BackgroundGrowing evidence indicates significant alterations in fatty acid metabolism in patients with relapsing-remitting multiple sclerosis (RRMS). However, the metabolic status of long-chain fatty acids (LCFAs), including mono-unsaturated fatty acids (MUFAs) and poly-unsaturated fatty acids (PUFAs), and their potential link to immune-inflammatory responses during RRMS relapses, remain unclear. This study aims to uncover the aberrant metabolic signatures of LCFAs, potential LCFA biomarkers during RRMS relapses, and their interactive network with peripheral inflammatory responses.MethodsIn this study, plasma samples from 20 RRMS patients and 22 age- and sex-matched healthy controls (HCs) were analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based untargeted metabolomics method.ResultsMetabolomics analysis revealed marked changes in the LCFA metabolic profile of RRMS patients. Compared to HCs, 26 differentially abundant metabolites (DAMs) belonging to amino acids, fatty acids, and their derivatives were identified in RRMS samples, including significantly upregulated LCFA palmitic acid (FA 16:0) (Padj < 0.001), MUFA oleic acid (FA 18:1) (Padj < 0.05), PUFA arachidonic acid (FA 20:4) (Padj < 0.01), and significantly downregulated dodecanoic acid (FA 12:0) (Padj < 0.01). These DAMs were mainly enriched in amino acid, fatty acid, and lipid synthesis/metabolism pathways. Additionally, the circulating levels of pro-inflammatory factors TNF-α and IL17A were significantly elevated (Padj < 0.001), while the concentrations of chemokines such as IL1RA, CCL2, CCL3, CCL4, CCL5, PDGFB, IL7, CXCL8, IL9, and IL12A were significantly reduced (Padj < 0.01) in RRMS compared to HC samples. Linear regression analysis showed significant positive correlations between FA 20:4 and IL17A (r = 0.370, Padj < 0.05), and significant negative correlations between FA 16:0 and PDGFB (r = -0.339, Padj < 0.05). Receiver operating characteristic (ROC) curve analysis indicated that individual fatty acids (e.g., FA 12:0 [AUC = 0.881], FA 18:1 [AUC = 0.833], FA 16:0 [AUC = 0.881]) have high potential for predicting RRMS, with higher accuracy, specificity, and sensitivity when combining two (FA 12:0 and FA 18:1 [AUC = 0.929]) or four (FA 12:0, FA 18:1, FA 16:0, and FA 20:4 [AUC = 0.952]) fatty acids.ConclusionOur results uncover the aberrant metabolic features of LCFAs and potential biomarkers in RRMS patients, and the interactive network and key molecular nodes between LCFAs and peripheral immune-inflammatory responses. The interplay between LCFAs and immuno-inflammation may drive the migration of inflammatory events from the periphery to the CNS, reigniting CNS neuroinflammation and causing RRMS relapses. These findings offer valuable insights for RRMS diagnosis and novel therapeutic development.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis and progressive joint destruction. Although conventional therapies effectively alleviate clinical symptoms, they are largely incapable of reversing irreversible joint damage and the underlying immune dysregulation. Mesenchymal stem cells (MSCs), with their dual capabilities in immunomodulation and tissue repair, have emerged as a promising new therapeutic strategy. This review delineates how MSCs and their derived extracellular vesicles exert multifaceted anti-inflammatory and immunosuppressive effects in RA. Locally, these mechanisms include modulating the Treg/Th17 cell balance, inhibiting the proliferation and invasion of fibroblast-like synoviocytes, and regulating the RANKL/OPG system to suppress osteoclast activity, while orchestrating the repair and regeneration of damaged joints primarily through the secretion of trophic factors and paracrine regulation of local bone metabolism. Importantly, beyond these local effects, this review highlights the novel ‘gut-MSC-immune’ axis, elucidating the potential pathway through which MSCs might systemically modulate immune homeostasis by influencing gut microbiota composition and mucosal barrier integrity. Although preliminary clinical trials have demonstrated a favorable safety profile and potential therapeutic feasibility of MSC-based interventions, its therapeutic outcomes are significantly influenced by patient heterogeneity and the hostile inflammatory microenvironment. To address these clinical bottlenecks and overcome interpatient therapeutic heterogeneity, we discuss the synergistic potential of microbiota-targeted interventions combined with MSC therapy. Finally, key priorities for future research are proposed, including standardizing MSC preparation protocols, optimizing administration regimens, and validating long-term efficacy and safety via large-scale multicenter clinical trials—efforts that will ultimately accelerate the clinical translation and clinical application of precision MSC-based therapy for RA.

The APOE4 variant was the strongest genetic risk factor for sporadic Alzheimer’s disease (AD). Individuals with APOE4 have an increased risk of developing the disease at an early age of onset. Similarly, APOE4 carriers are predisposed to high cholesterol levels and tend to have an increased risk of cardiovascular disease (CVD). The global allele frequency of APOE4 was 13.7

Inflammation and bacterial infection are important causes of implant failure, and the development of multifunctional titanium surfaces to address these issues is an effective means of treating infected bone defects. In this study, polyphenols (EGCG) and Zn2+ were first loaded onto the titanium surface to construct an EGCG/Zn2+ polyphenol metal network coating. Then melatonin (MT) was loaded into the EGCG/Zn2+ network structure to prepare the EGCG/Zn2+/MT composite coating. The results proved that the EGCG/Zn2+/MT coating had good mechanical properties, hydrophilicity, corrosion resistance and bioactivity. In vitro, the inhibition rates of EGCG/Zn2+/MT against E. coli and S. aureus were about 97 % and 81 %, respectively. In vitro experiments revealed that EGCG/Zn2+/MT could regulate the polarization of macrophages (RAW264.7) to M2 type, could induce vascularization of human umbilical vein endothelial cells (HUVEC), and could promote the differentiation of pro-osteoblasts (MC3T3-E1) to osteogenesis. Meanwhile, EGCG/Zn2+/MT achieved effective ROS scavenging within HUVEC and MC3T3-E1. In vivo experiments demonstrated that the EGCG/Zn2+/MT coatings possessed favorable biosafety, anti-inflammatory, antimicrobial, and bone repair capabilities. This study provides a simple and versatile strategy for designing multifunctional surfaces with both antimicrobial, anti-inflammatory, antioxidant, angiogenic and osteogenic properties.

Background and ObjectiveParental chromosomal structural variations (SVs) represent a primary genetic factor contributing to recurrent spontaneous abortion (RSA). Individuals carrying SVs with complex chromosomal rearrangements (CCRs) typically exhibit a normal phenotype but are at an increased risk of miscarriage. Current standard clinical detection methods are insufficient for the identification and interpretation of all SV types, particularly complex and occult SVs, thereby presenting a significant challenge for clinical genetic counseling. Leveraging the high-resolution capabilities of optical genome mapping (OGM) technology, this study aims to rapidly and accurately identify complex SVs in RSA couples. Furthermore, it seeks to conduct an in-depth analysis of the genetic information within the breakpoint regions, thereby providing a more comprehensive scientific foundation for genetic counseling of RSA couples at both the cellular and genetic levels.Material and MethodsThis study involved the selection of nine subjects from two families who underwent genetic counseling at our hospital. Family 1 comprised a couple with the wife as a SVs carrier, and both her parents and brother were simultaneously analyzed for chromosomal karyotype. Family 2 included a couple with the husband as the SVs carrier, with his parents also undergoing chromosomal karyotype analysis. For SVs carriers whose karyotype analysis did not elucidate the recombination pattern, optical genome mapping (OGM) technology was utilized for further investigation, followed by Sanger sequencing to validate the OGM findings.ResultsIn Family 1, only the wife was identified as an SVs carrier. Initial chromosomal karyotype analysis suggested a karyotype of 46,XX,t (5; 6;8; 13; 15) (?). However, OGM analysis ultimately confirmed the karyotype as 46,XY,der (5)t (5; 13) (q35.2; q21.32), der (6)t (6; 8) (q25.3; q13.1)ins (6; 13) (q25.3; q21.32q21.33),der (8)t (6; 8) (q26; q13.1)ins (8; 13) (q13.1; q21.33q22.1),der (13)t (13; 15) (q21.32; q26.1)ins (13; 6) (q21.32; q25.3q26), der (15)t (5; 15) (q35.2; q26.1). Furthermore, OGM identified a novel translocation variant of the KIF7 gene that is associated with recurrent miscarriage. In Family 2, both the husband and his maternal parent were identified as SVs carriers. Nuclear type analysis revealed a karyotype of 46,XY,?t (1; 6) (q42; p21) (husband) and 46,XX,?t (1; 2) (p31.1; q24.1),?t (1; 6) (q42; p21) (mother). Through OGM detection and analysis, the final karyotype was determined to be 46,XY,ins (1; 6) (q42.2; p22.3p11.3) (husband) and 46,XX,der (1)t (1; 2) (p31.1; q24.1)ins (1; 6) (q42.2; p22.3p11.3), der (2) t (1; 2), der (6)ins (1; 6) (mother).ConclusionOGM technology facilitates the rapid and precise identification of complex chromosomal structural variations, effectively overcoming the limitations associated with traditional karyotype G-banding techniques in detecting intricate and cryptic SVs. This advancement substantially enhances the diagnostic rates of genetic etiology in patients experiencing RSA. The present study elucidates the specific manifestations of complex SVs using OGM technology, accurately pinpointing breakpoints and interpreting affected gene information. This provides novel reference approaches and evidence for disease assessment and genetic counseling in RSA patients. However, it is important to acknowledge certain limitations of this research: the study’s inclusion of only two RSA family cohorts (comprising nine participants) may limit the generalizability of its conclusions due to the small sample size, necessitating further validation through large-scale studies. Additionally, the causal relationship between KIF7 gene dysfunction and recurrent miscarriage remains to be experimentally verified in subsequent research.

Pulmonary fibrosis (PF) is a common and multidimensional devastating interstitial lung disease. The development of novel and more effective interventions for PF is an urgent clinical need. A previous study has found that miR-181a-5p plays an important role in the development of PF, and human amniotic mesenchymal stem cells (hAMSCs) exert potent therapeutic potential on PF. However, whether hAMSCs act on PF by delivering miR-181a-5p and its detailed mechanism still remain unknown. Thus, this study was designed to investigate the underlying possible mechanism of hAMSCs on PF in bleomycin (BLM)-induced mouse PF model, and a co-culture system of hAMSCs and A549 cells epithelial mesenchymal transition (EMT) model, focusing on its effects on collagen deposition, EMT, and epithelial cell cycle regulation. hAMSCs with different miR-181a-5p expression levels were constructed. BLM (4 mg/kg) was used to create a PF model, while TGF-β1 was used to induce A549 cells to construct an EMT model. Furthermore, the effects of different miR-181a-5p expression in hAMSCs on collagen deposition and EMT during lung fibrosis were assessed in vivo and in vitro. We found that hAMSCs exerted anti-fibrotic effect in BLM-induced mouse PF model. Moreover, hAMSCs also exerted protective effect on TGFβ1-induced A549 cell EMT model. Furthermore, hAMSCs ameliorated PF by promoting epithelial cell proliferation, reducing epithelial cell apoptosis, and attenuating EMT of epithelial cells through paracrine effects. hAMSCs regulated EMT in PF through delivering miR-181a-5p targeting TGFBR1. Our findings reveal for the first time that hAMSCs inhibit PF by promoting epithelial cell proliferation, reducing epithelial cell apoptosis, and attenuating EMT. Mechanistically, the therapeutic effect of hMASCs on PF is achieved through delivering miR-181a-5p targeting TGFBR1.

Microglia-evoked neuroinflammation contributes to neurodegenerative diseases such as multiple sclerosis (MS). Metabolic reprogramming, including changes in polyunsaturated fatty acids (PUFAs), plays a critical role in MS pathophysiology. Previous studies identified reduced plasma α-dimorphecolic acid (α-DIPA), a linoleic acid derivative, in MS patients. This study investigated the anti-inflammatory effects of α-DIPA on microglia and the underlying pathways. Lipopolysaccharide (LPS)-induced BV-2 microglial inflammation was used as an in vitro model. α-DIPA effects were assessed via ELISA for nitric oxide (NO) release, flow cytometry was used to examine cell proliferation, activation and polarization, and transcriptomic analysis was applied to identify key signaling pathways regulated by α-DIPA. ELISA results showed that exogenous α-DIPA treatment significantly inhibited LPS-induced NO release from BV-2 cells in a concentration-dependent manner. Moreover, flow cytometry analysis suggested that 40 µM α-DIPA treatment significantly repressed LPS-induced BV-2 cell proliferation, activation, as well as M1 and M2 type polarization. Furthermore, transcriptome analysis revealed that exogenous α-DIPA extensively and drastically decreased the transcriptional level of numerous genes that are involved in the regulation of inflammatory responses, for instance, proinflammatory genes such as Tnf and Ccl3 related to IL-17 and TNF-α signaling. In addition, we also observed that the expression of multiple genes in NF-κB signaling were also inhibited greatly by α-DIPA, such as Nfkb2 and Nfkbia. Notably, α-DIPA robustly suppressed LPS-induced mRNA expression of abundant genes participating in the ferroptosis pathway, including Acsl4, Slc7a11, Me1, and Hmox1. Interestingly, the expressions of multiple ferroptosis-related genes were regulated specifically by α-DIPA but not LPS, such as Acsl5, Acsl6, Alox5, Cars, Dpp3, Dpp10, Slc2a5, and Slc7a1. α-DIPA inhibits microglial inflammation likely through regulating the pathways of the ferroptosis and NF-κB signaling. These results provided preliminary evidence for α-DIPA as a potential therapeutic candidate for neurodegenerative diseases like MS.

Multiple sclerosis (MS) is an autoimmune disorder caused by chronic inflammatory reactions in the central nervous system. Currently, little is known about the changes of plasma proteomic profiles in Chinese patients with MS (CpwMS) and its relationship with the altered profiles of multi-omics such as metabolomics and gut microbiome, as well as potential molecular networks that underlie the etiology of MS. To uncover the characteristics of proteomics landscape and potential multi-omics interaction networks in CpwMS, Plasma samples were collected from 22 CpwMS and 22 healthy controls (HCs) and analyzed using a Tandem Mass Tag (TMT)-based quantitative proteomics approach. Our results showed that the plasma proteomics pattern was significantly different in CpwMS compared to HCs. A total of 90 differentially expressed proteins (DEPs), such as LAMP1 and FCG2A, were identified in CpwMS plasma comparing to HCs. Furthermore, we also observed extensive and significant correlations between the altered proteomic profiles and the changes of metabolome, gut microbiome, as well as altered immunoinflammatory responses in MS-affected patients. For instance, the level of LAMP1 and ERN1 were significantly and positively correlated with the concentrations of metabolite L-glutamic acid and pro-inflammatory factor IL-17 (Padj < 0.05). However, they were negatively correlated with the amounts of other metabolites such as L-tyrosine and sphingosine 1-phosphate, as well as the concentrations of IL-8 and MIP-1α. This study outlined the underlying multi-omics integrated mechanisms that might regulate peripheral immunoinflammatory responses and MS progression. These findings are potentially helpful for developing new assisting diagnostic biomarker and therapeutic strategies for MS.

BackgroundChondrocyte ferroptosis plays a critical role in the pathogenesis of osteoarthritis (OA), regulated by the SLC7A11/GPX4 signaling pathway. Icariin (ICA), a flavonoid glycoside, exhibits strong anti-inflammatory and antioxidant activities. This study investigated whether ICA could modulate the SLC7A11/GPX4 signaling to inhibit chondrocyte ferroptosis and alleviate OA.PurposeThe objective was to explore the impact of ICA on chondrocyte ferroptosis in OA and its modulation of the SLC7A11/GPX4 signaling pathway.MethodsThe anti-ferroptosis effects of ICA were evaluated in an interleukin-1β (IL-1β)-treated SW1353 cell model, using Ferrostatin-1 (Fer-1) and Erastin (Era) as ferroptosis inhibitor and inducer, respectively, along with GPX4 knockdown via lentivirus-based shRNA. Additionally, the therapeutic efficacy of ICA on OA-related articular cartilage damage was assessed in rats through histopathology and immunohistochemistry (IHC).ResultsIL-1β treatment upregulated the expression of OA-associated matrix metalloproteinases (MMP3 and MMP1), a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS-5), and increased intracellular ROS, lipid ROS, and MDA levels while downregulating collagen II and SOX9 expression in SW1353 cells. ICA treatment countered the IL-1β-induced upregulation of MMPs and ADAMTS-5, restored collagen II and SOX9 expression, and reduced intracellular ROS, lipid ROS, and MDA levels. Furthermore, IL-1β upregulated P53 but downregulated SLC7A11 and GPX4 expression in SW1353 cells, effects that were mitigated by ICA or Fer-1 treatment. Significantly, ICA also alleviated Era-induced ferroptosis, whereas it had no effect on GPX4-silenced SW1353 cells. In vivo, ICA treatment reduced articular cartilage damage in OA rats by partially restoring collagen II and GPX4 expression, inhibiting cartilage extracellular matrix (ECM) degradation and chondrocyte ferroptosis.ConclusionICA treatment mitigated chondrocyte ferroptosis and articular cartilage damage by enhancing the SLC7A11/GPX4 signaling, suggesting its potential as a therapeutic agent for OA interventions.

Background/Aim: The research of hematopoietic stem cells (HSCs) has been broadly used in the technical fields of biochemistry, cytology and clinical medicine. Mice is an important tool in the research of HSCs. However, it is not clear that the difference quantity and composition of HSCs among different species mice, and its affects on the experimental results.Materials and Methods: The proportion and content of HSCs in bone marrow (BM) and peripheral blood (PB) from KM, BALB/c and C57BL/6J mice were observed respectively. Cell counts in PB and histopathology of bone marrow were assessed by staining paraffin sections with H & E. HSCs from BM and PM were analyzed by flow cytometry.Results: The peripheral WBC and lymphocyte counts were significantly higher in C57BL/6J mice than the counts in KM and BALB/C mice (P < 0.01 or P < 0.05). Whereas there was no significant difference between the three species mice in BM. In addition, both in PB and BM, the percentage of LSK cells in KM mice was the highest compared with BALB/c and C57BL/6J mice, and the lowest was BALB/c mice.Conclusions: The study reveals that the distinction in HSCs among the three species mice may be helpful in the selection of experimental animals in the research field of HSCs.

When exposed to various microenvironmental stimuli, macrophages are highly plastic and primarily polarized into the pro-inflammatory M1-type and the anti-inflammatory M2-type, both of which perform almost entirely opposing functions. Due to this characteristic, macrophages perform different functions at different stages of immunity and inflammation. Inflammatory immune skin diseases usually show an imbalance in the M1/M2 macrophage ratio, and altering the macrophage polarization phenotype can either make the symptoms worse or better. Therefore, this review presents the mechanisms of macrophage polarization, inflammation-related signaling pathways (JAK/STAT, NF-κB, and PI3K/Akt), and the role of both in inflammatory immune skin diseases (psoriasis, AD, SLE, BD, etc.) to provide new directions for basic and clinical research of related diseases.

Objective: DNA methylation plays a potential role in the pathogenesis of Alzheimer's disease (AD). However, little is known about the global changes of blood leukocyte DNA methylome profiles from Chinese patients with mild cognitive impairment (MCI) and with AD, or the specific DNA methylation-based signatures associated with MCI and AD. In this study, we sought to dissect the characteristics of blood DNA methylome profiles in MCI- and AD-affected Chinese patients with the aim of identifying novel DNA methylation biomarkers for AD. Methods: In this study, we profiled the DNA methylome of peripheral blood leukocytes from 20 MCI- and 20 AD-affected Chinese patients and 20 cognitively healthy controls (CHCs) with the Infinium Methylation EPIC BeadChip array. Results: We identified significant alterations of the methylome profiles in MCI and AD blood leukocytes. A total of 2,582 and 20,829 CpG sites were significantly and differentially methylated in AD and MCI compared with CHCs (adjusted p < 0.05), respectively. Furthermore, 441 differentially methylated positions (DMPs), aligning to 213 unique genes, were overlapped by the three comparative groups of AD versus CHCs, MCI versus CHCs, and AD versus MCI, of which 6 and 5 DMPs were continuously hypermethylated and hypomethylated in MCI and AD relative to CHCs (adjusted p < 0.05), respectively, such as FLNC cg20186636 and AFAP1 cg06758191. The DMPs with an area under the curve >0.900, such as cg18771300, showed high potency for predicting MCI and AD. In addition, gene ontology and pathway enrichment results showed that these overlapping genes were mainly involved in neurotransmitter transport, GABAergic synaptic transmission, signal release from synapse, neurotransmitter secretion, and the regulation of neurotransmitter levels. Furthermore, tissue expression enrichment analysis revealed a subset of potentially cerebral cortex-enriched genes associated with MCI and AD, including SYT7, SYN3, and KCNT1.Conclusion: This study revealed a number of potential biomarkers for MCI and AD, also highlighted the presence of epigenetically dysregulated gene networks that may engage in the underlying pathological events resulting in the onset of cognitive impairment and AD progression. Collectively, this study provides prospective cues for developing therapeutic strategies to improve cognitive impairment and AD course.

Background and Aims: Diabetic kidney disease (DKD) is a prevalent and intractable microvascular complication of diabetes mellitus (DM), the process of which is closely related to abnormal expression of angiogenesis-regulating factors (ARFs). Stem cell transplantation might be a novel strategy for treating DKD. This study aims to explore the effect of transplantation of human amniotic mesenchymal stem cells (hAMSCs) on renal microangiopathy in a type 1 DKD rat model (T1DRM).Methods: Seventy-two rats were randomly divided into three groups, including normal control group, DKD group, and hAMSCs transplantation group. T1DRM was established using a rat tail vein injection of streptozotocin (STZ) (55 mg/kg). hAMSCs were obtained from placental amniotic membranes during cesarean delivery and transplanted at 3 and 4 weeks through penile veins. At 6, 8, and 12 weeks following transplantation, blood glucose levels, renal function, pathological kidney alterations, and the expressions of ARFs' mRNA and protein were analyzed.Results: In T1DRM, transplanted hAMSCs that were homed at the injured site of kidneys increased ARFs' expression and decreased blood glucose levels. Compared to the DKD group, the levels of 24-h urinary protein, serum creatinine, urea, and kidney injury molecule-1 (KIM-1) were reduced in hAMSCs transplantation group. In terms of renal pathology such as the degree of basement membrane thickening, hAMSCs transplantation was also less severe than the DKD group, thereby alleviating kidney injury.Conclusion: hAMSCs transplantation might ameliorate STZ-induced chronic kidney injury through increasing ARFs' expression in kidneys and lowering blood glucose levels.

Calcium-sensing receptor (CaSR) is a G protein-coupled receptor, widely distributed in various tissues, including vascular endothelial cells and smooth muscle cells, which plays an important role in the migration and homing of stem/progenitor cells and the proliferation of tissue cells. Restenosis after Percutaneous coronary intervention (PCI) seriously affects its prognosis and application. Our previous research has found that ginsenoside Rg1 (GS-Rg1) can inhibit the occurrence of restenosis after balloon injury of the common carotid artery in rats, but the mechanism is still unclear. In this study, it was found that GS-Rg1 (4, 8, 16 mg/kg) inhibited vascular restenosis caused by balloon injury, and mobilize endothelial progenitor cells (EPCs) to promote reendothelialization and inhibit intimal hyperplasia, which significantly reduced after administration of CaSR antagonist NPS 2143. Interestingly, CaSR and its downstream JNK, P38 were highly expressed in the proliferative intima and participated in the abnormal proliferation of vascular smooth muscle cells mediated by smooth muscle progenitor cells (SMPCs). GS-Rg1 inhibited intimal hyperplasia, while it decreased the expression of CaSR, JNK, and P38. This might relate to the distribution of CaSR and the facilitation of GS-Rg1 on the vascular endothelial repair. It is concluded that CaSR plays a key role in GS-Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon Injury.

Background: Short tandem repeats (STR) are highly polymorphic DNA markers utilised in forensic personal identification and human population genetic research. Guizhou Tujia is one of the ancient minority groups in southwest China, however, the population has not been studied using the highly discriminating 23 STR Huaxia Platinum Kit. Aim: To obtain genetic data from 23 autosomal STRs in Guizhou Tujia and examine the population's relationship with others. Subjects and methods: A total of 480 individuals from the Guizhou Tujia population were analysed using 23 STR loci of Huaxia Platinum Kit. Allele frequencies and forensic parameters were estimated. Population genetic relationships were calculated by Nei's genetic distances and visualised using a variety of biostatistical methods. Results A total of 264 alleles were found, with allelic frequencies ranging from 0.0010 to 0.5104. The combined discrimination power (CDP) and the combined probability of paternity (CPE) of 23 STR loci were 0.9999999999999999999999999996 and 0.999999999710422, respectively. Guizhou Tujia showed closer genetic relationships with Hubei Tujia, Guizhou Gelao, and Guizhou Miao than with other populations. Conclusion: We first obtained the population genetic data of Guizhou Tujia using the 23 STR system and demonstrated its value in forensic applications. Comprehensive population comparisons showed an evident genetic affinity pattern between populations that are geographically, ethnically and linguistically related.

Spinal Cord Injury (SCI), with its morbidity characteristics of high disability rate and high mortality rate, is a disease that is highly destructive to both the physiology and psychology of the patient, and for which there is still a lack of effective treatment. Following spinal cord injury, a cascade of secondary injury reactions known as ischemia, peripheral inflammatory cell infiltration, oxidative stress, etc. create a microenvironment that is unfavorable to neural recovery and ultimately results in apoptosis and necrosis of neurons and glial cells. Mesenchymal stem cell (MSC) transplantation has emerged as a more promising therapeutic options in recent years. MSC can promote spinal cord injury repair through a variety of mechanisms, including immunomodulation, neuroprotec-tion, and nerve regeneration, giving patients with spinal cord injury hope. In this paper, it is discussed the neuroprotection and nerve regeneration components of MSCs' therapeutic method for treating spinal cord injuries.

目的 基于15个常染色体短串联重复序列(STR)基因座,探究贵州汉族与苗族与5个不同民族人群的遗传关系.方法 通过15个STR基因座的等位基因频率数据,应用Arlequin v3.5软件计算各基因座的遗传分化系数Fst及P值,应用Phylip 3.695软件计算7个群体的Nei's遗传距离,应用TBtools软件进行可视化热图和聚类分析;基于Nei's遗传距离,分别采用MEGA 7.0和SPSS 26.0软件构建系统发生树和主成分分析.结果 遗传分化系数Fst及P值显示,贵州汉族或苗族群体分别与布依、水、仡佬、侗和土家族5个群体比较,遗传分化程度都较低(Fst分别介于0.00002～0.02567和0.0002～0.0377),但是汉族与苗族群体比较时显示出相对较高的遗传分化程度(Fst介于0.00111～0.01861).Fst及P值、Nei's遗传距离、热图、系统发生树和主成分分析的结果均显示,贵州汉族与仡佬族、侗族和土家族的遗传关系最近,与水族和布依族的遗传关系相对较远,与苗族的遗传关系最远.且苗族与布依、水、仡佬、侗和土家族5个民族之间遗传关系较远.结论 贵州汉族与苗族群体之间遗传差异最大,而苗族与布依族、水族、仡佬族、侗族和土家族5个少数民族之间遗传差异均较大.

Recent studies have revealed that activated astrocytes (AS) are divided into two distinct types, termed A1 and A2. A2 astrocytes are neuroprotective and promote tissue repair and regeneration following spinal cord injury. Whereas, the specific mechanism for the formation of the A2 phenotype remains unclear. This study focused on the PI3K/Akt pathway and examined whether TGF-β secreted by M2 macrophages could mediate A2 polarization by activating this pathway. In this study, we revealed that both M2 macrophages and their conditioned medium (M2-CM) could facilitate the secretion of IL-10, IL-13 and TGF-β from AS, and this effect was significantly reversed after the administration of SB431542 (a TGF-β receptor inhibitor) or LY294002 (a PI3K inhibitor). Moreover, immunofluorescence results demonstrated that TGF-β secreted by M2 macrophages could facilitate the expression of A2 biomarker S100A10 in AS; combined with the results of western blot, it was found that this effect was closely related to the activation of PI3K/Akt pathway in AS. In conclusion, TGF-β secreted by M2 macrophages may induce the conversion of AS to the A2 phenotype through the activation of the PI3K/Akt pathway.

项目式学习教学新模式在医学检验教改课程中的应用研究,旨在提升教学质量及学习效果.针对教学过程中因内容多、抽象,实验设备多、流程精细、程序复杂以及传统的"满堂灌"或"一言堂"等教学的不足,文章拟从教学方案设计、教学方法 及流程优化等方面进行改革,利用"互联网+雨课堂"学习平台传递学习内容,以图片、文字、典型案例及视频导学等方式实现项目式教学,在学习情境中以小组合作的方式进行探究式学习,强调对重、难点知识的理解与熟记,形成具有专业特色的教学改革新模式.通过系统学习掌握所需知识与技能,培养学生对目标事物的判断力、对团队合作的协作力、对解决问题的创造力,提升学习氛围及教学质量.

Small-diameter vascular grafts (SDVGs) cannot meet current clinical demands owing to their suboptimal long-term patency rate. Various materials have been employed to address this issue, including nanomaterials (NMs), which have demonstrated exceptional capabilities and promising application potentials. In this review, the utilization of NMs in different forms, including nanoparticles, nanofibers, and nanofilms, in the SDVG field is discussed, and future perspectives for the development of NM-loading SDVGs are highlighted. It is expected that this review will provide helpful information to scholars in the innovative interdiscipline of cardiovascular disease treatment and NM.