Cancer has become a significant global public health issue， severely impacting public health and societal development. Despite advances in tumor treatment methods in recent years and a gradual decline in cancer mortality rates， drug-related adverse reactions and drug resistance remain substantial challenges. Traditional Chinese medicine （TCM） has demonstrated significant clinical efficacy in cancer treatment and small side effects， making it widely applied in the field of oncology. Xuefu Zhuyutang， derived from Yilin Gaicuo， is known for its abilities to invigorate blood circulation， dispel blood stasis， promote Qi flow， and alleviate pain. It was specifically formulated by the esteemed WANG Qingren of the Qing dynasty for the "blood stasis syndrome in the blood mansion" and is commonly used to treat Qi stagnation and blood stasis syndrome. Clinical studies have shown that Xuefu Zhuyutang， when combined with conventional Western medications， produces significant effects in the treatment of malignant tumors such as liver cancer， lung cancer， and cervical cancer. It substantially reduces the incidence of adverse reactions following Western treatments， including radiation esophagitis， radiation encephalopathy， radiation-induced oral mucositis， and edema. Additionally， it alleviates cancer-related pain and fever， blood hypercoagulability， and associated complications such as depression and anxiety， and also mitigates chemotherapy-induced side effects like hand-foot syndrome. Basic research has demonstrated its potential anti-tumor mechanisms， including the inhibition of Wnt/β-catenin signaling pathway activation， suppression of mitogen-activated protein kinase （MAPK） pathway activation， and anti-tumor angiogenesis. Pharmacological studies have revealed that its active components inhibit tumor cell proliferation and migration， induce tumor cell apoptosis， suppress tumor angiogenesis， enhance the cytotoxicity of natural killer cells against tumors， improve the tumor microenvironment， and regulate immune function. This paper reviewed the latest research progress on Xuefu Zhuyutang in the treatment of malignant tumors from four aspects： theoretical exploration， clinical studies， mechanisms of action， and pharmacological basis， aiming to provide insights and methods for the clinical diagnosis and treatment of malignant tumors.

Cancer has become a significant global public health issue， severely impacting public health and societal development. Despite advances in tumor treatment methods in recent years and a gradual decline in cancer mortality rates， drug-related adverse reactions and drug resistance remain substantial challenges. Traditional Chinese medicine （TCM） has demonstrated significant clinical efficacy in cancer treatment and small side effects， making it widely applied in the field of oncology. Xuefu Zhuyutang， derived from Yilin Gaicuo， is known for its abilities to invigorate blood circulation， dispel blood stasis， promote Qi flow， and alleviate pain. It was specifically formulated by the esteemed WANG Qingren of the Qing dynasty for the "blood stasis syndrome in the blood mansion" and is commonly used to treat Qi stagnation and blood stasis syndrome. Clinical studies have shown that Xuefu Zhuyutang， when combined with conventional Western medications， produces significant effects in the treatment of malignant tumors such as liver cancer， lung cancer， and cervical cancer. It substantially reduces the incidence of adverse reactions following Western treatments， including radiation esophagitis， radiation encephalopathy， radiation-induced oral mucositis， and edema. Additionally， it alleviates cancer-related pain and fever， blood hypercoagulability， and associated complications such as depression and anxiety， and also mitigates chemotherapy-induced side effects like hand-foot syndrome. Basic research has demonstrated its potential anti-tumor mechanisms， including the inhibition of Wnt/β-catenin signaling pathway activation， suppression of mitogen-activated protein kinase （MAPK） pathway activation， and anti-tumor angiogenesis. Pharmacological studies have revealed that its active components inhibit tumor cell proliferation and migration， induce tumor cell apoptosis， suppress tumor angiogenesis， enhance the cytotoxicity of natural killer cells against tumors， improve the tumor microenvironment， and regulate immune function. This paper reviewed the latest research progress on Xuefu Zhuyutang in the treatment of malignant tumors from four aspects： theoretical exploration， clinical studies， mechanisms of action， and pharmacological basis， aiming to provide insights and methods for the clinical diagnosis and treatment of malignant tumors.

Objective: To investigate the efficacy of magnesium-strontium co-doped hydroxyapatite mineralized collagen (MSHA/Col) in improving the bone repair microenvironment and enhancing bone regeneration capacity, providing a strategy to address the insufficient biomimetic composition and limited bioactivity of traditional hydroxyapatite mineralized collagen (HA/Col) scaffolds. Methods: A high-molecular-weight polyacrylic acid-stabilized amorphous calcium magnesium strontium phosphate precursor (HPAA/ACMSP) was prepared. Its morphology and elemental distribution were characterized by high-resolution transmission electron microscopy (TEM) and energy-dispersive spectroscopy. Recombinant collagen sponge blocks were immersed in the HPAA/ACMSP mineralization solution. Magnesium-strontium co-doped hydroxyapatite was induced to deposit within collagen fibers (experimental group: MSHA/Col; control group: HA/Col). The morphological characteristics of MSHA/Col were observed using scanning electron microscopy (SEM). Its crystal structure and chemical composition were analyzed by X-ray diffraction and Fourier transform infrared spectroscopy, respectively. The mineral phase content was evaluated by thermogravimetric analysis. The scaffold's porosity, ion release, and in vitro degradation performance were also determined. For cytological experiments, CCK-8 assay, live/dead cell staining, alkaline phosphatase staining, alizarin red S staining, RT-qPCR, and western blotting were used to evaluate the effects of the MSHA/Col scaffold on the proliferation, viability, early osteogenic differentiation activity, late mineralization capacity, and gene and protein expression levels of key osteogenic markers [runt-related transcription factor 2 (Runx2), collagen type Ⅰ (Col-Ⅰ), osteopontin (Opn), and osteocalcin (Ocn)] in mouse embryonic osteoblast precursor cells (MC3T3-E1). Results: HPAA/ACMSP appeared as amorphous spherical nanoparticles under TEM, with energy spectrum analysis showing uniform distribution of carbon, oxygen, calcium, phosphorus, magnesium, and strontium elements. SEM results of MSHA/Col indicated successful complete intrafibrillar mineralization. Elemental analysis showed the mass fractions of magnesium and strontium were 0.72% (matching the magnesium content in natural bone) and 2.89%, respectively. X-ray diffraction revealed characteristic peaks of hydroxyapatite crystals (25.86°, 31°-34°). Infrared spectroscopy results showed characteristic absorption peaks for both collagen and hydroxyapatite. Thermogravimetric analysis indicated a mineral phase content of 78.29% in the material. The scaffold porosity was 91.6% ± 1.1%, close to the level of natural bone tissue. Ion release curves demonstrated sustained release behavior for both magnesium and strontium ions. The in vitro degradation rate matched the ingrowth rate of new bone tissue. Cytological experiments showed that MSHA/Col significantly promoted MC3T3-E1 cell proliferation (130% increase in activity at 72 h, P < 0.001). MSHA/Col exhibited excellent efficacy in promoting osteogenic differentiation, significantly upregulating the expression of osteogenesis-related genes and proteins (Runx2, Col-Ⅰ, Opn, Ocn) (P < 0.01). Conclusion The MSHA/Col scaffold achieves dual biomimicry of natural bone in both composition and structure, and effectively promotes osteogenic differentiation at the genetic and protein levels, breaking through the functional limitations of pure hydroxyapatite mineralized collagen. This provides a new strategy for the development of functional bone repair materials

ObjectiveThis study systematically analyzed the arginine metabolic dysregulation in the rat model of heart failure （HF）， providing a modern scientific basis for elucidating the pathogenesis of HF and offering new insights for the prevention and treatment of HF with traditional Chinese medicine （TCM）. MethodsA thoracotomy was performed to ligate the left anterior descending coronary artery of rats， which induced acute myocardial ischemia and thus led to the development of post-myocardial infarction heart failure. The rats were divided into a sham surgery group and a model group， with eight rats in each group. Serum targeted metabolomics analysis was performed using ultra-performance liquid chromatography-triple quadrupole mass spectrometry （UPLC-TQ-S）， and the spatial distribution of metabolites in cardiac tissue was observed using airflow-assisted desorption electrospray ionizationmass spectrometry imaging （AFADESI-MSI）. Targets associated with HF and arginine metabolism were screened from databases including GeneCards and the Gene Expression Omnibus （GEO）， a protein-protein interaction （PPI） network was constructed， and enrichment analysis of the Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway and Gene Ontology （GO） was performed. Finally， molecular docking was conducted to verify the binding between core metabolic components and key targets， and potential TCMs were predicted based on the core pathways and targets. ResultsCompared with the sham surgery group， the levels of arginine and citrulline in the serum of model rats were significantly decreased （P<0.01）， while those of proline， ornithine， creatine， creatinine and glutamate were significantly increased （P<0.05， P<0.01）. Cardiac mass spectrometry imaging showed a decreased abundance of arginine in the local myocardial tissue. Bioinformatics analysis identified 24 core functional targets， such as the angiotensin-converting enzyme （ACE）， neuronal nitric oxide synthase （NOS1）， 5-hydroxytryptamine receptor 2A （HTR2A）， and epidermal growth factor receptor （EGFR）， and enrichment analysis indicated that these targets were significantly involved in the calcium signaling pathway， neuroactive ligand-receptor interactions， and phosphatidylinositol signaling pathway. Molecular docking confirmed strong binding activities between arginine， citrulline and HTR2A， as well as between creatine， creatinine and EGFR. Based on pathway-target prediction， potential TCM interventions， such as ginseng and magnolia， were identified. ConclusionThis study revealed characteristic arginine metabolic disorder in HF， and the core targets of HF were closely associated with the phosphatidylinositol signaling pathway. It provides a modern biological interpretation of the pathogenesis of HF in TCM from the perspectives of metabolites and signaling pathways， and offers valuable insights for targeted therapy of HF and the development of TCM.

ObjectiveThis study systematically analyzed the arginine metabolic dysregulation in the rat model of heart failure （HF）， providing a modern scientific basis for elucidating the pathogenesis of HF and offering new insights for the prevention and treatment of HF with traditional Chinese medicine （TCM）. MethodsA thoracotomy was performed to ligate the left anterior descending coronary artery of rats， which induced acute myocardial ischemia and thus led to the development of post-myocardial infarction heart failure. The rats were divided into a sham surgery group and a model group， with eight rats in each group. Serum targeted metabolomics analysis was performed using ultra-performance liquid chromatography-triple quadrupole mass spectrometry （UPLC-TQ-S）， and the spatial distribution of metabolites in cardiac tissue was observed using airflow-assisted desorption electrospray ionizationmass spectrometry imaging （AFADESI-MSI）. Targets associated with HF and arginine metabolism were screened from databases including GeneCards and the Gene Expression Omnibus （GEO）， a protein-protein interaction （PPI） network was constructed， and enrichment analysis of the Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway and Gene Ontology （GO） was performed. Finally， molecular docking was conducted to verify the binding between core metabolic components and key targets， and potential TCMs were predicted based on the core pathways and targets. ResultsCompared with the sham surgery group， the levels of arginine and citrulline in the serum of model rats were significantly decreased （P<0.01）， while those of proline， ornithine， creatine， creatinine and glutamate were significantly increased （P<0.05， P<0.01）. Cardiac mass spectrometry imaging showed a decreased abundance of arginine in the local myocardial tissue. Bioinformatics analysis identified 24 core functional targets， such as the angiotensin-converting enzyme （ACE）， neuronal nitric oxide synthase （NOS1）， 5-hydroxytryptamine receptor 2A （HTR2A）， and epidermal growth factor receptor （EGFR）， and enrichment analysis indicated that these targets were significantly involved in the calcium signaling pathway， neuroactive ligand-receptor interactions， and phosphatidylinositol signaling pathway. Molecular docking confirmed strong binding activities between arginine， citrulline and HTR2A， as well as between creatine， creatinine and EGFR. Based on pathway-target prediction， potential TCM interventions， such as ginseng and magnolia， were identified. ConclusionThis study revealed characteristic arginine metabolic disorder in HF， and the core targets of HF were closely associated with the phosphatidylinositol signaling pathway. It provides a modern biological interpretation of the pathogenesis of HF in TCM from the perspectives of metabolites and signaling pathways， and offers valuable insights for targeted therapy of HF and the development of TCM.

Methods: Fifty patients who underwent UBE-TLIF and 50 patients who underwent W-TLIF, each with >2 years of follow-up, were retrospectively analyzed. Outcomes included operative parameters, time to postoperative mobilization, paravertebral muscle atrophy and fat infiltration rates, clinical scores (Visual Analog Scale [VAS], Oswestry Disability Index [ODI], Japanese Orthopaedic Association [JOA]), modified Macnab criteria, fusion rates, and complications. Results: Compared with W-TLIF, the UBE-TLIF group had significantly less intraoperative blood loss, shorter operative times, and lower postoperative drainage volumes (p <0.05). The UBE-TLIF group showed faster postoperative recovery and shorter hospital stays. At 6 months, 1 year, and 2 years, W-TLIF patients had higher multifidus and erector spinae atrophy, and greater paravertebral muscle fat infiltration (p <0.05). The UBE-TLIF group also had lower VAS and ODI scores at 1 year and 2 years (p <0.05) and fewer surgical complications (6% vs. 10%). Fusion rates (94% vs. 92%) and modified Macnab outcomes (88% vs. 86%) were comparable (p >0.05). Conclusions UBE-TLIF is associated with reduced intraoperative trauma, quicker recovery, and fewer complications. In the long-term, it better preserves paravertebral muscle integrity and provides superior pain and functional outcomes.

Amyotrophic lateral sclerosis (ALS) is a chronic, progressive degenerative disease affecting both upper and lower motor neurons, primarily characterized by skeletal muscle weakness and atrophy. Notably, the same muscle group may exhibit asynchronous involvement. This study aims to investigate the involvement patterns of the orbicularis oculi (OOc) and orbicularis oris (OOr) in ALS patients, compare the findings with healthy controls (HCs) and myasthenia gravis (MG) patients, and explore the characteristics and clinical significance of facial muscle involvement in ALS.

Objective To explore the predictive value of forkhead box P3 (FOXP3) mRNA expression in cord blood derived regulatory T cells (Tregs) and the associated cytokines interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) for early-onset atopic dermatitis (AD) in infants. Methods The healthy full-term newborns delivered vaginally at Shanghai Fifth People’s Hospital from September 2023 to April 2024 were enrolled. Umbilical vein blood was collected at birth to measure FOXP3 mRNA expression by RT-PCR and IL-10 and TGF-β concentrations by ELISA. Follow-up was performed at 6 weeks, 3 months, and 6 months postnatally via telephone or outpatient visits to assess the occurrence of AD in infants. Based on the occurrence of AD at 6 months of age, the infants were divided into an AD group and a control group. The indicators related to mothers and infants were compared between the two groups. Logistic regression analysis was used to identify risk factors for the development of AD in infants within 6 months after birth, and a predictive model was constructed. The performance of the model in predicting early-onset AD was evaluated using receiver operating characteristic (ROC) curve analysis. Results A total of 59 infants completed 6-month follow-up, with 17 (28.8%) diagnosed with AD. No significant differences were observed in gestational age, sex, birth weight, presence of siblings, smoking expossure, maternal dietary preferences (egg, milk, or seafood intake), maternal age and education level, or cord blood IL-10 levels between two groups. There were significant differences in season of birth, family history of atopic disease, feeding method, and cord blood levels of FOXP3 mRNA and TGF-β between two groups (P＜0.05). Logistic regression analysis showed low levels of cord blood FOXP3 mRNA and TGF-β, and family history of atopic disease were risk factors for early-onset AD in infants (P＜0.05). A predictive model was constructed using risk factors. The area under the curve of the combined model was 0.821 (95%CI 0.680–0.962), with a sensitivity of 76.5% and a specificity of 85.7%. Conclusion Reduced cord blood FOXP3 mRNA and TGF-β level, and a family history of atopic diseases could be used to predict early-onset AD in infants.

ObjectiveThis study aimed to evaluate the effects of cycloastragenol （CAG） on mitochondrial dysfunction during cardiac remodeling and to elucidate its regulatory role in myocardial energy metabolic homeostasis and the associated transcriptional regulatory axis. MethodsA rat model of heart failure （HF） was established by ligation of the left anterior descending coronary artery. Rats were randomly divided into a control group， a model group， a captopril group （3.25 mg·kg^-1）， a low-dose CAG group （10 mg·kg^-1， CAG-L）， and a high-dose CAG group （20 mg·kg^-1， CAG-H）. After 28 days of treatment， left ventricular ejection fraction （LVEF）， left ventricular fractional shortening （LVFS）， left ventricular end-diastolic diameter （LVIDd）， and left ventricular end-systolic diameter （LVIDs） were assessed by echocardiography. Serum levels of N-terminal pro-brain natriuretic peptide （NT-proBNP）， creatine kinase-MB （CK-MB）， cardiac troponinⅠ （cTnI）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and cyclic adenosine monophosphate （cAMP） were measured by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） and Masson's trichrome staining were used to evaluate myocardial histopathology and fibrosis. Wheat germ agglutinin （WGA）， reactive oxygen species （ROS）， and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining were performed to assess cardiomyocyte hypertrophy， oxidative stress， and apoptosis. Adenosine triphosphate （ATP） content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ were determined by colorimetric assays. The mRNA expression of α-smooth muscle actin （α-SMA）， Col Ⅰ， and Col Ⅲ was detected by Real-time quantitative polymerase chain reaction （Real-time PCR）， while the protein levels of β₂-adrenergic receptor （ADRB2）， protein kinase A （PKA）， phosphorylated cAMP response element-binding protein/total cAMP response element-binding protein （p-CREB/CREB）， peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）， nuclear respiratory factor 1 （NRF1）， and mitochondrial transcription factor A （TFAM） were analyzed by Western blot. ResultsCompared with the control group， the model group exhibited significantly decreased LVEF， LVFS， and ATP levels （P<0.05）， and markedly increased LVIDd， LVIDs， NT-proBNP， CK-MB， cTnI， IL-1β， IL-6， TNF-α， ROS levels， TUNEL-positive rate， Col deposition area， and the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ （P<0.05）. In addition， the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， the protein expression of ADRB2， PKA， p-CREB， PGC-1α， NRF1， and TFAM， as well as the cAMP content， were significantly reduced （P<0.05）. Compared with the model group， both low- and high-dose CAG significantly increased LVEF and LVFS， and decreased LVIDd， LVIDs， and the levels of NT-proBNP， CK-MB， and cTnI （P<0.05）. CAG treatment alleviated myocardial disarray and Collagen deposition， and downregulated the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ. The treatment markedly reduced ROS generation and the TUNEL-positive rate （P<0.05）， thereby attenuating cardiomyocyte hypertrophy and inflammatory responses. Furthermore， CAG treatment increased ATP content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， accompanied by upregulation of PGC-1α， NRF1， TFAM， ADRB2， PKA， and p-CREB protein expression as well as cAMP levels （P<0.05）. The CAG-H group showed the most pronounced improvements， which were superior to those of the captopril group and the CAG-L group. ConclusionCycloastragenol delays adverse cardiac remodeling and improves cardiac function by activating the ADRB2-mediated GPCR/cAMP/PKA/CREB signaling pathway， enhancing the PGC-1α/NRF1/TFAM activity， promoting mitochondrial energy metabolism remodeling， and suppressing oxidative stress， inflammation， and myocardial fibrosis.

Coronary heart disease （CHD） has a distinct circadian rhythmicity in its onset， which is closely related to the waxing and waning of qi and blood in the channel passages of the human body. Grounded in the circadian rhythm theory of "correspondence between heaven and humankind"， this paper explores the pathogenic evolution rules of qi-blood disharmony， channel obstruction， interacting as cause and effect with circadian rhythm disorders in CHD. Clinically， CHD can be observed to attack in the early morning， at night， in the afternoon， and at fixed or unfixed circadian intervals. The pathogenesis rhythms at different time nodes can correspondingly reflect the susceptibility tendencies and pathological stress responses of the human body to core pathogeneses such as yang deficiency with cold congelation， yin deficiency with yang floating， qi and yin deficiency， and liver constraint with qi stagnation under specific temporal states. Treatment should be adapted to the season and time， regulating yin and yang in accordance with biological rhythms. It is recommended to regulate qi during the daytime by promoting ascending and dispersing to unblock the channel passages， and select the appropriate timing for administration to harness natural timing. At the Mao （卯） hour， yang ascends while yin descends， and taking medication at this time conforms to the ascending of yang qi. At the Wu （午） hour， the heart meridian is active， and taking medication at this time warms the channel passages and assists heart yang， which can be treated with modified Buzhong Yiqi Decoction （补中益气汤） or Shengyang Yiwei Decoction （升阳益胃汤）. At night， blood should be harmonized， when the channel passages are unblocked through nourishing， restraining， and searching， with Lianmei Decoction （连梅汤） combined with Dahuang Zhechong Pill （大黄䗪虫丸）. Following the temporal rhythm， the focus is put on the transitional time of day and night and the four seasons to treat disease before it arises， resonating and corresponding with the natural rhythm.