Objective: To explore the setting of gray zone of Treponema pallidum (TP) testing by retrospective analysis of blood donors with single reagent reactive anti-TP results, so as to improve blood utilization and supply safety. Methods: Blood samples were collected from 112 blood donors previously deferred due to single reagent reactive TP antibody results between January 2020 and December 2023, and subjected to dual ELISA reagents and TPPA test. The gray zone panel analysis was performed on the two ELISA reagents currently used in our department. The detection rate at each concentration of the gray zone panle was counted, and the corresponding concentrations for C , C , and C and gray zone cut-off were calculated. Results: Among the 50 samples deferred by reagent 1, 19 were confirmed reactive and 31 non-reactive in supplementary testing. Among the 62 samples deferred by reagent 2, 12 were confirmed reactive and 50 non-reactive in supplementary testing. For reagent 1, the detection rate of was 56% for S/CO≥1 and 20% for 0.5≤S/CO<1, retrospectively. For reagent 2, the detection rate was 27% for S/CO≥1 and 12.5% for 0.5≤S/CO<1, retrospectively. The detection rate for S/CO≥1 was higher than those for 0.5≤S/CO<1 for both reagents. All the 112 samples were negative in TPPA test. The C concentration of reagent 1 was 1.51 mIU/mL, and the concentration range of C ±20% was 1.21-1.81 mIU/mL. The C concentration of reagent 2 was 1.45 mIU/mL, and the concentration range of C ±20% was 1.16-1.74 mIU/mL. The C and C concentration of both reagents were within the C ±20% range, suggesting that the gray zone cutoff for both Reagent 1 and Reagent 2 should be set at S/CO=0.8 (80% of the CO value). Conclusion: All anti-TP single reagent reactive samples with S/CO value within the gray zone was tested negative by TPPA. It is necessary to consider the rationality and necessity of establishing the gray zone, so as to ensure blood safety and improve the utilization rate of blood resources.

Malignant tumors represent a major threat to global health. Conventional anti-tumor pharmacotherapy often encounters challenges such as drug resistance, highlighting an urgent need for the development of novel therapeutic strategies. Fatty acid synthase (FASN), the key enzyme catalyzing de novo fatty acid synthesis, is subject to precise regulation at multiple levels, including transcriptional control, various post-translational modifications such as ubiquitination and phosphorylation, as well as modulation by diverse signaling pathways. Recent studies have revealed that FASN is aberrantly overexpressed in various malignant tumors and is closely associated with tumor progression and poor patient prognosis. FASN is a homodimer composed of seven functional domains that catalyzes the NADPH-dependent condensation of acetyl-CoA and malonyl-CoA to generate saturated fatty acids, primarily palmitic acid. Its stability is regulated by multiple ubiquitin ligases and deubiquitinating enzymes. Additionally, FASN is subject to upstream regulation via neural precursor cell-expressed developmentally downregulated 8 (Nedd8) modification and the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway, thereby establishing a metabolic-signaling positive feedback loop. As a core executor of metabolic reprogramming, FASN promotes tumorigenesis through dual mechanisms. First, its fatty acid synthesis product, palmitate, participates in membrane phospholipid synthesis, lipid raft formation, and protein palmitoylation, thereby activating several key oncogenic signaling pathways, including PI3K/AKT/mTOR, wingless-type MMTV integration site family member (Wnt)/β‑catenin, and signal transducer and activator of transcription 3 (STAT3)/matrix metalloproteinase (MMP), leading to tumor development and progression. Second, FASN plays a pivotal role in modulating the anti-tumor functions of immune cells and remodeling the tumor immune microenvironment. Specifically, FASN enhances immune checkpoint inhibition by inducing programmed death-ligand 1 (PD-L1) palmitoylation, suppresses the activation of cytotoxic T lymphocytes and natural killer cells, and promotes the polarization of M2-type macrophages, consequently facilitating tumor immune evasion and malignant progression. Precisely due to its significant overexpression in tumor cells, its critical functional role, and its differential expression compared to normal cells, FASN has emerged as a highly promising target for anti-tumor drug development. Highly selective small-molecule inhibitors, notably represented by TVB-2640, have advanced to clinical trial stages and demonstrated favorable anti-tumor activity. Furthermore, the combination of FASN inhibitors with other chemotherapeutic agents or targeted drugs can overcome the limitations of monotherapy through synergistic effects or by resensitizing tumor cells to conventional drugs, achieving a “1+1>2” therapeutic outcome. With the advancement of modern traditional Chinese medicine (TCM), numerous active ingredients derived from TCM have been confirmed to exert anti-tumor effects by modulating FASN-related pathways. This integrated approach leverages the precision of Western medicine while simultaneously harnessing the holistic regulatory benefits of TCM to alleviate the side effects of radiotherapy and chemotherapy. Despite the promising prospects of FASN-targeted therapies, challenges remain, including tumor cell metabolic plasticity, tumor context-dependent responses, and heterogeneity. This review systematically summarizes the molecular structure, physiological functions, and mechanisms of FASN in tumorigenesis, as well as recent advances in targeted therapies. Future directions—including the precise identification of responsive patient populations using spatial transcriptomics, the development of novel combination regimens, and the active exploration of integrative strategies combining traditional Chinese and Western medicine—will facilitate the clinical translation of FASN-targeted therapies and open new avenues for improving the quality of life and prognosis of cancer patients.

Objective: To analyze the status of Treponema pallidum (TP) infection among blood donors in Hefei area by evaluating anti-TP reactive donors, and to provide data support for blood screening strategies, evaluation of reagent application, and public health prevention and control strategies. Methods: TPPA confirmation test were performed on 338 anti-TP positive samples of voluntary blood donors at Anhui Blood Center from February to April 2022, July to October 2022, February to June 2023. RPR tests were conducted on samples positive for TPPA. The test results, co-reactivity of TP with HBV, HCV, and HIV, and demographic characteristics of the donors were statistically analyzed. Results: The unqualified rate of anti-TP among blood donors in Hefei area was 0.30% (405/133 587), and the positive rate for TPPA was 67.46% (228/338). Among the TPPA-positive donors, 31.67% were RPR-positive. The co-positive rates of HBV, HCV and HIV in anti-TP reactive blood donors were 0.74% (3/405), 0.49% (2/405), and 1.73% (7/405), respectively, with HIV copositivity being the most common. Most co-positive donors were males aged 31-50 years with a high school education or lower, and all were first-time whole blood donors. Conclusion: The anti-TP unqualified rate among blood donors in Hefei area is at a low-to-mederate level. HIV is the most common co-infection with TP among anti-TP positive donors. The majority of co-infected donors are middle-aged men donating whole blood for the first time.

Background: and Purpose Live cell-based assays (LCBA) are increasingly used for serological antibody detection due to their ability to preserve antigen conformation, offering moderately higher sensitivity than fixed cell-based assays. However, the clinical necessity of prioritizing LCBA for the detection of aquaporin-4 immunoglobulin G (AQP4-IgG) in neuromyelitis optica spectrum disorder (NMOSD) remains unclear, especially when compared to its established role in diagnosing myelin oligodendrocyte glycoprotein antibody-associated disease. Methods: We compared the performance of live cell-based assays using immunofluorescence (LCBA-IF) and fixed cell-based assays using immunofluorescence (FCBA-IF) in detecting AQP4-IgG in 90 cases of NMOSD meeting 2015 International Panel for Neuromyelitis Optica Diagnosis criteria, alongside 40 controls. Additionally, we further investigated the relationship between AQP4-IgG titers as measured by LCBA-IF and FCBA-IF and clinical parameters in NMOSD patients. Results: Results showed 96.9% agreement between LCBA-IF and FCBA-IF (Cohen’s κ=0.935), with a strong Spearman correlation (0.977, p<0.001). Both methods demonstrated 100% specificity, with LCBA-IF showing slightly higher sensitivity compared to FCBA-IF. Within LCBAIF-tested groups, statistically significant differences in annualized relapse rates were observed across all pairwise comparisons (low-titer vs. moderate-titer, low-titer vs. high-titer, and moderate-titer vs. high-titer; all p<0.050). However, this association reached statistical significance in some FCBA-IF-tested groups. Conclusions Overall, there is a strong concordance between LCBA-IF and FCBA-IF in detecting AQP4-IgG, where LCBA-IF shows slightly higher sensitivity. Furthermore, there is a potential link between elevated AQP4-IgG titers and an increased risk of relapse, and this correlation may appear more pronounced when using LCBA-IF.

Alzheimer’s disease (AD) is a central neurodegenerative disease characterized by progressive cognitive decline and memory impairment in clinical. Currently, there are no effective treatments for AD. In recent years, a variety of therapeutic approaches from different perspectives have been explored to treat AD. Although the drug therapies targeted at the clearance of amyloid β-protein (Aβ) had made a breakthrough in clinical trials, there were associated with adverse events. Neuroinflammation plays a crucial role in the onset and progression of AD. Continuous neuroinflammatory was considered to be the third major pathological feature of AD, which could promote the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles. At the same time, these toxic substances could accelerate the development of neuroinflammation, form a vicious cycle, and exacerbate disease progression. Reducing neuroinflammation could break the feedback loop pattern between neuroinflammation, Aβ plaque deposition and Tau tangles, which might be an effective therapeutic strategy for treating AD. Traditional Chinese herbs such as Polygonum multiflorum and Curcuma were utilized in the treatment of AD due to their ability to mitigate neuroinflammation. Non-steroidal anti-inflammatory drugs such as ibuprofen and indomethacin had been shown to reduce the level of inflammasomes in the body, and taking these drugs was associated with a low incidence of AD. Biosynthetic nanomaterials loaded with oxytocin were demonstrated to have the capability to anti-inflammatory and penetrate the blood-brain barrier effectively, and they played an anti-inflammatory role via sustained-releasing oxytocin in the brain. Transplantation of mesenchymal stem cells could reduce neuroinflammation and inhibit the activation of microglia. The secretion of mesenchymal stem cells could not only improve neuroinflammation, but also exert a multi-target comprehensive therapeutic effect, making it potentially more suitable for the treatment of AD. Enhancing the level of TREM2 in microglial cells using gene editing technologies, or application of TREM2 antibodies such as Ab-T1, hT2AB could improve microglial cell function and reduce the level of neuroinflammation, which might be a potential treatment for AD. Probiotic therapy, fecal flora transplantation, antibiotic therapy, and dietary intervention could reshape the composition of the gut microbiota and alleviate neuroinflammation through the gut-brain axis. However, the drugs of sodium oligomannose remain controversial. Both exercise intervention and electromagnetic intervention had the potential to attenuate neuroinflammation, thereby delaying AD process. This article focuses on the role of drug therapy, gene therapy, stem cell therapy, gut microbiota therapy, exercise intervention, and brain stimulation in improving neuroinflammation in recent years, aiming to provide a novel insight for the treatment of AD by intervening neuroinflammation in the future.

Acute respiratory distress syndrome(ARDS)is a common respiratory emergency,but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures.Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS,but the application of hydrogen has flammable and explosive safety concerns.Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance,thus improving ARDS in patients and animal models.Coral calcium hydrogenation(CCH)is a new solid molecular hydrogen carrier prepared from coral calcium(CC).Whether and how CCH affects acute lung injury in ARDS re-mains unstudied.In this study,we observed the therapeutic effect of CCH on lipopolysaccharide(LPS)induced acute lung injury in ARDS mice.The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable,demonstrating a significant improvement compared to the untreated ARDS model group.CCH treatment significantly reduced pulmonary hemorrhage and edema,and improved pulmonary function and local microcirculation in ARDS mice.CCH promoted mitochon-drial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2(Trx2),improved lung mitochondrial dysfunction induced by LPS,and reduced oxidative stress damage.The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

Objective:To explore the diagnostic value of a clinical-radiomics model based on the T 1 mapping and apparent diffusion coefficient (ADC)-based radiomics, and the clinical indicator for renal fibrosis (RF) caused by chronic kidney disease (CKD). Methods:This cross-sectional study prospectively and consecutively enrolled 122 patients with CKD at the Second Affiliated Hospital of Soochow University from September 2021 to December 2023 who were randomly allocated to a training set ( n=85) or a validation set ( n=37) in an approximate 7∶3 ratio using simple random sampling. Patients underwent T 1 mapping and diffusion-weighted imaging scans. Renal biopsy was performed within 3 days after the MRI scans. Patients were categorized into three groups based on the degree of RF: no RF ( n=25), mild RF ( n=55), and moderate to severe RF ( n=42). To differentiate the presence of RF (no RF vs. any RF) and the severity of RF (mild RF vs. moderate to severe RF), univariate and multivariate logistic regression were used to optimize the independent clinical predictor, which constituted the clinical model. Radiomics features were extracted from regions of interest delineated within the renal parenchyma of the right kidney on T 1 mapping and ADC maps. Features were selected using least absolute shrinkage and selection operator regression to build the radiomics model. A clinical-radiomics model was subsequently constructed by integrating the independent clinical predictors with the selected radiomics features. Model diagnostic performance was evaluated using the area under the receiver operating characteristic curve (AUC). Calibration curve was plotted to assess model calibration, and decision curve analysis was performed to evaluate clinical net benefit. Results:Univariate logistic regression analysis revealed that estimated glomerular filtration rate (eGFR), serum creatinine, and blood urea nitrogen exhibited statistically significant differences ( P0.05) in distinguishing both the presence and severity of RF. Multivariate analysis identified eGFR as an independent clinical predictor for both the presence of RF ( OR=0.939, 95% CI 0.898-0.982, P=0.006) and RF severity ( OR=0.956, 95% CI 0.917-0.997, P=0.037). From the MRI images, 7 radiomics features were selected to build the radiomics model for distinguishing the presence of RF, and 8 features were selected for the model assessing RF severity. These radiomics models were then combined with eGFR to construct the clinical-radiomics models. The clinical-radiomics models demonstrated the highest diagnostic performance, with an AUC of 0.935 (95% CI 0.859-0.977) for RF presence and 0.967 (95% CI 0.891-0.995) for RF severity in the training set, and 0.914 (95% CI 0.774-0.981) and 0.908 (95% CI 0.748-0.981) in the validation set. Calibration curves and decision curve analysis confirmed that the clinical-radiomics models exhibited excellent calibration and provided the highest clinical net benefit for assessing RF in CKD patients. Conclusion:The clinical-radiomics model integrating T 1 mapping and ADC-based radiomics and eGFR can effectively improve the diagnostic performance for RF in CKD patients.

Objective To investigate the risk factors of hemodynamic instability after carotid artery stenting by meta-analysis.Methods Ten databases were searched:PubMed,ProQuest,ScienceDirect,Embase,Cochrane Library,Web of Science,China Knowledge Network,Wanfang Data,VIP Information Database,and China Biomedical Database.The search date was from inception until 2 February 2024,and meta-analysis was performed using Stata 16.0 statistical software.Results A total of 27 studies with 4199 subjects and 22 influencing factors were included.The studies showed a 37.4％(95％CI 30.3％-44.8％)incidence of haemodynamic instability after carotid stenting,Meta-analysis determined that age＞60 years(P＜0.001),hypertension(P＜0.001),calcified plaque(P＜0.001),stenosis＞70％(P=0.008),eccentric plaque(P=0.002),distance from the largest stenosis to the carotid bifurcation≤ 10 mm(P＜0.001),stenosis involvement of the balloon or bifurcation(P＜0.001),balloon post-dilation(P=0.003),open-loop stenting(P＜0.001),dilated balloon diameter≥5 mm(P=0.002),repeat balloon dilation(P=0.011)and balloon dilation pressure≥8 atm(P＜0.001)are risk factors for intraoperative and postoperative haemodynamic instability in patients undergoing carotid artery stenting surgery.Statin use was a protective factor(P＜0.001).Conclusions Medical staff working in the clinic should assess the patient's condition preoperatively,identify risk factors that may lead to haemodynamic instability,and avoid unnecessary intraoperative stimulation of patients who are already in a high-risk state.Reduce postoperative clinical complications in patients with carotid artery stenosis and improve patient recovery.

AIM To study the chemical constituents from Euphorbia humifusa Willd.and their in vitro anti-hepatoma activity.METHODS Silica gel,D101 macroporous adsorption resin and semi-preparative RP-HPLC were used for isolated and purified,then the structures of obtained compounds were identified by physicochemical properties and spectral data.The anti-hepatocellular carcinoma activity was determined by MTT mothod.RESULTS Eighteen compounds were isolated and identified as 22-O-angeloyl-R1-barrigenol(1),dimethyl 3,3'-[oxybis(4,1-phenylene)](2E,2'E)-diacrylate(2),N-(3-methoxy-1,3-dioxopropyl)-D-tryptophan methyl ester(3),N-acetyltryptophan methyl ester(4),N-(methoxycarbonyl)-tryptophan methyl ester(5),(3β,5α,17β)-4,4,8,14-tetramethyl-18-norandrostane-3,17-diol(6),3β,18,19β-trihydroxylupane(7),pregnenolone(8),3-hydroxy-5,6-epoxy-7-megastigmen-9-one(9),dehydrovomifoliol(10),loliolide(11),2,2'-oxybis(1,4-di-tert-butylbenzene)(12),dibutyl phthalate(13),4-methoxycinnamic acid(14),3,4-dimethoxycinnamic acid(15),methyl 4-hydroxybenzoate(16),kaempferol(17),quercetin(18).The IC50 values of compounds 1,7 and 8 on HepG2 cells were(17.27±0.92),(19.11±2.14)and(7.53±1.09)μmol/L,respectively.CONCLUSION Compounds 1-16 are first isolated from this plant.Compounds 1,7 and 8 have anti-hepatoma activity.

Objective To investigate the causal relationship between abnormal placental lipid metabolism and trophoblast dysfunction in patients with preeclampsia(PE),and to explore the regulatory effects of PPARγ on trophoblast function under hypoxic conditions.Methods Placental tissues were collected from 30 patients with PE and 30 individuals with normal pregnancies at the General Hospital of Ningxia Medical University between October 2020 and November 2021 for the analysis of lipid deposition.A rat model of PE was established,comprising a sham-operated(Sham)group and a reduced uterine perfusion pressure(Rupp)group,with six rats in each group(n=12 total).Human trophoblast cells(HTR-8/SVneo)were cultured in vitro and randomly assigned to four experimental groups:normoxic control,hypoxia,hypoxia+PPARγ agonist(Rosiglitazone),and hypoxia+PPARγ antagonist(T0070907).The expression levels of lipid metabolism-related genes and transcription factors(FASN,FABP4,PPARγ,LXRα)were assessed using RT-qPCR.Western blotting was performed to determine the protein expression levels of PPARγ.Cell migration and invasion capacities were evaluated using scratch wound healing and Transwell assays,respectively.Results Placental lipid deposition in the PE group was significantly higher than that in the control group,particularly in the Rupp model mice(P<0.001).Under hypoxic conditions,the expression levels of FASN and FABP4 were upregulated in trophoblast cells(P<0.001),whereas the expression of PPARγ and LXRα was downregulated(P<0.001).Furthermore,treatment with the PPARγ antagonist T0070907 exacerbated the inhibitory effects of hypoxia on cell function(P<0.001),significantly reducing cell invasion and migration capacity(P<0.001).Additional siRNA-mediated knockdown experiments confirmed that PPARγ deficiency further aggravated hypoxia-induced impairments in cell migration and invasion,and this detrimental effect could not be reversed by Rosiglitazone.Conclusions Abnormal placental lipid metabolism in PE is closely linked to PPARγ-mediated enhancement of lipid synthesis and metabolic dysregulation under hypoxic conditions,which may subsequently impair trophoblast invasion and migration.