Work-related musculoskeletal disorders (WMSDs) represent a significant occupational health challenge among healthcare professionals globally, posing substantial threats to physical and mental well-being as well as work sustainability. Adopting preventive behaviors—including ergonomic postural adjustments, optimized work-rest scheduling, proper use of protective and assistive equipment, and regular physical activity—is essential for mitigating the risk of WMSDs. Guided by the social ecological model, the review synthesized current evidence on the determinants of WMSDs preventive behaviors across four levels: intrapersonal characteristics, work environment conditions, interpersonal support, and policy/institutional factors. The findings suggest that higher educational attainment, favorable health-related behavioral patterns, optimized ergonomic work environments, adoption of supportive collaborative systems, strong organizational support, as well as policy safeguards facilitate preventive behavior adoption. Conversely, limited prevention-related knowledge, low risk perception, insufficient physical activity, excessive workload, lack of appropriate protective equipment, inadequate ergonomic training, a prevailing culture of presenteeism, and inadequate policy implementation constitute significant barriers. Multi-dimensional intervention strategies targeting these determinants are warranted to enhance preventive behaviors, reduce the risk of WMSDs, and strengthen occupational health protection for healthcare professionals.

Objective: To investigate the regulatory role of miR-6824-3p in macrophage function and its molecular mechanism in inhibiting hepatitis B virus (HBV) replication, thereby providing experimental evidence to elucidate the immune regulatory mechanisms underlying persistent HBV infection. Methods: miR-6824-3p mimic and inhibitor were transfected into human THP-1-induced macrophages. Real-time quantitative PCR (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), neutral red uptake, reactive oxygen species (ROS) production, and fluorescent latex particle phagocytosis assays were employed to evaluate the effects of miR-6824-3p on macrophage phenotype and function. Through a combination of bioinformatics analysis, dual luciferase reporter assays, western blot, and siRNA interference techniques, we identified the target gene of miR-6824-3p and examined their effects on downstream signaling pathways. qRT-PCR and western blot analyses were performed to assess the impact of miR-6824-3p-regulated macrophages on HBV DNA, pgRNA, cccDNA, and HBV-associated antigen levels in HepAD38 cells. Key effector molecules were identified through neutralization assays. Results: miR-6824-3p mimic significantly promoted the expression and secretion of proinflammatory factors, such as TNF-α and IL-1β, in macrophages (P<0.001), while concurrently reducing ROS production and phagocytosis (P<0.05). Furthermore, miR-6824-3p downregulated NRAS expression in macrophages, which was accompanied by a reduction in MAPK signalling path-way activity (p-MEK, p-ERK). Compared to the control group, the medium of macrophages with overexpressed miR-6824-3p inhibited the expression of HBV DNA, pgRNA, cccDNA, and HBV-associated antigens HBsAg, HBeAg, and HBcAg in HepAD38 cells (P<0.01). Similar results were also observed in the co-culture system of macrophages with HepAD38 cells. The addition of TNF-α neutralizing antibodies markedly attenuated the aforementioned antiviral effects (P<0.001). Conclusion: miR-6824-3p targets NRAS to affect the downstream MAPK signaling pathway, regulating the immune function of macrophages. The TNF-α induced by miR-6824-3p is one of the key molecules that suppress HBV replication. This study provides evidence for further elucidating the molecular mechanisms by which miRNAs influence HBV replication via modulating the host immune microenvironment.

ObjectiveTo investigate the effects of Huayu Jiedu prescription on brain microvascular endothelial cells （BMECs） after oxygen-glucose deprivation （OGD） injury and to explore its intervention mechanisms. MethodsThe cell counting kit-8 （CCK-8） assay was used to determine the optimal OGD duration and the effective concentration of Huayu Jiedu prescription-containing serum. Cells were randomly divided into the blank serum medium group （KBXQ）， model group （OGD）， HYXQ group （OGD + Huayu Jiedu prescription-containing serum）， and 3-methyladenine （3-MA） group （OGD + 3-MA）. Cell morphology was observed under an inverted microscope. The numbers of autophagosomes and autolysosomes in cells were observed by transmission electron microscopy. Cell viability was determined using the CCK-8 assay. Cell apoptosis rate was detected using the TdT-mediated dUTP nick-end labeling （TUNEL） assay. The expression levels of microtubule-associated protein 1 light chain 3 （LC3） and Occludin were detected by immunofluorescence. The permeability of the cell monolayer was also measured. Cells were further randomly divided into the KBXQ group， model group （OGD）， HYXQ group， phosphatidylinositol-3 kinase （PI3K） inhibitor （LY294002） group （OGD + LY294002）， and HYXQ + LY294002 group （OGD + Huayu Jiedu prescription-containing serum + LY294002）. Western blot analysis was used to detect the expression levels of the autophagy-related key molecule yeast Atg6 homolog 1 （Beclin1）， LC3Ⅱ/LC3Ⅰ， selective autophagy adaptor protein （p62）， Occludin， phosphorylated （p）-PI3K， PI3K， phosphorylated protein kinase B （p-Akt）， Akt， phosphorylated mammalian target of rapamycin （p-mTOR）， and mTOR. ResultsOGD for 6 h was selected as the optimal modeling condition， and 5% was determined as the optimal volume fraction of Huayu Jiedu prescription-containing serum. Compared with the KBXQ group， the model group showed obvious cell damage under the inverted microscope， and transmission electron microscopy revealed markedly increased numbers of autophagosomes and autolysosomes. Cell viability was significantly decreased （P<0.01）， apoptosis rate was significantly increased （P<0.01）， LC3 fluorescence intensity was significantly increased （P<0.01）， Occludin fluorescence intensity was significantly decreased （P<0.01）， and monolayer permeability was significantly increased （P<0.01）. Compared with the model group， cell damage in the HYXQ group and the 3-MA group was significantly improved， the numbers of autophagosomes and autolysosomes were markedly reduced， cell viability was significantly increased （P<0.01）， apoptosis rate was significantly decreased （P<0.01）， LC3 fluorescence intensity was significantly decreased （P<0.01）， Occludin fluorescence intensity was significantly increased （P<0.01）， and monolayer permeability was reduced （P<0.05）. Western blot results showed that， compared with the KBXQ group， the model group exhibited significantly increased expression of Beclin1 and LC3Ⅱ/LC3Ⅰ （P<0.01）， while the expression levels of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR were significantly decreased （P<0.01）. Compared with the model group， the HYXQ group showed significantly decreased expression of Beclin1 and LC3Ⅱ/LC3Ⅰ （P<0.01） and significantly increased expression of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR （P<0.01）. In the LY294002 group， Beclin1 and LC3Ⅱ/LC3Ⅰ expression were significantly increased （P<0.05， P<0.01）， whereas the expression levels of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR were significantly decreased （P<0.01）. Compared with the LY294002 group， the HYXQ + LY294002 group showed significantly decreased expression of Beclin1 and LC3Ⅱ/LC3Ⅰ （P<0.01） and significantly increased expression of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR （P<0.01）. ConclusionHuayu Jiedu prescription has a protective effect on BMECs after OGD injury， which may be achieved by activating the PI3K/Akt/mTOR autophagy-related signaling pathway and inhibiting excessive autophagy， thereby protecting Occludin protein expression and endothelial barrier function.

Objective: To evaluate the effects of green tea extract (GTE) and its main catechin monomers on erythrocyte lesion (such as hemolysis, decreased energy metabolism and oxidative stress) during in vitro storage, and to explore its potential as a novel additive for erythrocyte preservation solutions. Methods: The composition of GTE was analyzed by high-performance liquid chromatography (HPLC). Using an in vitro simulated storage model, erythrocytes were stored in CPDA-1 preservation solution supplemented with GTE and the three most abundant catechin monomers (EGCG, ECG, EGC) for 60 days. Hemolysis rate and ATP content were dynamically monitored during storage. Flow cytometry was used to analyze phosphatidylserine (PS) exposure. Meanwhile, the protective effects of each component were verified in an acute oxidative stress model, and erythrocyte membrane stability was assessed by osmotic fragility test. Results: After 60 days of storage at 4℃, the hemolysis rate at the end of storage in the GTE group was <0.8%, which was superior to that in the control group and the single catechin-supplemented groups. Erythrocyte osmotic fragility assay showed that GTE could enhance the stability of erythrocyte membranes. In the acute oxidative stress experiment, the protective rate of GTE against erythrocyte injury exceeded 99%, which was better than that of the single catechin groups. At the initial stage of storage, ATP content decreased in all catechin-treated groups, but PS exposure was not significantly increased. Conclusion: The addition of GTE can effectively alleviate storage lesions of erythrocytes, with efficacy superior to that of single catechins. GTE enhances the antioxidant capacity and membrane stability of stored erythrocytes. Our results provide new experimental evidence for the development of GTE-based erythrocyte preservation additives.

Objective: To develop and validate a clinically actionable prediction model for postoperative pulmonary complications (PPCs) in cardiac surgery patients, focusing on modifiable preoperative risk factors amenable to targeted optimization. Methods: In this prospective observational cohort study, 492 adults undergoing open-chest cardiac surgery between August 15, 2023 and December 31, 2023 were analyzed. Prespecified predictors included gas exchange variables, pulmonary function, inspiratory muscle strength, and physical performance. Univariable and multivariable logistic regression analyses were used to develop the prediction model. Discrimination was assessed by the area under the receiver operating characteristic curve (AUC). Results: A total of 90 patients (14.1%) developed PPCs after surgery. Five independent predictors were identified: elevated arterial PaCO2 (odds ratio [OR] 1.12, 95% confidence interval [CI] 1.00–1.26), oxygen desaturation (SpO2<93%) (OR 12.47, 95% CI 3.51–48.13), reduced gait speed (OR 0.17, 95% CI 0.04–0.71), lower FEV1/FVC ratio (OR 0.96, 95% CI 0.92–1.00), and diminished inspiratory muscle strength (MIP % predicted) (OR 0.96, 95% CI 0.92–0.99). The model demonstrated good discriminative ability with an AUC of 0.86 (95% CI 0.80–0.93) in the training cohort and 0.87 (95% CI 0.74–0.93) in the validation cohort. Conclusion This parsimonious model achieved high predictive accuracy using five modifiable physiological variables. By targeting abnormalities in gas exchange, pulmonary mechanics, muscle strength, and functional reserve, the model offers a practical tool to guide individualized prehabilitation strategies for reducing PPC risk in cardiac surgery patients.

ObjectiveTo investigate the effect of icariin （ICA） on the phenotype of dendritic cells （DCs） in heart tissue of the Dahl salt-sensitive myocardial remodeling model of rats and its regulation on the vitamin D system. MethodsMale Dahl salt-resistant rats were divided into a normal group， and male Dahl salt-sensitive rats were divided into a model group， low-， medium-， and high-dose ICA groups （30， 60， 120 mg·kg^-1·d^-1）， and Vitamin D group （3×10^-5 mg·kg^-1·d^-1）. In addition to the normal group， the other groups were given an 8% high salt diet to establish a myocardial remodeling model and received intragastric administration after successful modelling once a day for six weeks. The dynamic changes in tail artery blood pressure were monitored， and detection of cardiac ultrasound function in rats was performed. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the morphological changes in rat heart tissue. The phenotype of DCs and T helper cell 17 （Th17）/regulatory T cell （Treg） ratio were detected by flow cytometry. The mRNA and protein expression of vitamin D receptor （VDR）， 1α-hydroxylase （CYP27B1）， 24-hydroxylase （CYP24A1）， forkhead frame protein 3 （FoxP3）， solitaire receptor γt （RORγt）， myocardial type Ⅰ collagen （ColⅠ）， and type collagen （ColⅢ） in heart tissue was detected by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot. ResultsCompared with the normal group， the model group showed disordered arrangement and rupture of myocardial cells， nuclear condensation， significant edema of myocardial tissue， significant proliferation of collagen fibers in a network distribution， and a significant increase in tail artery blood pressure， left ventricular end diastolic diameter （LVEDD）， and left ventricular end systolic diameter （LVESD） （P<0.05）. The phenotype of cardiac DCs was CD40， CD80， and CD86， and the levels of major histocompatibility complex Ⅱ （MHC-Ⅱ）， Th17 cells， and Th17/Treg were significantly increased （P<0.05）. The mRNA and protein expression of CYP24A1 and RORγt in the heart， as well as the mRNA expression of ColⅠ and ColⅢ， were significantly increased （P<0.05）. The left ventricular ejection fraction （LVEF）， interventricular septal thickness （IVSD）， and left ventricular posterior wall thickness （LVPWD） were significantly decreased （P<0.05）. The phenotype of cardiac DCs such as CD11， CD11b， and Treg cells， were significantly reduced （P<0.05）， while the mRNA and protein expression of cardiac VDR， CYP27B1， and FoxP3 were significantly decreased （P<0.05）. Compared with the model group， the low-， medium-， and high-dose ICA groups and vitamin D group significantly reduced myocardial cell rupture and nuclear consolidation in rats. The high-dose ICA group and vitamin D group showed a small amount of myocardial cell rupture and nuclear consolidation， improving myocardial fiber arrangement to varying degrees and significantly reducing myocardial fiber rupture and proliferation. The tail artery blood pressure， LVEDD， and LVESD were significantly decreased in the low-， medium-， and high-dose ICA groups and vitamin D group （P<0.05）， and the phenotype of cardiac DCs including CD40， CD80， CD86， MHC-Ⅱ， Th17 cells， and Th17/Treg were significantly decreased （P<0.05）. The mRNA and protein expression of CYP24A1 and RORγt， and the mRNA expression of ColⅠ and ColⅢ in the heart were significantly decreased in the medium- and high-dose ICA groups and vitamin D group （P<0.05）. The LVEF， IVSD， and LVPWD of myocardial remodeling model rats in the low-， medium-， and high-dose ICA groups and vitamin D group were significantly increased （P<0.05）. The phenotypes of cardiac DCs including CD11， CD11b， and Treg cells were significantly increased in the medium- and high-dose ICA groups and the Vitamin D group （P<0.05）. The mRNA and protein expressions of VDR， CYP27B1， and FoxP3 in the heart were significantly increased in the medium- and high-dose ICA groups and vitamin D group （P<0.05）. ConclusionICA can regulate tail artery blood pressure， cardiac structural and functional damage， and myocardial tissue fibrosis and inhibit phenotype and functional maturation of DCs in heart tissue in the myocardial remodeling model of Dahl salt-sensitive rats. It can also affect the gene and protein expression of VDR， CYP24A1， and CYP27B1， achieving its intervention in Th17/Treg balance in the immune process of myocardial remodeling possibly by regulating vitamin D/VDR in heart tissue.

Objective To evaluate the effectiveness and safety of endovascular treatment(EVT)for acute tandem vertebrobasilar artery occlusions(tVBAO).Methods A computerized retrieval of academic papers concerning the EVT treatment for acute tVBAO from the databases of PubMed,Cochrane Library,CNKI,Wanfang database was conducted.The retrieval time period was from the establishment of the database to September 30,2024.The outcome indexes included successful recanalization of responsible vessels(mTICI≥grade 2b),good clinical prognosis in 90 days(mRS:0-2 points),symptomatic intracranial hemorrhage(sICH)and mortality.The clinical outcomes were compared between the tVBAO patients and non-tVBAO patients.A random effects model was used to calculate the pooled risk ratio(RR).Results Nine eligible academic papers with 1 725 patients were finally included in this study,including 314 tVBAO patients and 1 411 non-tVBAO patients.There were no significant differences in the successful recanalization of responsible blood vessels(RR=0.99,95％CI:0.94-1.04,P=0.67),good clinical prognosis at 90 days(RR=0.99,95％CI:0.74-1.34,P=0.96),and mortality(RR=1.18,95％CI:0.88-1.59,P=0.28)between the tVBAO group and the non-tVBAO group.The sICH in the tVBAO group was significantly higher than that in the non-tVBAO group(RR=1.76,95％CI:1.12-2.78,P=0.02).Conclusion After EVT,there are no significant differences in the successful recanalization of responsible blood vessels,90d good clinical prognosis,and mortality rate between tVBAO patients and non-tVBAO patients.However,after EVT the risk of sICH in tVBAO patients is significantly higher than that in the non-tBBAO patients.

Objective To investigate the mechanism of circ-001209 on retinal angiogenesis in rats with diabetic retinopathy(DR)by regulating the interleukin-33/suppression of tumorigenicity 2(IL-33/ST2)signaling pathway.Methods Fifty rats were randomly divided into Col group,DR group,si-circ-NC group,si-circ-001209 group,and si-circ-001209+IL-33 group,with 10 rats in each group.The levels of fasting plasma glucose(FPG)and fasting insulin(FINS)in rats were detec-ted;fundus fluorescein angiography(FFA)was used to detect retinal angiogenesis;the enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of angiogenesis-related factors and inflam-matory factors in serum;the hematoxylin-eosin(HE)staining was used to detect histopathological chan-ges in the retina;the periodic acid-Schiff(PAS)staining was used to detect the number of retinal micro-vascular formations;the Western blotting was used to detect the protein expression levels of IL-33,ST2,vascular endothelial growth factor(VEGF),hypoxia-inducible factor-lα(HIF-1α),and intercellular adhesion molecule-1(ICAM-1)in retinal tissues.Results Compared with the Col group,the DR group and si-circ-NC group showed significant increase in levels of FPG,FINS,serum VEGF,an-giopoietin-1(Ang-1),IL-6,IL-33,tumor necrosis factor-α(TNF-α),the number of microvascular formation,and the protein expression levels of IL-33,ST2,VEGF,HIF-1α,and ICAM-1 in retinal tissues(P＜0.05);the si-circ-001209 group showed significant decrease in levels of FPG,FINS,serum VEGF,Ang-1,IL-6,IL-33,TNF-α,the number of microvascular formation,and the protein expression levels of IL-33,ST2,VEGF,HIF-1α,and ICAM-1 in retinal tissues compared with the si-circ-NC group(P＜0.05);the si-circ-001209+IL-33 group showed significant increase in levels of FPG,FINS,serum VEGF,Ang-1,IL-6,IL-33,TNF-α,the number of microvascular forma-tions,and the protein expression levels of IL-33,ST2,VEGF,HIF-1α,and ICAM-1 in retinal tis-sues compared with the si-circ-001209 group(P＜0.05).Conclusion Knockdown of circ-001209 can inhibit retinal angiogenesis in rats with DR,potentially through inhibiting the activation of the IL-33/ST2 signaling pathway and reducing inflammation.

Objective To investigate the value of C-X-C motif chemokine ligand 16(CXCL16)combined with C-C motif chemokine ligand 21(CCL21)in predicting pulmonary function impairment and disease control in children with childhood allergic rhinitis-asthma syndrome(CARAS).Methods A total of 108 children with CARAS(CARAS group),108 children with simple asthma(asthma group),and 108 children with simple allergic rhinitis(AR group)admitted to Baoji People's Hospital of Shaanxi Province from January 2022 to December 2024 were prospectively selected.The levels of CXCL16 and CCL21 in peripheral blood and pulmonary function indicators[peak expiratory flow(PEF),percentage of predicted forced expiratory volume in one second(FEV1％pred),and ratio of forced expiratory volume in one second to forced vital capacity(FEV1/FVC)]were compared among the groups.Pearson correlation analysis was used to explore the correlations of the levels of CXCL16 and CCL21 in peripheral blood with pulmonary function indicators in children with CARAS.After com-pletion of treatment,a 3-month follow-up was conducted,and the children with CARAS were divid-ed into poorly controlled group and well-controlled group according to disease control status.Multi-variate Logistic regression and receiver operating characteristic(ROC)curve analyses were used to analyze the relationships of the levels of CXCL16 and CCL21 in peripheral blood with poor disease control in children with CARAS and their predictive efficacy.Results The levels of CXCL16 and CCL21 in peripheral blood in the AR group,asthma group,and CARAS group increased sequential-ly,while PEF,FEV1％pred,and FEV1/FVC decreased sequentially(P＜0.05).There were no statistically significant differences in the levels of CXCL16 and CCL21 in peripheral blood,PEF,FEV 1％pred,and FEV1/FVC among the pollen group,dust mite group,animal dander group,and other groups(P＞0.05).Pearson correlation analysis showed that the levels of CXCL16 and CCL21 in peripheral blood in children with CARAS were negatively correlated with PEF,FEV 1％pred,and FEV1/FVC(r=-0.629,-0.668,-0.710,-0.645,-0.672,-0.697,P＜0.001).After a 3-month follow-up,the rate of poor disease control after treatment among the 108 children with CARAS was 47.22％(51/108).Univariate analysis showed that total immunoglobulin E(IgE),eosinophil(EOS)count,fractional exhaled nitric oxide(FeNO),PEF,FEV1％pred,FEV1/FVC,CXCL16,and CCL21 were associated with poor disease control in children with CARAS(P＜0.05).Logistic regression analysis showed that high EOS count,high FeNO,high CXCL16,and high CCL21 were independent risk factors for poor disease control in children with CARAS(P＜0.05).ROC curve analysis showed that the areas under the curve for peripheral blood CXCL16 lev-el,CCL21 level,and their combination in predicting poor disease control in children with CARAS were 0.843,0.820,and 0.917,respectively.The predictive efficacy of their combination was bet-ter than that of peripheral blood CXCL16 level or CCL21 level alone(Z=2.054,2.312;P=0.040,0.021).Conclusion Elevated levels of CXCL16 and CCL21 in peripheral blood are close-ly associated with decreased pulmonary function and poor disease control in children with CARAS,and their combination has a high predictive efficacy for poor disease control.

BACKGROUND: Renal osteodystrophy (ROD) is a skeletal pathology associated with chronic kidney disease-mineral and bone disorder (CKD-MBD) that is characterized by aberrant bone mineralization and remodeling. ROD increases the risk of fracture and mortality in CKD patients. The underlying mechanisms of ROD remain elusive, partially due to the absence of an appropriate animal model. To address this gap, we established a stable mouse model of ROD using an optimized adenine-enriched diet and conducted exploratory analyses through ribonucleic acid sequencing (RNA-seq). METHODS: Eight-week-old male C57BL/6J mice were randomly allocated into three groups: control group ( n = 5), adenine and high-phosphate (HP) diet group ( n = 20), and the optimized adenine-containing diet group ( n = 20) for 12 weeks. We assessed the skeletal characteristics of model mice through blood biochemistry, microcomputed tomography (micro-CT), and bone histomorphometry. RNA-seq was utilized to profile gene expression changes of ROD. We elucidated the functions of differentially expressed genes (DEGs) using gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and gene set enrichment analysis (GSEA). DEGs were validated via quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: By the fifth week, adenine followed by an HP diet induced rapid weight loss and high mortality rates in the mouse group, precluding further model development. Mice with optimized adenine diet-induced ROD displayed significant abnormalities in serum creatinine and blood urea nitrogen levels, accompanied by pronounced hyperparathyroidism and hyperphosphatemia. The femur bone mineral density (BMD) of the model mice was lower than that of control mice, with substantial bone loss and cortical porosity. ROD mice exhibited substantial bone turnover with an increase in osteoblast and osteoclast markers. Transcriptomic profiling revealed 1907 genes with upregulated expression and 723 genes with downregulated expression in the femurs of ROD mice relative to those of control mice. Pathway analyses indicated significant enrichment of upregulated genes in the sphingolipid metabolism pathway. The significant upregulation of alkaline ceramidase 1 ( Acer1 ), alkaline ceramidase 2 ( Acer2 ), prosaposin-like 1 ( Psapl1 ), adenosine A1 receptor ( Adora1 ), and sphingosine-1-phosphate receptor 5 ( S1pr5 ) were successfully validated in mouse femurs by qRT-PCR. CONCLUSIONS Optimized adenine diet mouse model may be a valuable proxy for studying ROD. RNA-seq analysis revealed that the sphingolipid metabolism pathway is likely a key player in ROD pathogenesis, thereby providing new avenues for therapeutic intervention.
Animals ; Mice ; Chronic Kidney Disease-Mineral and Bone Disorder/genetics* ; Male ; Disease Models, Animal ; Mice, Inbred C57BL ; Sphingolipids/metabolism* ; Transcriptome/genetics* ; Signal Transduction/genetics* ; X-Ray Microtomography ; Adenine