacological inhibition of ferroptosis as a therapeutic target for brain injury after Ischemic stroke through activating nuclear factor erythroid 2-related factor 2 (Nrf2), which transcriptionally controls many key components of the ferroptosis pathway. In this review, briefly describe ferroptosis processes and the roles they play in contributing to brain injury after ischemic stroke in the brain. We then provide a critical overview of the relationship between Nrf2 signalling and ferroptosis. With a focus on discuss how therapeutic modulation of the Nrf2 pathway is a viable strategy to explore in the treatment of ferroptosis-driven brain injury after Ischemic stroke.

Targeting ferroptosis for treatment of Alzheimer' s disease / 中国药理学通报

Alzheimer' s disease (AD) is a progressive neurodegenerative disorder histologically characterized by the presence of senile plaques and neurofibrillary tangles (NFTs) found in and around pyramidal neurons in cortical tissue. Mounting evidence suggests regional increased iron load and dyshomeostasis have been associated with oxidative stress, oxidation of proteins and lipids, and cell death, and appears to be a risk factor for more rapid cognitive decline, thereby involved in multiple aspects of the pathophysiology of AD. Ferroptosis is a newly identified iron-dependent lipid peroxidation-driven cell death and emerging evidences have demonstrated the involvement of ferroptosis in the pathological process of AD. Notably, some novel compounds targeting ferroptosis can relieve AD-related pathological symptoms in AD cells and animal model and exhibit potential clinical benefits in AD patients. This review systematically summarizes the growing molecular and clinical evidence implicating ferroptosis in the pathogenesis of AD, and then reviews the application of ferroptosis inhibitors in mouse/cell models to provide valuable information for future treatment and prevention of AD.

Research progress of targeted pulmonary vascular endothelial dysfunction in treatment of pulmonary hypertension / 中国药理学通报

Pulmonary hypertension (PH) is a progressive and fatal disease. The dysfunction of pulmonary artery endothelial cells (PAECs) is one of its important pathogenic factors. PAECs are monolayer flat epithelial cells, which play an important role in maintaining pulmonary vascular homeostasis. Studies have found that PAECs show damage and apoptosis at the early stage of PH development, while PAECs show anti-apoptotic characteristics at the late stage of PH development. The transition of PAECs into mesenchymal cells induced by hypoxic and inflammatory factors is also involved in the pathogenesis of PH. Carcinoid metabolism and mitochondrial dysfunction, bone mor- phogenic type 2 receptor mutation, epigenetic changes and inflammation of PAECs are the main pathogenesis of pulmonary vascular endothelial dysfunction in PH patients. New therapeutic measures targeting PAECs dysfunction are expected to play an important role in the treatment of PH in the future.

Functional near infrared imaging of college students on speech fluency tasks in traumatized / 中国学校卫生

Objective@#The study aims to explore the neural mechanism of cognitive differences in college students with posttraumatic stress disorder under verbal fluency task based on functional near infrared spectroscopy (fNIRS), so as to provide neuroimaging support for the evaluation, diagnosis and treatment of posttraumatic stress disorder(PTSD).@*Methods@#Posttaumatic Stress Disorder Checklist Combat(PCL-C) was used to screen the subjects, including 21 students in PTSD group (PCL-C≥38) and 30 students in control group from September to Novenber in 2020. A 53 channel near infrared spectroscopy device was used to collect cerebral blood oxygen signals under the verbal fluency task, and correlation analysis, Mann Whitney U test and independent sample t test were performed on the results.@*Results@#The difference in the total average score of PCL-C Scale between PTSD group and the control group(46.38±6.96，25.57±6.09) was statistically significant ( t=11.33, P <0.05). Correlation analysis showed that Avg-HbO in left dorsolateral prefrontal lobe was negatively correlated with PCL-C Score ( r=-0.37, P <0.05). Mann Whitney U test showed that in the left dorsolateral prefrontal lobe (Ch6), the Avg-HbO change in PTSD group [0.19(-0.09, 0.86)mmol/(L〖KG*7〗·mm)] was significantly lower than the control group [0.79( 0.37 , 1.47)mmol/(L ·mm)] ( Z=2.16, P <0.05), which was statistically significant.@*Conclusions@#The degree of PTSD was negatively correlated with the index of oxygenated hemoglobin in the left dorsolateral prefrontal lobe, and the oxygenated hemoglobin content in the PTSD group was lower than that in the normal group. In the future, fNIRS may be used to collect blood oxygen signals from the left dorsolateral prefrontal lobe in cognitive tasks to provide imaging evidence for the identification of PTSD.

Short-term efficacy of surgical treatment for multiple pulmonary nodules: A retrospective study in a single center / 中国胸心血管外科临床杂志

@#Objective To summarize and analyze the clinical diagnosis, surgical treatment and prognosis of multiple pulmonary nodules (MPNs). Methods The clinical data of lung cancer patients who received surgical treatment in our hospital from 2018 to 2020 were collected. The short-term efficacy of surgical treatment for MPNs was analyzed. Results A total of 97 patients were enrolled, including 30 males and 67 females with an average age of 56.1±10.0 years at onset ill. There were 62 patients with double lesions, 22 patients with three lesions, 4 patients with four lesions, and 9 patients with more than four lesions. A total of 213 lesions were surgically treated, including 88 pure ground-glass nodules, 81 partially solid nodules, and 7 solid nodules. There were 87 simultaneous surgeries and 10 staged surgeries, with an average operation interval of 5.2 months. The pathological combination type included adenocarcinoma-adenocarcinoma in 96 (99.0%) patients, squamous cell carcinoma-squamous cell carcinoma in 1 (1.0%) patient, and no lymph node metastasis was found. The 2-year disease-free survival (DFS) rate was 92.1%, and the overall survival (OS) rate was 100.0%. Univariate analysis showed that high-risk lesion size>2 cm (P=0.316), residual lesions (P=0.782) and pathological combination type (P=0.913) had statistical effect on the 2-year DFS rate. Conclusion MPNs are mainly diagnosed with multiple primary lung cancers, and the pathological combination is mostly adenocarcinoma-adenocarcinoma combination. Imaging examination is of great help to the surgical approach selection, diagnosis and differential diagnosis of MPNs. During the operation, maximal preservation of lung function and complete resection of high-risk nodules should be taken as the principle, and the prognosis is satisfactory.

Progress in diagnosis and treatment of biliary anastomotic stricture after liver transplantation / 器官移植

In recent years, with the development of organ preservation, surgical techniques, perioperative management and immunosuppression regimens, the success rate of liver transplantation and survival rate of the recipients have been significantly enhanced. Liver transplantation has become the optimal treatment for patients with end-stage liver disease. However, biliary complications still commonly occur after liver transplantation, especially biliary anastomotic stricture. Severe biliary anastomotic stricture will not only increase the cost of treatment, but also lead to graft loss and even affect the survival rate of recipients. Therefore, timely diagnosis and treatment of biliary anastomotic stricture play a significant role in improving the survival rate of liver transplant recipients. In this article, the risk factors, clinical symptoms, diagnosis and treatment of biliary anastomotic stricture after liver transplantation were reviewed, aiming to provide novel ideas for the research, diagnosis and treatment of biliary anastomotic stricture after liver transplantation, and further enhance clinical efficacy of liver transplantation and the quality of life of recipients.

Intratumoral delivery of a Tim-3 antibody-encoding oncolytic adenovirus engages an effective antitumor immune response in liver cancer.

BACKGROUND AND PURPOSE: The use of oncolytic viruses as a gene therapy vector is an area of active biomedical research, particularly in the context of cancer treatment. However, the actual therapeutic success of this approach to tumor elimination remains limited. As such, the present study was developed with the goal of simultaneously enhancing the antitumor efficacy of oncolytic viruses and the local immune response by combining the Ad-GD55 oncolytic adenovirus and an antibody specific for the TIM-3 immune checkpoint molecule (α-TIM-3). APPROACH AND KEY RESULTS: The results of Virus and cell-mediated cytotoxicity assay, qPCR, and Western immunoblotting showed that Ad-GD55-α-Tim-3 oncolytic adenovirus is capable of inducing α-TIM-3 expression within hepatoma cells upon infection, and Ad-GD55-α-TIM-3 exhibited inhibitory efficacy superior to that of Ad-GD55 when used to treat these tumor cells together with the induction of enhanced intracellular immunity. In vivo experiments revealed that Ad-GD55-α-TIM-3 administration was sufficient to inhibit tumor growth and engage in a more robust local immune response within the simulated tumor immune microenvironment. CONCLUSION AND IMPLICATIONS: These results highlighted the promising therapeutic effects of Ad-GD55-α-TIM-3 oncolytic adenovirus against HCC in vitro and in vivo. As such, this Ad-GD55-α-TIM-3 oncolytic adenovirus may represent a viable approach to the treatment of hepatocellular carcinoma.

Numerical simulation and experiment of double chamber brake based on CFD.

The artillery firing process will instantly produce high-temperature and high-pressure gunpowder gas, this process will produce shock waves. The gunpowder gas has a limited effect on the projectile during the firing and ballistic after-effects period, however, it has a very obvious effect on the stability of the gun body, and the reduction of the stability of the gun body directly affects the firing accuracy and the safety of the firing personnel. Based on the method of Computational Fluid Dynamics (CFD), numerical simulation is carried out, and the structure and flow parameters of the muzzle flow field are obtained by using three-dimensional Euler's control equation, gas equation of state, and k-epsilon model, as well as dynamic mesh technology. By comparing the flow parameters of the brake before and after optimization, and analyzing the results obtained from the 8-round firing experiments, the efficiency of the optimized brake is increased by 8.2%, and the deviation between the experimental data and the simulation results is only 10.5%, which not only verifies the accuracy of the numerical simulation calculations but also verifies the optimized brake's good retracting effect. The results of the study can provide a reference for the optimization and design of the double-chamber brake.

A glimpse of the connection between PPARγ and macrophage.

Nuclear receptors are ligand-regulated transcription factors that regulate vast cellular activities and serve as an important class of drug targets. Among them, peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor family and have been extensively studied for their roles in metabolism, differentiation, development, and cancer, among others. Recently, there has been considerable interest in understanding and defining the function of PPARs and their agonists in regulating innate and adaptive immune responses and their pharmacological potential in combating chronic inflammatory diseases. In this review, we focus on emerging evidence for the potential role of PPARγ in macrophage biology, which is the prior innate immune executive in metabolic and tissue homeostasis. We also discuss the role of PPARγ as a regulator of macrophage function in inflammatory diseases. Lastly, we discuss the possible application of PPARγ antagonists in metabolic pathologies.

Correlation between the setting of gating window width and setup accuracy in left breast cancer radiotherapy based on deep inspiration breath hold.

Personalized precision irradiation of patients with left-sided breast cancer is possible by examining the setup errors of 3- and 4-mm gated window widths for those treated with deep inspiration breath-hold (DIBH) treatment. An observational study was performed via a retrospective analysis of 250 cone-beam computed tomography (CBCT) images of 60 left-breast cancer patients who underwent whole-breast radiotherapy with the DIBH technique between January 2021 and 2022 at our hospital. Among them, 30 patients had a gated window width of 3 mm, while the remaining 30 had a gated window width of 4 mm; both groups received radiotherapy using DIBH technology. All patients underwent CBCT scans once a week, and the setup errors in the left-right (x-axis), inferior-superior (y-axis), and anterior-posterior (z-axis) directions were recorded. The clinical-to-planning target volume (CTV-PTV) margins of the two gating windows were calculated using established methods. The setup error in the Y direction was 1.69 ± 1.33 mm for the 3-mm - wide gated window and 2.42 ± 3.02 mm for the 4-mm - wide gated window. The two groups had statistically significant differences in the overall mean setup error (Dif 0.7, 95% CI 0.15-1.31, t = 2.48, p= 0.014). The Z-direction setup error was 2.32 ± 2.12 mm for the 3-mm - wide gated window and 3.15 ± 3.34 mm for the 4-mm - wide gated window. The overall mean setup error was statistically significant between the two groups (Dif 0.8, 95% CI 0.13-1.53, t= 2.34, p = 0.020). There was no significant difference in the X-direction setup error (p > 0.05). Therefore, the CTV-PTV margin values for a 3-mm gated window width in the X, Y, and Z directions are 5.51, 5.15, and 7.28 mm, respectively; those for a 4-mm gated window width in the X, Y, and Z directions are 5.52, 8.16, and 10.21 mm, respectively. The setup errors of the 3-mm - wide gating window are smaller than those of the 4-mm - wide gating window in the three dimensions. Therefore, when the patient's respiratory gating window width is reduced, the margin values of CTV-PTV can be reduced to increase the distance between the PTV and the organs at risk (OARs), which ensures adequate space for the dose to decrease, resulting in lower dose exposure to the OARs (heart, lungs, etc.), thus sparing the OARs from further damage. However, some patients with poor pulmonary function or unstable breathing amplitudes must be treated with a slightly larger gating window. Therefore, this study lays a theoretical basis for personalized precision radiotherapy, which can save time and reduce manpower in the delivery of clinical treatment to a certain extent. Another potential benefit of this work is to bring awareness to the potential implications of a slightly larger gating window during treatment without considering the resulting dosimetric impact.

Deciphering the decline of metabolic elasticity in aging and obesity.

Organisms must adapt to fluctuating nutrient availability to maintain energy homeostasis. Here, we term the capacity for such adaptation and restoration "metabolic elasticity" and model it through ad libitum-fasting-refeeding cycles. Metabolic elasticity is achieved by coordinate versatility in gene expression, which we call "gene elasticity." We have developed the gene elasticity score as a systematic method to quantify the elasticity of the transcriptome across metabolically active tissues in mice and non-human primates. Genes involved in lipid and carbohydrate metabolism show high gene elasticity, and their elasticity declines with age, particularly with PPARγ dysregulation in adipose tissue. Synchronizing PPARγ activity with nutrient conditions through feeding-timed agonism optimizes their metabolic benefits and safety. We further broaden the conceptual scope of metabolic and gene elasticity to dietary challenges, revealing declines in diet-induced obesity similar to those in aging. Altogether, our findings provide a dynamic perspective on the dysmetabolic consequences of aging and obesity.

PPARγ Acetylation in Adipocytes Exacerbates BAT Whitening and Worsens Age-Associated Metabolic Dysfunction.

Aging and obesity are the two prominent driving forces of metabolic dysfunction, yet the common underlying mechanisms remain elusive. PPARγ, a central metabolic regulator and primary drug target combatting insulin resistance, is hyperacetylated in both aging and obesity. By employing a unique adipocyte-specific PPARγ acetylation-mimetic mutant knock-in mouse model, namely aKQ, we demonstrate that these mice develop worsened obesity, insulin resistance, dyslipidemia, and glucose intolerance as they age, and these metabolic deregulations are resistant to intervention by intermittent fasting. Interestingly, aKQ mice show a whitening phenotype of brown adipose tissue (BAT) manifested in lipid filling and suppressed BAT markers. Diet-induced obese aKQ mice retain an expected response to thiazolidinedione (TZD) treatment, while BAT function remains impaired. This BAT whitening phenotype persists even with the activation of SirT1 through resveratrol treatment. Moreover, the adverse effect of TZDs on bone loss is exacerbated in aKQ mice and is potentially mediated by their increased Adipsin levels. Our results collectively suggest pathogenic implications of adipocyte PPARγ acetylation, contributing to metabolic dysfunction in aging and thus posing as a potential therapeutic target.

Unraveling the pathophysiology of schizophrenia: insights from structural magnetic resonance imaging studies.

Background: Schizophrenia affects about 1% of the global population. In addition to the complex etiology, linking this illness to genetic, environmental, and neurobiological factors, the dynamic experiences associated with this disease, such as experiences of delusions, hallucinations, disorganized thinking, and abnormal behaviors, limit neurological consensuses regarding mechanisms underlying this disease. Methods: In this study, we recruited 72 patients with schizophrenia and 74 healthy individuals matched by age and sex to investigate the structural brain changes that may serve as prognostic biomarkers, indicating evidence of neural dysfunction underlying schizophrenia and subsequent cognitive and behavioral deficits. We used voxel-based morphometry (VBM) to determine these changes in the three tissue structures: the gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF). For both image processing and statistical analysis, we used statistical parametric mapping (SPM). Results: Our results show that patients with schizophrenia exhibited a significant volume reduction in both GM and WM. In particular, GM volume reductions were more evident in the frontal, temporal, limbic, and parietal lobe, similarly the WM volume reductions were predominantly in the frontal, temporal, and limbic lobe. In addition, patients with schizophrenia demonstrated a significant increase in the CSF volume in the left third and lateral ventricle regions. Conclusion: This VBM study supports existing research showing that schizophrenia is associated with alterations in brain structure, including gray and white matter, and cerebrospinal fluid volume. These findings provide insights into the neurobiology of schizophrenia and may inform the development of more effective diagnostic and therapeutic approaches.