Objective To compare the clinical efficacy of typeⅡhybrid surgery versus Sun’s surgery in treating acute Stanford A aortic dissection. Methods A retrospective analysis was conducted on the clinical data of patients with acute Stanford A aortic dissection who were treated at the Central Hospital of Wuhan affiliated to Tongji Medical College, Huazhong University of Science and Technology from 2016 to 2022. According to the surgical method, patients were divided into a typeⅡhybrid group and a Sun’s surgery group, and the clinical efficacy of the two groups was compared. Results A total of 52 patients were included, with 22 in the typeⅡhybrid surgery group and 30 in the Sun’s surgery group. The typeⅡhybrid group consisted of 18 males and 4 females, with an average age of (58.18±6.00) years, while the Sun’s surgery group consisted of 22 males and 8 females, with an average age of (53.03±11.89) years. All surgeries were successfully completed. There were 4 (13.3%) perioperative deaths in the Sun’s surgery group, including 2 patients of multiple organ failure, 1 patient of paraplegia, and 1 patient of uncontrollable postoperative bleeding. There was 1 (4.5%) perioperative death in the typeⅡhybrid surgery group, who was suspected of acute coronary syndrome and took a loading dose of dual antiplatelet drugs preoperatively. The patient underwent secondary thoracotomy for hemostasis, was re-cannulated during the operation, and finally died of circulatory failure after implantation of intra-aortic balloon pumping. There was no statistical difference in perioperative mortality between the two groups (P=0.381). Compared with the Sun’s surgery group, the typeⅡhybrid surgery group had shorter cardiopulmonary bypass time [153.00 (135.00, 185.25) min vs. 182.50 (166.50, 196.75) min, P=0.013], aortic cross-clamping time [77.00 (70.50, 92.00) min vs. 102.50 (93.50, 109.75) min, P<0.001], postoperative ICU stay [4.00 (2.83, 6.00) days vs. 8.00 (6.38, 11.78) days, P<0.001], postoperative ventilator support time [72.00 (29.50, 93.25) h vs. 87.65 (39.13, 139.13) h, P=0.138], less intraoperative blood loss [(1586.82±209.41) mL vs. (1 806.00±292.62) mL, P=0.004], postoperative 24 h drainage volume [612.50 (507.50, 762.50) mL vs. 687.50 (518.75, 993.75) mL, P=0.409], and shorter postoperative hospital stay [18.00 (13.00, 20.25) days vs. 22.00 (17.00, 29.25) days, P=0.013]. There was no statistically significant difference in the incidence of other early postoperative complications such as secondary thoracotomy for hemostasis, tracheotomy, renal dysfunction requiring dialysis, stroke, and paraplegia between the two groups (P>0.05). Conclusion For patients with acute Stanford A aortic dissection, typeⅡhybrid surgery is safe and effective; compared with traditional Sun’s surgery, typeⅡhybrid surgery has relatively less trauma, lower incidence of complications, satisfactory short-term results, and further research is needed on long-term prognosis.

This study aims to investigate the effect of Chaijin Jieyu Anshen Formula on the neuroinflammation of rats with insomnia complicated with depression through the regulation of triggering receptor expressed on myeloid cells 2(TREM2)/complement protein C1q signaling pathway. Rats were randomly divided into a normal group, a model group, a positive drug group, as well as a high, medium, and low-dose groups of Chaijin Jieyu Anshen Formula, with 10 rats in each group. Except for the normal group, the other groups were injected with p-chlorophenylalanine and exposed to chronic unpredictable mild stress to establish the rat model of insomnia complicated with depression. The sucrose preference experiment, open field experiment, and water maze test were performed to evaluate the depression in rats. Enzyme-linked immunosorbent assay was employed to detect serum 5-hydroxytryptamine(5-HT), dopamine(DA), and norepinephrine(NE) levels. Hematoxylin and eosin staining and Nissl staining were used to observe the damage in nucleus accumbens neurons. Western blot and immunofluorescence were performed to detect TREM2, C1q, postsynaptic density 95(PSD-95), and synaptophysin 1(SYN1) expressions in rat nucleus accumbens, respectively. Golgi-Cox staining was utilized to observe the synaptic spine density of nucleus accumbens neurons. The results show that, compared with the model group, Chaijin Jieyu Anshen Formula can significantly increase the sucrose preference as well as the distance and number of voluntary activities, shorten the immobility time in forced swimming test and the successful incubation period of positioning navigation, and prolong the stay time of space exploration in the target quadrant test. The serum 5-HT, DA, and NE contents in the model group are significantly lower than those in the normal group, with the above contents significantly increased after the intervention of Chaijin Jieyu Anshen Formula. In addition, Chaijin Jieyu Anshen Formula can alleviate pathological damages such as swelling and loose arrangement of tissue cells in the nucleus accumbens, while increasing the Nissl body numbers. Chaijin Jieyu Anshen Formula can improve synaptic damage in the nucleus accumbens and increase the synaptic spine density. Compared to the normal group, the expression of C1q protein was significantly higher in the model group, while the expression of TREM2 protein was significantly lower. Compared to the model group, the intervention with Chaijin Jieyu Anshen Formula significantly downregulated the expression of C1q protein and significantly upregulated the expression of TREM2. Compared with the model group, the PSD-95 and SYN1 fluorescence intensity is significantly increased in the groups receiving different doses of Chaijin Jieyu Anshen Formula. In summary, Chaijin Jieyu Anshen Formula can reduce the C1q protein expression, relieve the TREM2 inhibition, and promote the synapse-related proteins PSD-95 and SNY1 expression. Chaijin Jieyu Anshen Formula improves synaptic injury of the nucleus accumbens neurons, thereby treating insomnia complicated with depression.
Animals ; Male ; Rats ; Nucleus Accumbens/metabolism* ; Drugs, Chinese Herbal/administration & dosage* ; Depression/complications* ; Membrane Glycoproteins/genetics* ; Rats, Sprague-Dawley ; Sleep Initiation and Maintenance Disorders/complications* ; Neurons/metabolism* ; Receptors, Immunologic/genetics* ; Signal Transduction/drug effects* ; Synapses/metabolism*

OBJECTIVE: Glucocorticoid-induced osteoporosis (GIOP) is a common complication of prolonged glucocorticoid therapy. Chlorogenic acid (CGA), a polyphenol with antioxidant properties that is extracted from traditional Chinese medicines such as Eucommiae Cortex, has potential anti-osteoporotic activity. This study aimed to investigate the possible effects of CGA on GIOP in mice and murine long bone osteocyte Y4 (MLO-Y4) cells and explore the underlying molecular mechanisms. METHODS: The protective effects of CGA were initially evaluated in the GIOP mouse model induced by dexamethasone (Dex). The micro-computed tomography, hematoxylin-eosin staining, silver nitrate staining, and serum detection were used to assess the efficacy of CGA for improving bone formation in vivo. Then, network pharmacology analysis was used to predict the potential targets and molecular mechanisms underlying the therapeutic efficacy of CGA against GIOP. After that, 2',7'-dichlorofluorescein diacetate staining, flow cytometry, real-time quantitative reverse transcription polymerase chain reaction, and Western blotting were used to verify the mechanisms of CGA against GIOP in vitro. RESULTS: Animal experiments showed that CGA treatment effectively attenuated Dex-induced decreases in bone mass and strength and improved disrupted osteocyte morphology in mice. The protein-protein interaction analysis highlighted erb-b2 receptor tyrosine kinase (ERBB2), which is also known as human epidermal growth factor receptor 2 (HER2), caspase-3, kinase insert domain receptor, matrix metallopeptidase 9, matrix metallopeptidase 2, proto-oncogene tyrosine-protein kinase Src, and epidermal growth factor receptor as core targets. The Kyoto Encyclopedia of Genes and Genomes analysis revealed several significantly enriched pathways (P < 0.05), including the ERBB, phosphoinositide 3 kinase-AKT serine/threonine kinase 1 (AKT), and mechanistic target of rapamycin kinase (mTOR) pathways. Cellular experiments verified that CGA enhanced bone formation and promoted autophagy while inhibiting apoptosis in MLO-Y4 cells exposed to Dex, which was associated with the upregulated expression of HER2 and activation of the HER2/AKT/mTOR signaling pathway. CONCLUSION CGA exerted anti-osteoporotic effects against GIOP, partially through targeting osteocytes and modulating the HER2/AKT/mTOR signaling pathway. Please cite this article as: Xie AN, Zhang SZY, Zhang Y, Cao JL, Wang CL, Wang LB, Wu HJ, Zhang J, Dai WW. Chlorogenic acid mitigates glucocorticoid-induced osteoporosis via modulation of HER2/AKT/mTOR signaling pathway. J Integr Med. 2025; 23(6):670-682.
Animals ; Chlorogenic Acid/therapeutic use* ; Osteoporosis/metabolism* ; Signal Transduction/drug effects* ; Proto-Oncogene Proteins c-akt/metabolism* ; TOR Serine-Threonine Kinases/metabolism* ; Mice ; Glucocorticoids/adverse effects* ; Receptor, ErbB-2/metabolism* ; Proto-Oncogene Mas ; Dexamethasone/adverse effects* ; Osteocytes/drug effects* ; Osteogenesis/drug effects* ; Male ; Cell Line ; Mice, Inbred C57BL ; Humans

Objective:To investigate the role of alkylation repair homolog 5(ALKBH5)-mediated N6-methyladenosine(m6A)modifi-cation in endometrial decidualization.Methods:The mouse models of pregnancy and pseudopregnancy were established,and quantita-tive real-time PCR and Western blot were used to measure the expression pattern of ALKBH5 in the endometrium.The mouse and cell models of artificially induced decidualization were established,and quantitative real-time PCR,Western blot,and immunohistochemis-try were used to measure the expression levels of decidualization-related markers.The EpiQuik m6A RNA methylation quantification kit was used to measure the level of m6A.The mouse and cell models of artificially induced decidualization with interference of ALKBH5 expression were established,and quantitative real-time PCR,Western blot,and immunohistochemistry were used to measure the expression levels of decidualization-related markers,cell proliferation marker molecules,and apoptosis molecules.Flow cytometry was used to measure cell apoptosis rate.Results:In the mouse model of pregnancy,the expression level of ALKBH5 at the uterine em-bryo implantation site was significantly higher than that adjacent to the implantation site,and in the mouse and cell models of artifi-cially induced decidualization,compared with the control group,the induction group had a significant increase in the expression level of ALKBH5 and a significant reduction in the level of m6A.Inhibiting the expression of ALKBH5 led to an increase in the level of m6A,which in turn inhibited the proliferation of stromal cells,induced cell apoptosis,and ultimately impaired the normal process of en-dometrial decidualization.Conclusion:ALKBH5 deficiency leads to an increase in the level of m6A and decidualization injury in the en-dometrium,which lays a foundation for the research on m6A modifi-cation in decidualization.

The concept of "qi deficiency with stagnation" refers to a pathological state characterized by the depletion of primordial qi， impaired qi transformation， and the development of internal stagnation. Under the cyclic chemotherapy regimen in oncology， chemotherapy-induced myelosuppression follows a progressive pathological course from qi deficiency to increasing stagnation. This sequential evolution from mild to severe myelosuppression closely aligns with the dynamic syndrome differentiation and treatment framework of "qi deficiency with stagnation". "Qi deficiency" reflects the gradual depletion of qi， blood， and essence， while "stagnation" refers to the accumulation of phlegm， turbid dampness， and blood stasis. These two components interact reciprocally， forming a vicious cycle where deficiency leads to stagnation， and stagnation further damages the healthy qi. In the early stage of mild myelosuppression， chemotoxicity begins to accumulate in the bone marrow， leading to qi consumption， blood deficiency， yin injury， and the gradual formation of turbid phlegm and damp stagnation. In the advanced stage of severe myelosuppression， the accumulation of toxicity causes qi sinking， exhaustion of essence， and marrow depletion， along with blood stasis obstructing the collaterals. Treatment strategies should be based on syndrome differentiation， with an emphasis on assessing the severity of the condition， balancing deficiency and excess， and achieving both symptomatic relief and root cause resolution.

Establishing a scientific talent classification evaluation mechanism is of great significance for public hospitals to motivate and guide the career development of various types of talents and to promote the high-quality development of the health and medical care industry. However, university-affiliated hospitals had long faced issues such as an imperfect talent classification evaluation system, difficulty in setting evaluation indicators, a relatively monolithic evaluation method, and insufficient application of evaluation results. In 2019, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, initiated a talent stratification and classification management mechanism. The hospital established separate evaluation indicator systems for clinical, research, and teaching talents, and adhered to a value orientation that equally emphasizes medical care, teaching, and research. Additionally, a diversified evaluation mode was constructed, led by the hospital with the participation of peers and the public. Emphasis was also placed on linking evaluation results with talent development, rewards, and excellence awards. The initiative has achieved positive outcomes and can serve as a reference for talent management in other university-affiliated hospitals and relevant departments.

Objective:To evaluate the feasibility of the novel programmed death-ligand 1 (PD-L1)-targeted PET/CT molecular probe for evaluating PD-L1 expression and tumor heterogeneity in patients with non-small cell lung cancer (NSCLC).Methods:From October 2023 to October 2024, 30 patients (21 males, 9 females; age 69(58, 75) years) with newly diagnosed NSCLC at the First Affiliated Hospital of Xiamen University were prospectively enrolled. All patients underwent PET/CT imaging 1 h after intravenous administration of 68Ga-1, 4, 7-triazacyclononane-1, 4, 7-triacetic acid (NOTA)-DK224, and SUV max was calculated. Immunohistochemical staining on biopsy samples of patients were performed and the PD-L1 tumor proportion score (TPS) was calculated. The differences of SUV max between two groups were compared by using Mann-Whitney U test. Results:Of 30 patients, 31 biopsy specimens were obtained including 24 primary lesion biopsies, 1 lymph node lesion biopsy, and 6 metastatic lesion biopsies, with 16 TPS<1%, 9 1%≤TPS<50% and 6 TPS≥50%. PD-L1-positive tumors showed relatively high uptake of 68Ga-NOTA-DK224. The SUV max of TPS≥1% group was significantly higher than that of TPS<1% group (6.9(5.1, 7.7) vs 3.8(3.1, 4.2); Z=-4.47, P<0.001), and SUV max of TPS≥50% group was significantly higher than that of TPS<50% group (8.6(7.3, 12.4) vs 4.2(3.7, 5.3); Z=-3.65, P<0.001). Of 30 patients, 24 had multiple metastatic lesions with 212 lesions in total. The median fold difference was 2.3 (range: 1.4-6.0), and the median CV was 28.3% (range: 11.7%-61.6%). Conclusion:68Ga-NOTA-DK224 PET/CT is able to accurately and comprehensively reflect PD-L1 expression and tumor heterogeneity in primary and metastatic NSCLC.