The widespread implementation of low-dose computed tomography screening has led to a substantial rise in the detection of pulmonary nodules,with multiple pulmonary nodules(MPNs)now representing a common clinical presentation.Conventional diagnostic and therapeutic paradigms,characterized by sequential,multi-site processes,are often limited by inefficiency,safety concerns,and suboptimal patient outcomes.In contemporary thoracic surgery,a transformative"one-stop"precision management strategy has emerged within hybrid operating theaters.This integrated approach synergizes intraoperative imaging,advanced navigation,and surgical intervention to address these limitations.Cone-beam CT plays a pivotal role in this model by leveraging its maneuverability,low radiation,and high spatial resolution to greatly facilitate the development of precise diagnosis and treatment for MPNs.

The widespread implementation of low-dose computed tomography screening has led to a substantial rise in the detection of pulmonary nodules,with multiple pulmonary nodules(MPNs)now representing a common clinical presentation.Conventional diagnostic and therapeutic paradigms,characterized by sequential,multi-site processes,are often limited by inefficiency,safety concerns,and suboptimal patient outcomes.In contemporary thoracic surgery,a transformative"one-stop"precision management strategy has emerged within hybrid operating theaters.This integrated approach synergizes intraoperative imaging,advanced navigation,and surgical intervention to address these limitations.Cone-beam CT plays a pivotal role in this model by leveraging its maneuverability,low radiation,and high spatial resolution to greatly facilitate the development of precise diagnosis and treatment for MPNs.

BACKGROUND:Prolyl hydroxylase domain 2(PHD2)inhibitors can regulate bone metabolism and relieve osteoporosis in ovariectomized rats.cpd17 is a small molecule oral PHD2 inhibitor newly developed by China Pharmaceutical University.It is effective in the treatment of renal anemia with few side effects,but its effect on bone formation and bone resorption is still unclear. OBJECTIVE:To investigate the effects of cpd17 on mouse osteogenic precursor cells. METHODS:Osteogenic precursor cells were treated with cpd17.Alkaline phosphatase activity and extracellular matrix mineralization were measured,and the expression levels of osteogenesis-and osteoclastogenesis-related markers,as well as PHD2 and hypoxia-inducible factor 1α,were detected.After inhibition of the hypoxia-inducible factor 1α pathway using LW6(a hypoxia-inducible factor 1α pathway inhibitor),alkaline phosphatase activity and extracellular matrix mineralization were detected again,as well as the expression levels of osteogenesis-and osteoclastogenesis-related markers,PHD2 and hypoxia-inducible factor 1α. RESULTS AND CONCLUSION:cpd17 significantly enhanced alkaline phosphatase activity and extracellular matrix mineralization,up-regulated the expression of osteogenesis-related markers,down-regulated the expression of osteoclastogenesis-related markers,up-regulated the expression of hypoxia-inducible factor 1α,down-regulate the expression of PHD2.However,cpd17's effects were significantly attenuated by LW6.To conclude,the PHD2 inhibitor cpd17 promotes osteogenic differentiation and inhibits osteoclastic differentiation through activation of the hypoxia-inducible factor 1α signaling pathway.

OBJECTIVES: Wild-caught Microtus fortis (M. fortis) at the age of 9-15 months can develop epithelial ovarian cancers similar to human epithelial ovarian cancers under natural conditions during experimental animal breeding, but its pathological types and biological characteristics remain unclear. This study aims to analyze the biological characteristics of spontaneous ovarian cancer in M. fortis, intending to develop M. fortis as an animal model for human epithelial ovarian cancer. METHODS: The female M. fortis (9-15 months old) with spontaneous ovarian cancer were selected as the experimental group, and healthy M. fortis from the same litter were selected as the control group. The ovarian pathological changes of the two groups were observed by dissection. Blood routine and biochemical indicators were measured by biochemical analysis. Hematoxylin and eosin (HE) staining was performed to observe the pathological changes in the ovarian cancer tissue of M. fortis. Immunohistochemical staining was used to detect the protein expression of common ovarian cancer markers, and real-time RT-PCR was used to analyze the transcription levels of ovarian cancer-related genes. RESULTS: Spontaneous ovarian cancer in M. fortis mainly affects both ovaries, with tumors appearing solid or cystic. HE staining and histopathological analysis confirmed that the ovarian tumors originated from ovarian surface epithelium. Compared to the control group, the experimental group showed significantly decreased hemoglobin (P<0.01), hematocrit (P<0.05), albumin (P<0.05), and blood glucose levels (P<0.01), while lymphocyte percentage (P<0.05), monocyte percentage (P<0.05), cholesterol (P<0.01), and progesterone (P<0.01) levels were significantly increased. Expression of ovarian cancer-related genes, including ID3, CDC42, RHOA, RB1CC1, NF1, PIN1, MIB1, PDS5A, MCM7, and MLH1, was significantly downregulated (all P<0.05), while PAX8 gene expression was significantly upregulated (P<0.05). Immunohistochemical results showed that Wilms' tumor gene 1 (WT1) protein was mainly distributed throughout the cell, with significantly higher expression in ovarian cancer M. fortis. Tumor protein 53 (TP53) was expressed in both healthy and ovarian cancer M. fortis and was distributed throughout the cell. Hepatocyte nuclear factor 1 beta (HNF1B) and progesterone receptor (PR) protein were highly expressed in the ovarian tissue of healthy M. fortis but were significantly reduced in the ovarian cancer M. fortis, though both were located in the cytoplasm. CONCLUSIONS Spontaneous ovarian cancer in M. fortis is serous ovarian cancer. Compared to healthy M. fortis, significant differences were observed in ovarian tissue morphology, biochemical indicators, ovarian cancer-related gene expression, and protein expression, which show similarity to the biological characteristics of human serous ovarian cancer. This suggests that M. fortis could be an ideal animal model for studying human serous ovarian cancer.
Female ; Ovarian Neoplasms/metabolism* ; Animals ; Carcinoma, Ovarian Epithelial ; Disease Models, Animal ; Humans ; Neoplasms, Glandular and Epithelial/metabolism* ; Ovary/pathology*

OBJECTIVES: To explore the mechanism of cinnamic acid (CA) for improving doxorubicin-induced myocardial injury (DIC) in mice. METHODS: Network pharmacology analysis was used to obtain the key targets of CA and DIC. Male C57BL/6J mice were randomized into Sham, DOX, CA (25, 50 and 100 mg/kg)+DOX, and CA+Ferrostatin-1+DOX groups, and their myocardial function and pathology were examined by echocardiography and HE staining. Serum levels of CK-MB, LDH, MDA, IL-6, TNF‑α and myocardial ROS level were detected, and the expression levels of TLR4 and ferroptosis pathway proteins in myocardial tissue were detected by Western blotting. Cultured murine cardiomyocytes (HL-1 cells) with or without transfection with a small interfering RNA targeting TLR4 (si-TLR4) were treated with DOX or Erastin, and the cellular ROS content was measured by DCFH-DA staining; the expression level of GPX4 was detected using immunofluorescence staining. RESULTS: Network pharmacology analysis suggested that CA may improve DIC through TLR4 signaling. DOX treatment caused obvious myocardial injury in mice, which showed significantly increased serum levels of CK-MB, LDH, MDA, IL-6, TNF-α and myocardial ROS level with decreased myocardial levels of SLC7A11 and GPX4 proteins and increased levels of TLR4 and PTGS2 proteins. All these changes in the mouse models were significantly alleviated by treatment with CA, and the mice receiving CA or ferrostatin-1 treatment exhibited increased myocardial expressions of SLC7A11 and GPX4 proteins and lowered expressions of TLR4 and PTGS2 proteins. In cultured HL-1 cells, treatment with DOX and Erastin both obviously increased intracellular ROS level and decreased cellular GPX4 expression level, and these changes were strongly attenuated by TLR4 interference. CONCLUSIONS CA, as a potent herbal monomer, can effectively alleviate DIC in mice by inhibiting TLR4-mediated ferroptosis.
Animals ; Ferroptosis/drug effects* ; Toll-Like Receptor 4/metabolism* ; Myocytes, Cardiac/metabolism* ; Mice, Inbred C57BL ; Mice ; Male ; Doxorubicin/adverse effects* ; Cinnamates/pharmacology* ; Signal Transduction ; Reactive Oxygen Species/metabolism*

Objective:To explore the efficacy of long intramedullary nails versus short intramedullary nails in the treatment of AO/OTA 31-A3 intertrochanteric fractures.Methods:A retrospective analysis was conducted on 60 patients with AO/OTA 31-A3 intertrochanteric femur fractures treated between March 2019 and August 2022. The patients were randomly divided into two groups (the long nail group and the short nail group). Thirty-four patients were treated with long intramedullary nails, including 16 males and 18 females, aged 68.41±17.84 years old (range 31-96 years). Twenty-six patients were treated with short intramedullary nails, including 13 males and 13 females, aged 72.23±13.97 years old (range 31-90 years). The causes of injury, fracture classification (AO/OTA classification), intraoperative blood loss, operation time, fracture healing time, imaging indexes (fracture reduction quality, postoperative neck trunk angle, and medial support), Harris score of the hip joint at the last follow-up, one-year mortality rates and complications were compared between the two groups.Results:The follow-up time was 24.26±6.67 months in the long nail group and 24.31±5.60 months in the short nail group, and the general information of the two groups were comparable. Between the long nail and short nail group, the intraoperative blood loss was 281.47±235.28 ml vs. 121.92±84.14 ml and the operation time was 110.44±24.63 min vs. 81.15±28.54 min with significant differences ( P<0.05). While the length of hospital stay was 12.35±4.81 d vs. 10.89±4.30 d, the good rate of fracture reduction was 55.9% vs. 61.53%, the fracture healing time was 120.44±16.43 d vs. 128.07±18.33 d, the presence rate of medial support was 67.6% vs. 79.4%, and the excellent rate of Harris score was 65.4% vs. 65.4% with no significant difference between the two groups ( P>0.05). One-year mortality rates was 5.3% vs. 7.1% and complications was 11.7% vs. 15.4% with no significant difference between the two groups ( P>0.05). Conclusion:Both long intramedullary nails and short intramedullary nails are effective in the treatment of AO/OTA 31-A3 intertrochanteric femur fractures. However, surgical time and intraoperative blood loss was less in the short nail group.

Objective:To design a fully integrated multi-channel implantable brain-computer interface electrical stimulation system.Methods:The human-computer interaction interface of the upper computer was set by users, and the data was packaged via a self-built protocol. When parameters were transmitted to the field programmable gate array (FPGA) chip through the Bluetooth module, the stimulation chip was controlled after the parameter analysis was completed. Eventually the user-set current stimulation was output. To verify the system feasibility, the accuracy of the single-channel stimulation waveform, the multi-channel output capability, and the adjustable range of the parameter were tested separately.Results:It realized 16 channels of time-sharing differential stimulation current output, the output stimulation current waveform was dual-phase equal-width pulse, the amplitude ranged within 4~1 000 μA, the pulse single-phase width range was 10~1 000 μs, the cycle time was 1~1 000 ms, thus the current parameters could be accurately adjusted.Conclusions:A fully integrated multi-channel implantable brain-computer interface electrical stimulation system was completed.

Osteoarthritis (OA) is a chronic degenerative joint disease whose main characteristic is the destruction of articular cartilage, causing pain and disability in patients and seriously affecting their quality of life. OA can be induced by a variety of causes, and pathological changes in articular cartilage are considered to be one of the key driving factors for the occurrence of OA. High mobility group box-1 protein (HMGB1), as a non-histone protein in eukaryotic cells, can participate in regulating the inflammation and apoptosis process of OA chondrocytes, thus leading to the occurrence of OA. This article reviews the research on the mechanism of HMGB1 in OA chondrocytes, with a view to providing new ideas for the clinical prevention and treatment of OA.

Objective To generate a stable kidney-specific deletion of augmenter of liver regeneration(ALR)mice and provide an animal model for further studying the biological function of ALR in the kidney.In addition,we further explored the effect of ALR on renal tubulointerstitial fibrosis.Methods Mating and identification of ALRflox/+/Ggt1-Cre mice with ALRflox/flox mice was carried out,and the ALRflox/flox/Ggt1-Cre mice were screened.Mating and identification of ALRflox/flox/Ggt1-Cre mice with ALRflox/flox mice were carried out,and screening the ALRflox/flox/Ggt1-Cre mice was performed.The ALRflox/flox/Ggt1-Cre mouse was a kidney-specific ALR knockout mouse and the ALRflox/flox mouse was a control mouse.The mouse genotypes were identified by PCR;the expression of ALR protein and mRNA levels in mouse liver were detected by Western blotting and real-time PCR;ALR expression in mouse kidney was detected by immunofluorescence.The kidney tissue morphology of the mouse kidney was observed using hematoxylin-eosin staining,periodic acid Schiff's reaction and Masson stain.Flow cytometry,immunohistochemistry,immunofluorescence and real time PCR analyses were used to determine macrophage phenotype.Results PCR results indicate that mouse genotypes are consistent with ALRflox/flox/Ggt1-Cre.Compared with ALRflox/flox mice,ALRflox/flox/Ggt1-Cre mice showed lower levels of ALR mRNA and protein,more interstitial inflammatory cells in kidney tissue,broken basement membrane of the renal tubules,the brush-border damage and significant interstitial fibrosis.After the kidney-specific ALR gene was knocked out,macrophages infiltrated the kidney tissue o and the polarization process of macrophages from M1 to M2 was reduced.Conclusion In this study,the kidney-specific deletion of ALR mouse was successfully constructed using the Cre/Loxp technology,which providing an important animal model for further study of the role of ALR genes.And ALR deficiency promotes renal fibrosis in physiological conditions.

Objective To generate a stable kidney-specific deletion of augmenter of liver regeneration(ALR)mice and provide an animal model for further studying the biological function of ALR in the kidney.In addition,we further explored the effect of ALR on renal tubulointerstitial fibrosis.Methods Mating and identification of ALRflox/+/Ggt1-Cre mice with ALRflox/flox mice was carried out,and the ALRflox/flox/Ggt1-Cre mice were screened.Mating and identification of ALRflox/flox/Ggt1-Cre mice with ALRflox/flox mice were carried out,and screening the ALRflox/flox/Ggt1-Cre mice was performed.The ALRflox/flox/Ggt1-Cre mouse was a kidney-specific ALR knockout mouse and the ALRflox/flox mouse was a control mouse.The mouse genotypes were identified by PCR;the expression of ALR protein and mRNA levels in mouse liver were detected by Western blotting and real-time PCR;ALR expression in mouse kidney was detected by immunofluorescence.The kidney tissue morphology of the mouse kidney was observed using hematoxylin-eosin staining,periodic acid Schiff's reaction and Masson stain.Flow cytometry,immunohistochemistry,immunofluorescence and real time PCR analyses were used to determine macrophage phenotype.Results PCR results indicate that mouse genotypes are consistent with ALRflox/flox/Ggt1-Cre.Compared with ALRflox/flox mice,ALRflox/flox/Ggt1-Cre mice showed lower levels of ALR mRNA and protein,more interstitial inflammatory cells in kidney tissue,broken basement membrane of the renal tubules,the brush-border damage and significant interstitial fibrosis.After the kidney-specific ALR gene was knocked out,macrophages infiltrated the kidney tissue o and the polarization process of macrophages from M1 to M2 was reduced.Conclusion In this study,the kidney-specific deletion of ALR mouse was successfully constructed using the Cre/Loxp technology,which providing an important animal model for further study of the role of ALR genes.And ALR deficiency promotes renal fibrosis in physiological conditions.