From the perspective of transfusion medicine and based on the vision and framework of patient blood management, this article combines the advances in basic science, blood transfusion, laboratory, and clinical medicine. It aims to systematically review the key elements and characteristics of patient fibrinogen management by maintaining and optimizing patients' hemostatic function while reducing blood transfusions. This review enriches the connotation of transfusion medicine, especially patient blood management, and provides valuable insights for clinical practice.

ObjectiveThe present study aimed to investigate alterations in white matter microstructure and spontaneous neural activity in male college smokers, and to further explore their associations with nicotine dependence. Given that adolescence and early adulthood represent critical periods for brain maturation, particularly for white matter development, understanding the neural correlates of smoking behavior during this stage is of substantial importance for both neuroscience and public health. MethodsA total of 115 male undergraduate students were initially recruited for this study. After quality control and exclusion procedures, 52 male college smokers and 42 demographically matched healthy non-smokers were included in the final analysis. All participants underwent multimodal magnetic resonance imaging (MRI), including diffusion tensor imaging (DTI) and resting-state functional MRI (rs-fMRI). White matter fiber tracts were reconstructed using the automated fiber quantification (AFQ) method, which enables precise identification and quantification of major fiber bundles. Eighteen major white matter tracts were segmented for each participant. Along the core trajectory of each tract, 100 equidistant nodes were sampled. Fractional anisotropy (FA) was calculated at each node to assess white matter microstructural integrity, while amplitude of low-frequency fluctuation (ALFF) was computed to evaluate spontaneous neural activity within white matter tracts. Between-group differences in FA and ALFF were assessed using two-sample t-tests, with appropriate corrections applied for multiple comparisons. Furthermore, Pearson correlation analyses were conducted to examine the relationships between imaging-derived metrics (FA and ALFF values in regions showing significant group differences) and nicotine dependence severity, as measured by the Fagerström test for nicotine dependence (FTND). ResultsCompared with healthy non-smokers, male college smokers exhibited significantly increased FA values in several white matter tracts, including the left thalamic radiation, right corticospinal tract, forceps major of the corpus callosum, left uncinate fasciculus, and right arcuate fasciculus. These findings suggest altered microstructural organization or increased directional coherence within these pathways. In addition, smokers demonstrated significantly elevated ALFF values in the forceps major, right uncinate fasciculus, and left arcuate fasciculus, indicating enhanced spontaneous neural activity in these white matter regions. Correlation analyses revealed that FA values in the left thalamic radiation and right corticospinal tract were negatively correlated with FTND scores, suggesting that higher levels of nicotine dependence were associated with reduced microstructural integrity or altered fiber organization in these regions. In contrast, ALFF values in the forceps major and right uncinate fasciculus were positively correlated with FTND scores, indicating that greater nicotine dependence was associated with increased spontaneous neural activity in specific white matter pathways. ConclusionThe present study provides evidence that male college smokers exhibit distinct alterations in both white matter microstructure and functional activity. These abnormalities are not uniformly distributed but rather localized to specific fiber tracts implicated in sensorimotor processing, interhemispheric communication, and higher-order cognitive and emotional regulation. Importantly, the observed associations between imaging metrics and nicotine dependence severity suggest that these structural and functional alterations may reflect neurobiological mechanisms underlying addiction. The combination of AFQ-based tract profiling and multimodal MRI offers a sensitive approach for detecting subtle changes along white matter pathways, highlighting its potential utility in identifying neuroimaging biomarkers of nicotine dependence. Overall, these findings indicate that smoking during early adulthood may disrupt ongoing white matter maturation, potentially leading to long-term consequences for brain function. This study provides novel insights into the neural basis of nicotine dependence and underscores the importance of early intervention and prevention strategies targeting young smokers.

BACKGROUND:Acupoint embedding and floating needle therapy are two methods for the treatment of knee osteoarthritis,but there are few reports on the combined treatment of the two methods. OBJECTIVE:To investigate the therapeutic effect of acupoint embedding combined with floating needle therapy on different stages of knee osteoarthritis using generalized estimating equations. METHODS:A total of 436 patients with knee osteoarthritis admitted to Dongguan Hospital of Traditional Chinese Medicine from February 2019 to February 2023 were selected as the research subjects.All patients were randomly divided into a control group with floating needle therapy(n=218)and an observation group with acupoint embedding method combined with floating needle therapy(n=218).Staging was performed according to the K-L staging method.In the control group,there were 57 cases in stage Ⅰ,62 in stage Ⅱ,49 in phase Ⅲ,and 50 in stage Ⅳ,while in the observation group,there were 48 cases in stage Ⅰ,66 in stage Ⅱ,63 in phase Ⅲ,and 41 in stage Ⅳ.The levels of indexes and clinical efficacy were compared between groups before and after treatment.Generalized estimating equation model was used to analyze the influencing factors of clinical efficacy and the interaction effect of different time points,different methods and different stages on therapeutic efficacy. RESULTS AND CONCLUSION:There was no significant difference in baseline data between the observation group and the control group,as well as between the patients of different stages(P>0.05).After treatment,the cure rate of stage Ⅰ patients was the highest after treatment,and the total improvement rate in the observation group was significantly higher than that in the control group.There were significant differences in the cure rate among different stages in each group(P<0.05).After treatment,all indicators in the two groups were significantly decreased.In the control group,there were significant differences in various indicators of patients at different stages after 4 weeks of treatment(P<0.05).In the observation group,after 2 weeks of treatment,there were significant differences in various indicators of patients at different stages(P<0.05),and all the indexes in the observation were lower than those in the control group after 4 weeks of treatment(P<0.05)and the therapeutic effect in the observation group was better than that in the control group.Generalized estimating equation model analysis showed that trauma history,interleukin-6 level,treatment method,treatment time and K-L stage all significantly affected the clinical efficacy in patients.In the interaction effect analysis,after 2 weeks of treatment,there was a significant difference in the visual analogue scale score between the two groups in stages Ⅲ and Ⅳ(P<0.05).After 4 weeks of treatment,there was a significant difference in the visual analogue scale score between the two groups in stages Ⅱ,Ⅲ,and Ⅳ(P<0.05).To conclude,acupoint embedding combined with floating needle therapy is superior to floating needle therapy alone in the treatment of different stages of knee osteoarthritis.Trauma history,interleukin-6 level,treatment method,treatment time and K-L stage significantly influence the therapeutic effect.

Objective To investigate the effect of miR-29b-3p targeting insulin-like growth factor-1(IGF-1)on high glucose-induced injury in human retinal microvascular endothelial cells(HRMECs)and the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTOR)signaling pathway.Methods HRMECs were di-vided into the following groups:control group(normal culture),high glucose(HG)group(treated with 30.0 mmol·L-1 glucose for 48 h),inhibitor-NC group,miR-29b-3p inhibitor group,miR-29b-3p inhibitor+si-NC group,miR-29b-3p inhib-itor+si-IGF-1 group(all transfected with corresponding plasmids for 24 h after HG treatment),and LY294002 group(treated with 40 μmol·L-1 LY294002 for 24 h).The expression level of miR-29b-3p was detected by quantitative real-time PCR(qRT-PCR).Cell viability was assessed using the Cell Counting Kit-8(CCK-8)assay.Intracellular reactive oxygen species(ROS)levels were measured by immunofluorescence.The expression levels of malondialdehyde(MDA),superox-ide dismutase(SOD),and glutathione peroxidase(GSH-Px)were determined using enzyme-linked immunosorbent assay(ELISA).Cell apoptosis was analyzed by flow cytometry.Autophagosome formation was observed under a transmission electron microscope.The protein expression levels related to apoptosis,autophagy,IGF-1,and the PI3K/Akt/mTOR path-way were examined by Western blot.The targeting relationship between miR-29b-3p and IGF-1 was verified by a dual-lucif-erase reporter assay.Results Compared with the Control group,the HG group showed significant increases in the ex-pression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;whereas the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the number of autophagosomes were significantly decreased(all P＜0.05).Compared with the in-hibitor-NC group,the miR-29b-3p inhibitor group exhibited significant decreases in the expression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;while the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the num-ber of autophagosomes were significantly increased(all P＜0.05).Compared with the miR-29b-3p inhibitor+si-NC group,the miR-29b-3p inhibitor+si-IGF-1 group demonstrated significant increases in the expression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;whereas the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the number of autophagosomes were significantly decreased(all P＜0.05).Compared with the HG group,the LY294002 group showed significant decreases in the expression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;while the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the number of autophagosomes were significantly increased(all P＜0.05).The dual-luciferase activity was significantly lower in cells co-transfected with IGF-1-WT and miR-29b-3p mimic compared to miR-NC cells(P＜0.05).Conclusion Inhibition of miR-29b-3p can target upregulation of IGF-1 expression levels,thereby inhibiting the PI3K/Akt/mTOR pathway and improving high glucose induced cell damage in HRMECs.

This study aims to innovate a homogeneous outpatient service management system across multiple hospital campuses to enhance service quality.Based on the practical experience of a tertiary general hospital in Guangdong Province and in accordance with the"Interim Regulations on Outpatient Quality Management in Healthcare Institutions,"we constructed a"6+1"homogeneous outpatient service management system.This system includes:① a multi-stakeholder co-governance outpa-tient management system,②a vertical and cross-hierarchical management network,③ a democratic-centralized clinical coordina-tion strategy,④ a guidance-encouragement performance evaluation standard,⑤a collaborative dynamic supervision mechanism,⑥a spiral retrospective evaluation and improvement method,and ⑦ an integrated outpatient diagnosis and treatment system.Af-ter over two years of implementation,the hospital's outpatient volume has grown by an average of over 15％annually,patient waiting time after appointment has been reduced to 20 minutes,and patient satisfaction in the tertiary public hospital performance evaluation achieved full marks.The electronic medical record system functionality reached Level 6,significantly improving healthcare service efficiency and quality while enhancing homogeneous management across campuses.

The concept of amplification feedback pathways represents an intersection between electronics and control theory,involving both amplification and feedback processes.It reveals the dynamic evolution mechanisms of systems under the combined influence of these two processes.In Traditional Chinese Medicine(TCM),Chest Bi syndrome is considered a"ben xu biao shi"condition,with its primary pathology located in the heart and closely related to other organs such as the liver,spleen and kidneys.This article focuses on the interrelationship between organ dysfunction and the imbalance of the Five Elements Theory.By applying amplification feedback theory and models,the study constructs and analyzes single-stage amplification feedback pathways involving the heart,liver and kidneys,as well as double-stage amplification feedback pathways involving the heart,liver,kidneys and spleen,in the context of multifactorial interactions such as heart and kidney Yang deficiency,Qi stagnation in the heart and chest,and spleen-stomach dysfunction.Particular emphasis is placed on analyzing the phenomena of deep feedback and self-excited oscillation,and specific formulas and clinical evidence are used to validate the analysis results,clarifying the role of relevant organ function changes in the pathogenesis of Chest Bi syndrome.The article aims to provide new insights into the complex pathogenesis of refractory diseases from a control theory perspective,offering new directions for modernizing TCM research with digital technology and theoretical support for future simulation-based digital systems guided by TCM theory.

Objective·To explore the effects and potential molecular mechanisms of blocking cannabinoid receptor 1(CB1)in acute lung injury(ALI)in mice.Methods·Forty mice were randomly divided into blank control group,AM281(CB1 antagonist)control group,lipopolysaccharide(LPS)group,and LPS+AM281 group,with ten mice in each group.ALI models were induced by LPS.The pathological manifestations of lung tissues were observed in each group of mice by hematoxylin and eosin(H-E)staining and the inflammation scores were calculated.The mRNA levels of M1 markers[tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),IL-12]and M2 markers[arginase(Arg),mannose receptor,C type 2(Mrc2),macrophage galactose-type lectin 1(Mgl1)]in lung macrophages were measured by reverse transcription and real-time fluorescence quantitative polymerase chain reaction(qPCR).Human myeloid leukemia monocytes THP-1 cells were cultured in vitro,and the expression of CB1 and CB2 in THP-1 cells was detected by immunofluorescence.After further blocking CB1 and inhibiting the Gαi/o/RhoA signaling pathway,the mRNA levels of M1 markers were assessed.Results·The LPS group showed significant lung tissue damage and a significant increase in inflammation scores in mice.After blocking CB1,compared with the LPS group,the LPS+AM281 group of mice showed improvements in lung injury,manifested as improved congestion of alveolar wall capillaries,reduced infiltration of inflammatory cells in the lung interstitium and alveolar cavity,and a decreased inflammation score(P=0.007).Compared with the control group,the levels of M1 marker in the lung tissue of the LPS group were upregulated,while the polarization of macrophages changed and the M1/M2 ratio was reversed after blocking CB1(all P<0.05).In vitro studies found that macrophages expressed CB1 and CB2.Activation of CB1 by arachidonyl-2-chloroethylamide(ACEA)upregulated the expression of M1 markers.Blocking CB1 and selectively inhibiting Gαi/o/RhoA signaling significantly downregulated M1 markers(all P<0.05).Conclusion·CB1 promotes the polarization of macrophage towards the M1 phenotype through the Gαi/o/RhoA signaling pathway in ALI,and blocking CB1 can improve lung injury.

To investigate the in vitro inhibitory mechanism of Nymphaea candida total flavonoids(NCTF)against Staphylococcus aureus(S.aureus)and its safety in mice,this study first deter-mined the antibacterial effect of NCTF on the clinically isolated strain S.aureus-C1.Subsequently,the inhibitory mechanism of NCTF on S.aureus-C1 was explored by measuring its effects on bac-terial growth curves,microstructure,intracellular AKP and LDH levels,and biofilm formation.Safety evaluation included determination of LD50 and MDT in mice,as well as analysis of serum biochemical parameters,organ indices,and histopathological observations.Results showed that NCTF effectively inhibited S.aureus-C1 proliferation,with an inhibition zone diameter of(18.98±0.67)mm and a MIC of 6.25 g/L.A concentration of 2×MIC nearly completely suppressed bacte-rial growth.Scanning electron microscopy revealed structural damage to bacterial cells,including collapse and shrinkage.AKP and LDH assays indicated significantly increased AKP activity(P＜0.05)and decreased intracellular LDH activity(P＜0.05)in the supernatant of drug-treated groups,demonstrating NCTF-induced disruption of cell walls and membranes leading to leakage of AKP and LDH.Crystal violet staining of biofilms showed significant inhibition rates of(43.77±9.16)％and(61.71±9.82)％at 2 × MIC and 4 × MIC concentrations,respectively(P＜0.05).Safe-ty assessments indicated low toxicity of NCTF in mice,with transient effects that returned to nor-mal levels within a short period.These findings demonstrate that NCTF exhibits potent antibacte-rial activity against S.aureus-C1 by damaging bacterial cell structures,increasing cell wall/mem-brane permeability,reducing biofilm formation,and displaying low toxicity.This study provides scientific evidence for clinical drug screening against bovine mastitis and the development of Nym-phaea candida resources.

Objective To investigate the effect of miR-29b-3p targeting insulin-like growth factor-1(IGF-1)on high glucose-induced injury in human retinal microvascular endothelial cells(HRMECs)and the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTOR)signaling pathway.Methods HRMECs were di-vided into the following groups:control group(normal culture),high glucose(HG)group(treated with 30.0 mmol·L-1 glucose for 48 h),inhibitor-NC group,miR-29b-3p inhibitor group,miR-29b-3p inhibitor+si-NC group,miR-29b-3p inhib-itor+si-IGF-1 group(all transfected with corresponding plasmids for 24 h after HG treatment),and LY294002 group(treated with 40 μmol·L-1 LY294002 for 24 h).The expression level of miR-29b-3p was detected by quantitative real-time PCR(qRT-PCR).Cell viability was assessed using the Cell Counting Kit-8(CCK-8)assay.Intracellular reactive oxygen species(ROS)levels were measured by immunofluorescence.The expression levels of malondialdehyde(MDA),superox-ide dismutase(SOD),and glutathione peroxidase(GSH-Px)were determined using enzyme-linked immunosorbent assay(ELISA).Cell apoptosis was analyzed by flow cytometry.Autophagosome formation was observed under a transmission electron microscope.The protein expression levels related to apoptosis,autophagy,IGF-1,and the PI3K/Akt/mTOR path-way were examined by Western blot.The targeting relationship between miR-29b-3p and IGF-1 was verified by a dual-lucif-erase reporter assay.Results Compared with the Control group,the HG group showed significant increases in the ex-pression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;whereas the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the number of autophagosomes were significantly decreased(all P＜0.05).Compared with the in-hibitor-NC group,the miR-29b-3p inhibitor group exhibited significant decreases in the expression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;while the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the num-ber of autophagosomes were significantly increased(all P＜0.05).Compared with the miR-29b-3p inhibitor+si-NC group,the miR-29b-3p inhibitor+si-IGF-1 group demonstrated significant increases in the expression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;whereas the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the number of autophagosomes were significantly decreased(all P＜0.05).Compared with the HG group,the LY294002 group showed significant decreases in the expression levels of miR-29b-3p,ROS,MDA,Bax,Cleaved-caspase 3,p62,the p-PI3K/PI3K ratio,the p-Akt/Akt ratio,the p-mTOR/mTOR ratio,and the cell apoptosis rate;while the expression levels of IGF-1,SOD,GSH-Px,the LC3Ⅱ/LC3Ⅰ ratio,cell viability,and the number of autophagosomes were significantly increased(all P＜0.05).The dual-luciferase activity was significantly lower in cells co-transfected with IGF-1-WT and miR-29b-3p mimic compared to miR-NC cells(P＜0.05).Conclusion Inhibition of miR-29b-3p can target upregulation of IGF-1 expression levels,thereby inhibiting the PI3K/Akt/mTOR pathway and improving high glucose induced cell damage in HRMECs.

To investigate the in vitro inhibitory mechanism of Nymphaea candida total flavonoids(NCTF)against Staphylococcus aureus(S.aureus)and its safety in mice,this study first deter-mined the antibacterial effect of NCTF on the clinically isolated strain S.aureus-C1.Subsequently,the inhibitory mechanism of NCTF on S.aureus-C1 was explored by measuring its effects on bac-terial growth curves,microstructure,intracellular AKP and LDH levels,and biofilm formation.Safety evaluation included determination of LD50 and MDT in mice,as well as analysis of serum biochemical parameters,organ indices,and histopathological observations.Results showed that NCTF effectively inhibited S.aureus-C1 proliferation,with an inhibition zone diameter of(18.98±0.67)mm and a MIC of 6.25 g/L.A concentration of 2×MIC nearly completely suppressed bacte-rial growth.Scanning electron microscopy revealed structural damage to bacterial cells,including collapse and shrinkage.AKP and LDH assays indicated significantly increased AKP activity(P＜0.05)and decreased intracellular LDH activity(P＜0.05)in the supernatant of drug-treated groups,demonstrating NCTF-induced disruption of cell walls and membranes leading to leakage of AKP and LDH.Crystal violet staining of biofilms showed significant inhibition rates of(43.77±9.16)％and(61.71±9.82)％at 2 × MIC and 4 × MIC concentrations,respectively(P＜0.05).Safe-ty assessments indicated low toxicity of NCTF in mice,with transient effects that returned to nor-mal levels within a short period.These findings demonstrate that NCTF exhibits potent antibacte-rial activity against S.aureus-C1 by damaging bacterial cell structures,increasing cell wall/mem-brane permeability,reducing biofilm formation,and displaying low toxicity.This study provides scientific evidence for clinical drug screening against bovine mastitis and the development of Nym-phaea candida resources.