Dormant tumor cells constitute a population of cancer cells that reside in a non-proliferative or low-proliferative state, typically arrested in the G0/G1 phase and exhibiting minimal mitotic activity. These cells are commonly observed across multiple cancer types, including breast, lung, and ovarian cancers, and represent a central cellular component of minimal residual disease (MRD) following surgical resection of the primary tumor. Dormant cells are closely associated with long-term clinical latency and late-stage relapse. Due to their quiescent nature, dormant cells are intrinsically resistant to conventional therapies—such as chemotherapy and radiotherapy—that preferentially target rapidly dividing cells. In addition, they display enhanced anti-apoptotic capacity and immune evasion, rendering them particularly difficult to eradicate. More critically, in response to microenvironmental changes or activation of specific signaling pathways, dormant cells can re-enter the cell cycle and initiate metastatic outgrowth or tumor recurrence. This ability to escape dormancy underscores their clinical threat and positions their effective detection and elimination as a major challenge in contemporary cancer treatment. Hypoxia, a hallmark of the solid tumor microenvironment, has been widely recognized as a potent inducer of tumor cell dormancy. However, the molecular mechanisms by which tumor cells sense and respond to hypoxic stress—initiating the transition into dormancy—remain poorly defined. In particular, the lack of a systems-level understanding of the dynamic and multifactorial regulatory landscape has impeded the identification of actionable targets and constrained the development of effective therapeutic strategies. Accumulating evidence indicates that hypoxia-induced dormancy tumor cells are accompanied by a suite of adaptive phenotypes, including cell cycle arrest, global suppression of protein synthesis, metabolic reprogramming, autophagy activation, resistance to apoptosis, immune evasion, and therapy tolerance. These changes are orchestrated by multiple converging signaling pathways—such as PI3K-AKT-mTOR, Ras-Raf-MEK-ERK, and AMPK—that together constitute a highly dynamic and interconnected regulatory network. While individual pathways have been studied in depth, most investigations remain reductionist and fail to capture the temporal progression and network-level coordination underlying dormancy transitions. Systems biology offers a powerful framework to address this complexity. By integrating high-throughput multi-omics data—such as transcriptomics and proteomics—researchers can reconstruct global regulatory networks encompassing the key signaling axes involved in dormancy regulation. These networks facilitate the identification of core regulatory modules and elucidate functional interactions among key effectors. When combined with dynamic modeling approaches—such as ordinary differential equations—these frameworks enable the simulation of temporal behaviors of critical signaling nodes, including phosphorylated AMPK (p-AMPK), phosphorylated S6 (p-S6), and the p38/ERK activity ratio, providing insights into how their dynamic changes govern transitions between proliferation and dormancy. Beyond mapping trajectories from proliferation to dormancy and from shallow to deep dormancy, such dynamic regulatory models support topological analyses to identify central hubs and molecular switches. Key factors—such as NR2F1, mTORC1, ULK1, HIF-1α, and DYRK1A—have emerged as pivotal nodes within these networks and represent promising therapeutic targets. Constructing an integrative, systems-level regulatory framework—anchored in multi-pathway coordination, omics-layer integration, and dynamic modeling—is thus essential for decoding the architecture and progression of tumor dormancy. Such a framework not only advances mechanistic understanding but also lays the foundation for precision therapies targeting dormant tumor cells during the MRD phase, addressing a critical unmet need in cancer management.

Acute respiratory distress syndrome (ARDS) is the leading cause of respiratory failure with high morbidity and mortality. Pulmonary surfactant (PS)-based complementary therapies have exhibited potential for ARDS healing and applied as an adjunctive therapy strategy. Coacervate (Coac) has the characteristics of softness, deformability and excellent molecular enrichment properties, and has attracted extensive attention in the biomedical field. Here PS and coacervate were combined for the potential ARDS treatment. The Coac, fabricated from polyallylamine hydrochloride (PAH) and adenosine triphosphate (ATP) by simple mixing, exhibited soft droplet property and high enrichment for dexamethasone sodium phosphate (DSP). To avoid the fusion effect of membraneless coacervate and endow it with biological functions of PS, liposomes with PS-biomimetic lipid components (PS-lipo) were further introduced to construct PS-biomimetic membranized coacervate (DSP@PS-Coac). The DSP@PS-Coac demonstrated high lung targeting effect and significant penetration efficiency after intravenous injection. Furthermore, PS-lipo replenished the endogenous PS pool and facilitated the distribution of DSP in inflammatory cells in the lung. In the ARDS mouse model, PS-Coac and DSP exerted synergetic anti-inflammatory functions, via reducing the recruitment of inflammatory neutrophils and modulating macrophages into anti-inflammatory phenotype. The overall results confirmed that DSP@PS-Coac may provide a promising delivery option for the treatment of ARDS.

The plant F-box protein more axillary growth 2 (MAX2) is a key factor in the signal transduction of strigolactones (SLs) and karrinkins (KARs). As the main component of the SKP1-CUL1-FBX (SCF) complex ubiquitin ligase E3, MAX2 is responsible for specifically recognizing the target proteins, suppressor of MAX2 1/SMAX1-like proteins (SMAX1/SMXLs), which would be degraded after ubiquitination. It can thereby regulate plant morphogenesis and stress responses. There exist homologous genes of MAX2 in the important grain and oil crop soybean (Glycine max). However, its role in plant defense responses has not been investigated yet. Here, GmMAX2b, a homologous gene of MAX2, was successfully cloned from stressed soybean. Bioinformatics analysis revealed that there were two MAX2 homologous genes, GmMAX2a and GmMAX2b, with a similarity of 96.2% in soybean. Their F-box regions were highly conserved. The sequence alignment and cluster analysis of plant MAX2 homologous proteins basically reflected the evolutionary relationship of plants and also suggested that soybean MAX2 might be a multifunctional protein. Expression analysis showed that plant pathogen infection and salicylic acid treatment induced the expression of GmMAX2b in soybean, which is consistent with that of MAX2 in Arabidopsis. Ectopic expression of GmMAX2b compensated for the susceptibility of Arabidopsis max2-2 mutant to pathogen, indicating that GmMAX2b positively regulated plant disease resistance. In addition, yeast two hybrid technology was used to explore the potential target proteins of GmMAX2b. The results showed that GmMAX2b interacted with SMXL6 and weakly interacted with SMXL2. In summary, GmMAX2b is a positive regulator in plant defense responses, and its expression is induced by pathogen infection and salicylic acid treatment. GmMAX2b might exert its effect through interaction with SMXL6 and SMXL2. This study expands the theoretical exploration of soybean disease resistant F-box and provides a scientific basis for future soybean disease resistant breeding.
Glycine max/metabolism* ; Disease Resistance/genetics* ; Plant Diseases/immunology* ; Plant Proteins/genetics* ; Cloning, Molecular ; Gene Expression Regulation, Plant ; F-Box Proteins/genetics* ; Arabidopsis/genetics* ; Phylogeny

As the social pressure is increasing,the incidence of depression is growing.Testosterone is synthesized and secreted through the hypothalamic-pituitary-gonadal axis,which plays a regulatory role in men's mental health.Studies have shown that low testosterone levels,clinical hypogonadism,and androgen deprivation therapy-induced testosterone deficiency are significantly associated with male depression,while there are still many uncertainties about the mechanism of their effects.Given that low testosterone levels may serve as a characteristic biomarker of male depression risk,testosterone replacement therapy may have a good therapeutic effect on male depression.This article focuses on assessing the role of testosterone levels and related clinical therapies in mood regulation in men.
Humans ; Testosterone/physiology* ; Male ; Depression/etiology* ; Hormone Replacement Therapy

Inflammasome is a kind of intracellular polyprotein complex,which is an important component of the complex system of local inflammatory microenvironment after human tissue damage.When the inflammasome is activated,it induces the activation of cysteine aspartate proteinase 1(caspase-1),mediates the maturation and secretion of proinflammatory cytokines,such as interleukin(IL)-1 β and IL-18,and induces cell death,which plays an important role in regulating the host immune response to pathogen infection and tissue repair of cell damage.Nod-like receptor protein 3(NLRP3)inflammatory body,which is composed of NLRP3,pro-cysteine aspartic acid specific protease-1(pro-caspase-1)and apoptosis-related spot-like protein(ASC),is the most deeply and widely studied type of inflammatory body,which plays an important role in the regulation of inflammation.When NLRP3 inflammatory bodies are activated,inflammatory mediators are produced and released,which participate in the occurrence and development of a variety of inflammatory diseases.Some studies have shown that traditional Chinese medicine can improve the pathological state of a variety of diseases by inhibiting NLRP3 inflammatory bodies,and play a role in the prevention and treatment of a variety of inflammatory diseases,including cardiovascular diseases,joint inflammation,diabetes and so on.This paper systematically combs the mechanism of NLRP3 inflammatory bodies,and summarizes the latest research reports on the effects of traditional Chinese medicine compound prescription,traditional Chinese medicine monomers and traditional Chinese medicine extracts on NLRP3 inflammatory bodies in the treatment of inflammatory diseases,in order to provide new ideas for the further study of the pathogenesis and drug treatment of many inflammatory diseases.

Eighteen compounds were isolated from the methanol extract of the fruits of Litsea cubeba by silica gel, ODS, Sephadex LH-20 column chromatography, semi-preparative RP-HPLC, chiral HPLC and recrystallization. Their structures were elucidated by spectroscopic analyses and by comparison with reported spectroscopic data and physicochemical properties, and the absolute configurations of the enantiomers were established by experimental and calculated electronic circular dichroism spectra. These compounds were identified as (+)-(R)-4-hydroxypiperitenone (1a), (-)-(S)-4-hydroxypiperitenone (1b), (3S,4S,6R)-3,6-dihydroxy-1-menthene (2), (4S,5R)-4-hydroxy-5-isopropyl-2-methylcyclohex-2-en-1-one (3), (R)-6-hydroxy-3-(2-hydroxypropan-2-yl)-6-methylcyclohex-2-enone (4), (4S,6R)-4-hydroxy-6-isopropyl-3-methylcyclohex-2-enone (5), (1R,3S,4R)-3-hydroxy isopulegol (6), subamone (7), (6S)-3,7-dimethyl-7-hydroxy-2(Z)-octen-6-olide (8), (6S)-6,7-dihydroxy-3,7-dimethyloct-2(Z)-enoate (9), holostylactone (10), sesamin (11), dimethylmatairesinol (12), p-hydroxybenzoylcarbinol (13), syringaldehyde (14), p-hydroxybenzaldehyde (15), 4-hydroxy-3-methoxybenzaldehyde (16), 5,4ʹ-dihydroxy-7-methoxyflavone (17). Among them, compounds 1a and 1b were a pair of new monoterpenoid enantiomers, 8 and 9 were new natural products, 2-7, 10, 11 and 17 were isolated from Litsea genus for the first time. The in vitro anti-inflammatory effects of compounds 1-17 were evaluated using lipopolysaccharide-stimulated RAW264.7 cells, the results showed that compound 14 exhibited significant anti-inflammatory activity with NO inhibitory rate of 66.27% at a concentration of 40 μmol·L^-1.

Objective:To investigate a new method for the reconstruction of hemifacial microsomia by sagittal osteotomy of the affected mandibular outer cortex combined with bone graft of mandibular outer cortex from healthy side.Methods:From March 2006 to March 2023, the clinical data of patients with hemifacial microsomia admitted to the Department of Craniomaxillofacial Surgery, Plastic Surgery Hospital, Chinese Academy of Medical Sciences were analyzed retrospectively. Preoperative diagnosis and surgical design were performed based on clinical manifestations and imaging findings. All cases were operated under general anesthesia. The affected mandibular outer cortex was previously split by an intraoral approach, and then the mandibular outer cortex of appropriate shape and size on the healthy side was harvested and grafted into the split bone space according to the preoperative design, following by internal rigid fixation. Complications, facial appearance improvement, and patient satisfaction were followed up. Photographs were taken preoperative, immediately postoperative and at the long-term(last) postoperative follow-up, and the severity of the deformity was analyzed. CT data from preoperative, immediate postoperative, and long-term follow-up visits were imported into Surgicase Proplan medical three-dimensional image workstation in Dicom format. The mandible was reconstructed using Segmentation, and the thickness of the mandible was measured during pre-operative, immediate post-operative and long-term follow-up visits. Anova with repeated measurement design was used to compare measurements and LSD test was used for multiple comparisons. The Kruskal-Wallis rank sum test were used to statistically analyze malformation severity. P< 0.05 is considered statistically significant. Results:A total of 39 patients were included in this study, including 13 females and 26 males, with an average age of (22.21±4.57) years (15-27 years). All patients were followed up for an average of (45.56±39.41) months (6-153 months) after surgery. The grafted mandibular outer cortex grows well with the adjacent bone tissue, and the mandibular angle and mandibular body are significantly wider. Of the 39 cases, 1 developed an infection 1 year after surgery, the titanium plate was exposed, and the patient healed after debridement and removal of the immobilizing splint. The facial appearance of the other patients improved significantly. Preoperative, immediate postoperative and long term follow up of mandibular thickness measurements were compared in pairs, and the differences were statistically significant (all P<0.05). The patient’s appearance satisfaction score: the preoperative score was [2.0(1.5, 2.0)] points, the immediate postoperative score was [4.0(4.0, 4.0)] points, the score of the last postoperative follow up was [4.0(4.0, 4.0)] points. There was statistical difference in satisfaction among the three groups ( P<0.01). The preoperative scores were compared with the scores of the immediate postoperative and the last postoperative follow-up respectively, and the differences were statistically significant( P<0.01). There was no statistical significance in satisfaction between the immediate postoperative score and the score of the last postoperative follow up ( P>0.05). Conclusion:The sagittal splitting osteotomy of the mandibular outer cortex is consistent with the features of mandibular anatomy, and provides a good condition for the grafting and healing of autogenous bone. Removing the outer cortex of the mandible on the healthy side not only increases the thickness of the affected side, but also decreases the width of the angle of the mandible on the healthy side, so as to effectively correct the asymmetric deformity of the mandible. The method is simple, with few complications and good results, and is one of the ideal treatments to correct hemofacial microsomia.

Objective:To investigate a new method for the reconstruction of hemifacial microsomia by sagittal osteotomy of the affected mandibular outer cortex combined with bone graft of mandibular outer cortex from healthy side.Methods:From March 2006 to March 2023, the clinical data of patients with hemifacial microsomia admitted to the Department of Craniomaxillofacial Surgery, Plastic Surgery Hospital, Chinese Academy of Medical Sciences were analyzed retrospectively. Preoperative diagnosis and surgical design were performed based on clinical manifestations and imaging findings. All cases were operated under general anesthesia. The affected mandibular outer cortex was previously split by an intraoral approach, and then the mandibular outer cortex of appropriate shape and size on the healthy side was harvested and grafted into the split bone space according to the preoperative design, following by internal rigid fixation. Complications, facial appearance improvement, and patient satisfaction were followed up. Photographs were taken preoperative, immediately postoperative and at the long-term(last) postoperative follow-up, and the severity of the deformity was analyzed. CT data from preoperative, immediate postoperative, and long-term follow-up visits were imported into Surgicase Proplan medical three-dimensional image workstation in Dicom format. The mandible was reconstructed using Segmentation, and the thickness of the mandible was measured during pre-operative, immediate post-operative and long-term follow-up visits. Anova with repeated measurement design was used to compare measurements and LSD test was used for multiple comparisons. The Kruskal-Wallis rank sum test were used to statistically analyze malformation severity. P< 0.05 is considered statistically significant. Results:A total of 39 patients were included in this study, including 13 females and 26 males, with an average age of (22.21±4.57) years (15-27 years). All patients were followed up for an average of (45.56±39.41) months (6-153 months) after surgery. The grafted mandibular outer cortex grows well with the adjacent bone tissue, and the mandibular angle and mandibular body are significantly wider. Of the 39 cases, 1 developed an infection 1 year after surgery, the titanium plate was exposed, and the patient healed after debridement and removal of the immobilizing splint. The facial appearance of the other patients improved significantly. Preoperative, immediate postoperative and long term follow up of mandibular thickness measurements were compared in pairs, and the differences were statistically significant (all P<0.05). The patient’s appearance satisfaction score: the preoperative score was [2.0(1.5, 2.0)] points, the immediate postoperative score was [4.0(4.0, 4.0)] points, the score of the last postoperative follow up was [4.0(4.0, 4.0)] points. There was statistical difference in satisfaction among the three groups ( P<0.01). The preoperative scores were compared with the scores of the immediate postoperative and the last postoperative follow-up respectively, and the differences were statistically significant( P<0.01). There was no statistical significance in satisfaction between the immediate postoperative score and the score of the last postoperative follow up ( P>0.05). Conclusion:The sagittal splitting osteotomy of the mandibular outer cortex is consistent with the features of mandibular anatomy, and provides a good condition for the grafting and healing of autogenous bone. Removing the outer cortex of the mandible on the healthy side not only increases the thickness of the affected side, but also decreases the width of the angle of the mandible on the healthy side, so as to effectively correct the asymmetric deformity of the mandible. The method is simple, with few complications and good results, and is one of the ideal treatments to correct hemofacial microsomia.

Objective Viral encephalitis is an infectious disease severely affecting human health.It is caused by a wide variety of viral pathogens,including herpes viruses,flaviviruses,enteroviruses,and other viruses.The laboratory diagnosis of viral encephalitis is a worldwide challenge.Recently,high-throughput sequencing technology has provided new tools for diagnosing central nervous system infections.Thus,In this study,we established a multipathogen detection platform for viral encephalitis based on amplicon sequencing. Methods We designed nine pairs of specific polymerase chain reaction(PCR)primers for the 12 viruses by reviewing the relevant literature.The detection ability of the primers was verified by software simulation and the detection of known positive samples.Amplicon sequencing was used to validate the samples,and consistency was compared with Sanger sequencing. Results The results showed that the target sequences of various pathogens were obtained at a coverage depth level greater than 20×,and the sequence lengths were consistent with the sizes of the predicted amplicons.The sequences were verified using the National Center for Biotechnology Information BLAST,and all results were consistent with the results of Sanger sequencing. Conclusion Amplicon-based high-throughput sequencing technology is feasible as a supplementary method for the pathogenic detection of viral encephalitis.It is also a useful tool for the high-volume screening of clinical samples.

Objective To observe the effects of"Sleep Recipe"on the behavior,brain tissue and central neurotransmitters of insomnia rats.Methods The male rats with SD were randomly divided into control group,model group,sleep formula group,and eszolam group,with 10 rats in each group,and the insomnia model was constructed by intraperitoneal injection of P-chlorphenylalanine(PCPA).After successful modeling,the control group and the model group were given saline gavage,and the medylom group and eszolam group were given drug gavage.The insomnia-like behavior of rats in each group was evaluated by pentobarbital sodium correction experiment and open field experiment,Hematoxlin and eosin(HE)staining observed the pathological changes of rat cerebral cortex,hippocampus,and hypothalamic tissue,and Enzyme-linked mmunosorbent assay(ELISA)was used to determine the expression levels of Gamma-aminobutyric acid(GABA),5-hydroxytryptamine(5-HT).Results The sleep latency of rats in the model group was significantly elongated(P<0.01),while the sleep time was less(P<0.01),and the mental state and fur color were poor,significantly decreased in body weight(P<0.01).Compared with the model group,the sleep latency was significantly shortened(P<0.01),the sleep duration was significantly prolonged(P<0.01),and the body mass was significantly increased(P<0.05,P<0.01);In the open field experiment,the total activity distance of rats in the model group increased,the average speed and central region residence time decreased(P<0.05),the total activity distance of rats in the Sleep Formula group and Eszolam group decreased significantly(P<0.05),the average speed increased and the central region residence time increased(P<0.05).HE results showed that the number of neurons,morphological structure and arrangement of neurons,such as cerebral cortex,hippocampus and hypothalamus in the model group,were damaged to varying degrees,and the sleep formula group and estazolam group were significantly improved.ELISA results showed that the expression of 5-HT and GABA in the cerebral cortex and hypothalamus of rats in the model group was significantly reduced(P<0.01,P<0.05),and the expression of GABA in hippocampal tissues was also significantly reduced(P<0.01).The protein expression levels of cerebral cortical GABA,hypothalamic GABA and 5-HT in the Sleep Formula group were significantly increased(P<0.01).Conclusion Sleep Formula can improve the mental state,restore normal body weight,improve sleep efficiency,and reduce anxiety and tension in insomnia rats.The mechanism may be related to increasing the content of 5-HT and GABA,and inhibiting the spread and conduction of hypothalamic and brainstem pro-awakening nuclei.