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Enhancement of Microglial Phagocytosis by Scaffold Protein PDLIM5 and Its Role in Multiple Sclerosis
Abstract：ObjectiveTo investigate the expression of scaffold protein PDLIM5 in multiple sclerosis （MS） patients and the mouse microglial cell line BV2， and to explore its effects on the phagocytosis of microglial cells.MethodsPeripheral blood samples were collected from 24 MS patients and 6 healthy volunteers as controls. The expression levels of PDLIM5 were detected by real-time quantitative PCR. A neuroinflammation cell model was established by treating the mouse microglial cell line BV2 with lipopolysaccharide （LPS， 1 µg/mL）. The expression levels of PDLIM5 were measured by Western Blot. The effect of PDLIM5 expression on phagocytosis was analyzed by transfecting BV2 cells with PDLIM5 shRNA plasmids or PDLIM5 overexpression plasmids.ResultsReal-time quantitative PCR results showed that compared with the healthy control group， the expression level of PDLIM5 from the MS patients was significantly increased in monocytes ［2.78 （0.70-6.86） vs. 0.54 （0.39-1.51）， P=0.036］ and lymphocytes ［1.62 （0.90-2.26） vs. 0.11 （0.05-0.21）， P<0.001］. Western Blot results indicated that PDLIM5 expression was significantly upregulated in BV2 cells following LPS stimulation （P<0.05）. Plasmid transfection experiments demonstrated that knockdown of PDLIM5 inhibited the phagocytic capacity of BV2 cells as measured by trypan blue uptake （P<0.05）， while overexpression of PDLIM5 enhanced the phagocytic ability of BV2 cells （P<0.001）.ConclusionUnder neuroinflammatory conditions， PDLIM5 expression is elevated， and this upregulation promotes the phagocytosis of microglial cell.Keywords：PDLIM5;multiple sclerosis;microglia;phagocytosis;neuroinflammation283|369|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20- Abstract：ObjectiveTo explore the effects of astragalin （AST） on autophagy and apoptosis of astrocytes in the L4-5 dorsal horn of the spinal cord in mice with inflammatory pain induced by complete Freund's adjuvant （CFA）.MethodsTwenty-four male C57BL/6 mice， aged six months， were randomly assigned to four groups： control group， saline group， CFA model group， and CFA+AST group， six mice in each group. The inflammatory pain model was established by injection of 10 µL CFA into the right lateral malleolus fossa. The saline group were injected with an equal amount of normal saline at the same site. The inflammatory pain mice in CFA+AST group were further treated with AST （60 mg/kg） intraperitoneally once a day for 21 consecutive days. Multiplex immunofluorescence staining was used to detect the coexpression of autophagy-related factors including ATG 12 and Beclin-1， apoptosis-related factors including Cleaved-Caspase3 and Caspase9， and the astrocyte marker such as GFAP in the L4-5 spinal dorsal horn of the mice in each group. Western blot was used to examine the protein expression levels of autophagy-related proteins（ATG12， Beclin-1） and apoptosis-related proteins（Caspase 3， Caspase 9） in the L4-5 spinal dorsal horn of mice.ResultsImmunofluorescent staining showed that in the L4-5 dorsal horn of the spinal cord， the fluorescence intensity of ATG12 （P<0.000 1） and Beclin-1 （P<0.000 1） was significantly increased， while that of Cleaved-Caspase 3 （P<0.001） and Caspase 9 （P<0.000 1） was decreased in the CFA+AST group when compared to the CFA model group. Furthermore， AST could inhibit the activation of astrocytes. Western blot further confirmed that AST significantly upregulated the expression of ATG12 （P<0.000 1） and Beclin-1 （P<0.000 1） in the L4-5 spinal cord of CFA mice， and downregulated the expression of Caspase 3 （P<0.01） and Caspase 9 （P<0.001）.ConclusionsAST promotes autophagy of astrocytes and inhibits their apoptosis in the L4-5 spinal dorsal horn of CFA mice.Keywords：astragalin;inflammatory pain;spinal dorsal horn;astrocytes;autophagy;apoptosis293|200|103<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：Chronic pain patients often experience varying degrees of negative emotions， such as anxiety and depression， and the persistent presence of these negative emotions may further exacerbate chronic pain. When treating chronic pain， improving either aspect of pain or negative emotions， the other symptom will also be alleviated. The brain regions involved in chronic pain and negative emotions partially overlap and share similar neurophysiological mechanisms， which may be one of the important reasons for their interaction. Multiple brain regions play synergistic roles in pain-related emotional， cognitive， and motivational processing， especially brain regions such as the amygdala， prefrontal cortex， nucleus accumbens， and ventral tegmental area in the cerebral cortex-limbic system， which are critical for the recognition and processing of emotional information. Currently， the clinical treatment of chronic pain remains challenging， especially the limitations of existing pharmacologic treatments. Therefore， benign regulation of negative emotions occupies an important place in the treatment of chronic pain as one of the important intervention targets. In this paper， on the basis of summarizing the neural mechanisms that generate negative emotions in chronic pain， a variety of current therapeutic options for chronic pain related negative emotions are summarize and organized， including pharmacotherapy， non-invasive neuromodulation， psychotherapy， and acupuncture. The combined application of these options not only helps to alleviate patients' negative emotions， but also provides more precise therapeutic targets and more effective strategies for future research. The aim of this article is to deepen beginners' understanding of the background of chronic pain pathophysiology and to provide a reference for clinical practice and research.Keywords：chronic pain;negative emotions;pharmacotherapy;non-invasive neuromodulation;psychotherapy;acupuncture490|7647|4<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：Alzheimer’s disease （AD） is a neurodegenerative disorder associated with aging， characterized by neurofibrillary tangles， accumulation of amyloid-β （Aβ） plaques， and neuronal death. These pathological changes lead to a gradual decline in cognitive function， ultimately impairing the ability to perform daily activities. Currently， treatment options for AD are limited， with pharmacological interventions often being ineffective and frequently accompanied by side effects. Therefore， the study of non-pharmacological therapies， especially nutritional interventions， has become particularly important. Omega-3 polyunsaturated fatty acids （ω-3PUFAs） are essential fatty acids crucial for health， primarily found in fish oil and certain plant oils. They play a key role in anti-inflammatory， antioxidant， neuroprotective， and immunomodulatory activities. Epidemiological evidence and clinical trials have shown that supplementation with ω-3PUFAs is associated with improved cognitive function， with particularly positive effects demonstrated in the use of docosahexaenoic acid （DHA） and eicosapentaenoic acid （EPA）. This article reviews the role of ω-3PUFAs in AD and the latest advances in their mechanism of action， with a particular focus on their ability to reduce brain Aβ deposition and Tau protein phosphorylation， inhibit oxidative stress and neuroinflammation， maintain the integrity of the blood-brain barrier， and regulate energy metabolism. However， current research findings remain inconsistent， especially regarding the significant differences in effects among individuals with different genotypes. Therefore， future studies need to further explore the role of ω-3PUFAs in early intervention and optimize their dosage and formulations to achieve the best neuroprotective effects. Additionally， this article provides dietary recommendations and dosage suggestions based on existing research， hoping to offer new directions for the prevention and treatment of AD.Keywords：Alzheimer's disease;omega-3 polyunsaturated fatty acids;neuroprotection;cognitive function;non-pharmacological treatment387|2461|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：Vascular dementia （VD） is a chronic progressive cognitive impairment caused by cerebrovascular diseases. Its pathogenesis is complex， primarily involving brain tissue damage due to factors such as neuronal apoptosis， oxidative stress response， inflammatory reaction， ferroptosis， and mitochondrial damage. Among these， oxidative stress plays a crucial role in the development of VD. It leads to the accumulation of free radicals， disrupts cellular structures， and is closely related to inflammatory reactions， mitochondrial damage， ferroptosis， and neuronal apoptosis， together forming a complex pathogenic network. In recent years， monomeric compounds from traditional Chinese medicine （TCM） have shown significant therapeutic effects on VD through the regulation of oxidative stress. This article reviews the relevant research progress and explores the mechanisms of oxidative stress in VD. Oxidative stress regulates inflammatory reactions through factors such as Nrf2， NLRP3， and NF-κB； mediates mitochondrial damage by disrupting mitochondrial function and dynamics through excessive reactive oxygen species （ROS）； induces ferroptosis through lipid peroxidation， iron metabolism， and glutathione metabolism； and activates apoptotic proteins via pathways such as protein denaturation， DNA modification， endoplasmic reticulum stress， and death receptors， thereby inducing neuronal apoptosis. Additionally， this article summarizes the therapeutic approaches of TCM monomers in treating VD through the regulation of oxidative stress and its related mechanisms. For example， curcumin reduces ROS levels and enhances antioxidant and anti-inflammatory capacities； gastrodin alleviates mitochondrial damage mediated by oxidative stress， improves energy metabolism， and inhibits ferroptosis； dendrobium polysaccharides mitigate oxidative stress and subsequently inhibit ferroptosis； and triptolide enhances antioxidant capacity， reduces cell apoptosis， and slows the progression of VD. It is hoped that this review will provide insights for future experimental mechanism studies and clinical applications of TCM monomers targeting oxidative stress in the treatment of VD.Keywords：oxidative stress;inflammatory response;mitochondria;ferroptosis;neuronal apoptosis236|1625|2<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
Hot Spot Tracking: Neuromedicine
- Abstract：Copper is a trace element in the human body and is closely related to various signaling pathways and tumor-related biological behaviors. However， when its concentration exceeds the threshold maintained by homeostatic mechanisms， it becomes toxic and triggers cell death. Cuproptosis is a novel form of cell death， distinct from all other known cell death pathways. It occurs through the direct binding of copper to the lipoic acid components of the tricarboxylic acid cycle， leading to the aggregation of lipoic-acylated proteins and the loss of iron-sulfur cluster proteins. This triggers protein toxicity stress， ultimately resulting in cell death. Cuproptosis plays a role in the occurrence， development， and prognosis of digestive tract tumors. Noncoding RNAs （ncRNAs） such as long non-coding RNA （lncRNA）， micro RNA （miRNA） and circular RNA （circRNA） directly or indirectly regulate the expression of cuproptosis-related genes （FDX1，LIPT1，LIAS，DLD，DLAT，PDHA1，PDHB，MTF1，GLS and CDKN2A） in digestive tract tumors based on ceRNA mechanism， thereby inducing copper ion accumulation， driving oxidative stress response， protein fatty acylation and ubiquitin-proteasome system， inhibiting the occurrence and development of digestive tract tumor cells. NcRNAs’ implication in the genesis of tumor cells via regulating cuproptosis-related genes provides a new insight into precision-targeted therapy for tumors. This article introduces cuproptosis， outlines the various regulatory mechanisms of cuproptosis， and provides an overview of ncRNAs and their roles. It reviews recent research on ncRNAs involved in regulating cuproptosis in digestive tract tumors such as esophageal squamous cell carcinoma， gastric cancer， hepatocellular carcinoma， colorectal carcinoma， pancreatic cancer， along with their molecular mechanisms. The article also presents clinical perspectives， aiming to provide a theoretical basis for the diagnosis and treatment of digestive tract tumors.Keywords：cuproptosis;non-coding RNAs;digestive tract tumors;signal axis;review332|1190|1<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：External counterpulsation （ECP） technology represents a non-invasive adjunctive circulation treatment approach implemented in clinical practice since 1962， initially focused on managing cardio-cerebrovascular diseases. Over the past four decades， continuous research and advancements in medical technology have facilitated the evolution of enhanced external counterpulsation （EECP）. This therapeutic modality can enhance the function of vascular endothelial cells， promote blood circulation， and improve metabolism by increasing organ perfusion pressure and blood flow. Given its demonstrated safety， efficacy， and cost-effectiveness， EECP has not only played a significant role in the clinical treatment of cardio-cerebrovascular diseases but also expanded into diverse domains， including andrology， which provides new therapeutic avenues for various health concerns. Particularly in the treatment of male erectile dysfunction （ED）， EECP has shown remarkable potential， and certain clinical practice experience and scientific research results are accumulated. Research indicates that the occurrence of ED is closely associated with endothelial dysfunction and microcirculatory issues. EECP has been shown to effectively alleviate symptoms in ED patients and improve treatment outcomes by optimizing endothelial function and overall systemic health.This article reviews relevant findings from both domestic and international sources， summarizing the current research on the application of EECP in treating andrological diseases. It focuses on analyzing its clinical effects and mechanisms in treating ED and explores potential applications in other male urological conditions. Additionally， this paper discusses the limitations of current research and offers insights into future research directions to provide a more robust scientific basis and references for the use of EECP in managing andrological diseases.Keywords：enhanced external counterpulsation;andrology;erectile dysfunction;vascular endothelial cell260|1460|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：Oral leukoplakia is a potentially malignant mucosal disease with a high incidence rate. Macrophages play a significant regulatory role in the malignant transformation of oral leukoplakia， yet there is a lack of research on the molecular mechanisms underlying this process. Recent studies have found that M2 polarization of macrophages has a significant impact on the malignant transformation of oral leukoplakia， and this process is regulated by a complex network involving immune cells， microorganisms， cytokines， and the extracellular matrix， etc. Therefore， this article reviews the biological functions， subtypes， and regulatory factors of macrophage polarization in oral leukoplakia. Building on the preliminary research foundation of our group on the relationship between oral intracellular colonizing bacteria and mucosal malignant tumors， it is proposed that oral intracellular colonizing bacteria， such as Porphyromonas gingivalis， may promote the malignant transformation of leukoplakia by inducing a macrophage M2 polarization that leads to an immunosuppressive microenvironment. This perspective explores potential intervention strategies from the angle of macrophage polarization， providing new research directions for the prevention and treatment of oral leukoplakia and oral cancer.Keywords：oral medicine;macrophages;oral leukoplakia;immunoregulation;malignant transformation;polarization236|1475|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：Allergic diseases pose an increasingly significant threat to children's health， with environmental pollutants playing a crucial role. Indoor and outdoor air pollution （such as particulate matter， nitrogen oxides， sulfur oxides， ozone， etc.）， chemical contamination （such as persistent organic pollutants， heavy metals， etc.）， and other environmental exposure factors （such as green spaces， viruses， meteorological conditions， diet， etc.） are all significant risk factors for allergic diseases in children. Particularly during the early life stages from the fetal period to infancy， exposure to environmental pollutants has a profound impact on the development of the immune system and the risk of future allergic diseases in children.It is worth noting that during these early life stages， certain specific dietary components （such as specific fatty acids， microorganisms， vitamins， etc.） and breastfeeding can provide some protection for children， reducing the incidence of allergic diseases. However， the mechanisms by which emerging persistent organic pollutants （such as chlorinated paraffins and perfluoroalkyl substances） interact with allergic diseases in children have not yet been fully elucidated. Additionally， the potential health impacts of green spaces and their components， as well as the relationship between household pet ownership and allergic diseases in children， remain key areas for future research.This article reviews the recent research progress on the correlation between environmental pollutants and allergic diseases in children， analyzes the mechanisms by which different environmental factors affect children's health， and aims to explore the impact of environmental pollutants on children's health in depth. It also provides a scientific basis for the prevention and treatment of allergic diseases in children.Keywords：environmental pollutants;emerging pollutants;allergic diseases;children;environmental exposure270|1436|1<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：Exosomes are small vesicles with a lipid bilayer membrane structure that have applied in precision medicine due to their non-invasive nature， high accessibility， and stability. Exosomes play a crucial role in processes such as tumor metastasis， invasion， and angiogenesis. Gynecological malignancies primarily include cervical cancer， ovarian cancer， and endometrial cancer， and their early diagnosis and treatment have long been a focus of research. As novel biological markers， exosomes exhibit high specificity and can effectively block the occurrence and progression of gynecological malignancies. This article explores the diagnostic and therapeutic applications of exosomes in cervical cancer， ovarian cancer， and endometrial cancer in detail. In cervical cancer， exosomes are involved in processes such as HPV infection， angiogenesis， and immune evasion， with specific miRNAs （such as miR-30d-5p and let-7d-3p） serving as diagnostic markers. Furthermore， exosomes can act as targeted drug delivery vehicles and vaccine development platforms. In ovarian cancer， the miRNAs carried by exosomes （such as miR-21 and the miR-200 family） have reference value for early diagnosis， and exosomes play an important role in chemotherapy resistance and tumor progression. For endometrial cancer， miRNAs in exosomes （such as miR-15a-5p and miR-106b-5p） can serve as biomarkers for early detection. Additionally， this article highlights the challenges faced by exosomes in clinical applications， such as the complexity of isolation and extraction and the identification of cell sources， and emphasizes the necessity for further basic research and clinical trials. This study provides new ideas and methods for the early diagnosis and precision treatment of gynecological malignancies， holding significant theoretical and clinical importance.Keywords：exosomes;gynecological malignancies;cervical cancer;ovarian cancer;endometrial cancer;clinical application232|1184|2<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
Review
- Abstract：ObjectiveTo investigate the regulatory effect and potential mechanisms of isocitrate dehydrogenase 3A （IDH3A） on cardiomyocyte hypertrophy.MethodsThe expression of IDH3A in the myocardium of healthy volunteers （n=10） and patients with heart failure （HF） （n=10）， and in the myocardium of mice subjected to transverse aortic constriction （TAC） surgery and sham operation， as well as in phenylephrine （PE）-induced neonatal rat ventricular cardiomyocytes （NRVCs）， was assessed by real-time quantitative polymerase chain reaction （RT-qPCR） and Western blot assay. The effect of adenovirus-mediated overexpression of IDH3A on the expression of hypertrophy-related genes in PE-induced NRVCs was also evaluated. The effect of IDH3A on NRVCs area was examined by phalloidin staining assay. A mutant of IDH3A with abolished enzymatic activity， IDH3A_D208A， was generated through site-directed mutagenesis. The impact of this IDH3A mutant on the hypertrophic phenotype， ATP and ROS levels in NRVCs was evaluated to investigate whether the regulatory role of IDH3A in cardiomyocyte hypertrophy was dependent on its enzymatic activity. The effect of exogenous α-ketoglutaric acid （AKG） on cardiomyocyte hypertrophy was also detected by Western blot and phalloidin staining assay， respectively.ResultsIDH3A was significantly decreased in the myocardium of HF patients， in the myocardium of TAC-operated mice， and in PE-induced NRVCs （P = 0.005 2，P = 0.026 6，P = 0.041 3 and P = 0.006 6， respectively）. Overexpression of IDH3A markedly suppressed the expression of hypertrophy-related genes and the increase of cell size of PE-induced NRVCs （P < 0.000 1， P = 0.000 1 and P = 0.000 2， respectively）. The ATP and ROS analysis indicated that IDH3A inhibited the increases of ATP and ROS levels in PE-induced NRVCs （P = 0.001 2 and P<0.000 1， respectively）， whereas the enzymatically inactive IDH3A mutant lacked this effect. Exogenous AKG provision could， but overexpression of IDH3A mutant failed to suppress PE-induced NRVCs hypertrophy.ConclusionIDH3A inhibits cardiomyocyte hypertrophy via elevating AKG level， providing scientific evidence for study on IDH3A-based treatment of cardiac hypertrophy.Keywords：cardiac hypertrophy;isocitrate dehydrogenase 3A;α-ketoglutarate;cardiomyocytes;mitochondria217|338|1<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo investigate the effect of blue light on emmetropization in guinea pigs， explore the potential mechanisms and assess its application in myopia prevention and control.MethodsThree-week-old male guinea pigs （n=20） were randomly assigned to the white light group and the blue light group. Refraction and ocular biological parameters were measured every 2 weeks until the experiment ended at week 8. And the 4D-data-independent acquisition （4D-DIA） proteomics technology was used to analyze retina from both the blue light and white light groups， exploring protein composition， expression differences， and biological functions.ResultsAfter 2 weeks， Guinea pigs exposed to white light gradually tended towards emmetropia， showing a statistically significant difference in refractive error compared to the blue light group （P<0.001）. From week 4， the axial length of the blue light group was significantly shorter than that of the white light group （P<0.05）. Meanwhile， the vitreous chamber length in the blue light group was significantly smaller than that of the white light group from week 2 （P<0.05）. A total of 161 differentially expressed proteins were identified by proteomics technology in the retina， with 98 proteins upregulated and 63 proteins downregulated. These proteins were primarily enriched in biosynthetic pathways such as vesicle transport， redox reaction， niacin and nicotinamide metabolism and NAD+ metabolism.ConclusionsGuinea pigs raised under blue light exhibit hyperopic drift and slowed axial elongation， which slows the procession of emmetropization. Based on the 4D-DIA technology， the differentially expressed proteins between the blue light and white light groups are primarily involved in NAD+ metabolism， niacin and nicotinamide metabolism. Especially in NAD+ salvage synthesis， nicotinamide phosphoribosyl transferase （NAMPT） is upregulated， while sirtuin 2 （SIRT2） is downregulated. It provides new insights into the mechanism of blue light in emmetropization and a theoretical basis for myopia prevention and control.Keywords：blue light;emmetropization;myopia;refractive development;proteomics203|472|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo investigate the demyelination induced by Angiostrongylus cantonensis （AC） infection in the brain of Balb/c mice and analyze the untargeted metabolomic changes in the corpus callosum， aiming to elucidate the underlying mechanisms.MethodsBalb/c mice were randomly assigned to a control group （n=6） and an infection group （n=6）. The infection group was orally administered 30 third-stage larvae of AC， while the control group received an equal volume of saline. Body weight， visual function， and behavioral scores were measured on post-infection 3， 6， 9， 12， 15， 18， and 21 days to assess neurological alterations. After 21 days， brain tissues were harvested for immunofluorescence staining， hematoxylin-eosin （HE） staining， and transmission electron microscopy to examine morphological changes in brain myelin and retina. Metabolomics analysis was performed， and differential metabolites were identified using volcano plots and heatmaps. The distribution of fold changes and bar charts were used to profile the key metabolites. These differential metabolites were then subjected to Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and regulatory network analysis.ResultsOn the 9th day after AC infection， Balb/c mice showed a decline in neurological behavioral scores （P<0.05）. By day 15， visual scores decreased （P<0.05）， and by day 21， significant weight loss （P＜0.001） and mortality were observed. Concurrently， transmission electron microscopy and immunofluorescence staining revealed significant myelin damage in the corpus callosum and a marked reduction in oligodendrocytes （P<0.001）. HE staining showed severe retinal ganglion cell damage. Metabolomic analysis revealed that glycerophospholipids were the most abundant differential metabolites， with steroids and sphingolipids being relatively less abundant. Cholesteryl ester CE （20：2） was significantly upregulated （P<0.001）， while phosphatidylmethanol （18：0_18：1） was significantly downregulated （P<0.01）. KEGG enrichment and regulatory network analyses demonstrated that the differential metabolites were mainly enriched in metabolic pathways like steroid biosynthesis， bile secretion， and cholesterol metabolism， and were involved in key metabolic pathways such as sphingolipid metabolism， neural signal regulation， and glycerophospholipid metabolism.ConclusionsAC infection affects the metabolic state of mice via multiple pathways， modifying the levels of metabolites crucial for myelination and myelin stability. Demyelination may be closely linked to the disruption of these key metabolic pathways， particularly the dysregulation of cholesterol and sphingolipid metabolism， potentially playing a central role in demyelination onset. Furthermore， alterations in phospholipid metabolism and abnormal nerve signaling regulation may exacerbate myelin damage.Keywords：Angiostrongylus cantonensis;metabolomics;demyelination;cholesterol;phospholipids226|258|2<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo explore the incremental cost of central line-associated bloodstream infections （CLABSI） after central venous catheterization （CVC） in critically ill patients in the intensive care unit （ICU）， as well as the main cost of nosocomial infection prevention and control. By comparing these two costs， the medical personnel to pay more attention should CLABSI prevention and control from the perspectives of medical quality and economic benefits， and promote the implementation of prevention and control measures.MethodsCluster sampling was used to select 126 critically ill patients who underwent CVC in the ICU of a tertiary traditional Chinese medicine hospital from January 2021 to December 2023， including 65 cases in the CLABSI group and 61 in the non-CLABSI group. Patients’ data were retrospectively collected from the hospital medical records， including the disease type， gender， age， length of hospital stay， outcome， and hospitalization expenses. The costs of different hand hygiene methods and differing approaches to environmental cleaning and disinfection were analyzed and compared.ResultsThere were significant differences in the length of hospital stay （Z=-5.35， P<0.05） and total hospitalization expenses （Z=-6.79， P<0.05） between the CLABSI and non-CLABSI group. Total hospitalization expenses showed significant differences among patients with different lengths of hospital stay （H=43.01， P<0.05）， with much higher median one in those with 60 or more days of hospital stay than other patients. Greater differences of median total hospitalization expenses were found in males than in females （Z=-3.98， P<0.05）， as well as in patients aged 60-80 years than in patients of other ages （Z=-5.79， P<0.05）.ConclusionsThe occurrence of CLABSI significantly increases the ICU patients’ length of hospital stay and hospitalization expenses. There are differences in the costs of different hand hygiene methods and differing approaches to environmental cleaning and disinfection， but these costs are acceptable compared to the incremental costs directly attributable to CLABSI. Therefore， medical institutions should attach importance to the investment in prevention and control of nosocomial infections such as hand hygiene and environmental cleaning and disinfection， formulate practical， reasonable and feasible plans， and ensure their implementation， in order to avoid nosocomial infections， improve the medical quality， effectively control patients’ length of hospital stay and hospitalization costs， and strive to maintain patient safety.Keywords：intensive care unit;central line-associated bloodstream infections;hospitalization expenses;prevention and control;cost213|333|2<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
Preclinic Research
- Abstract：ObjectiveTo evaluate the application of prostate-specific membrane antigen （PSMA）PET/CT in prostate biopsy screening， and propose effective strategies for prostate biopsy decision making based on PSMA PET/CT detection.MethodsA retrospective analysis was conducted on PSMA PET/CT imaging and clinical pathological data from 155 patients with suspected prostate cancer between January 2020 and December 2023. PRIMARY score was used as the standardized evaluation method for PSMA PET/CT in the diagnosis of prostate cancer. And compared the positive prostate biopsy rates， missed diagnosis rates and biopsy reduction rates were compared regarding different PRIMARY scores. Receiver operating characteristic （ROC） curves were used to analyze prostate-specific antigen （PSA） and its derived parameters and identify the most suitable supplementary screening indicators for combined use with the PRIMARY score.ResultsAmong patients with PRIMARY scores of 1 to 5， the proportions of patients diagnosed with prostate cancer were 15.8% （3/19）， 17.1% （7/41）， 50% （12/24）， 95.2% （20/21） and 98% （49/50）， respectively. Using PRIMARY score of 3-5 as the biopsy screening strategy resulted in a positive prostate biopsy rate of 85.3% and biopsy reduction rate of 38.7%， but a missed diagnosis rate of 11%. PSA density > 0.15 ng/（mL·cm³） was selected as a supplementary screening criterion to detect prostate cancer from patients with PRIMARY scores of 1-2. The combined application of the above two screening criteria reduced the missed diagnosis rate to 2.2%.ConclusionThis study proposes a novel biopsy screening strategy for suspected prostate cancer patients using PSMA PET/CT， that is， a PRIMARY score of 3-5 or a PRIMARY score of 1-2 but PSA density>0.15 ng/（mL·cm³）， which can effectively avoid unnecessary biopsies and significantly reduce the missed diagnosis rate.Keywords：prostate biopsy;prostate cancer;PET/CT;prostate-specific membrane antigen;prostate-specific antigen density208|698|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo explore the value of the Model for End-Stage Liver Disease （MELD） 3.0 in predicting survival outcomes for patients with alcoholic cirrhosis and to establish an effective mortality prediction model.MethodsClinical data of 788 hospitalized patients who were first diagnosed with alcoholic cirrhosis at the Third Affiliated Hospital of Sun Yat-sen University between January 1， 2011 and December 31， 2019 were analyzed. Patients were followed up until December 31， 2023 and divided into survival and mortality groups based on the survival outcomes at 30 days， 90 days， 1 year， and 3 years after admission. The prognostic values of the MELD 3.0， MELD， MELD-Sodium （MELD-Na） for survival in alcoholic cirrhosis patients were assessed and compared by using the receiver operating characteristic （ROC） curve and the area under the curve （AUC）. Additional risk factors associated with mortality in alcoholic cirrhosis patients were identified， and a novel mortality prediction model based on MELD 3.0 was developed.ResultsThe AUC of the MELD 3.0 score in predicting 30-day， 90-day， 1-year， and 3-year survival was 0.823， 0.730， 0.686， and 0.658， respectively， which were superior to those of the MELD-Na （0.802， 0.708， 0.666， and 0.645， respectively） and MELD scores （0.698， 0.668， 0.654， and 0.633， respectively） （all P < 0.05）. MELD 3.0 demonstrated better performance at 30 and 90 days （AVC=0.823，0.730； both P < 0.05） than at 1 year and 3 years （AVC=0.686，0.658； both P < 0.05）. Binary logistic regression combined with LASSO regression indicated that the independent risk factors associated with the 1-year outcome included MELD 3.0， baseline ascites and hepatocellular carcinoma. A survival prediction model was then established with AUC of 0.748， sensitivity of 0.695， and specificity of 0.775.ConclusionsMELD 3.0 has a superior predictive ability for 30-day， 90-day， 1-year， and 3-year survival in patients with alcoholic cirrhosis than MELD-Na and MELD. The prediction model incorporating MELD 3.0， ascites and hepatocellular carcinoma improves the prediction of 1-year survival outcomes for alcoholic cirrhosis patients.Keywords：alcoholic liver disease;prognosis;end-stage liver disease （MELD） 3.0;MELD;MELD-sodium （MELD-Na）170|908|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo clarify the application value of nutritional scoring in patients with sepsis and explore the impact of the modified Nutritional Risk in Critically Ill （mNUTRIC） score on the in-hospital fatality of sepsis patients in the emergency intensive care unit （EICU）.MethodsA retrospective analysis was conducted on the clinical data and laboratory examination results of 436 sepsis patients treated in the EICU of Sun Yat-sen Memorial Hospital of Sun Yat-sen University from January 2021 to May 2024. The patients were divided into survival group （298 cases） and death group （138 cases） according to whether they died or not during hospital treatment， and then compared the two groups’ data. Logistic multi-factor regression analysis was used to analyze the risk factors for in-hospital death and the ROC curve to evaluate the predictive value of each risk factor for the prognosis of sepsis patients.ResultsThe death group exhibited higher Acute Physiology and Chronic Health EvaluationⅡ（APACHE Ⅱ） score， Nutritional Risk Screening 2002 （NRS 2002） score， mNUTRIC score， Sequential Organ Failure Assessment （SOFA） score， Padua Prediction Score for Venous Thromboembolism， the proportions of chronic kidney failure and pneumonia patients， C-reactive protein （CRP） level， lactate concentration and neutrophil count， but lower prognostic nutritional index， cholinesterase level， cholinesterase-albumin ratio and lymphocyte count than the survival group， with statistical significance （all P<0.05）. Logistic regression analysis revealed that the mNUTRIC score ［OR=1.254， 95%CI （1.109，1.417）］， CRP ［OR=1.004， 95%CI （1，1.007）］， and pneumonia ［OR=1.82， 95%CI （1.017， 3.257）］ were independent risk factors for in-hospital death in sepsis patients. ROC curve analysis showed that the area under the curve （AUC） of the mNUTRIC score for predicting in-hospital death in sepsis patients was 0.683 ［95%CI （0.623，0.742）］， with a sensitivity of 83% and a specificity of 49.3%. The AUC for CRP and pneumonia were 0.602 ［95%CI （0.533， 0.671）］， and 0.582 ［95%CI （0.516，0.647）］.ConclusionThe mNUTRIC score is an independent predictive indicator for in-hospital death in sepsis patients in the EICU.Keywords：modified Nutritional Risk in Critically Ill （mNUTRIC） score;sepsis;risk factor;nutrition;prognosis223|643|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo investigate the prognostic role of radiotherapy in women aged 70 years or older with breast cancer.MethodsA total of 311 women aged 70 years or older with breast cancer undergoing breast-conserving surgery in the Second Affiliated Hospital of Nanchang University between February 28， 2011 and February 28， 2021， were divided into two groups： 183 patients in the control group were given postoperative radiotherapy， and 128 patients in the case group were not treated by radiotherapy. The nonparametric Mann-Whitney U test or χ2 test was used to compare the general clinicopathological data of the two groups， the Kaplan-Meier method and log-rank test to analyze the disease-free survival （DFS） and overall survival （OS）， multivariate Cox proportional hazards regression model to examine the factors affecting DFS and OS. Additional subgroup analysis was performed.ResultsThere were no statistically significant differences between the control and case groups in age， T-stage， N-stage， tumor clinical stage， estrogen receptor （ER）， progesterone receptor （PR） and human epidermal growth factor receptor type 2 （HER2） statuses， Ki-67， tumor histological grade， tumor pathological type， and whether they received adjuvant chemotherapy or postoperative endocrine therapy （all P > 0.05）. The median follow-up was 110.0 （95%CI： 98.9， 121.1） months for the control group and 93.0 （95% CI： 86.1， 100.0） months for the case group. Differences between the two groups in DFS rate were significant （92.9% vs. 85.2%， P = 0.024）， but in OS rate insignificant （92.3% vs. 88.3%， P=0.199）. Multivariate Cox proportional hazards regression analysis showed that T-stage， N-stage （N2 and N3）， HER2 status， Ki-67， tumor histological grade （grade Ⅱ and Ⅲ）， and no radiotherapy were independent risk factors for DFS in elderly breast cancer patients （all P < 0.05）， while ER status was an independent protective factor （P < 0.05）. The independent risk factors for OS in elderly breast cancer patients included tumor stage， N-stage （N2 and N3）， HER2 status， and Ki-67 （all P < 0.05）， and ER status was an independent protective factor （P < 0.05）. Subgroup analysis revealed that in elderly hormone receptor （HR）-negative breast cancer patients， the median follow-ups of the control and case groups were 123.0 （95% CI： 116.8， 129.2） months and 88.0 （95% CI： 75.2， 100.8） months， respectively， with a statistically significant difference both in DFS （91.3% vs. 68.6%， P=0.008） and OS rates （89.1% vs. 71.4%， P=0.027）.ConclusionsPost-breast-conserving radiotherapy provides a limited survival benefit in the overall elderly breast cancer patients， but a significant survival benefit in the elderly HR-negative breast cancer patients， which suggests the need for a prospective randomized controlled trial of a stratified step-down strategy for radiotherapy in elderly breast cancer patients.Keywords：elderly breast cancer;breast-conserving surgery;radiotherapy;disease-free survival;overall survival182|315|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo investigate the changes of intestinal flora in children with food allergy and constipation by high-throughput sequencing， and to analyze the function of intestinal flora， to provide a basis for the prevention and treatment of food allergy and constipation in children.MethodsTotally 33 children with food allergy and constipation in Longgang District of Shenzhen were selected as the disease group （CPFA group）， another 59 healthy children of the same age were recruited as the HC group. Stool samples were collected and subjected to high-throughput sequencing of 16SrRNA genes， followed by bioinformatics analysis.Results① The species abundance of HC group was higher than that of CPFA group， and the diversity of intestinal microbial community was different between the two groups； ② At the phylum level， the relative abundance of Bacteroidota， Desulfobacterota in CPFA group was lower than that in HC group， and the relative abundance of Firmicutes， Actinobacteria and Proteobacteria in CPFA group was higher than that in HC Group（P< 0.05）； ③ At the genus level， the relative abundance of Bacteroids， Parabacteroides in the CPFA group was lower than that in the HC group， and the relative abundance of Bifidobacterium， Escherichia-Shigella and Veillonella in the CPFA group was higher than that in the HC group； ④ Functional analysis showed that there were significant differences in functional genes between the two groups. Compared with those in the HC group， the abundance of functional genes in valine， leucine and isoleucine biosynthesis， cysteine and methionine metabolism， fatty acid metabolism and Staphylococcus aureus infection were significantly increased in the CPFA group （P<0.05）. The abundance of functional pathways related to bile acid biosynthesis and retinol metabolism was significantly decreased （P<0.05）.ConclusionThere are differences in intestinal flora and function between children with CPFA and HC， which may help to explore the pathogenesis of food allergy and constipation， and provide a theoretical basis for new therapeutic interventions.Keywords：food allergy;constipation;intestinal flora;microbiota function;high-throughput sequencing186|1093|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
- Abstract：ObjectiveTo evaluate a third-generation applicator template for intracavitary combined with interstitial brachytherapy （IC-ISBT） suitable for locally advanced cervical cancer， aiming to improve therapeutic outcomes.MethodsA retrospective study was conducted on patients with stage IB3-ⅣB cervical cancer treated at Sun Yat-sen University Cancer Center from January 2023 to October 2023. Magnetic resonance imaging data before and after external beam radiation therapy were collected and analyzed. According to the residual tumor after external beam radiation， high-risk clinical target volumes （HR-CTV） were delineated， based on which a third-generation IC-ISBT applicator template was designed. The dosimetric and therapeutic differences between using this applicator template （template implantation group） and traditional freehand interstitial implantation （freehand implantation group） were further compared. Statistical methods were used to analyze the data from both groups to test the efficacy and safety of the two approaches.ResultsThe third-generation applicator template could accommodate different cervical structures and optimize needle path layout. The tumor volume in the template implantation group was significantly larger than in the freehand implantation group， showing statistical differences. In terms of dosimetric coverage （V100%）， the template implantation group exhibited significant statistical differences compared with the freehand implantation group， demonstrating superior dose coverage. Additionally， the third-generation template showed advantages in protecting the rectum and sigmoid colon by potentially reducing high-dose points， while there were no significant differences in bladder dosimetry between the two methods. The primary cervical lesion remission rates were similar between the two groups.ConclusionThe third-generation IC-ISBT applicator template is scientifically and rationally designed， especially for patients with larger tumor volumes and later stages. It is easy to operate， highly reproducible， and shows significant advantages in dose distribution and protection of surrounding critical organs. The template has the potential to be widely applied as a routine treatment option.Keywords：cervical cancer;intracavitary combined with interstitial;brachytherapy applicator template;freehand insertion;dosimetry190|764|0<HTML><L-PDF> <Meta-XML>Updated：2025-03-20
Clinical Research
