Sleep is an instinctive behavior alternating awakening state, sleep entails many active processes occurring at the cellular, circuit and organismal levels. The function of sleep is to restore cellular energy, enhance immunity, promote growth and development, consolidate learning and memory to ensure normal life activities. However, with the increasing of social pressure involved in work and life, the incidence of sleep disorders (SD) is increasing year by year. In the short term, sleep disorders lead to impaired memory and attention; in the longer term, it produces neurological dysfunction or even death. There are many ways to directly or indirectly contribute to sleep disorder and keep the hormones, including pharmacological alternative treatments, light therapy and stimulus control therapy. Exercise is also an effective and healthy therapeutic strategy for improving sleep. The intensities, time periods, and different types of exercise have different health benefits for sleep, which can be found through indicators such as sleep quality, sleep efficiency and total sleep time. So it is more and more important to analyze the mechanism and find effective regulation targets during sleep disorder through exercise. Dopamine (DA) is an important neurotransmitter in the nervous system, which not only participates in action initiation, movement regulation and emotion regulation, but also plays a key role in the steady-state remodeling of sleep-awakening state transition. Appreciable evidence shows that sleep disorder on humans and rodents evokes anomalies in the dopaminergic signaling, which are also implicated in the development of psychiatric illnesses such as schizophrenia or substance abuse. Experiments have shown that DA in different neural pathways plays different regulatory roles in sleep behavior, we found that increasing evidence from rodent studies revealed a role for ventral tegmental area DA neurons in regulating sleep-wake patterns. DA signal transduction and neurotransmitter release patterns have complex interactions with behavioral regulation. In addition, experiments have shown that exercise causes changes in DA homeostasis in the brain, which may regulate sleep through different mechanisms, including cAMP response element binding protein signal transduction, changes in the circadian rhythm of biological clock genes, and interactions with endogenous substances such as adenosine, which affect neuronal structure and play a neuroprotective role. This review aims to introduce the regulatory effects of exercise on sleep disorder, especially the regulatory mechanism of DA in this process. The analysis of intracerebral DA signals also requires support from neurophysiological and chemical techniques. Our laboratory has established and developed an in vivo brain neurochemical analysis platform, which provides support for future research on the regulation of sleep-wake cycles by movement. We hope it can provide theoretical reference for the formulation of exercise prescription for clinical sleep disorder and give some advice to the combined intervention of drugs and exercise.

ObjectiveTo investigate the role of mature-tRNA-Asp-GTC and pre-tRNA-Arg-TCT in the ferroptosis phenotype of ovarian cancer （OC） cells and the regulatory mechanism of gypenoside L （Gyp-L） on mature-tRNA-Asp-GTC and pre-tRNA-Arg-TCT in OC cells. MethodsThe proliferation of human ovarian adenocarcinoma OVCAR3 cells was detected by cell counting kit-8 （CCK-8） assay， and the half-maximal inhibitory concentration （IC₅₀） values of cisplatin （DDP）， Gyp-L， and DDP in the presence of Gyp-L were calculated to determine the intervention concentration for subsequent experiments. Cell cloning assay and scratch assay reflected the proliferation and migration ability of OVCAR3 cells. PANDORA-seq small RNA sequencing was used to detect the differentially expressed transfer RNA-derived small RNAs （tsRNAs） in the cells after Gyp-L intervention， and the corresponding target genes of the tsRNAs were found by the RNAhybrid software. Malondialdehyde （MDA）， glutathione （GSH）， and lipid peroxide （LPO） levels were measured by colorimetry or enzyme linked immunosorbent assay （ELISA） method， Fe²⁺ content by FerroOrange fluorescent probe， and reactive oxygen species （ROS） content by DCFH-DA fluorescent probe to reflect the occurrence of ferroptosis in OVCAR3 cells. OVCAR3 cells were divided into a control group， a 50 µmol·L^-1 Gyp-L group， and a 100 µmol·L^-1 Gyp-L group. Quantitative real-time polymerase chain reaction （PCR） was performed to detect the expression of mature-tRNA-Asp-GTC， mature-tRNA-Leu-CAA， mature-mt_tRNA-Tyr-GTA_5_end， mature-tRNA-Val-CAC， mature-mt_tRNA-Glu-TTC， pre-tRNA-Arg-TCT， mature-tRNA-Asn-GTT， hydroxymethylbilane synthase （HMBS）， Wnt， β-catenin， glutathione peroxidase 4 （GPX4）， Kelch-like ECH-associated protein 1 （KEAP1）， nuclear factor erythroid 2-related factor 2 （Nrf2）， activating transcription factor 3 （ATF3）， cystine/glutamate antiporter xCT， lysophosphatidylcholine acyltransferase 3 （LPCAT3）， and arachidonate 15-lipoxygenase （ALOX15）. Western blot was performed to detect the expression of HMBS， Wnt， β-catenin， GPX4， KEAP1， Nrf2， ATF3， xCT， LPCAT3， and ALOX15 proteins. ResultsThe 50 µmol·L^-1 Gyp-L， 100 µmol·L^-1 Gyp-L， DDP， 50 µmol·L^-1 Gyp-L+DDP， and 100 µmol·L^-1 Gyp-L+DDP groups showed significantly inhibited proliferation and migration of OVCAR3 cells （P<0.05） and exacerbated cell ferroptosis as reflected by the increase in the content of ROS， MDA， LPO， and Fe²⁺， as well as a decrease in the content of GSH （P<0.05）. Compared with the control group， Gyp-L effectively interfered with the expression of 25 tsRNAs in OVCAR3 cells （P<0.05， |log₂Fc|>1）. Pre-tRNA-Arg-TCT/HMBS/Wnt/β-catenin/GPX4， pre-tRNA-Arg-TCT/KEAP1/NRF2/xCT， mature-tRNA-Asp-GTC/ATF3/KEAP1/NRF2/xCT， and mature-tRNA-Asp-GTC/LPCAT3/ALOX15 axial expression was significantly aberrant after Gyp-L intervention （P<0.05）. ConclusionThe pre-tRNA-Arg-TCT/HMBS/Wnt/β-catenin/GPX4， pre-tRNA-Arg-TCT/KEAP1/Nrf2/xCT， mature-tRNA-Asp-GTC/ATF3/KEAP1/Nrf2/xCT， and mature-tRNA-Asp-GTC/LPCAT3/ALOX15 signaling pathways are involved in OC development. Gyp-L inhibits OC development by activating OVCAR3 cell ferroptosis onset mainly through the mature-tRNA-Asp-GTC/ATF3/KEAP1/Nrf2/xCT and mature-tRNA-Asp-GTC/LPCAT3/ALOX15 signaling axes.

ObjectiveTo investigate the role of mature-tRNA-Asp-GTC and pre-tRNA-Arg-TCT in the ferroptosis phenotype of ovarian cancer （OC） cells and the regulatory mechanism of gypenoside L （Gyp-L） on mature-tRNA-Asp-GTC and pre-tRNA-Arg-TCT in OC cells. MethodsThe proliferation of human ovarian adenocarcinoma OVCAR3 cells was detected by cell counting kit-8 （CCK-8） assay， and the half-maximal inhibitory concentration （IC₅₀） values of cisplatin （DDP）， Gyp-L， and DDP in the presence of Gyp-L were calculated to determine the intervention concentration for subsequent experiments. Cell cloning assay and scratch assay reflected the proliferation and migration ability of OVCAR3 cells. PANDORA-seq small RNA sequencing was used to detect the differentially expressed transfer RNA-derived small RNAs （tsRNAs） in the cells after Gyp-L intervention， and the corresponding target genes of the tsRNAs were found by the RNAhybrid software. Malondialdehyde （MDA）， glutathione （GSH）， and lipid peroxide （LPO） levels were measured by colorimetry or enzyme linked immunosorbent assay （ELISA） method， Fe²⁺ content by FerroOrange fluorescent probe， and reactive oxygen species （ROS） content by DCFH-DA fluorescent probe to reflect the occurrence of ferroptosis in OVCAR3 cells. OVCAR3 cells were divided into a control group， a 50 µmol·L^-1 Gyp-L group， and a 100 µmol·L^-1 Gyp-L group. Quantitative real-time polymerase chain reaction （PCR） was performed to detect the expression of mature-tRNA-Asp-GTC， mature-tRNA-Leu-CAA， mature-mt_tRNA-Tyr-GTA_5_end， mature-tRNA-Val-CAC， mature-mt_tRNA-Glu-TTC， pre-tRNA-Arg-TCT， mature-tRNA-Asn-GTT， hydroxymethylbilane synthase （HMBS）， Wnt， β-catenin， glutathione peroxidase 4 （GPX4）， Kelch-like ECH-associated protein 1 （KEAP1）， nuclear factor erythroid 2-related factor 2 （Nrf2）， activating transcription factor 3 （ATF3）， cystine/glutamate antiporter xCT， lysophosphatidylcholine acyltransferase 3 （LPCAT3）， and arachidonate 15-lipoxygenase （ALOX15）. Western blot was performed to detect the expression of HMBS， Wnt， β-catenin， GPX4， KEAP1， Nrf2， ATF3， xCT， LPCAT3， and ALOX15 proteins. ResultsThe 50 µmol·L^-1 Gyp-L， 100 µmol·L^-1 Gyp-L， DDP， 50 µmol·L^-1 Gyp-L+DDP， and 100 µmol·L^-1 Gyp-L+DDP groups showed significantly inhibited proliferation and migration of OVCAR3 cells （P<0.05） and exacerbated cell ferroptosis as reflected by the increase in the content of ROS， MDA， LPO， and Fe²⁺， as well as a decrease in the content of GSH （P<0.05）. Compared with the control group， Gyp-L effectively interfered with the expression of 25 tsRNAs in OVCAR3 cells （P<0.05， |log₂Fc|>1）. Pre-tRNA-Arg-TCT/HMBS/Wnt/β-catenin/GPX4， pre-tRNA-Arg-TCT/KEAP1/NRF2/xCT， mature-tRNA-Asp-GTC/ATF3/KEAP1/NRF2/xCT， and mature-tRNA-Asp-GTC/LPCAT3/ALOX15 axial expression was significantly aberrant after Gyp-L intervention （P<0.05）. ConclusionThe pre-tRNA-Arg-TCT/HMBS/Wnt/β-catenin/GPX4， pre-tRNA-Arg-TCT/KEAP1/Nrf2/xCT， mature-tRNA-Asp-GTC/ATF3/KEAP1/Nrf2/xCT， and mature-tRNA-Asp-GTC/LPCAT3/ALOX15 signaling pathways are involved in OC development. Gyp-L inhibits OC development by activating OVCAR3 cell ferroptosis onset mainly through the mature-tRNA-Asp-GTC/ATF3/KEAP1/Nrf2/xCT and mature-tRNA-Asp-GTC/LPCAT3/ALOX15 signaling axes.

Neuroscience is a significant frontier discipline within the natural sciences and has become an important interdisciplinary frontier scientific field. Brain is one of the most complex organs in the human body, and its structural and functional analysis is considered the “ultimate frontier” of human self-awareness and exploration of nature. Driven by the strategic layout of “China Brain Project”, Chinese scientists have conducted systematic research focusing on “understanding the brain, simulating the brain, and protecting the brain”. They have made breakthrough progress in areas such as the principles of brain cognition, mechanisms and interventions for brain diseases, brain-like computation, and applications of brain-machine intelligence technology, aiming to enhance brain health through biomedical technology and improve the quality of human life. Due to limited understanding and comprehension of neuroscience, there are still many important unresolved issues in the field of neuroscience, resulting in a lack of effective measures to prevent and protect brain health. Therefore, in addition to actively developing new generation drugs, exploring non pharmacological treatment strategies with better health benefits and higher safety is particularly important. Epidemiological data shows that, exercise is not only an indispensable part of daily life but also an important non-pharmacological approach for protecting brain health and preventing neurodegenerative diseases, forming an emerging research field known as motor neuroscience. Basic research in motor neuroscience primarily focuses on analyzing the dynamic coding mechanisms of neural circuits involved in motor control, breakthroughs in motor neuroscience research depend on the construction of dynamic monitoring systems across temporal and spatial scales. Therefore, high spatiotemporal resolution detection of movement processes and movement-induced changes in brain structure and neural activity signals is an important technical foundation for conducting motor neuroscience research and has developed a set of tools based on traditional neuroscience methods combined with novel motor behavior decoding technologies, providing an innovative technical platform for motor neuroscience research. The protective effect of exercise in neurodegenerative diseases provides broad application prospects for its clinical translation. Applied research in motor neuroscience centers on deciphering the regulatory networks of neuroprotective molecules mediated by exercise. From the perspectives of exercise promoting neurogenesis and regeneration, enhancing synaptic plasticity, modulating neuronal functional activity, and remodeling the molecular homeostasis of the neuronal microenvironment, it aims to improve cognitive function and reduce the incidence of Parkinson’s disease and Alzheimer’s disease. This has also advanced research into the molecular regulatory networks mediating exercise-induced neuroprotection and facilitated the clinical application and promotion of exercise rehabilitation strategies. Multidimensional analysis of exercise-regulated neural plasticity is the theoretical basis for elucidating the brain-protective mechanisms mediated by exercise and developing intervention strategies for neurological diseases. Thus,real-time analysis of different neural signals during active exercise is needed to study the health effects of exercise throughout the entire life cycle and enhance lifelong sports awareness. Therefore, this article will systematically summarize the innovative technological developments in motor neuroscience research, review the mechanisms of neural plasticity that exercise utilizes to protect the brain, and explore the role of exercise in the prevention and treatment of major neurodegenerative diseases. This aims to provide new ideas for future theoretical innovations and clinical applications in the field of exercise-induced brain protection.

As China accelerates its efforts in deep space exploration and long-duration space missions, including the operationalization of the Tiangong Space Station and the development of manned lunar missions, safeguarding astronauts’ physiological and cognitive functions under extreme space conditions becomes a pressing scientific imperative. Among the multifactorial stressors of spaceflight, microgravity emerges as a particularly potent disruptor of neurobehavioral homeostasis. Dopamine (DA) plays a central role in regulating behavior under space microgravity by influencing reward processing, motivation, executive function and sensorimotor integration. Changes in gravity disrupt dopaminergic signaling at multiple levels, leading to impairments in motor coordination, cognitive flexibility, and emotional stability. Microgravity exposure induces a cascade of neurobiological changes that challenge dopaminergic stability at multiple levels: from the transcriptional regulation of DA synthesis enzymes and the excitability of DA neurons, to receptor distribution dynamics and the efficiency of downstream signaling pathways. These changes involve downregulation of tyrosine hydroxylase in the substantia nigra, reduced phosphorylation of DA receptors, and alterations in vesicular monoamine transporter expression, all of which compromise synaptic DA availability. Experimental findings from space analog studies and simulated microgravity models suggest that gravitational unloading alters striatal and mesocorticolimbic DA circuitry, resulting in diminished motor coordination, impaired vestibular compensation, and decreased cognitive flexibility. These alterations not only compromise astronauts’ operational performance but also elevate the risk of mood disturbances and motivational deficits during prolonged missions. The review systematically synthesizes current findings across multiple domains: molecular neurobiology, behavioral neuroscience, and gravitational physiology. It highlights that maintaining DA homeostasis is pivotal in preserving neuroplasticity, particularly within brain regions critical to adaptation, such as the basal ganglia, prefrontal cortex, and cerebellum. The paper also discusses the dual-edged nature of DA plasticity: while adaptive remodeling of synapses and receptor sensitivity can serve as compensatory mechanisms under stress, chronic dopaminergic imbalance may lead to maladaptive outcomes, such as cognitive rigidity and motor dysregulation. Furthermore, we propose a conceptual framework that integrates homeostatic neuroregulation with the demands of space environmental adaptation. By drawing from interdisciplinary research, the review underscores the potential of multiple intervention strategies including pharmacological treatment, nutritional support, neural stimulation techniques, and most importantly, structured physical exercise. Recent rodent studies demonstrate that treadmill exercise upregulates DA transporter expression in the dorsal striatum, enhances tyrosine hydroxylase activity, and increases DA release during cognitive tasks, indicating both protective and restorative effects on dopaminergic networks. Thus, exercise is highlighted as a key approach because of its sustained effects on DA production, receptor function, and brain plasticity, making it a strong candidate for developing effective measures to support astronauts in maintaining cognitive and emotional stability during space missions. In conclusion, the paper not only underscores the centrality of DA homeostasis in space neuroscience but also reflects the authors’ broader academic viewpoint: understanding the neurochemical substrates of behavior under microgravity is fundamental to both space health and terrestrial neuroscience. By bridging basic neurobiology with applied space medicine, this work contributes to the emerging field of gravitational neurobiology and provides a foundation for future research into individualized performance optimization in extreme environments.

Objective To investigate the effect of grape seed proanthocyanidins(GSPs)on nuclear factor erythroid 2-related factor 2(Nrf2)antioxidant system and mitochondrial biosynthesis in testes of arsenic-exposed mice.Methods ICR mice were randomly divided into four groups:Control group,model group,GSPs group and experimental group.The mice in the model group and the experimental group drank sodium arsenite solution(10 mg·L-1 arsenic)to induce testicular injury.GSPs group and experimental group were given 100 mg·kg-1 GSPs by gavage,control group and model group were given equal volume of distilled water by gavage once a day for 8 weeks.The histological parameters of testes were measured by hematoxylin-eosin(HE)staining.The contents of malondialdehyde(MDA),superoxide dismutase(SOD)and adenosine triphosphate(ATP)in testicular tissue were determined by kit method.The expression levels of heme oxygenase 1(HO-1)and quinone oxidoreductase 1(NQ01)were detected by real-time quantitative reverse transcription polymerase chain reaction(RT-PCR).The expression of Nrf2 protein in testicular tissue was detected by immunohistochemistry.The expressions of mitochondrial synthesis-related proteins were detected by Western blot.Results The diameters of seminiferous tubules in control group,model group,GSPs group and experimental group were(184.32±14.14),(170.41±10.70),(186.87±8.03)and(181.70±9.15)μm;the contents of MDA were(2.30±0.26),(3.28±0.64),(2.32±0.40)and(2.74±0.31)nmol·mg-1;the proportions of Nrf2 positive cells were(46.50±11.98)％,(22.33±8.82)％,(51.67±12.44)％and(39.83±8.35)％;the mRNA expression levels of HO-1 were 1.00±0.21,0.51±0.10,1.00±0.28 and 0.80±0.06;the mRNA expression levels of NQO1 were 1.00±0.18,0.59±0.11,1.09±0.28 and 0.81±0.08;the contents of ATP were(491.83±67.16),(368.81±69.93),(512.44±70.96)and(472.20±68.24)μmol·g-1;the relative expression levels of PGC-1α protein were 1.00±0.06,0.22±0.03,0.94±0.05 and 0.48±0.05;the relative expression levels of TFAM were 1.00±0.07,0.32±0.05,0.80±0.05 and 0.67±0.06.The above indexes in the experimental group were statistically significant compared with the model group(all P＜0.05,P＜0.01).Conclusion GSPs has a protective effect against arsenic-induced testicular injury in mice by activating the Nfr2 antioxidant system and promoting mitochondrial biosynthesis.

ObjectiveTo investigate the influencing factors for rebleeding after endoscopic therapy and the effect of the number of sequential treatment sessions on postoperative rebleeding in patients with liver cirrhosis receiving secondary prevention of gastroesophageal varices （GOV）. MethodsA total of 1 717 patients with liver cirrhosis who received secondary prevention of GOV and attended The 960th Hospital of the PLA Joint Logistice Support Force from January 2017 to December 2021 were enrolled， and according to the presence or absence of bleeding after endoscopic therapy， they were divided into non-bleeding group and rebleeding group. The influencing factors for rebleeding were analyzed， as well as the association between the number of endoscopic treatment sessions and rebleeding. The chi-square test was used for comparison of categorical data between groups； the independent-samples t test or the Mann-Whitney U test was used for comparison of continuous data between the two groups； the Kruskal-Wallis H test was used for comparison bertween multiple groups， and the Wilcoxon test was used for further comparison between two groups. The Cox regression model was used to investigate the influencing factors for rebleeding， and the Kaplan-Meier method was used to plot survival curves， while the Log-rank test was used for comparison between groups. ResultsOf all patients， 286 （16.7%） experienced rebleeding after endoscopic therapy， and 1 431 （83.3%） did not experience bleeding. There were significant differences between the two groups in history of smoking and drinking， etiology of liver cirrhosis， hemoglobin （Hb）， prothrombin time （PT）， prothrombin activity （PTA）， international normalized ratio （INR）， albumin （Alb）， fasting blood glucose， blood urea nitrogen， Child-Pugh class， aspartate aminotransferase-to-platelet ratio index （APRI） score， albumin-bilirubin （ALBI） score， use of non-selective beta-blocker （NSBB） before surgery， treatment modality， type of varices， and maximal varicose vein diameter （all P<0.05）. The univariate Cox regression analysis showed that in the patients with liver cirrhosis who received secondary prevention of GOV， rebleeding was associated with history of smoking and drinking， etiology of liver cirrhosis， use of NSBB before surgery， treatment modality， maximal varicose vein diameter， Hb， platelet count， PT， PTA， INR， Alb， total bilirubin （TBil）， alkaline phosphatase （ALP）， gamma-glutamyl transpeptidase， blood glucose， Child-Pugh class， and ALBI score （all P<0.05）. The multivariate Cox regression analysis showed that Hb （hazard ratio ［HR］=0.989， 95% confidence interval ［CI］： 0.983‍ ‍—‍ ‍0.994， P<0.001）， TBil （HR=1.020， 95%CI： 1.006‍ ‍—‍ ‍1.034， P=0.005）， Alb （HR=0.868， 95%CI： 0.758‍ ‍—‍ ‍0.994， P=0.041）， treatment modality （sclerosing agent： HR=2.158， 95%CI： 1.342‍ ‍—‍ ‍3.470， P=0.002； tissue adhesive： HR=2.709， 95%CI： 1.343‍ ‍—‍ ‍5.462， P=0.005； ligation+sclerosing agent： HR=3.181， 95%CI： 1.522‍ ‍—‍ ‍6.645， P=0.002； sclerosing agent+tissue adhesive： HR=1.851， 95%CI： 1.100‍ ‍—‍ ‍3.113， P=0.020）， ALP （HR=1.003， 95%CI： 1.001‍ ‍—‍ ‍1.004， P=0.002）， and maximal varicose vein diameter （HR=1.346， 95%CI： 1.119‍ ‍—‍ ‍1.618， P=0.002） were independent influencing factors for rebleeding after endoscopic therapy. Comparison of rebleeding rate after different numbers of sequential treatment sessions showed that the patients treated for three sessions had a significantly lower rebleeding rate than those treated for one or two sessions （χ²=8.643 and 5.277， P=0.003 and 0.022）. The survival analysis showed that with the increase in the number of treatment sessions， there was a significantly longer interval between rebleeding （P=0.006） and a significantly lower mortality rate （P<0.001）. ConclusionThe levels of TBil， ALP， Hb， and Alb on admission， endoscopic treatment modality， and maximal varicose vein diameter were the main predictive factors for rebleeding after endoscopic therapy for GOV in liver cirrhosis， and such predictive factors should be closely monitored in clinical practice. Regular endoscopic therapy can reduce the rebleeding and mortality rates of patients with liver cirrhosis and GOV and prolonmg the interval between rebleeding.

【Objective】 To explore the feasibility of using autologous platelet-rich plasma (PRP) in the treatment of deep second-degree burns complicated with wound infection. 【Methods】 A retrospective analysis was conducted on the treatment process of a patient with deep second-degree burns and bacterial infection on the wound using autologous PRP. Clinical treatment highlights and outpatient follow-up were combined to discuss the feasibility and clinical effects of using autologous PRP in the treatment of burn wounds complicated with infection. 【Results】 The patient had a deep second-degree burn with a coagulase-negative Staphylococcus infection on the left lower limb. After one week of conventional wound dressing and antibiotic treatment, the patient's body temperature returned to normal. However, wound healing was slow and yellow secretion persisted. Subsequently, the burn wound was treated combined with topical autologous PRP. The wound pain score gradually decreased from 8 to 1. After 2 weeks, the bacterial culture of the wound secretion was negative, and the wound healed completely after 18 days. The wound scar score decreased from 5 to 2 at 1, 3 and 6 months after PRP treatment, and no obvious scar formation was observed. In the course of PRP treatment, there were no adverse reactions such as increased wound inflammation, abnormal blood routine and liver and kidney function test results. 【Conclusion】 For deep second-degree burn patients with localized wound bacterial infections who either refuse surgery or are not suitable for surgery, autologous PRP is a safer alternative that can effectively promote tissue regeneration and wound healing. The patient in this case achieved a curative effect in a short period of time.

【Objective】 To establish a blood quality monitoring indicator system, in order to continuously improve blood quality and standardized management. 【Methods】 Based on the research of literature and standards, and guided by the key control points of blood collection and supply process, the blood quality monitoring indicator system was developed. Through two rounds of Delphi expert consultation, the indicator content was further revised and improved according to expert opinions after six months of trial implementation. The indicator weight was calculated by questionnaire and analytic hierarchy process. 【Results】 A blood quality monitoring indicator system covering the whole process of blood collection and supply was constructed, including five primary indicators, namely blood donation service, blood component preparation, blood testing, blood supply and quality control, as well as 72 secondary indicators, including definitions, calculation formulas, etc. Two rounds of expert consultation and two rounds of feasibility study meeting were held to revise 17 items and the weight of each indicator was obtained through the analytic hierarchy process. After partial adjustments, a blood quality monitoring indicator system was formed. 【Conclusion】 A blood quality monitoring indicator system covering the whole process of blood collection and supply has been established for the first time, which can effectively evaluate the quality management level of blood banks and coordinate blood quality control activities of blood banks in Shandong like pieces in a chess game, thus improving the standardized management level

【Objective】 To objectively evaluate the quality control level of blood testing process in blood banks through quantitative monitoring and trend analysis, and to promote the homogenization level and standardized management of blood testing laboratories in blood banks. 【Methods】 A quality monitoring indicator system covering the whole process of blood collection and supply, including blood donation service, blood component preparation, blood testing, blood supply and quality control was established. The questionnaire Quality Monitoring Indicators for Blood Collection and Supply Process with clear definition of indicators and calculation formulas was distributed to 17 blood banks in Shandong province. Quality monitoring indicators of each blood bank from January to December 2022 were collected, and 31 indicators in terms of blood testing were analyzed using SPSS25.0 software. 【Results】 The proportion of unqualified serological tests in 17 blood bank laboratories was 55.84% for ALT, 13.63% for HBsAg, 5.08% for anti HCV, 5.62% for anti HIV, 18.18% for anti TP, and 1.65% for other factors (mainly sample quality). The detection unqualified rate and median were (1.23±0.57)% and 1.11%, respectively. The ALT unqualified rate and median were (0.74±0.53)% and 0.60%, respectively. The detection unqualified rate was positively correlated with ALT unqualified rate (r=0.974, P<0.05). The unqualified rate of HBsAg, anti HCV, anti HIV and anti TP was (0.15±0.09)%, (0.05±0.04)%, (0.06±0.03)% and (0.20±0.05)% respectively. The average unqualified rate, average hemolysis rate, average insufficient volume rate and the abnormal hematocrit rate of samples in 17 blood bank laboratories was 0.21‰, 0.08‰, 0.01‰ and 0.02‰ respectively. There were differences in the retest concordance rates of four HBsAg, anti HCV and anti HIV reagents, and three anti TP reagents among 17 blood bank laboratories (P<0.05). The usage rate of ELISA reagents was (114.56±3.30)%, the outage rate of ELISA was (10.23±7.05) ‰, and the out of range rate of ELISA was (0.90±1.17) ‰. There was no correlation between the out of range rate, outrage rate and usage rate (all P>0.05), while the outrage rate was positively correlated with the usage rate (r=0.592, P<0.05). A total of 443 HBV DNA positive samples were detected in all blood banks, with an unqualified rate of 3.78/10 000; 15 HCV RNA positive samples were detected, with an unqualified rate of 0.13/10 000; 5 HIV RNA positive samples were detected, with an unqualified rate of 0.04/10 000. The unqualified rate of NAT was (0.72±0.04)‰, the single NAT reaction rate [(0.39±0.02)‰] was positively correlated with the single HBV DNA reaction rate [ (0.36±0.02) ‰] (r=0.886, P<0.05). There was a difference in the discriminated reactive rate by individual NAT among three blood bank laboratories (C, F, H) (P<0.05). The median resolution rate of 17 blood station laboratories by minipool test was 36.36%, the median rate of invalid batch of NAT was 0.67%, and the median rate of invalid result of NAT was 0.07‰. The consistency rate of ELISA dual reagent detection results was (99.63±0.24)%, and the median length of equipment failure was 14 days. The error rate of blood type testing in blood collection department was 0.14‰. 【Conclusion】 The quality monitoring indicator system for blood testing process in Shandong can monitor potential risks before, during and after the experiment, and has good applicability, feasibility, and effectiveness, and can facilitate the continuous improvement of laboratory quality control level. The application of blood testing quality monitoring indicators will promote the homogenization and standardization of blood quality management in Shandong, and lay the foundation for future comprehensive evaluations of blood banks.