Objective: To explore the possibility of performing allogeneic platelet-rich plasma (PRP) treatment for patients who were not suitable for autologous PRP collection through case reports of two patients with refractory wounds treated with allogeneic PRP. Methods: The ABO-compatible allogeneic whole blood was centrifuged 3 times to obtain allogeneic PRP within 6 hours of blood collection. Then the qualified allogeneic PRP was applied to 2 cases of refractory wound on the same day. Results: The platelet concentration in allogeneic PRP was higher than 1 000×10 /L, and the test results of infectious diseases, as well as the mixing of red blood cells and white blood cells, met the standard of quality control. Both patients achieved satisfactory wound healing outcomes (3 d). Conclusions: For patients who were not suitable for autologous PRP treatment, allogeneic PRP might be a new option.

Myelodysplastic syndrome (MDS), a myeloid tumor derived from the malignant clones of hematopoietic stem cells, has an annually increasing incidence. The contemporary research direction has shifted to analyzing the synergistic effect of immune surveillance collapse and abnormal bone marrow microenvironment in the pathological process of MDS. Against this backdrop, the immune checkpoint molecule TIM3 has emerged as a key target because of its persistently high expression on the surface of important immune cells such as T and NK cells. The abnormal activation of the TIM3 pathway is the mechanism by which solid tumors and hematological malignancies achieve immune escape and is a key hub in the formation of immune exhaustion phenotypes. This work integrates the original discoveries of our team with the latest international progress, systematically demonstrating the bidirectional regulatory network of TIM3 between the malignant clone proliferation of MDS and the immunosuppressive microenvironment. Integrating the evidence from emerging clinical trials allows us to consider the clinical significance of TIM3-targeted blocking for MDS, providing a transformative path to overcome the resistance of traditional treatments and marking a new chapter in the active immune reconstitution of MDS treatment.

Hearing loss is the most prevalent disabling disease. Cochlear implantation（CI） serves as the primary intervention for severe to profound hearing loss. This consensus systematically explores the value of genetic diagnosis in the pre-operative assessment and efficacy prognosis for CI. Drawing upon domestic and international research and clinical experience, it proposes an evidence-based medicine three-tiered prognostic classification system（Favorable, Marginal, Poor）. The consensus focuses on common hereditary non-syndromic hearing loss（such as that caused by mutations in genes like GJB2, SLC26A4, OTOF, LOXHD1） and syndromic hereditary hearing loss（such as Jervell & Lange-Nielsen syndrome and Waardenburg syndrome）, which are closely associated with congenital hearing loss, analyzing the impact of their pathological mechanisms on CI outcomes. The consensus provides recommendations based on multiple round of expert discussion and voting. It emphasizes that genetic diagnosis can optimize patient selection, predict prognosis, guide post-operative rehabilitation, offer stratified management strategies for patients with different genotypes, and advance the application of precision medicine in the field of CI.
Humans ; Cochlear Implantation ; Prognosis ; Hearing Loss/surgery* ; Consensus ; Connexin 26 ; Mutation ; Sulfate Transporters ; Connexins/genetics*

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation and joint damage, accompanied by the accumulation of plasma cells, which contributes to its pathogenesis. Understanding the genetic alterations occurring during plasma cell differentiation in RA can deepen our comprehension of its pathogenesis and guide the development of targeted therapeutic interventions. Here, our study elucidates the intricate molecular mechanisms underlying plasma cell differentiation by demonstrating that PRDX1 interacts with DOK3 and modulates its degradation by the autophagy-lysosome pathway. This interaction results in the inhibition of plasma cell differentiation, thereby alleviating the progression of collagen-induced arthritis. Additionally, our investigation identifies Salvianolic acid B (SAB) as a potent small molecular glue-like compound that enhances the interaction between PRDX1 and DOK3, consequently impeding the progression of collagen-induced arthritis by inhibiting plasma cell differentiation. Collectively, these findings underscore the therapeutic potential of developing chemical stabilizers for the PRDX1-DOK3 complex in suppressing plasma cell differentiation for RA treatment and establish a theoretical basis for targeting PRDX1-protein interactions as specific therapeutic targets in various diseases.

Hearing loss is one of the most prevalent sensory disorders affecting the human nervous system. Liquid-liquid phase separation (LLPS) is a physiological process that facilitates the reversible and dynamic assembly of biomolecular condensates. Increasing evidence suggests that LLPS plays a significant role in the pathogenesis of hereditary hearing loss. Nevertheless, there is a conspicuous lack of systematic investigations exploring the impact of LLPS abnormalities on the etiology of hereditary hearing loss. In this review, we examine the mechanisms by which dysfunctions in LLPS contribute to hereditary hearing loss, specifically focusing on its effects on mechanoelectrical transduction in hair bundles, transcriptional regulation, post-transcriptional modifications, the actin cytoskeleton, ion homeostasis within the inner ear, and energy and redox homeostasis. Furthermore, we evaluate the considerable potential of targeting LLPS as a therapeutic approach for hearing loss and propose innovative perspectives on LLPS that may guide future research initiatives in the field of auditory disorders.
Humans ; Animals ; Hearing Loss/physiopathology* ; Phase Separation

Objective: For patients with elevated hematocrit (Hct), platelet-rich plasma (PRP) apheresis is prone to red blood cell contamination—commonly referred to as “flushing” or erythrocyte carryover—which compromises product quality and therapeutic efficacy. This study reports two clinicaly derived measures to mitigate this issue. Methods: For 21 patients with Hct ≥53%, intravenous 0.9% sodium chloride infusion before apheresis process (replacement method, n=13) or 0.9% sodium chloride fluids hemodilution within the centrifuge bowl during PRP apheresis process (dilution method, n=8) were given, respectively. The collection time, adverse reactions, and the celluar composition of PRP—including white blood cells, red blood cells, and platelet counts—were recorded and compared. Results: Neither method resulted in visible RBC contamination (“flushing”). The red blood cell counts [(0.021±0.014)×10 /L vs (0.019±0.011)×10 /L, P>0.05], white blood cell counts [(2.258±3.288) ×10 /L vs (0.557 5±1.203) ×10 /L, P>0.05], and platelet counts [(1 140±308.2)×10 /L vs (1 105±309.9)×10 /L, P>0.05] in the PRP products obtained by two methods all met the control standards of PRP. There was no significant difference [(2.268±0.927) vs (2.438±0.762) mL/min, P=0.669 2] between the two methods in terms of the speed of PRP collection. One case of adverse reaction occurred with the fluid replacement method, while no adverse reaction occurred with the dilution method. Conclusion: For patients with elevated Hct, both fluid replacement and dilution methods can effectively prevent RBC contamination during PRP collection, yielding products that meet clinical quality standards.

Objective: To summarize the treatment methods and efficacy of a patient with pure red cell aplasia (PRCA) after allogeneic hematopoietic stem cell transplantation (allo-HSCT), and to accumulate relevant case data. Methods: The clinical treatment and laboratory test data of a patient with PRCA after allo-HSCT in our hospital were retrospectively collected. The therapeutic strategy, monitoring parameters, and treatment outcomes were summarized. Results: Upon suspicion of post-transplant PRCA, the patient was promptly treated with intravenous injection of human immunoglobulin and three sessions of plasma exchange. The titer of blood group antibodies in the patient decreased, and the hemolytic symptoms were relieved. Over one year post-transplantation, the patient exhibited a sustained impairment of erythropoiesis, necessitating continued red blood cell transfusions. After treatment with intravenous daratumumab (400 mg twice weekly for 4 weeks), the pateint's hemoglobin (Hb) and reticulocyte (Ret) levels normalized rapidly, the ABO blood type converted from the recipient to the donor type, and the titer of IgM blood group antibodies returned to normal. The patient was successfully weaned off red blood cell transfusions, indicating the clinical efficacy of the treatment. Conclusion: Daratumumab shows effectiveness in the treatment of refractory PRCA after allo-HSCT in the case. It is essential to monitor Hb, Ret and the titer of blood group antibodies during treatment. Nevertheless, the interference of daratumumab with the titer of blood group antibodies should be considered.

Centrifugal therapeutic plasma exchange (CTPE), as an important therapeutic plasma separation technique, has gained widespread application in clinical treatment in recent years due to its high efficiency, safety, and operational flexibility. By utilizing centrifugal force to separate plasma from cellular blood components, CTPE demonstrates significant advantages over conventional membrane-based therapeutic plasma exchange (MTPE), particularly regarding therapeutic efficacy and procedural rapidity in managing complex diseases. This article provides a systematic review of the principles, operational procedures, and differences between CTPE and MTPE from the professional perspective of transfusion medicine specialists. It focuses on its applications in various clinical conditions and introduces advanced techniques in CTPE. By integrating the latest research findings and clinical practice experience, this article aims to provide theoretical basis and practical guidance for transfusion medicine specialists and related clinical personnel, thereby promoting the standardisation and optimisation of CTPE technology.

Cancer is a leading cause of mortality in children and results in a significant disease burden. Lipid metabolic reprogramming emerges as a pivotal cancer hallmark, bearing profound implications for understanding tumorigenesis, developing treatment strategies, and improving prognoses. However, research on lipid metabolism and lipid nutritional interventions related to childhood cancers is notably limited compared to adult cancers. This review focused on the current understanding of fatty acid, cholesterol, and phospholipid metabolism in childhood cancers and discussed the correlation between major lipid dietary patterns (such as high-fat, ketogenic, and Mediterranean diets) and the development and progression of childhood cancers. This review also highlighted existing research gaps on the mechanisms of lipid metabolism and the effects of major lipid dietary patterns, and warranted improved research depth, experimental design, and sample size. Therefore, we advocate for future epidemiological, basic science, and multidisciplinary research in the field of childhood cancers to understand more comprehensively and profoundly the role of lipid nutrition in the prevention and treatment of pediatric cancers.

Background Natural pyrethrins have long been widely used in the fields of environmental and household hygiene. Studies have reported that natural pyrethrins have potential liver toxicity, but their specific mechanisms are still unclear yet. Objective To explore the effect of natural pyrethrins on DNA damage in human liver cells. Methods This study used human liver cell QSG7701 as an in vitro testing model. After exposure to DMSO and a series of concentrations of natural pyrethrins (5, 10, 20, and 40 μg·mL⁻¹) for 6 and 24 h, reactive oxygen species (ROS) was detected by fluorescence microscopy using a fluorescence probe, thiobarbituric acid reactive substance (TBARS) by colorimetric method using a microplate reader, DNA damage by comet assay through observing DNA fragment migration under microscope, and phospho H2AX (γH2AX) and 8-oxoguanine (8-oxoG) by immunofluorescence assay using a laser confocal microscope. Results As the exposure concentration of natural pyrethrins increased, the fluorescence intensity of ROS significantly increased in a concentration-dependent manner. The differences in ROS between the 10 μg·mL⁻¹ and above groups and the control group were statistically significant (P<0.01), and the ROS levels in the 20 μg·mL⁻¹ and 40 μg·mL⁻¹ treatment groups were 2.17 and 3.05 times higher than that in the control group respectively. The TBARS level increased in a concentration-dependent manner in natural pyrethrins treated cells (P<0.01), and the levels in the 20 μg·mL⁻¹ and 40 μg·mL⁻¹ treatment groups were 2.46 and 3.01 times higher than that in the control group respectively. The results of comet assay showed trailing formation of cellular DNA in each dose group; as the exposure concentration of natural pyrethrins increased, indicators such as tail DNA content (TDNA%), tail length (TL), tail moment (TM), and Olive tail moment (OTM) increased in a concentration-dependent manner. Compared with the control group, the differences in the indicators between the 20 μg·mL⁻¹ and above groups and the control group were statistically significant (P<0.01), especially in the 40 μg·mL⁻¹ treatment groups, where TDNA%, TL, TM, and OTM were (46.92 ± 3.52) %, (64.67± 4.16) μm, 30.96 ± 2.94, and 22.64 ± 3.89, respectively. The cellular immunofluorescence results showed that natural pyrethrins induced the formation of γH2AX and 8-oxoG, the fluorescence intensities of γH2AX and 8-oxoG increased in a concentration-dependent manner, and the differences between the 10 μg·mL⁻¹ and above groups and the control group were statistically significant (P<0.01). Conclusion Natural pyrethrins could induce DNA damage in human liver cells, and ROS-mediated oxidative stress may play an important role in its liver cell genotoxicity.