It has been demonstrated that long-term space flights have a significantly greater impact on the cardiovascular, skeletal, and nervous systems of astronauts. The structural and functional alterations in the skeletal and muscular systems resulting from exposure to weightlessness can lead to the development of low back pain, significantly impairing the ability of astronauts to perform tasks and respond to emergencies. Both space flight and simulated microgravity have been shown to result in low back pain among astronauts, with the following factors identified as primary contributors to this phenomenon. The occurrence of intervertebral disc (IVD) edema results in the stimulation of type IV mechanoreceptors, which subsequently activate nociceptive afferents. The protrusion of an IVD causes compression of the spinal nerve roots. Furthermore, the elongation of the vertebral column and/or the diminished lumbar curvature of the spine exert traction on the dorsal root nerves. Paravertebral muscle degeneration leads to the inhibition of decreased nociceptive activity of the wide-dynamic range neurons of the spinal dorsal horn. Moreover, endogenous pain descending facilitation triggered by conditioning stimulation can be enhanced via the thalamic mediodorsal nuclei, while endogenous pain descending inhibition triggered by conditioning stimulation can be weakened via the thalamic ventromedial nuclei. Psychological factors may contribute to the development of low back pain. The mechanisms governing the generation, maintenance, and alleviation of low back pain in weightlessness differ from those observed in normal gravitational environments. This presents a significant challenge for space medicine research. Therefore, the elucidation of the occurrence and development mechanism of low back pain in weightlessness is important for the prevention and treatment during space flight. To reduce the incidence of low back pain during long-term missions on the space station, astronauts may choose to wear specialized space clothing that can provide axial physiological loads, designed to stimulate both musculature and skeletal structures, mitigating potential increases in vertebral column length, diminished lumbar curvature, and intervertebral disc edema and/or muscular atrophy. Additionally, assuming a “fetal tuck position” described as the knees to chest position may increase lumbar IVD hydrostatic pressure, subsequently reducing disc volume, rectifying diminished lumbar curvature, and alleviating dorsal root nerve tensions. Moreover, this position may reduce type IV mechanoreceptor facilitation and nerve impulse propagation from the sinuvertebral nerves of the annulus fibrosus. Elongated posterior soft tissues (apophyseal joint capsules and ligaments) with spinal flexion may potentially stimulate type I and II mechanoreceptors. It is also recommended to exercise the paraspinal muscles to prevent and alleviate the decrease in their cross-sectional area and maintain their structure and function. Photobiomodulation has been proved to be an effective means of activating the pain descending inhibition pathway of the central nervous system. In addition, astronauts should be encouraged to participate in mission-related activities and strive to avoid psychological problems caused by the long-term confinement in a small space station. The article presents a concise review of potential causes and targeted treatment strategies for low back pain induced by space flight or simulated microgravity in recent years. Its objective is to further elucidate the mechanisms underlying the occurrence and development of low back pain in weightless environments while providing scientific evidence to inform the development of guidelines for preventing, treating, and rehabilitating low back pain during long-term space flights.

Sarcopenia is a clinical syndrome characterized by a decrease in skeletal muscle strength and quality， often accompanied by adverse outcomes such as falls， loss of function and weakness. The pathogenesis of sarcopenia is complex， and studies have shown that dysfunction due to impaired mitochondrial quality control is an important pathological factor in the occurrence and development. Traditional Chinese medicine（TCM） has been widely favoured for regulating mitochondrial homeostasis and preventing sarcopenia by virtue of its multi-target and multi-pathway advantages. They can play a role in the prevention and treatment of sarcopenia by regulating the mitochondrial quality control system to inhibit the occurrence of mitochondrial oxidative stress， regulate the balance of mitochondrial dynamics， inhibit mitochondrial autophagy， promote mitochondrial biosynthesis， resist the occurrence of mitochondrial apoptosis， and maintain the mitochondrial calcium and protein homeostasis. Based on this， the paper reviewed the relationship between mitochondrial quality control and sarcopenia， as well as the mechanism of TCM in intervening the mitochondrial quality control system to treat sarcopenia， in order to provide a new idea for the prevention and treatment of sarcopenia by TCM and to a theoretical basis for the clinical research on TCM intervention in sarcopenia.

Objective To analyze the medication rules of Professor HUANG Feng for the treatment of low back pain using data mining methods.Methods The information of prescriptions for the effective cases of outpatients with low back pain treated by Professor HUANG Feng were collected and screened.Microsoft Excel 2019 was used to analyze the frequency of medication and the distribution of properties,flavors and meridian tropism of the drugs in the included prescription.IBM SPSS Modeler 18.0 was used for association rule analysis,and IBM Statistics 26.0 was used for cluster analysis.Results A total of 239 prescriptions and 75 Chinese medicines were included.There were 23 high-frequency Chinese medicines with the medication frequency being or over 20 times,and the top 10 Chinese medicines were Glycyrrhizae Radix et Rhizoma,vinegar-processed Corydalis Rhizoma,Cibotii Rhizoma,Atractylodis Macrocephalae Rhizoma,Zanthoxyli Radix,salt-processed Achyranthis Bidentatae Radix,Rehmanniae Radix,Dipsaci Radix,Coicis Semen,and Salviae Miltiorrhizae Radix et Rhizoma.The medicines were mainly warm in nature,and were sweet,bitter and pungent in flavor.Most of the drugs had the meridian tropism of liver,stomach and spleen meridians.Among the drug combinations obtained from association rule analysis with the top 20 highest support,vinegar-processed Corydalis Rhizoma,Cibotii Rhizoma,Atractylodis Macrocephalae Rhizoma and Zanthoxyli Radix were the core drugs.Cluster analysis yielded 6 clustering combinations.Conclusion For the treatment of low back pain,Professor HUANG Feng follows the principle of"treatment adapting to the climate,individuality,and environment"and"treating the root cause of the disease",usually adopts the drugs for activating blood,moving qi and relieving pain,nourishing the liver and kidney,and also uses the medicines for replenishing qi and strengthening the spleen.The ideas of HUANG Feng for the treatment of low back pain can be used as a reference for the clinical treatment.

Four pyrazines were isolated from the n-butanol fraction of Hypecoum erectum L. by using various chromatographic methods, including MCI gel, ODS, silica gel and semi-preparative HPLC. The structures of the isolated compounds were identified as hyperectpyrazin A (1), 1′S-(6-methylpyrazin-2-yl)-ethane-1′,2′-diol (2), 2-hydroxymethyl-6-methylpyrazin (3) and pyrazine-2-carboxylic acid (4) by spectroscopy methods (1D NMR, 2D NMR, UV, IR, MS, etc.). The absolute configuration of compound 2 was determined by using the Mo₂(OAc)₄ induced CD analysis for the first time. Compound 1 was a new compound, compounds 2-4 were isolated from H. erectum for the first time. Compounds 1-4 were evaluated for their inhibition against acetylcholinesterase and nitric oxide generation induced by lipopolysaccharide-RAW264.7 macrophage cells. At a concentration of 50 μmol·L^-1, compounds 2 and 4 displayed inhibitory effects on acetylcholinesterase with the inhibition rates of 44.40% and 43.99%, respectively.

Objective:To explore the scientificity of the public hospital liability policy governance from the perspective of policy tools,and to provide evidence for the optimization and adjustment of subsequent policies.Methods:Policy texts at the national and regional levels from 2009-2022 were selected,and the coding results were statistically analyzed using Excel 2019 based on Rothwell and Zegveld's classification of policy tools.Results:A total of 128 policy texts were included in the analysis,with 29.96%,34.16%,and 35.88%of the policy tools in the policy instrument dimension being demand-based,supply-based,and environment-based,respectively.The system mechanism dimension focused primarily on compensation mechanisms.Conclusion:The use of the three policy instruments is mainly dominated by environmental policies,with a relative lack of policies from demand side.It is recommended that the use of policies from demand side could be strengthened and the internal structure of policy tools be optimized,to improve the consistency and coupling of policies.

Objective:To analyze the changes in the income structure of public hospitals at all levels in Hebei Province,evaluate the effectiveness of the compensation mechanism reform in public hospitals of Hebei Province,and provide policy recommendations for optimizing the compensation mechanism.Methods:Select some public hospitals at all levels in Hebei Province as samples,and use structural change analysis to analyze the income structure of the sample hospitals.Result:From 2016 to 2021,the proportion of medical income in tertiary and primary hospitals increased by 2.6 and 9.8 percentage points respectively,while the proportion of medical income in secondary hospitals decreased by 0.6 percentage points.The proportion of consumables revenue in hospitals at all levels has increased,and drug revenue remains the main driving factor for the growth of medical revenue in hospitals at all levels.The contribution rate of drug revenue to the growth of medical revenue in tertiary hospitals is 50％.Conclusion:The optimization of medical income structure in public hospitals in Hebei Province is significant,but the compensation mechanism still needs to be further improved,and the income structure still needs further adjustment.On the basis of consolidating and improving the policy of canceling consumable markup,it is needed to further standardize medical service behavior,improve precise and sustainable financial compensation mechanisms,adjust medical service prices,and broaden financing channels.

ATG8-binding proteins play a key role in autophagy, selective autophagy or non-autophagy process by interacting between ATG8 and the ATG8-interacting motif (AIM) or the ubiquitin-interacting motif (UIM). There is great progress of ATG8-binding proteins in yeast and mammalian studies. However, the plant domain is still lagging behind. Therefore, the structure characteristics of plant ATG8 binding protein were firstly outlined. Unlike the single copy of ATG8 gene in yeast, many homologous genes have been identified in plant. The LIR/ AIM-docking site (LDS) of ATG8 protein contains W and L pockets and is responsible for binding to AIM. The ATG8 protein binds to UIM-containing proteins via UIM-docking site (UDS) instead of LDS. UDS is in the opposite position to LDS, so the ATG8 can bind both AIM and UIM proteins. Secondly, the structure and function of ATG8-binding proteins, especially the selective autophagy receptors, were systematically described. The protein NBR1 and Joka2, as proteaphagy receptors, guide ubiquitination protein aggregates to autophagosome for degradation by binding to AIM and ATG8 in Arabidopsis and tobacco, respectively. AtNBR1 also promotes plant immunity by binding the capsid protein of cauliflower mosaic virus and silencing suppressor HCpro of turnip mosaic virus, mediating pathogen autophagy. AtNBR1 still degrades chloroplast by microautophagy under photoinjure or chlorophagy during ibiotic stress. And the protein ORM mediates the degradation of plant immune receptor flagellin sensing 2 (FLS2) through AIM binding to ATG8. Interestingly, ATI1 and ATI2 participate in both chlorophagy and ERphagy. Otherwise, ER membrane protein AtSec62, soluble protein AtC53, and ubiquitin-fold modifier1-specific ligase 1 (UFL1) can be directly bound to ATG8 as ER autophagy receptors. As pexophagy receptor, AtPEX6 and AtPEX10 bind to ATG8 via AIM and participate in pexophagy. RPN10, as a 26S proteasome subunit, whose C-terminal UIM1 and UIM2 bind ubiquitin and ATG8, respectively, mediates the selective autophagy degradation of 26S proteasome inactivation when fully ubiquitinated. Plant-specific mitochondrial localization proteins FCS-like zinc finger (FLZ) and friendly (FMT) may also be mitophagy receptors. CLC2 binds to ATG8 via the AIM-LDS docking site and is recruited to autophagy degradation on the Golgi membrane. The tryptophan-rich sensory protein (TSPO) in Arabidopsis was involved in clearing free heme, porphyrin and plasma membrane intrinsic protein 2;7 (PIP2;7) through the combination of AIM and ATG8. The conformation of GSNOR1 changes during anoxia, exposing the interaction between AIM and ATG8, leading to selective degradation of GSNOR1. At last, the ATG8 binding proteins involved in autophagosome closure, transport and synthetic synthesis was summarized. For example, plant-specific FYVE domain protein required for endosomal sorting 1 (FREE1) is involved in the closure of autophagosomes during nutrient deficiency. Therefore, according to the recent research advances, the structure and function of plant ATG8-binding proteins were systematically summarized in this paper, in order to provide new ideas for the study of plant selective autophagy and autophagy.

DNA polymerase theta (Polθ), also known as DNA polymerase θ, is the member of the DNA polymerase A family and plays a crucial role in the repair of DNA double-strand breaks (DSB). Polθ has 3 distinct structural domains: the N-terminal helicase-like domain with a conserved sequence, the C-terminal polymerase domain, and the central domain, which is a disordered sequence connecting these two regions. Notably, Polθ is the only known polymerase in eukaryotes that possesses helicase activity. However, it is also an error-prone polymerase. When DNA DSBs occur, a specialized network consisting of at least 4 pathways, including classical-non homologous end joining (C-NHEJ), homologous recombination (HR), single-strand annealing (SSA), and alternative-end joining (Alt-EJ), is responsible for repairing DNA damage caused by DSBs. In the absence of major DNA repair pathways like HR, cells rely on Alt-EJ pathway mediated by Polθ to repair damaged DNA and maintain genomic stability. Nevertheless, due to the low fidelity of Polθ, Alt-EJ repair often leads to errors. Depletion of Polθ has shown to increases DSB formation and compromise genomic stability. Conversely, overexpression of Polθ has been associated with increases DNA damage markers and impairs cell cycle progression. As a result, the impact of Polθ on genome stability remains controversial. Furthermore, overexpression of Polθ is frequently observed in cancer and is associated with a characteristic mutational signature and poor prognosis. Depleting Polθ in an HR-deficient background has been shown to impair cell viability, suggesting a synthetic lethal (SL) relationship between Polθ and HR factors. In recent years, targeted chemotherapy drugs that inhibit tumor growth have gained significant attention. However, off-target effects and drug resistance pose challenges for clinical application, particularly with poly-ADP-ribose polymerase inhibitor (PARPi). Blocking Polθ activity in HR-deficient tumor cells has been found to reverse PARPi resistance, making Polθ a very promising therapeutic target in cancer treatment. The availability of crystal structures for both helicase and polymerase domain has facilitated the design of potent inhibitors of Polθ. Currently, several highly specific and effective small molecule inhibitors targeting Polθ, such as Novobiocin, RP-6685, and ART558, have been reported to effectively block various cancers with HR deficiency. The initial success of these inhibitors points to new directions for treating BRCA1/2-mutated tumors. Additionally, reducing the Alt-EJ repair pathway mediated by Polθ can improve HR repair efficiency and increase the chance of exogenous gene target integration (TI), suggesting potential new applications for Polθ inhibitors. This article reviews the recent research progress on the molecular function of Polθ and its involvement in the Alt-EJ pathway modification mechanism, providing insights for a deeper understanding of this field.

【Objective】 To explore the distribution of serological markers related to samples whose serological test results were inconsistent with HBV DNA test results among voluntary blood donors in Xi′an. 【Methods】 A total of 71 HBsAg ELISA positive and NAT non-reactive (ELISA+ /NAT-)blood samples were collected from Shaanxi Blood Center from November 1, 2022 to April 30, 2023. The serological markers of hepatitis B were detected by electrochemiluminescence method, and the HBV S region and C region gene fragments were amplified by nested-PCR. 【Results】 The positive rate of nested-PCR in double ELISA+ /NAT- group(n=30) was statistically higher than that of ELISA+ /NAT- group(n=41)(60% vs 24.4%, P<0.05). Donors in double ELISA+ /NAT- group were all first-time blood donors, with the positive rate of anti-HBc in serum of 100%, and the serological pattern was mainly positive for items 1, 4 and 5 items(80%). Among the ELISA+ /NAT- group, 31.7% were repeat blood donors, with the positive rate of anti-HBc in serum of only 19.51%, and the serological patterns were mainly single anti-HBs positive (43.90%) and all negative (36.58%). 【Conclusion】 There are false positives in the test results of ELISA+ /NAT- group, which leads to unnecessary blood discarding. Meanwhile, the samples with negative NAT may have low levels of HBV DNA, which may lead to missed detection. It is suggested that multiple systems and methods should be applied to trace the blood donors who are HBsAg positive and NAT non-reactive, so as to improve the accuracy of HBV screening of blood donors and reduce blood waste.

Objective To investigate the effects and the mechanisms of sulforaphane(SFN)on endothelin-1(ET-1)-induced proliferation in rat vascular smooth muscle cell(VSMC).Methods Rat VSMC were cultured by using the modified tissue explant technique in vitro and were randomly divided into control group(normal culture),model group(treated with 0.1 μmol·L-1 ET-1)and experimental-L,-M,-H groups(treated with 5,10,20 SFN+0.1 μmol·L-1 ET-1).The survival rate of VSMC were measured by methyl thiazolyl tetrazolium.The proliferation and apoptosis related genes in mRNA level in VSMC were respectively examined with real-time quantitative polymerase chain reaction;the relative fluorescence intensity of reactive oxygen species(ROS)in VSMC were measured by fluorescent probe 2',7'-dichlorodihydrofluorescein diacetate;the protein expression of B-cell lymphoma-2(Bel-2),cysteinyl aspartate-specific proteinase-3(caspase-3),p38 mitogen-activated protein kinases(p38MAPK),phosphorylated p38 mitogen-activated protein kinases(p-p38MAPK),and p53 in VSMC were investigated by Western blot.Results The proliferation activities of the control group,model group,experimental-L,-M,-H groups were 0.27±0.02,0.50±0.04,0.40±0.03,0.38±0.03 and 0.34±0.03;the expression levels of Bcl-2 mRNA were 1.57±0.28,1.00±0.00,0.87±0.05,0.75±0.08 and 0.41±0.18;the expression levels of caspase-3 mRNA were 0.84±0.10,1.00±0.00,1.33±0.10,1.61±0.15 and 1.83±0.16;the relative fluorescence intensities of ROS in VSMC were 6.05±1.50,31.45±3.12,30.03±1.85,18.39±5.62 and 17.18±1.97;the relative expression levels of Bel-2 protein were 0.65±0.02,0.60±0.02,0.49±0.02,0.48±0.03 and 0.49±0.01;the relative expression levels of caspase-3 protein were 0.03±0.00,0.25±0.01,0.42±0.01,0.46±0.02 and 0.64±0.03;the protein expression ratios of p-p38MAPK/p38MAPK were 0.97±0.05,1.44±0.04,1.62±0.10,2.18±0.05 and 2.70±0.05;the relative expression levels of p53 protein were 0.20±0.01,0.30±0.01,0.34±0.02,0.37±0.01 and 0.42±0.01 respectively.There were statistically significant differences in the above indicators between model group and control group,between model group and experimental-M,-H groups(P＜0.05,P＜0.01).Conclusion These demonstrate that SFN may inhibit proliferation and prompt apoptosis in ET-1-stimulated VSMC by anti-oxidant and activating p38MAPK and p53-depended apoptosis signal pathway.