Ming-Xin He

Peripheral blood hematopoietic stem cell (PBHSC) cryopreservation is critical for autologous stem cell transplantation (ASCT), but traditional cryoprotective agents (TCPAs) containing 10% dimethyl sulfoxide (DMSO) raise safety concerns due to toxicity risk. This study aimed to validate a novel low-DMSO cryoprotective agent (CPA, 2% DMSO) for PBHSC preservation at -80 °C, eliminating the need for liquid nitrogen storage. PBHSCs from six donors were divided into CPA and TCPA groups. The CPA was mixed with PBHSCs (1:1 vol/vol) and directly stored at -80 °C. TCPA (10% DMSO + 5% human albumin) underwent gradual cooling (1 °C/min) and liquid nitrogen storage. After 1 month, both groups were thawed in a 37 °C water bath. Cell viability, cytoskeletal integrity (microfilaments/microtubules), mitochondrial activity, and colony-forming capacity were compared. After thawing, PBHSC survival was comparable between CPA (91.29%) and TCPA (90.07%). However, CPA outperformed TCPA in cell viability assays (CPA: 89.38% versus TCPA: 79.55%; p < 0.05). Cytoskeletal analysis revealed intact microfilaments and microtubules in CPA-preserved cells, with structural clarity exceeding TCPA. Mitochondrial activity in CPA-treated cells mirrored fresh PBHSCs, exhibiting 8.5% higher activity than TCPA (p < 0.05) and increased mitochondrial complex numbers. Colony-forming assays further confirmed CPA's superiority, with higher colony counts post-induction. CPA enables safe, convenient PBHSC cryopreservation at -80 °C using ultralow DMSO (2%), eliminating liquid nitrogen reliance. Its enhanced cell viability and mitochondrial preservation suggest clinical advantages by reducing infusion toxicity risks. This protocol offers a transformative strategy for ASCT, optimizing safety and operational efficiency.

Peripheral blood hematopoietic stem cell (PBHSC) cryopreservation is critical for autologous stem cell transplantation (ASCT), but traditional cryoprotective agents (TCPAs) containing 10% dimethyl sulfoxide (DMSO) raise safety concerns due to toxicity risk. This study aimed to validate a novel low-DMSO cryoprotective agent (CPA, 2% DMSO) for PBHSC preservation at -80 °C, eliminating the need for liquid nitrogen storage. PBHSCs from six donors were divided into CPA and TCPA groups. The CPA was mixed with PBHSCs (1:1 vol/vol) and directly stored at -80 °C. TCPA (10% DMSO + 5% human albumin) underwent gradual cooling (1 °C/min) and liquid nitrogen storage. After 1 month, both groups were thawed in a 37 °C water bath. Cell viability, cytoskeletal integrity (microfilaments/microtubules), mitochondrial activity, and colony-forming capacity were compared. After thawing, PBHSC survival was comparable between CPA (91.29%) and TCPA (90.07%). However, CPA outperformed TCPA in cell viability assays (CPA: 89.38% versus TCPA: 79.55%; p < 0.05). Cytoskeletal analysis revealed intact microfilaments and microtubules in CPA-preserved cells, with structural clarity exceeding TCPA. Mitochondrial activity in CPA-treated cells mirrored fresh PBHSCs, exhibiting 8.5% higher activity than TCPA (p < 0.05) and increased mitochondrial complex numbers. Colony-forming assays further confirmed CPA's superiority, with higher colony counts post-induction. CPA enables safe, convenient PBHSC cryopreservation at -80 °C using ultralow DMSO (2%), eliminating liquid nitrogen reliance. Its enhanced cell viability and mitochondrial preservation suggest clinical advantages by reducing infusion toxicity risks. This protocol offers a transformative strategy for ASCT, optimizing safety and operational efficiency.

Liver diseases have long been a prevalent cause of morbidity and mortality, and their development and progression involve multiple vital organs throughout the body. Recent studies on the oral–gut–liver axis have revealed that the oral microbiota is associated with the pathophysiology of chronic liver diseases. Since interventions aimed at regulating oral biological disorders may delay the progress of liver disease, it is crucial to better comprehend this process. Oral bacteria with potential pathogenicity have been extensively studied and are closely related to several types of chronic liver diseases. Therefore, this review will systemically describe the emerging role of oral pathogenic bacteria in common liver diseases, including alcoholic liver disease (ALD), non-alcoholic steatohepatitis (NASH), non-alcoholic fatty liver disease (NAFLD), cirrhosis, autoimmune liver diseases (AILD), and liver cancer, and bring in new perspectives for future research.

Microorganisms have long been known to play key roles in the initiation and development of tumors. The oral microbiota and tumorigenesis have been linked in epidemiological research relating to molecular pathology. Notably, some bacteria can impact distal tumors by their gastrointestinal or blood-borne transmission under pathological circumstances. Certain bacteria drive tumorigenesis and progression through direct or indirect immune system actions. This review systemically discusses the recent advances in the field of oral microecology and tumor, including the oncogenic role of oral microbial abnormalities and various potential carcinogenesis mechanisms (excessive inflammatory response, host immunosuppression, anti-apoptotic activity, and carcinogen secretion) to introduce future directions for effective tumor prevention.