To prepare all-trans retinoic acid (ATRA) and irinotecan (IRI) co‑loaded liposomes (ATRA-IRI@Lip) and evaluate their in vitro therapeutic effects against anaplastic thyroid carcinoma (ATC) and their ability to eliminate cancer stem cells (CSCs).

Objective: To investigate the effect of exogenous supplementation of umbilical cord blood (UCB) immune cells on immune function reconstruction and hematopoietic function recovery in elderly high-risk myeloid neoplasms (MN) patients. Methods: The research includes clinical studies and cell experiments. Clinical data of elderly high-risk MN patients aged >60 years admitted to the Department of Hematology at the Second Hospital of Tianjin Medical University from January 2023 to June 2025 were retrospectively included. Based on treatment regimens, the patients were categorized into chemotherapy group ("3+7"regimen), demethylation therapy (HMA) group (decitabine-based therapy), and UCB group (venetoclax combined with azacitidine plus UCB reinfusion). At 28 days post-treatment, differences were compared among the groups regarding disease remission (complete remission rate), hematopoietic function reconstruction (recovery time of white blood cells and platelets), survival outcomes (overall survival rate and event-free survival rate), and cellular immune function reconstruction [levels of various CD4+T cells, CD8+T cells, natural killer (NK)cells, etc.]. To further confirm the role of UCB in the bone marrow microenvironment of MN patients, primary bone marrow cells were collected from 3 elderly high-risk MN patients in the UCB group (ileal bone marrow aspiration was performed on day 15 post-treatment and before UCB infusion, with 10 ml of bone marrow aspirated each time); additionally, UCB cells were obtained from 3 healthy donors (sourced from the Shandong Umbilical Cord Blood Hematopoietic Stem Cell Bank of China, all HLA 2/10 matched male donors). Based on different seeding methods of patient primary bone marrow cells and healthy donor UCB mononuclear cells in Transwell chambers, the cells were divided into a control group (patient bone marrow mononuclear cells cultured separately), an indirect co-culture group (non-contact co-culture of patient bone marrow mononuclear cells and UCB cells), and a direct co-culture group (contact co-culture of patient bone marrow mononuclear cells and UCB cells). After 48 hours of culture, the cells from the lower chamber and the supernatant were collected from each group. The proportional differences among immune cell subsets (various T-cell, B-cell, and NK cell subsets) were compared among the three groups, and the differences in cytokine levels among the three groups of the supernatants [tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6] were also compared. Results: A total of 109 patients were enrolled, including 54 males and 55 females, with an age range [M (Q1, Q3)] of 68 (60, 87) years. There were 38, 39, and 32 cases in the chemotherapy group, HMA group, and UCB group, respectively. Analysis of disease response revealed that the complete response rates in the UCB group [43.8% (14/32) vs 28.2% (11/39), P<0.001] and the chemotherapy group [44.7% (17/38) vs 28.2% (11/39), P<0.001] were higher than those in the HMA group. In terms of hematopoietic function recovery, the median time to achieve target leukocyte counts in the UCB group was shorter than that in the chemotherapy group [22 (14, 28) vs 28 (24, 37) days, P<0.05] and the HMA group [22 (14, 28) vs 31 (21, 42) days, P<0.05]. Similarly, the median time to achieve target platelet counts in the UCB group was shorter than that in the chemotherapy group [24 (17, 29) vs 28 (23, 33) days, P<0.05] and the HMA group [24 (17, 29) vs 29 (22, 37) days, P<0.05]. The survival analysis demonstrated that the 3-year overall survival rate in the UCB group was higher than that in the HMA group (39.1% vs 19.7%, P<0.05), while no statistically significant difference was observed compared to the chemotherapy group (P>0.05). Similarly, the 3-year event-free survival rate in the UCB group was higher than that in the HMA group (35.8% vs 25.5%, P<0.05), with no statistically significant difference compared to the chemotherapy group (P>0.05). Regarding the reconstruction of cellular immune function, the proportion of CD4+central memory T cells in the UCB group at 28 days post-treatment was lower than that in the chemotherapy group [20% (9%, 29%) vs 32%(23%, 39%), P<0.05], while no statistically significant difference was observed compared to the HMA group (P>0.05). At 28 days post-treatment, the proportions of CD4+naive T cells [45% (30%, 58%) vs 22% (10%, 34%)] and CD8+naive T cells [41% (31%, 52%) vs 22% (8%, 36%)] in the UCB group were significantly higher than those in the HMA group (both P<0.05), while no statistically significant difference was observed compared to the chemotherapy group (both P>0.05). At 28 days post-treatment, the UCB group exhibited higher proportions of CD8+effector T cells [40% (33%, 50%) vs 18% (8%, 28%)], CD19+B cells [20% (13%, 27%) vs 12% (7%, 14%)], and NK cells [20% (15%, 26%) vs 14% (7%, 21%)] compared to the chemotherapy group (all P<0.05). However, the UCB group showed lower proportions of regulatory T cells at 28 days post-treatment than both the chemotherapy group [4% (4%, 6%) vs 7% (7%, 8%), P<0.05] and the HMA group [4% (4%, 6%) vs 8% (6%, 12%), P<0.05]. In terms of cellular experiments, differential analysis of immune cells revealed that the indirect co-culture group exhibited higher levels of CD8+naive T cells, CD4+naive T cells, NK cells, and CD19+B cell subsets compared to the control group; conversely, the levels of regulatory T cells and CD4+central memory T cells were lower than those in the control group (all P<0.05). Cytokine level analysis demonstrated that the direct co-culture group showed higher levels of TNF-α and IFN-γ, as well as lower levels of IL-6 compared to the control group (P<0.001). Conclusion: Immunocytes such as NK cells in UCB may promote immune function reconstruction and hematopoietic recovery in patients, thereby improving their prognosis.

To explore the promotion of dynamic distraction on osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMMSCs) in three-dimensional culture.

To investigate the mechanism by which polydatin ameliorates neurological damage in Wilson disease (WD) based on bioinformatics analysis and experimental validation.

To investigate the effect of Angelica sinensis on thymic cortical regeneration in rapamycin-treated mice and its underlying mechanisms.

Intrauterine adhesions (IUA) are gynecological disorders mainly characterized by menstrual abnormalities and infertility. At present, hysteroscopic adhesiolysis is the primary treatment for IUA; however, the postoperative recurrence rate remains high in patients with moderate to severe disease. In clinical practice, postoperative adjuvant therapies, including pharmacological treatment and intrauterine placement of physical barriers, are commonly applied to promote endometrial regeneration and reduce the risk of re-adhesion. These approaches show certain efficacy in patients with mild IUA, but their effects on restoring endometrial structure and improving pregnancy outcomes in moderate to severe cases remain limited. In recent years, stem cell therapy has demonstrated promising potential in endometrial repair, among which mesenchymal stem cells (MSCs) are considered the stem cell type with the greatest potential for clinical translation. MSCs can not only participate in tissue regeneration through differentiating into endometrial-related cells, but also exert indirect reparative effects through the secretion of extracellular vesicles (EVs), including anti-inflammatory, immunomodulatory, anti-fibrotic, pro-proliferative, and pro-angiogenic activities, thereby effectively promoting endometrial regeneration and improving pregnancy outcomes. However, most existing studies remain at the basic research or early clinical stage, and current clinical evidence is still insufficient. Their precise mechanisms of action and optimal application strategies also require further clarification. Future studies should focus on identifying potential therapeutic targets, systematically elucidating the mechanisms by which MSCs and their EVs contribute to IUA treatment, and promoting the standardized clinical translation of related research, with the ultimate goal of providing more effective therapeutic strategies for improving the endometrial environment and female reproductive function.

Thalassemia is one of the most common and harmful single-gene recessive disorders in the clinic. It is characterized by impaired or absent production of one globin chain of hemoglobin in adults. The most common form is beta-thalassemia, which is associated with defects in the production of beta-globin chain, resulting in an imbalance in the ratio of alpha-globin to beta-globin. As a result, unbound free alpha-globin chains precipitated in red blood cell precursors, resulting in iron overload, ineffective red blood cell production, and changes in mesenchymal stem cells, osteoblasts, osteoclasts, and other associated cells. Among them, iron overload and ineffective red blood cell production will destroy the bone marrow microenvironment, which will cause further damage to the hematopoietic system. Therefore, the correction of the bone marrow microenvironment plays an important role in the treatment of thalassemia. This review summarizes studies on the destruction of the bone marrow microenvironment in beta-thalassemia, treatment options for improving the microenvironment and stem cell transplantation.

Acute myeloid leukemia (AML) can be transformed by the malignant transformation of hematopoietic progenitor cells at different stages of normal myeloid cell differentiation and development, thus leading to infection, anemia, bleeding symptoms. It is a common highly heterogeneous hematologic malignancy, the incidence of which is on the rise year by year. The treatment of AML includes chemotherapy, hematopoietic stem cell transplantation and targeted therapy, etc. However, due to the highly heterogeneous nature of AML and the easy recurrence, the treatment is difficult and the cure rate is low. In recent years, combination therapy based on venetoclax has become one of the important research directions for the treatment of AML, and its efficacy has gradually received the attention of clinical researchers. This paper reviews the mechanism of action of venetoclax and its application in the current treatment of AML. Through an in-depth discussion of venetoclax and its combination therapy AML related clinical trials, the emergence of resistance mechanisms to venetoclax and potential strategies to overcome its resistance are summarized.

To investigate Cyclophosphamide (CTX)-induced pulmonary toxicity using a human lung organoid model and explore its effects on DNA damage, inflammatory response, and early fibrosis.

To evaluate the effects of Bone Morphogenetic Protein 4(BMP4) overexpression mediated by an adenoviral vector on immunophenotype features, migration ability, colony-forming ability, and early osteogenic differentiation potential of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs).

To explore the repair effect and its related mechanism of exosomes derived from embryonic stem cell-induced mesenchymal stromal cells (ESC-MSC) on radiation-induced lymphocyte damage.

To investigate the damaging effect of 5-fluorouracil (5-FU) on human intestinal organoids (HIOs) derived from human induced pluripotent stem cells (hiPSCs).

To compare the efficacy, safety, and pharmacoeconomic differences between Mecapeg-filgrastim and recombinant human granulocyte colony-stimulating factor （rhG-CSF） in mobilizing peripheral blood stem cells （PBSCs） from healthy donors.

To summarize the clinical characteristics, treatment outcomes, and prognosis of two children with STAT3 gene mutation-associated hyper-IgE syndrome(HIES) who underwent allogeneic hematopoietic stem cell transplantation(allo-HSCT).

To investigate the predictive indexes of blood transfusion after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in patients with blood diseases.

To investigate the efficacy, safety and cost-effectiveness of single high-dose etoposide (VP-16) combined with mecapegfilgrastim for mobilizing autologous peripheral blood stem cells (APBSC) in patients with lymphoma.

To report four cases of preneoplastic and neoplastic small lymphocytic proliferations concurrent with acute myeloid leukemia (AML), explore their clinical and laboratory characteristics, and improve the understanding of such diseases.

Objective: To investigate the influence and mechanism of exosomes derived from rat bone marrow mesenchymal stem cells (BMSCs) on rat fibroblasts (Fbs) under high glucose conditions, with the aim of exploring a potential novel strategy for the treatment of diabetic wounds. Methods: This study was designed as grouped experimental study. The exosomes derived from BMSCs (BMSC-Exos) were extracted from the rat primary BMSCs and were identified successfully. The BMSC-Exos were divided into control group and high-glucose group. The BMSC-Exos in control group were cultured routinely, while the BMSC-Exos in high-glucose group were cultured in DMEM medium containing glucose at a final molarity of 30 mmol/L (hereinafter referred to as high-glucose medium). The eukaryotic mRNA sequencing was performed on BMSC-Exos in both groups, combined with multi-database prediction and enrichment analysis, differentially expressed genes that strongly interacted with the classical pyroptosis signaling pathway were screened and identified. The rat BMSCs of passages 1 to 3 were divided into microRNA-140-3p (miR-140-3p) mimic control group, miR-140-3p mimic group, miR-140-3p inhibitor control group, and miR-140-3p inhibitor group according to the random number table method, then the corresponding miR-140-3p mimic control, miR-140-3p mimic, miR-140-3p inhibitor control, and miR-140-3p inhibitor were transfected into cells, respectively, after 24 hours of culture. The BMSC-Exos were extracted at 24 hours post-transfection, and the expression of miR-140-3p in BMSC-Exos was detected by real-time fluorescence quantitative polymerase chain reaction. The rat Fbs in the logarithmic growth phase were divided into miR-140-3p mimic control group, miR-140-3p mimic group, miR-140-3p inhibitor control group, and miR-140-3p inhibitor group. After 24 hours of culture in high-glucose medium, the Fbs were added with the exosomes secreted by BMSCs after being transfected with miR-140-3p mimic control, miR-140-3p mimic, miR-140-3p inhibitor control, and miR-140-3p inhibitor, respectively (the same grouping and treatment below). At 24 hours post-transfection, the cell absorbance value was detected using cell counting kit-8, representing cell proliferation activity. The rat Fbs in the logarithmic growth phase were grouped and treated, then the cell migration rate at 24 hours after scratching was detected by scratch test. At 24 hours post-transfection, the protein expression levels of pyroptosis-related protein, including interleukin-1β (IL-1β), IL-18, NOD-like receptor pyrin domain-containing protein 3 (NLRP3), cysteine aspartic acid specific protease-1 (caspase-1), and gasdermin D in cells were detected by Western blotting. The sample size was 3. Results: Compared with that in control group, the expressions of miR-140-3p and miR-542-5p were significantly upregulated in BMSC-Exos of high-glucose group. MiR-140-3p was identified as the differentially expressed gene that strongly interacted with the classical pyroptosis signaling pathway. At 24 hours post-transfection, the expression of miR-140-3p in BMSC-Exos of miR-140-3p mimic group was significantly higher than that in miR-140-3p mimic control group (P<0.05), and the expression of miR-140-3p in BMSC-Exos of miR-140-3p inhibitor group was significantly lower than that in miR-140-3p inhibitor control group (P<0.05). At 24 hours post-transfection, the absorbance value of Fbs in miR-140-3p mimic group was 0.940±0.031, which was significantly higher than 0.781±0.020 in miR-140-3p mimic control group (P<0.05); the absorbance value of Fbs in miR-140-3p inhibitor group was 0.510±0.041, which was significantly lower than 0.822±0.061 in miR-140-3p inhibitor control group (P<0.05). The Fb migration rate at 24 hours after scratching in miR-140-3p mimic group was significantly higher than that in miR-140-3p mimic control group (P<0.05), and the Fb migration rate at 24 hours after scratching in miR-140-3p inhibitor group was significantly lower than that in miR-140-3p inhibitor control group (P<0.05). At 24 hours post-transfection, the protein expressions of NLRP3, IL-18, IL-1β, caspase-1, and gasdermin D in Fbs of miR-140-3p mimic group were significantly lower than those in miR-140-3p mimic control group (P<0.05); the protein expressions of NLRP3, IL-18, IL-1β, caspase-1, and gasdermin D in Fbs of miR-140-3p inhibitor group were significantly higher than those in miR-140-3p inhibitor control group (P<0.05). Conclusions: The rat BMSC-Exos can deliver miR-140-3p to promote the proliferation and migration of rat Fbs under high-glucose conditions, inhibit the expression of pyroptosis-related protein, and alleviate cell pyroptosis. This study provides a promising therapeutic target for diabetic wound repair.

Objective: To investigate the ameliorative effect of menstrual blood-derived mesenchymal stem cells (MenSCs) on liver fibrosis and injury, and further study whether it plays a role by regulating the Toll-like receptor (TLR) signaling pathway in a mouse model of alcoholic liver disease (ALD). Methods: A C57BL/6J mouse model of ALD was established using the gradient ethanol gavage method combined with pyrazole. A blank control group and a model group were established. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) activities, as well as inflammatory factors, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), were measured. The modeling effect was evaluated by combining Masson staining and Sirius red staining in liver tissue with Western blotting to detect the protein expression of α-smooth muscle actin (α-SMA) and collagen type I α1 chain (COL1A1). Simultaneously, qPCR was used to detect the mRNA expression of TLRs and transforming growth factor β-activated kinase 1 (TAK1) to explore the related mechanisms. ALD model mice were divided into a phosphate-buffered saline (PBS) control group and a MenSCs treatment group [2×10⁵ MenSCs (200 μL) injected via tail vein], with intervention once a week sustained for four weeks after successful modeling. Mice batches were sacrificed on the seventh day following each intervention to collect serum and liver tissues. Collagen deposition changes were observed using Sirius red staining. The expression of α-SMA and transforming growth factor-β1 (TGF-β1) proteins was detected by Western blotting. Serum biochemical indicators levels were also measured. The effects of MenSCs on TLRs and TAK1 mRNA expression were assessed using qPCR to comprehensively evaluate the MenSCs intervention effect. The two groups were compared using paired t-tests. Repeated measures analysis of variance (RM-ANOVA) combined with Tukey's multiple comparisons test was used for comparisons among multiple groups. Results: Compared with the blank control group, serum levels of ALT, AST, and GGT, as well as inflammatory factors TNF-α and IL-6, were significantly elevated, while IL-1β levels were significantly decreased in the mouse model of the ALD group. Collagen deposition in liver tissue was markedly increased. The expression of fibrosis markers α-SMA and COL1A1 proteins was significantly upregulated (α-SMA: P<0.001; COL1A1: P<0.001). The mRNA expression of TLR1, TLR2, TLR4, TLR6, TLR7, and TLR8 was significantly upregulated, and the expression of TLR9 and TAK1 was downregulated, while the expression of TLR3 and TLR5 remained unchanged. Liver function levels (ALT and AST) were significantly reduced; liver fibrosis degree was markedly improved; and TGF-β1 and α-SMA protein expression were suppressed (TGF-β1: P<0.001; α-SMA: P=0.026) following MenSC transplantation in mice. MenSC specifically down-regulated the mRNA expression of TLR1, TLR2, TLR4, TLR6, TLR7, and TLR9, with significant inhibition of TLR1, TLR2, and TLR9 expression (P<0.001), while TLR8 and TAK1 expression were not significantly affected at week 4 of intervention (P>0.05). Conclusion: MenSCs transplantation can effectively improve liver function and reduce fibrosis in a mouse model of ALD, and its mechanism may be related to the inhibition of the TLR signaling pathway activation.

Following Mycobacterium tuberculosis (Mtb) infection, the pathogen can establish a metabolically quiescent or replication-arrested dormant state within the host, leading to asymptomatic latent tuberculosis infection (LTBI). Under specific conditions, these dormant bacilli may reactivate and replicate, resulting in symptomatic clinical infection and constituting a major reservoir for active tuberculosis (TB). Dormant Mtb exhibits reduced susceptibility to conventional anti-TB drugs, and current TB vaccines fail to prevent the establishment or reactivation of dormant Mtb, rendering latent infection a major challenge in TB control. The formation of Mtb dormancy requires a unique microenvironment characterized by hypoxia, nutrient deprivation, and host immunosuppression. As an intracellular pathogen, Mtb primarily infects macrophages. Recent studies have revealed that Mtb can also infect mesenchymal stem cells (MSCs), where it persists in a dormant state for a long term. MSCs exhibit a microenvironment marked by hypoxia, cellular quiescence, lipid droplet biogenesis, and elevated autophagic activity. Moreover, MSCs exert immunosuppressive effects on the host immune response to Mtb, thereby facilitating the formation of bacterial dormancy and long-term intracellular survival, which further contributes to TB reactivation and relapse. This review summarizes current advances in understanding Mtb infection of MSCs and the underlying mechanisms associated with Mtb dormancy within this cellular niche.