Cord Blood Research Articles

Chimeric antigen receptor (CAR) natural killer (NK) cell therapy represents an emerging frontier in cancer immunotherapy. CAR-NK cells offer the potential for "off-the-shelf" treatments with a favorable safety profile, due in part to their innate capacity for HLA-unrestricted tumor targeting and an absence of graft-versus-host disease. Landmark clinical studies using cord blood - derived CAR-NK cells and another employing iPSC-derived CAR-NK cells have reported impressive response rates, durable remissions, and minimal toxicity. Furthermore, a growing landscape of ongoing clinical trials is exploring innovative strategies to enhance persistence, overcome solid tumor challenges, and prevent antigen escape. These advances collectively underscore the potential of CAR-NK therapies to revolutionize cancer treatment while addressing limitations associated with current CAR-T cell approaches.

Glucocorticoids are essential for fetal organ maturation and form the basis of antenatal corticosteroid therapy that has significantly reduced preterm-related morbidity such as respiratory distress syndrome (RDS). However, neonatal morbidity remains a clinical challenge regardless of antenatal corticosteroid therapy. Currently, it is thought that adverse intrauterine environments dysregulate glucocorticoid receptor (GR) homeostasis, yet the biological mechanisms remain poorly understood. Therefore, we aimed to study ex vivo glucocorticoid sensitivity in cord blood immune cells from two independent preterm cohorts to identify associations with neonatal morbidity and uncover potential mechanisms of dysregulated glucocorticoid homeostasis. In the first cohort, thawed cord blood mononuclear cells were exposed to betamethasone in the presence of lipopolysaccharides (LPS) for 4 h. In the second cohort, freshly isolated white blood cells were treated with dexamethasone under unstimulated and LPS-stimulated conditions for 48 h. GR isoform expression and regulation of transactivated and transrepressed genes were assessed via qPCR, immunoblotting, flow cytometry, and ELISA. In both cohorts, reduced GR expression, particularly of the GRα isoform, was observed in neonates with morbidity, but only with culture time and not in freshly isolated cells. Ex vivo impaired glucocorticoid-mediated transrepression of proinflammatory genes IL6 and TNF was also observed in the morbidity groups. In contrast, all samples were comparable in basal immune cell distributions and transactivation of glucocorticoid response element (GRE)-dependent genes GILZ and FKBP5, irrespective of neonatal morbidity. These findings suggest that neonates that develop morbidities experience an early postnatal GR dysfunction that is potentially programmed in utero. Moreover, under conditions of decreased GR abundance, classical transactivation functions appear to be preserved at the expense of more complex regulatory mechanisms such as transrepression.

Adiponectin and leptin are key adipokines that play crucial roles in metabolic regulation and in fetal and neonatal growth. In adults, lower adiponectin/leptin ratio (AdipoQ/Lep) has been suggested as a potential biomarker for metabolic risk. This study aimed to investigate whether the AdipoQ/Lep ratio in fetal blood correlates with the maternal and neonatal phenotypes and whether it holds predictive value for the cardiometabolic risk of the offspring in early life. Umbilical cord blood (UCB) samples were collected at birth, and the concentrations of adiponectin and leptin levels were measured using ELISA kits. Infants were evaluated echocardiographically at 5 ± 2 mo old (range: 1-12 mo), and these parameters were correlated with the AdipoQ/Lep levels. Results show that fetal AdipoQ/Lep ratio was lower in infants born to mothers with prepregnancy obesity. Both prepregnancy weight and maternal weight at the end of the gestation correlated with the AdipoQ/Lep ratio in UCB, whereas gestational weight gain showed no such association. In addition, birth weight, birth length, and body mass index (BMI)-for-age Z-score were negatively correlated with the AdipoQ/Lep ratio. Notably, lower levels of this adipokine-based biomarker were associated with reduced Z-score of left ventricular end-diastolic diameter. However, multiple linear regression analysis showed that maternal obesity and somatometry at birth influence infants' cardiac function and structure, independent of UCB AdipoQ/Lep ratio, adiponectin, or leptin alone. To our knowledge, this is the first investigation to explore the relationship between fetal AdipoQ/Lep levels, maternal-neonatal weight, and early cardiac alterations, highlighting the biomarker's potential predictive value for early-life cardiometabolic risk.NEW & NOTEWORTHY This study is the first to explore the association between fetal adiponectin/leptin (AdipoQ/Lep) ratio and maternal and neonatal anthropometrics and early alterations in cardiac structure. Although maternal and neonatal weight metrics impact infant heart development, this occurs independently of the AdipoQ/Lep. However, lower levels of AdipoQ/Lep ratio were associated with reduced Z-score of left ventricular end-diastolic diameter, offering insights into fetal programming mechanisms linked to maternal metabolic status during pregnancy.

Gestational phthalate levels and biomarkers of aging in infants and children from New York City.

Prenatal exposures to persistent organic pollutants and menstrual characteristics in girls at age 12 in the French PELAGIE cohort.

ObjectiveTo characterise quantitative glucose-6-phosphate dehydrogenase (G6PD) activity in term and preterm neonates, compare activity by gestational age (GA) and sex and derive neonatal screening cut-offs using percentile and WHO methods.DesignRetrospective cross-sectional analysis of cord blood screening programme.SettingKing Abdulaziz Medical City, Riyadh, Saudi Arabia, January 2016 to May 2022.ParticipantsAll live births with cord blood G6PD and GA. Of 59 465 births, 58 139 (97.8%) were screened. For reference range derivation only, results below the adult threshold (<5.7 U/g haemoglobin (Hb); n=1163) were excluded, yielding 56 976.Main outcome measuresDistribution by GA and sex; prevalence under three definitions: adult cut-off (≤5.7 U/g Hb), neonatal percentile cut-off (2.5th percentile) and WHO bands (<30% deficient, 30–70% intermediate, >70% normal). Secondary measures were stratum medians and the male share among detected cases.ResultsMean activity was 15.33±2.67 U/g Hb, higher in preterm than term. Sex differences were absent in preterm strata but present at term (males lower than females; p=0.002). The neonatal 2.5th percentile cut-off was 9.9 U/g Hb. Using the adult cut-off, 2.00% (1163/58 139) were deficient, 80.9% male. Using the neonatal cut-off, prevalence rose to 4.97% (2888/58 139), adding 1725 infants (+583 males, +1142 females) and reducing the male share to 52.8%. WHO bands identified a small <30% group and a female intermediate (30–70%) group across strata. Medians were 15.0 (≥37 weeks), 16.0 (33–36), 17.0 (29–32) and 17.6 (≤28) U/g Hb.ConclusionsG6PD activity in neonates shows clear GA and sex effects. Adult cut-offs underestimate deficiency, especially in females. Neonatal thresholds (2.5th percentile plus GA-specific WHO bands) improve detection. Adoption within newborn screening, with reporting of a female intermediate band, should strengthen follow-up; external validation and linkage to bilirubin outcomes are needed.

Preeclampsia is amultisystem disorder involving in inflammatory responses and metabolic dysfunction of maternal-fetal circulation. Recently, researchers found it threatens renal health of offspring in adulthood. Growing evidence indicated chronic kidney disease is associated with glomeruli deficiencies during intrauterine development. Our previous study showed placenta-derived exosomes from cord plasma with preeclampsia impede fetal glomerular vascularization, during which we postulate microRNAs may function as epigenetic switches for gene silencing of human glomerular endothelial cells. However, the specific miRNAs in placenta-derived exosomes engaged in glomerular vascularization remain unclear. Small RNA sequencing of placental-derived exosomes and bioinformatics analysis were applied to identify differentially expressed miRNAs, followed by real-time polymerase chain reaction for verification. Transient expression and inhibition of candidate miRNA were performed by transfection with chemically synthesized miRNA oligonucleotides. Functional assays of HGECs including cell proliferation assays, EDU assays, migration assays, tube formation assays and monolayer cell barrier permeability assays were performed after transfection. Further, dual luciferase assay was used to explore the target genes of candidate miRNA, followed by RT-qPCR, western blot and rescue assays. Antagomirs transfection of C57BL/6J fetal mice via Amniotic cavity injection in vivo and C57BL/6J fetal mice kidney explants culture in vitro were performed to evaluate number of glomeruli, renal development. Preeclampsia downregulates miR-199a-3p in placenta-derived exosomes from cord plasma. Suppression of endogenous miR-199a-3p in HGECs inhibits angiogenesis, proliferation, migration and permeability. A dual luciferase assay and rescue assays confirmed that miR-199a-3p targets PH domain leucine-rich repeat-containing protein phosphatase 2, regulating the phosphorylation of Akt serine/threonine kinase 1 (S473). C57BL/6J fetal mice with miR-199a-3p downregulation have low glomerulus counts and relative growth rate. miR-199a-3p in placenta-derived exosomes from cord plasma controls VEGF-induced glomerular angiogenesis. Moreover, it provides a distinct perspective for the mechanisms underlying the increased risk for renal disease in the offspring of preeclampsia patients via placenta-derived exosomal miRNAs.

Associations between prenatal exposure to a mixture of lead, mercury and polychlorinated biphenyls and executive function in Inuit adolescents.

Low-dose aspirin (LDA) is an intervention recommended to prevent the development of hypertensive disorders of pregnancy (HDP) in high-risk pregnancies. Maternal conditions such as HDP have been associated with cord blood epigenetic changes including those related to cardiovascular processes; however, it is unclear whether maternal aspirin therapy may impact neonatal epigenetics in otherwise healthy high-risk pregnancy.This study aimed to determine if maternal LDA exposure in utero leads to altered DNA methylation in umbilical cord blood cells in term neonates compared with controls not exposed to aspirin, and to identify if these methylation changes alter key pathways in the development of chronic disease.Umbilical cord blood was collected from 10 neonates without LDA exposure and 13 neonates with LDA exposure in utero. Patients with hypertensive disorders of pregnancy, COVID-19, and chorioamnionitis were excluded. Genomic DNA was isolated from umbilical cord blood cells and genome-wide DNA methylation was performed using Illumina Methylation EPIC assay.A total of 155 differentially methylated loci (81 genes were hypermethylated and 74 were hypomethylated) were identified in LDA-exposed neonatal umbilical cord blood compared with the control group. Important canonical pathways identified by Ingenuity Pathway Analysis (IPA) were related to Th1 and Th2 signaling and classical (M1) macrophage activation. The genes affected by LDA exposure were associated with cardiac and renal systems.LDA exposure led to differential DNA methylation in umbilical cord blood. The differentially methylated genes were related to inflammatory pathways as well as cardiac and renal toxicity pathways. LDA exposure in utero may promote altered health programming in the neonate in areas impacting cardiovascular health. · Maternal aspirin exposure is associated with differential DNA methylation in cord blood.. · Cord blood epigenetic changes associated with maternal aspirin relate to anti-inflammatory pathways.. · Research on potential protective impact of maternal aspirin on neonatal epigenetics is warranted..

Hematopoietic stem cell transplantation has been conducted in clinical settings to treat patients with malignant or non-malignant blood diseases for decades. Cord blood (CB) has been recognized as an essential graft source with beneficial characteristics, such as a lower risk of relapse and a lower rate of chronic graft-versus-host disease. However, the limited number of cells in CB impedes its broader use and hinders the ability to harness its benefits. Various expansion strategies have emerged to address this barrier, based on a deeper understanding of fate decisions and the maintenance of stemness in hematopoietic stem cells. To achieve an efficient transition from the laboratory to clinical application, several strategies have successfully managed scale-up manufacturing to satisfy clinically relevant requirements for both quality and scale. These approaches have progressed to the clinical stage and have demonstrated promising results. Novel expanded CB-derived hematopoietic stem and progenitor cells (HSPCs) therapies, including OMISIRGE (Omidubicel onlv.), Zemcelpro (Dorocubicel), and upcoming products with International Nonproprietary Name designations, introduce innovative concepts and comprehensive considerations for improving CB transplantation. This progress enables novel therapeutic options and represents a breakthrough in traditional CB transplants. In this context, we summarize and explore representative techniques and products to provide insights that inspire future developments in CB-derived HSPC therapies.

Evaluation of total oxidant status/total antioxidant capacity and DNA damage in neonates with high lactate levels in umbilical cord blood gases

BackgroundEpigenetic alterations during fetal development have been proposed as key factors explaining associations between maternal lifestyle during pregnancy and later health outcomes in the offspring, pertaining to the developmental origin of health and disease hypothesis.ObjectivesTo assess the association of maternal lifestyle with offsprings’ birth weight and underlying epigenetic mediatory mechanisms in the NorthPop prospective birth cohort.MethodsA three-step analytic pipeline was applied. In 722 mother–child pairs, overall associations between ten maternal lifestyle factors and the offspring’s standardized birth weight were first evaluated by multiple linear regression. Three high-dimensional mediation methods, based on sure independence screening and penalized regression, were then applied on the beta methylation matrix to identify candidate CpG mediators in cord blood driving the significant overall associations. Finally, robust and ordinary least squares (OLS) regression-based classical mediation methods were used with candidate CpG probes to assess single- and multiple (parallel and serial)-mediator models on a low-dimensional space.ResultsGestational weight gain (GWG) (β-adj = 0.03; p = 2 × 10–5) and maternal BMI at the beginning of pregnancy (β-adj = 0.036; p = 1 × 10–4) were significantly associated with the offspring’s standardized birth weight. High-dimensional mediation analyses identified pooled sets of four (cg19242268 [TCEA2]; cg08461903 [N/A]; cg14798382 [CHERP/C19orf44] and cg21516291 [SLC35C2]) and five (cg17040807 [CYGB]; cg19242268 [TCEA2]; cg26552621 [CIRBP]; cg04457572 [CDH23] and cg06457011 [PLCG1]) candidate CpG mediators related to GWG and BMI at the beginning of pregnancy, respectively. For both exposures, classical mediation analyses revealed a range of significant single- and multiple (both serial and parallel)-mediator models via both robust and OLS regression based approaches. These indicated the likely presence of individual, causally linked multiple, and causally independent multiple mediatory pathways underlying the two significant overall associations.ConclusionsOur findings support the hypothesis that neonatal health effects related to maternal lifestyle may be partly mediated by epigenetic alterations. Findings also suggest the possible involvement of multiple DNA methylation sites via various mediatory pathways.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13148-025-02001-z.

HLA vaccine effect in double cord blood transplant: a Chinese cohort.

Two strains of the minute virus of mice (MVM) parvovirus (of the species Protoparvovirus rodent1), named i (immunosuppressive) and p (prototype), show disparate tropism and pathogenicity in mice. Unlike the virulent MVMi, the MVMp is attenuated and infection-restricted in primary mouse hematopoietic cells; however, it does infect human transformed, established, and stem cells. We thus seek here a putative MVMp natural tropism to humans compared to MVMi. Infectious purified MVMp virions suppress in vitro the clonogenic potential of human committed (erythroid and myeloid) and primitive CD34+ progenitors, regardless of the cell source (umbilical cord blood, G-CSF mobilized peripheral blood, or bone marrow), in a multiplicity of infection-dependent manner. Furthermore, primitive CD34+ progenitors in culture are permissive to the MVMp cytotoxic NS-1 protein expression and the synthesis of viral genome replicative intermediates. None of these features is shared by MVMi. In consistency, MVMp suppresses the pool of CD34+ progenitors in bone-marrow-humanized immunodeficient NSG mice and severely compromises their survival, whereas in basal NSG mice, it replicates to several thousand-fold lower levels than MVMi and undergoes evolution to variants carrying genetic changes at the capsid tropism determinant binding sialic acid types. We suggest that MVMp may have originated from a MVMi-like mouse parvovirus upon adaptation to human sialic acid receptors in immunocompromised individuals. Extensive serological and genetic screens failed to demonstrate circulating MVMp in Eurasian and African human populations, including hematopoietic patients. Nevertheless, the high MVMp cytotoxicity to human primitive hematopoietic progenitors and rapid evolvability deserve further epidemiological studies.IMPORTANCEAssigning the genuine natural viral host range may be uncertain without testing the susceptibility of primary cells. Parvoviridae, a family of ssDNA icosahedral viruses, harbors several members infecting humans, but only parvovirus B19 of the Erythroparvovirus genus shows tropism for human hematopoietic progenitors. Here, we evaluate the tropism of the MVMi and MVMp parvoviruses for humans, which are assumed to be mouse pathogens. We show that MVMp is remarkably cytotoxic for human primitive CD34+ and committed erythroid and myeloid hematopoietic progenitors. Infection of basal and bone marrow-humanized immunodeficient mice shows the emergence of viral strain-specific genetic changes at the capsid domain binding sialic-acid receptors, denoting adaptation to the respective host hematopoiesis. Although a large epidemiological survey failed to identify circulating MVMp sequences or antibodies in human populations, its high toxicity to human hematopoietic progenitors of different lineages and primitiveness and rapid evolutionary capacity demand in-depth characterization of its potential pathogenicity for humans.

Background: Evidence linking maternal vitamin D status with gestational hypertensive disorders and neonatal outcomes in Southern Europe remains limited. We evaluated maternal and cord 25-hydroxyvitamin D [25(OH)D] at birth in an urban Greek cohort and examined associations with gestational hypertension and preeclampsia. Methods: We conducted a cross-sectional study of 248 mother–infant dyads delivering at Tzaneio General Hospital of Piraeus, Greece. Eligible participants were of Greek origin or long-term residents (&gt;10 years). Maternal venous and umbilical cord blood were obtained at birth and analyzed for serum 25(OH)D. Postpartum questionnaires captured sun exposure, supplement use, and selected lifestyle factors; clinical and obstetric data, including diagnoses of gestational hypertension and preeclampsia, were abstracted from medical records. We classified 25(OH)D as deficient (&lt;20 ng/mL), insufficient (20–29 ng/mL), and, for risk-stratified analyses, treated values &lt; 30 ng/mL as low. Results: Maternal 25(OH)D concentrations varied seasonally (winter 16.96 ± 9.60 ng/mL; summer 24.22 ± 12.57 ng/mL) and correlated with cord concentrations (r = 0.80). Most mothers (75–89%) had &lt;30 ng/mL across seasons, and 73% of neonates were &lt;20 ng/mL despite supplementation. Gestational hypertension occurred in 29/248 (11.7%) and preeclampsia in 15/248 (6.0%), with low maternal 25(OH)D common among affected women. Conclusions: In this cross-sectional study of an urban Mediterranean population, hypovitaminosis D was highly prevalent among mothers and neonates, with seasonal variation and clustering among hypertensive pregnancies. These findings support prenatal care strategies beyond fixed supplementation, incorporating season- and environment-sensitive dosing with screening and dietary counseling. Prospective studies are needed to clarify causality and refine supplementation targets.

To characterize longitudinal vascular endothelial growth factor (VEGF) trajectories and establish time-discriminative thresholds for bronchopulmonary dysplasia (BPD) severity stratification in extremely preterm neonates. Prospective observational cohort study with serial biomarker assessments. Tertiary neonatal intensive care unit in Suzhou, China (February 2022–January 2023). The cohort comprised 157 infants born at < 30 weeks’ gestation with birth weights < 1250 g. After exclusions (n = 21), 136 infants completed the study protocol. BPD severity and weekly plasma VEGF levels (cord blood to postnatal day 28). Analyses included adjusted mixed-effects models for longitudinal trends and Receiver Operating Characteristic (ROC) curves with bootstrap 95% confidence intervals for discriminative accuracy. Infants developing moderate-to-severe BPD (n = 44) exhibited biphasic VEGF dysregulation: elevated cord blood levels (75.8 pg/mL, 95% CI: 63.2–88.4) followed by steep weekly decline (− 56.0 pg/mL/week, 95% CI: −62.5 to − 49.4), whereas no/mild BPD infants (n = 92) maintained stable trajectories (P < 0.001, partial η2 = 0.67). Discriminative performance varied temporally: at birth (AUC 0.88, 95% CI: 0.82–0.93; threshold ≥ 338.6 pg/mL), Day 14 (AUC 0.75, 95% CI: 0.66–0.84; threshold ≤ 232.2 pg/mL) and at Day 21 (AUC 0.91, 95% CI: 0.85–0.96; threshold ≤ 217.5 pg/mL), bootstrap validation confirmed robustness. Longitudinal VEGF trajectories from a parsimonious mixed‑effects model identified infants who developed moderate‑to‑severe BPD, supporting potential for early risk stratification requiring validation.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-21349-z.

Pericardial effusion (PCE) is a serious complication after allogeneic hematopoietic cell transplantation, but its etiology is not fully understood, particularly the role of viral reactivation. We investigated the presence of DNA viruses in pericardial fluid from nine umbilical cord blood transplant recipients who underwent pericardiocentesis. Multiplex PCR detected DNA viruses in seven patients (78%), with Epstein-Barr virus being most common. The clinical context of viral detection appeared to differ by onset timing. In early-onset PCE (< 100days), viral presence was often systemic and likely secondary to severe inflammation. In contrast, late-onset cases frequently occurred with chronic graft-versus-host disease and showed localized viral reactivation within the pericardium. These findings suggest DNA viruses are potential contributors to post-transplant PCE. Viral evaluation of pericardial fluid should be considered in these patients as it may influence therapeutic strategies.

A 53-year-old woman experienced relapse of diffuse large B cell lymphoma (DLBCL) 16years after achieving a first complete metabolic response (CMR). Despite initially being refractory to salvage chemotherapy, she achieved a second CMR and underwent umbilical cord blood transplantation (UCBT). On day 119 post-transplantation, she experienced a second relapse and received chimeric antigen receptor T (CAR T) cell therapy, achieving a third remission without cytokine release syndrome or graft-versus-host disease (GVHD). However, a third relapse occurred seven months after CAR T cell therapy. Epcoritamab treatment was initiated, resulting in CMR without severe complications. Subsequently, the patient underwent curative unrelated allogeneic peripheral blood hematopoietic stem cell transplantation (HSCT). She experienced no severe transplant-related complications, including serious GVHD or infections. She has remained in CMR for > 1year after the second transplant. Epcoritamab appears to be an effective and safe treatment option for DLBCL relapse, even after both UCBT and CAR T cell therapy, suggesting that bridging therapy with epcoritamab followed by a second allogeneic HSCT may achieve long-term survival.

Background Casein Kinase II Subunit Alpha (CK2α), the catalytic subunit of protein kinase CK2, is encoded by CSNK2A1 . This kinase catalyzes substrate phosphorylation and regulates diverse cellular processes including cell cycle progression, apoptosis, and transcription. CSNK2A1 is associated with Okur-Chung Neurodevelopmental Syndrome (OCNS, OMIM: 617062). Although CSNK2A1 functional deficiency is implicated in impaired embryonic development, prenatal case reports remain scarce. Methods Clinical data and fetal umbilical cord blood samples were collected. Whole-genome sequence (WGS) was used for potential pathogenic variants identification, followed by Sanger sequencing to validate the variant. Bioinformatic tools were employed to predict the 3D structure of the variant. Wild-type and mutant CSNK2A1 overexpression plasmids were constructed to investigate the functional consequences of the variant. Result A 33-year-old pregnant woman without adverse obstetric history. At 34 +4 weeks, ultrasound showed an intracranial abnormal echoes, multiple cardiovascular anomalies, and stillbirth had occurred at 35 weeks. WGS identified a novel frameshift mutation c.1020_1021delAG (p.Gly342Glnfs*57) in the CSNK2A1 gene. Bioinformatics analysis indicated structural modification in mutant proteins. In vitro kinase assays showed that the variant did not impair kinase activity. Quantitative analysis demonstrated significantly elevated mutant mRNA levels but reduced protein expression compared to wild-type. Elevated ubiquitination in mutants potentially explains diminished CSNK2A1 protein abundance. Conclusion We report a novel CSNK2A1 frameshift mutation that significantly reduces protein expression and impairs gene function. These findings expand our understanding of CSNK2A1 ’s genetic diversity and underscore the importance of comprehensive functional analyses to achieve accurate diagnosis. This study facilitates prenatal diagnosis of CSNK2A1 -related disorders and informs clinical decision-making for carriers.

ObjectiveThe purpose of this study is to analyze the changes of spinal artery blood flow (SCBF) and its potential impact on the safety of spinal cord function during spinal deformity osteotomy by using laser speckle imaging technology, and to monitor the changes of vertebral artery flow velocity and resistance index before and after operation by using color Doppler ultrasound technology, so as to preliminarily explore the correlation between vertebral artery and spinal cord vascular hemodynamic changes, and to explore the safety limit of osteotomy shortening.MethodsThe volunteers were divided into Group A and Group B according to their needs. Group A included 8 patients with spinal deformity who underwent vertebral artery ultrasound examination before and after spinal deformity correction surgery. Group B also included 8 patients with spinal deformity who underwent spinal osteotomy and 1/3 and 1/2 shortening of the spine, and 5 patients underwent 1/3 spinal distraction. Intraoperative laser speckle imaging system was used to monitor the changes of spinal cord blood perfusion and vascular diameter in real time, and the spinal cord function was evaluated with the help of neurophysiological monitoring. All patients in the study received SRS-22 and ODI scores before and after surgery; Rstudio software was used for statistical analysis.ResultsIn Group A, the postoperative vertebral artery flow velocity of 8 patients increased to varying degrees compared with that before operation, and the resistance index decreased or leveled to varying degrees, the difference was statistically significant (P < 0.05). In Group B, the SCBF of the left and right spinal arteries decreased to varying degrees after traction, and the diameter of spinal artery increased gradually with the increase of traction degree. In Group B, the SCBF of the left and right spinal artery increased first and then decreased after osteotomy and 1/3 and 1/2 spinal shortening, and the diameter of spinal artery gradually increased with the increase of shortening degree, the difference was statistically significant (P < 0.05). The SRS -22 scale and ODI scores of all patients before and after operation were significantly different (P < 0.05). Further analysis showed that there was a significant correlation between the SCBF of bilateral spinal artery and the diameter of bilateral spinal artery before and after 1/3 spinal distraction and 1/3 spinal shortening (P < 0.05). There were correlations between bilateral vertebral artery resistance index and flow velocity, SCBF and ODI scores, bilateral spinal artery diameter, and bilateral vertebral artery resistance index before and after operation (P < 0.05). However, there was no significant correlation between the SCBF of bilateral spinal cord blood vessels and the diameter of bilateral spinal cord blood vessels when the spine was shortened by 1/3 to 1/2 (P > 0.05). During the whole operation, no abnormality was found in the electrophysiological monitoring.ConclusionIn the process of spinal traction and shortening, the diameter of spinal cord blood vessels decreased and gradually increased. The pulling operation will lead to the decrease of SCBF, while the shortening operation will make the SCBF increase first and then decrease. Before and after operation, there were significant correlations between the resistance index and flow velocity of bilateral vertebral artery, SCBF and ODI scores, and the diameter of bilateral spinal artery and the resistance index of bilateral vertebral artery. When the degree of spinal shortening is controlled within 1/3 of that after single vertebral osteotomy in the lower thoracic spine, the change of SCBF is positively correlated with the increase of spinal cord vascular diameter, and the shortening of less than 1/2 after single vertebral osteotomy in the lower thoracic spine can be regarded as the safety threshold.