Knee osteoarthritis (KOA) is a prevalent degenerative joint disease characterized by synovial inflammation, cartilage loss. Often manifesting as joint pain and limited mobility, it severely affects the quality of life of patients. Traditional treatment methods such as pharmacological injections and surgical interventions primarily aim to alleviate symptoms but have limited effects on cartilage repair. Human umbilical cord mesenchymal stem cells (hUC-MSCs), due to their anti-inflammatory and chondrogenic capabilities, is considered a new hope for the treatment of KOA. This article synthesizes the latest research findings from both domestic and international sources to discuss the theoretical basis for the clinical application of hUC-MSCs in treating KOA, clinical study design, and efficacy evaluation. It also addresses the challenges in the clinical application of hUC-MSCs and explores future directions, in the hope of providing feasible theoretical support for the treatment of KOA with hUC-MSCs.

[Objective] To explore the strategy of blood management in patients with massive transfusion in the frigid plateau region. [Methods] The treatment process of a patient with liver rupture in the frigid plateau region was analyzed, and the blood management strategy of the frigid plateau region was discussed in combination with the difficulties of blood transfusion and literature review. [Results] The preoperative complete blood count (CBC) test results of the patient were as follows: RBC 3.14×10¹²/L, Hb 10⁶ g/L, HCT 30.40%, PLT 115.00×10⁹/L; coagulation function: PT 18.9 s, FiB 1.31 g/L, DD > 6 μg/mL, FDP 25.86 μg/mL; ultrasound examination and imaging manifestations suggested liver contusion and laceration / intraparenchymal hematoma, splenic contusion and laceration, and massive blood accumulation in the abdominal cavity; it was estimated that the patient's blood loss was ≥ 2 000 mL, and massive blood transfusion was required during the operation; red blood cell components were timely transfused during the operation, and the blood component transfusion was guided according to the patient's CBC and coagulation function test results, providing strong support and guarantee for the successful treatment of the patient. The patient recovered well after the operation, and the CBC test results were as follows: RBC 4.32×10¹²/L, Hb 144 g/L, HCT 39.50%, PLT 329.00×10⁹/L; coagulation function: APTT 29.3 s, PT 12.1 s, FiB 2.728 g/L, DD>6 μg/mL, FDP 25.86 μg/mL. The patient was discharged after 20 days, and regular follow-up reexamination showed no abnormal results. [Conclusion] Individualized blood management strategy should comprehensively consider the patient’s clinical symptoms, the degree of hemoglobin decline, dynamic coagulation test results and existing treatment conditions. Efficient and reasonable patient blood management strategies can effectively improve the clinical outcomes of massive transfusion patients in the frigid plateau region.

In recent years, growing interest has been directed toward the application of platelet derivatives in regenerative medicine, cell therapy and targeted drug delivery. This article analyzes the basis and classification of platelet derivatives, discusses their clinical applications, and addresses main challenges such as the quantification and standardization of preparation process— particularly when used as individualized biologics, as well as the uncertainty and lack of comparability across experimental results. Countermeasures and improvements are provided, suggesting that standardized and normative management may offer new opportunities for the clinical use of platelet derivatives.

Pre-admission is a critical initiative to optimize medical service processes and alleviate the challenge of "difficult access to healthcare. "However, there is currently a lack of standardized protocols for pre-admission procedures. This study aims to systematically analyze key nodes and risk factors in pre-admission process design and propose optimization strategies, providing a foundation for policy formulation and hospital practices. By constructing a "forward-reverse" dual-process model of pre-admission and identifying risk points based on stakeholder theory (patients, hospitals, healthcare administration, and insurance), the study reveals that while pre-admission can reduce the average length of stay, improve bed turnover rates, and enhance patient satisfaction, it also presents risks such as cross-period financial settlement, challenges in insurance policy adaptability, demands for information system integration, and the need for defining medical safety boundaries. To optimize the pre-admission process and mitigate these risks, this study explores framework improvements in areas including eligibility criteria, mode selection, cost settlement, transition between pre-admission and inpatient status, and cancellation of pre-admission, offering practical guidance for public hospitals. The authors argue that pre-admission requires tripartite collaboration among hospitals, insurers, and healthcare administrations: hospitals should establish top-level design, continuously refine processes, and implement dynamic risk assessment mechanisms; insurance providers should support cross-period settlement policies; and healthcare administrations should issue guiding policies or standardized protocols. Through multi-department coordination and collaborative efforts, the optimization and innovation of pre-admission processes can be advanced, ultimately delivering more efficient and convenient healthcare experiences for patients.

Circulating tumor cells (CTCs) have the ability to sow tumors and can be found in the peripheral blood of patients with precancerous lesions and healthy people. However, CTCs are not currently screened in the donors blood. A large number of allogeneic blood transfusions occurred worldwide each year, and allogeneic blood transfusions expose recipients to the risk of transmission and affect tumors associated with donor CTCs. Although leukocyte filtration can not completely remove tumor cells in the blood, it can effectively reduce the number of white blood cells in the blood and reduce their proliferation ability. Blood irradiation can effectively destroy the DNA of CTCs in the blood, and inhibit the occurrence and metastasis of tumors caused by the infusion of allogeneic blood containing CTCs. Therefore, we should pay attention to the potential risk of CTCs on clinical transfusion, and strengthen the preclinical treatment of blood to avoid donor-related tumor infection in blood recipients due to clinical transfusion.

[摘 要] 目的：探讨透明质酸介导运动受体（HMMR）在食管鳞状细胞癌（ESCC）细胞恶性进展中的作用及其潜在的分子机制。方法：收集2018年1月至2020年12月期间在河北医科大学第四医院手术切除的8例ESCC组织及癌旁组织标本，以及ESCC细胞KYSE-30和KYSE-150。利用WB法和免疫组化（IHC）法检测HMMR在ESCC组织中的表达情况。采用RNA干扰技术，在KYSE-30和KYSE-150细胞中敲低HMMR表达，qPCR法和WB法检测敲低效果，通过CCK-8实验和Transwell实验分别检测敲低HMMR对ESCC细胞增殖和侵袭能力的影响。4-硝基喹啉1-氧化物（4NQO）诱导小鼠致癌建立ESCC模型，H-E染色观察食管的形态变化，IHC法分析HMMR、序列相似性家族83成员D（FAM83D）、上皮钙黏素（E-cadherin）和神经钙黏素（N-cadherin）在小鼠不同癌变程度组织中的表达情况。结果：人ESCC组织中HMMR表达水平显著高于癌旁组织（均P < 0.05）。敲低HMMR后，KYSE-30和KYSE-150细胞的增殖和侵袭能力均显著降低（P < 0.05或P < 0.01），同时降低了FAM83D的表达水平（均P < 0.01）。裸鼠成瘤实验中，4NQO组小鼠体质量均低于对照组（均P < 0.05）；IHC法染色结果显示，肿瘤组织中HMMR呈高表达（P < 0.05），其中在高级别上皮内瘤变（HGIN）组织中的表达显著高于低级别上皮内瘤变（LGIN）组织（P < 0.001）。HMMR与FAM83D、N-cadherin表达呈显著正相关（r = 0.724、0.870，均P < 0.001），与E-cadherin表达呈显著负相关（r = -0.714，P < 0.001）。结论：HMMR在ESCC组织中呈高表达，其可能通过上调FAM83D表达水平促进ESCC的进展。

The paper summarizes Professor YANG Jun's thoughts on clinical treatment with acupuncture and moxibustion. Professor YANG Jun puts forward the "refined mode for diagnosis and treatment of diseases with acupuncture and moxibustion", aiming to improve the capacity of diagnosis and treatment in clinical practice. He advocates that the diagnosis and treatment should be guided by the identification of etiologies, syndromes and meridians; in accordance with regulating the shape/form, balancing yin and yang, and harmonizing the mind; and by means of skillful techniques of acupuncture and moxibustion, simplified selection of acupoints and delicate manipulations. Besides, he stresses on the combination of multiple techniques of acupuncture (such as penetrating technique with long needle, stuck needling by lifting and pulling, and micro-acupuncture systems) with moxibustion techniques (moxibustion for resolving stasis and unblocking collaterals, pressing moxibustion, borneol moxibustion, moxibustion with medicinal plaster) in clinical practice, so as to enhance the therapeutic effects.
Moxibustion/methods* ; Acupuncture Therapy/methods* ; Humans ; China ; Acupuncture Points

Metastatic dissemination is the major cause of death from breast-cancer (BC). Fusobacterium nucleatum (F.n) is widely enriched in BC and has recently been identified as one of the high-risk factors for promoting BC metastasis. Here, with an experimental model, we demonstrated that intratumoral F.n induced BC aggressiveness by transcriptionally activating Epithelial-mesenchymal transition-associated genes. Therefore, the F.n may be a potential target to prevent metastasis. Given the fact that cancer-associated fibroblasts (CAFs) are abundant in BC and located near blood vessels, we report an optogenetic system that drives CAF to in situ produce human antibacterial peptide LL37, with the characteristics of biosafety and freely intercellular trafficking, for depleting intratumoral F.n, leading to a 72.1% reduction in lung metastatic nodules number without affecting the balance of the systemic flora. Notably, mild photothermal treatment was found that could normalize CAF, contributing to synergistically inhibiting BC metastasis. In addition, the system can also simultaneously encode a gene of TNF-related apoptosis-inducing ligand to suppress the primary tumor. Together, our study highlights the potential of local elimination of tumor pathogenic bacteria to prevent BC metastasis.

OBJECTIVES: To investigate the mechanism by which Guijianyu ameliorates podocyte injury in a mouse model of diabetic kidney disease (DKD) induced by advanced glycation endproducts (AGEs). METHODS: Sixty db/db mouse models of DKD were randomized equally into 5 groups for treatment with saline, Guijianyu extract at 3 doses or irbesartan for 12 weeks, and the changes in renal pathology and structure were observed using transmission electron microscopy, and the expressions of related genes and key proteins were detected using RT-qPCR and immunohistochemistry. In cultured MPC-5 cells incubated with 50 mg/L AGEs-BSA for 24 h, the effect of different concentrations of Guijianyu extract on cell viability was examined with CCK-8 assay; Western blotting was performed to detect the protein expressions of RAGE, VEGFA, TNF-α, NF-κB(p65), IL-6 and caspase-3, and the mRNA expressions of RAGE, NF-κB (p65), VEGFA and IL-6 were detected with RT-qPCR. RESULTS: In mouse models of DKD, treatment with high-dose Guijianyu extract significantly reduced renal expressions of RAGE, VEGFA, NF-κB(p65), and IL-6 proteins and the mRNA expressions of RAGE, NF-κB, and IL-6. In MPC-5 cells, exposure to AGEs significantly reduced cell viability and increased the protein expressions of RAGE, NF‑κB (p65), VEGFA, TNF-α, IL-6 and caspase-3 (P<0.05) and mRNA expressions of RAGE, NF-κB (p65), VEGFA, and IL-6. Treatment with Guijianyu extract obviously improved cell viability and reduced the expressions of RAGE, NF-κB(p65), VEGFA, TNF-α, IL-6, and caspase-3. Furthermore, Guijianyu extract effectively reversed RAGE agonist-induced elevation of protein expressions of RAGE, VEGFA, TNF-α, IL-6, and caspase-3 and mRNA expressions of RAGE, NF-κB (p65), IL-6, and VEGFA in MPC-5 cells. CONCLUSIONS Guijianyu extract ameliorates AGEs-induced mouse renal podocyte injury in DKD by inhibiting the activation of AGEs-RAGE signaling pathway and reducing the expressions of pro-inflammatory cytokines and vascular endothelial growth factors.
Animals ; Glycation End Products, Advanced ; Drugs, Chinese Herbal/pharmacology* ; Mice ; Signal Transduction/drug effects* ; Podocytes/pathology* ; Diabetic Nephropathies/drug therapy* ; Receptor for Advanced Glycation End Products ; Vascular Endothelial Growth Factor A/metabolism* ; Interleukin-6/metabolism* ; Male

Approximately 20% to 30% of the global workforce is engaged in shift work. As a significant cause of circadian disruption, shift work is closely associated with an increased risk for periodontitis. Nevertheless, how shift work-related circadian disruption functions in periodontitis remains unknown. Herein, we employed a simulated shift work model constructed by controlling the environmental light-dark cycles and revealed that shift work-related circadian disruption exacerbated the progression of experimental periodontitis. RNA sequencing and in vitro experiments indicated that downregulation of the core circadian protein brain and muscle ARNT-like protein 1 (BMAL1) and activation of the Gasdermin D (GSDMD)-mediated pyroptosis were involved in the pathogenesis of that. Mechanically, BMAL1 regulated GSDMD-mediated pyroptosis by suppressing NOD-like receptor protein 3 (NLRP3) inflammasome signaling through modulating nuclear receptor subfamily 1 group D member 1 (NR1D1), and inhibiting Gsdmd transcription via directly binding to the E-box elements in its promoter. GSDMD-mediated pyroptosis accelerated periodontitis progression, whereas downregulated BMAL1 under circadian disruption further aggravated periodontal destruction by increasing GSDMD activity. And restoring the level of BMAL1 by circadian recovery and SR8278 injection alleviated simulated shift work-exacerbated periodontitis via lessening GSDMD-mediated pyroptosis. These findings provide new evidence and potential interventional targets for circadian disruption-accelerated periodontitis.
Pyroptosis/physiology* ; ARNTL Transcription Factors/metabolism* ; Animals ; Periodontitis/etiology* ; Mice ; Phosphate-Binding Proteins/metabolism* ; Shift Work Schedule/adverse effects* ; Intracellular Signaling Peptides and Proteins/metabolism* ; Mice, Inbred C57BL ; Male ; Disease Models, Animal ; Gasdermins