Objective To introduce the causes of accidents and the diagnosis and treatment of two patients with radiation-induced skin injury admitted to our hospital in 2023, and to provide a reference for the clinical treatment of subsequent radiation-induced skin injury. Methods The clinical treatment process of two patients with acute skin injury caused by external radiation exposure were summarized and analyzed. Results The exposure history of the two patients was reconstructed, the flaw detection scenario was simulated, the biological dose and hand skin exposure dose were estimated, and the infrared thermal imaging device was used for dynamic monitoring. A comprehensive analysis was conducted based on clinical manifestations and other data. The diagnosis of “Xie” was excessive exposure combined with acute radiation-induced skin injury on both hands (Grade IV for the right hand palm, index finger, and middle finger and Grade II for the left hand little finger). The diagnosis of “Hao” was acute radiation-induced skin injury on both hands (Grade I). The two patients received different clinical treatment measures: “Xie” was treated with both local and systemic therapies, while “Hao” was mainly treated with systemic therapy. Conclusion After systematic and effective treatment, the radiation-induced skin injuries healed in both patients.

Objective: To analyze the association between drinking behaviors and anxiety symptoms, with the mediating role of insomnia symptoms among college freshmen, so as to provide a reference basis for reducing the occurrence of anxiety symptoms in college freshmen. Methods: From October to December 2021, 31 856 freshmen were selected by the purposive sampling method in 22 colleges across 11 provinces (Fujian, Jiangsu, Guangdong, Henan, Anhui, Hubei, Shanxi, Jiangxi, Shaanxi, Yunnan, Chongqing) in China. The Semi quantitative Food Frequency Questionnaire was used to investigate college freshmen drinking behaviors. The Depression Anxiety Stress Scale 21 and the Insomnia Severity Index were used to assess anxiety symptoms and insomnia symptoms in college freshmen. The generalized linear model was employed to analyze the association between drinking behaviors and anxiety symptoms in college freshmen, and the structural equation modeling was used to assess the mediating effect of insomnia symptoms on the association. Results: The detection rate of anxiety symptoms among college freshmen was 28.2%, the detection rates of the mild, moderate, severe and extremely severe were 6.6%, 15.9%, 3.2% and 2.6%, respectively. While 23.6% of college freshmen reported drinking in the past month, the rates were 39.8% among boys and 15.9% among girls. After adjusting for demographic variables (ethnicity, education, major, etc.) and confounding variables (self evaluation of learning burden, number of close friends, screen time, etc.), the results of generalized linear model analysis showed that beer consumption was associated with anxiety symptoms in college freshmen( β =0.09, 95% CI =0.04-0.14), girls( β =0.14, 95% CI =0.07-0.21) and those aged 19-20 years ( β =0.12, 95% CI =0.05-0.19)(all P <0.05). Red wine consumption was associated with anxiety symptoms in male students ( β =0.13, 95% CI =0.02-0.24, P <0.05). Alcohol and beer consumption were associated with insomnia in college freshmen[ β (95% CI ) =0.22(0.08-0.36),0.31(0.23-0.39),both P <0.01]. Insomnia symptoms partially mediated the association between drinking behaviors and anxiety symptoms among college freshmen with a mediating effect value of 0.05, accounting for 50.49% of the total effect. Conclusions Insomnia symptoms partially mediates the association between drinking behaviors and anxiety symptoms in college freshmen. Measures should be taken to simultaneously intervene in the drinking behaviors and insomnia symptoms of college freshmen to prevent the occurrence of their anxiety symptoms.

Liver fibrosis is caused by various factors such as viral infection， alcohol intake， and metabolism-related damage， leading to the replacement of normal tissue by fibrous scars. As a regulatory factor for cell proliferation， insulin-like growth factor 1 （IGF-1） participates in the regulation of cell cycle， the promotion of cell proliferation and differentiation， and the inhibition of cell apoptosis by binding to its receptor insulin-like growth factor-1 receptor （IGF-1R）. Studies have shown that the IGF-1/IGF-1R signaling pathway can regulate the process of liver fibrosis by affecting the senescence and apoptosis of hepatocytes， the activation and proliferation of hepatic stellate cells， and the dysfunction of endothelial cells. In addition， the IGF-1/IGF-1R signaling system can also regulate multiple mechanisms such as DNA damage repair， cell proliferation， lipid metabolism， cell senescence， and oxidative stress， thereby providing new strategies and potential targets for the prevention and treatment of liver fibrosis. This article summarizes the mechanism of action of IGF-1/IGF-1R and its signal transduction system in mediating liver fibrosis by regulating DNA damage repair in different cells， in order to provide a theoretical basis for the treatment of liver fibrosis.

ObjectiveTo investigate the effect of quercetin on acute gouty arthritis （GA） in rats by inhibiting the reactive oxygen species （ROS）/NOD-like receptor protein 3 （NLRP3）/interleukin-1β （IL-1β） signaling pathway. MethodsSixty SPF-grade male SD rats were randomized into normal， model， colchicine （0.3 mg·kg^-1）， and low-， medium-， and high-dose （25， 50， 100 mg·kg^-1， respectively） quercetin groups （n=10）. The rats in the dosing groups were administrated with the corresponding drugs （10 mL·kg^-1） by gavage once a day for one week. An equal volume of normal saline was given by gavage to rats in normal and model groups. One hour after drug administration on day 5， an acute GA model was established in other groups except the control group via intra-articular injection of monosodium urate （MSU） suspension into the right posterior ankle joint cavity. The joint swelling and gait were scored at the time points of 6， 12， 24， 48 h after modeling. Histopathological alterations in the ankle joint tissue from each group were assessed by hematoxylin-eosin （HE） staining. Malondialdehyde （MDA）， xanthine oxidase （XOD）， and total superoxide dismutase （T-SOD） assay kits were used to assess the levels of MDA， XOD， and T-SOD in the serum. The levels of tumor interleukin-6 （IL-6）， necrosis factor-α （TNF-α）， and IL-1β in the rat serum， as well as ROS in the ankle joint tissue， were measured by enzyme-linked immunosorbent assay （ELISA）. Western blot was performed to determine the protein levels of NLRP3， thioredoxin-interacting protein （TXNIP）， apoptosis-associated speck-like protein containing a CARD domain （ASC）， precursor cysteinyl aspartate-specific proteinase-1 （pro-Caspase-1）， cleaved Caspase-1 （Caspase-1 p20）， and IL-1β in the ankle joint tissue. Real-time PCR was employed to assess the mRNA levels of TXNIP， NLRP3， ASC， IL-1β， and TNF-α in the ankle joint tissue. ResultsCompared with the normal group， the model group exhibited decreased spontaneous activity， mental fatigue， increased ankle joint swelling and gait scores （P<0.01）， aggravated synovial tissue edema and inflammatory cell infiltration （P<0.01）， elevated levels of XOD， MDA， TNF-α， IL-1β， and IL-6 in the serum and ROS in the joint tissue （P<0.01）， a declined level of T-SOD （P<0.01）， up-regulated protein levels of NLRP3， TXNIP， ASC， pro-Caspase-1， Caspase-1 p20， and IL-1β in the ankle joint tissue （P<0.01）， and up-regulated mRNA levels of NLRP3， TXNIP， ASC， IL-1β， and TNF-α in the ankle joint tissue （P<0.01）. Compared with the model group， the medium- and high-dose quercetin groups showed improved general conditions， decreased gait scores （P<0.05， P<0.01）， reduced joint swelling （P<0.01）， alleviated synovial tissue edema and inflammatory cell infiltration （P<0.05， P<0.01）， lowered levels of XOD， MDA， TNF-α， IL-1β， and IL-6 in the serum and ROS in the joint tissue （P<0.01）， increased levels of T-SOD （P<0.01）， down-regulated protein levels of TXNIP， NLRP3， ASC， pro-Caspase-1， Caspase-1 p20， and IL-1β in the ankle joint tissue （P<0.05， P<0.01）， and down-regulated mRNA levels of TXNIP， NLRP3， ASC， IL-1β， and TNF-α in the ankle joint tissue （P<0.01）. Low-dose quercetin also ameliorated some of the above parameters （P<0.05， P<0.01）. ConclusionQuercetin exerts anti-GA effects by blocking the ROS/NLRP3/IL-1β signaling pathway， downregulating NLRP3 inflammasome activation， and inhibiting the production of pro-inflammatory cytokines including TNF-α， IL-1β， and IL-6.

Objective This study reports on the obligatory parasitism of water mites Arrenurus sp. on Anopheles messeae at the Manzhouli Port, Inner Mongolia, China. Methods Duing July 2024, a survey on the mosquito diversity was conducted at the Manzhouli Port. Captured mosquitoes and their ectoparasites were identified to species level. Results A total of 1840 adult mosquitoes were collected, representing species from three genera: Culex(Cx. modestus, Cx. pipiens pallens), Aedes(Ae. dorsalis, Ae. flavidorsalis, Ae. flavescens), and Anopheles (An. messeae). Among all the mosqutioes specimens,3 out of 150 captured An. messeae were found to carry ectoparasitic mites, with number of 2,4,27 mites separately. Morphological and molecular identification reached the same result as water mites(Hydrachnidiae, Hydracrina). COI gene sequence showed 94% similarity with the closest species Arrenurus truncatellus. Conlusions Literature review suggests water mites are host-specific parasitism of mosquito species and herein with the first record of Arrenurus sp. parasiting on An. Messeae in the most high-latitude region globally.

Metabolic associated fatty liver disease （MAFLD） is a highly prevalent chronic liver disease worldwide， and the mechanism underlying its progression to metabolic associated steatohepatitis and liver fibrosis remain unclear. Endoplasmic reticulum stress （ERS） and ferroptosis （Fer） are deeply involved in the pathological evolution of MAFLD. This article systematically reviews the core regulatory mechanisms of ERS and its role in regulating lipid metabolism， inflammation response， and cell apoptosis in MAFLD. It also analyzes the core mechanism of Fer and discusses the predisposing factors for Fer in the pathological microenvironment of MAFLD， as well as the role of Fer in exacerbating hepatocyte death and activating the progression of liver fibrosis. This article proposes that the crosstalk between ERS and Fer is a key driver for the progression of MAFLD， which provides new references and ideas for the clinical intervention of MAFLD.

ObjectiveToll-like receptor 4 （TLR4）， a receptor for pathogen-associated molecular patterns of innate immunity， is associated with neurodegenerative diseases. Interleukin （IL）-6， IL-1β， and tumor necrosis factor-α （TNF-α） as common pro-inflammatory cytokines and high-sensitivity C-reactive protein （hs-CRP） are related to inflammatory responses. This study evaluated the clinical efficacy and possible mechanisms of therapeutic effects of Fengyintang on early and mid-stage PD with excessive heat generating wind by observing the effects of Fengyintang on the serum levels of TLR4， IL-6， IL-1β， TNF-α， and hs-CRP in the patients with PD. MethodsSixty-eight PD patients who met the inclusion criteria were randomly assigned into the control group and the observation group （n=34）. Both groups were treated with anti-PD Western medicine and the observation group was additionally treated with Fengyintang. Both groups were treated for 8 weeks. Before and after 8 weeks of treatment， the patients in the two groups were measured for their TCM symptom scores， International Movement Disorder Society Unified Parkinson's Disease Rating Scale （MDS-UPDRS） score， Parkinson's Disease Non-Motor Symptom Scale （NMSS） score， Patient Assessment of Constipation Symptom （PAC-SYM） score， Pittsburgh Sleep Quality Index （PSQI）， Hamilton Anxiety Scale （HAMA） score， Hamilton Depression Scale （HAMD） score， and changes in serum TLR4， IL-6， IL-1β， TNF-α， and hs-CRP levels. ResultsOne case in the control group was removed due to loss of visit， and a total of 67 PD patients （33 in the control group and 34 in the observation group） who met the criteria were included for analysis. After treatment， patients in the observation group showed decreases in scores of TCM symptoms， MDS-UPDRS， NMSS， PAC-SYM， PSQI， HAMA， and HAMD （P<0.05， P<0.01）. Moreover， the observation group had lower scores of TCM symptoms， MDS-UPDRS， NMSS， PAC-SYM， PSQI， HAMA， and HAMD than the control group （P<0.05， P<0.01）. The observation group showed higher efficacy in terms of TCM symptoms and MDS-UPDRS score than the control group （Z=-0.57， P<0.05）. The overall response rate was higher in the observation group than in the control group （Z=-0.62， P<0.05， P<0.01）. The serum TLR4， TNF-α， IL-1β， IL-6， and hs-CRP levels of the observation group were lower than those of the control group （P<0.05， P<0.01）. ConclusionFengyintang combined with Western medicine can safely and effectively alleviate the clinical symptoms， reduce the levels of inflammatory factors， improve the quality of life， and delay the disease progression of PD patients by inhibiting peripheral TLR4 expression and thus suppressing the downstream inflammatory response.

ObjectiveTo explore the mechanism by which aerobic exercise improves hippocampal neuroinflammation and learning and memory ability in brain-aged mice via interferon regulatory factor 7 (IRF7). MethodsA total of 60 male specific pathogen-free (SPF) C57BL/6J mice were enrolled in the experiment, including 30 young mice (2 months old) and 30 naturally aging mice (12 months old). Young mice and old mice were respectively randomly assigned to four groups: young control group (group C, n=15), young exercise group (group CE, n=15), and aging control group (group A, n=15), aging exercise group (group AE, n=15). Mice in the exercise groups received an 8-week continuous treadmill aerobic exercise intervention, while control mice were kept under routine feeding without exercise intervention. After the intervention, Barnes maze and Y-maze behavioral tests were performed to comprehensively assess the learning and memory abilities of each group of mice. Transmission electron microscopy was used to observe the ultrastructural morphological changes of hippocampal synapses. Western blot assay was utilized to detect the protein expression and phosphorylation levels of Janus kinase 1 (JAK1), signal transducer and activator of transcription 1 (STAT1), as well as the expression of postsynaptic density protein 95 (PSD95). Immunofluorescence staining was applied to quantify the fluorescence intensity of ionized calcium-binding adapter molecule 1 (IBA1) in hippocampal tissues. The expression levels of inflammatory cytokines including interferon-α (IFN-α), interferon-β (IFN-β), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured by enzyme-linked immunosorbent assay (ELISA). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the mRNA expression level of IRF7, and DNA methylation assay was further conducted to analyze the methylation level of the IRF7 gene in mouse hippocampus. ResultsAt the molecular level, compared with group C, the protein expression levels of JAK1, STAT1, p‑JAK1, and p‑STAT1 in group A were significantly increased (P<0.05), whereas PSD95 expression was decreased (P<0.05). ELISA assays showed that the levels of IFN‑α, IFN‑β, TNF‑α, and IL‑1β were significantly elevated in group A (P<0.001). RT‑PCR analysis revealed that, compared with group C, the mRNA expression of IRF7 in group A was markedly upregulated (P<0.000 1), while the CpG methylation rate of the IRF7 promoter was significantly reduced (P<0.05). In contrast, all the above parameters in the AE group showed improvements relative to those in group A. Immunofluorescence staining indicated positive IBA1 expression in the brain tissues of group A mice. Exercise intervention reversed these abnormal changes. ConclusionIn aged mice, aerobic exercise induces hypermethylation of the IRF7 promoter region, suppresses IRF7 expression and activation of the downstream IFN‑I/JAK1/STAT1 signaling pathway, accompanied by alleviated neuroinflammation, improved learning and memory, and ameliorated brain aging-related phenotypes.

Ischemic stroke accounts for approximately 80% of all stroke cases worldwide and remains a leading cause of long‑term neurological disability and mortality. Intravenous thrombolysis and endovascular thrombectomy constitute the mainstay of acute reperfusion therapies, yet their clinical utility is severely constrained by narrow therapeutic time windows. Even when large‑vessel recanalization is successfully achieved, a considerable proportion of patients still suffer poor functional outcomes due to futile reperfusion and ischemia‑reperfusion injury. Historically, preclinical studies have largely focused on direct neuronal protection against calcium overload, oxidative stress and ferroptosis. Unfortunately, most promising neuroprotective agents that exhibited robust benefits in rodent models have failed to demonstrate satisfactory efficacy in phase‑Ⅱ and phase‑Ⅲ clinical trials. One critical contributor to such translational failure is the disregard for the pathological disturbance within the cerebral vascular microenvironment. Instead of merely regarding neuronal death as an autonomous cellular event, accumulating evidence indicates that sequential biochemical disruption of perivascular microenvironment acts as an initiating amplifier that propagates damage toward brain parenchyma after ischemic insult. The cerebral vascular microenvironment centers on brain microvessels and comprises endothelial cells, endothelial glycocalyx, basement membrane, pericytes, astrocytic end‑feet, perivascular microglia, as well as interstitial ions, inflammatory mediators, reactive oxygen species and extracellular matrix components. Distinct from the concept of neurovascular unit which emphasizes functional coupling between neurons, glia and vessels, the vascular microenvironment highlights dynamic biochemical homeostasis in perivascular interstitial space. Following cerebral ischemia, injured brain tissue can be spatially divided into the irreversibly damaged infarct core, metabolically‑stressed ischemic penumbra and mildly‑affected peripheral regions. These three zones lack rigid anatomical boundaries and evolve dynamically depending on reperfusion timing, presenting divergent features in blood perfusion, blood‑brain barrier integrity, cellular viability and immune‑inflammatory profiles. Four interrelated pathological cascades jointly disrupt microenvironmental homeostasis: calcium‑overload‑triggered cytotoxic cascades; blood‑brain barrier breakdown resulting from glycocalyx shedding, tight‑junction dissociation and matrix metalloproteinase‑driven basement‑membrane degradation; inflammatory‑immune dysregulation dominated by microglial phenotypic reprogramming; and mutual crosstalk between coagulation disturbance and neuroinflammation that exacerbates secondary brain injury. Multiple molecular layers orchestrate these pathological alterations. Excessive activation of HIF‑1α, NF‑κB and MAPK/ERK signaling pathways promotes barrier leakage, pro‑inflammatory factor secretion and extracellular‑matrix remodeling. Epigenetic modulation mediated by non‑coding RNAs including miRNAs and lncRNAs reshapes vascular microenvironment via three major patterns: modulating endothelial‑pericyte barrier integrity, switching microglia‑astrocyte inflammatory phenotypes, and driving metabolic reprogramming among multiple cell populations within microdomains. In addition, metabolic shift toward glycolysis among endothelial cells, microglia, astrocytes and compromised neurons establishes self‑amplifying vicious cycles of energy depletion and oxidative stress in perivascular niches. Targeted theranostic approaches oriented toward vascular microenvironment bring new opportunities for precision medicine of ischemic stroke. Magnetic nanoprobes and near‑infrared fluorescent probes respond to elevated reactive oxygen species, pH shift and inflammatory signals, enabling in situ visualization of pathological signatures of microenvironment and risk evaluation of hemorrhagic transformation. Function‑tailored nanodelivery systems exert multi‑modal protective effects: reactive oxygen species‑responsive polymeric micelles deliver calcium chelators to block calcium‑overload‑initiated injury cascades; nanozymes scavenge reactive oxygen/nitrogen species and revert microglial pro‑inflammatory polarization; biomimetic membrane‑coated nanoparticles accumulate at micro‑thrombosis sites to break thrombo‑inflammatory loops and mitigate no‑reflow phenomenon; ferroptosis‑inhibitor‑loaded nanocarriers eliminate excessive labile iron within perivascular toxic microdomains. During subacute and recovery phases, spatiotemporally controlled release of angiogenic factors by nanocarriers facilitates maturation of newly‑formed microvessels rather than blind vascular sprouting, which helps reconstruct intact blood‑brain barrier and restore microenvironmental homeostasis. Nevertheless, substantial translational bottlenecks still impede clinical transformation of these nanomedicines, including potential biosafety risks caused by in vivo material accumulation, protein‑corona‑induced impairment of targeting capacity, intrinsic blood brain barrier transport obstacles, lack of unified quality‑control criteria for large‑scale manufacture, reliance on high‑end clinical imaging instruments, and prominent interspecies discrepancies between experimental animals and human patients. On the basis of summarizing spatiotemporal pathological characteristics, multi‑level regulatory mechanisms and cutting‑edge microenvironment‑oriented diagnostic and interventional strategies, the present review advocates a conceptual shift from isolated neuronal protection to comprehensive reconstruction of perivascular vascular microenvironment homeostasis. Such perspective provides theoretical foundations for expanding therapeutic time windows and inspires future development of novel therapeutic modalities for ischemic stroke.

Xiaoyao Powder has pharmacological action such as neuroprotection, anti-tumor, anti-depression, liver protection, regulation of intestinal flora, anti-fatigue and so on. Based on the five aspects of quality transfer and traceability, component measurability, component effectiveness, component specificity and compound compatibility environment, the quality marker (Q-marker) of Xiaoyao Powder was predicted and analyzed. It was considered that paeoniflorin, atractylenolide Ⅰ, atractylenolid Ⅱ, atractylenolide Ⅲ, liquiritin,glycyrrhizic acid, Saikosaponin A, Saikosaponin D, ferulic acid, Z-ligustilide, pachymic acid, Menthol,6-gingerol 8-gingerol and 10-gingerol have strong measurability and can be used as Q-marker of Xiaoyao Powder.